Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26General SciencesElectrical Measurements on Cadmium Selenite Nano Composites
English0105Nima Jessieba DanielEnglish N. ThangarajEnglish D. M. SureshEnglish N. Joseph JohnEnglishBy simple microwave irradiated solvothermal process using microwave oven Cadmium Selenite (CdSeO3) nanoparticles were prepared. Cadmium acetate and Sodium selenite were used as precursors in the molar ratio 1:3. The powder XRD result shows that particles are purely crystallized in hexagonal phase with the broadening of diffraction peaks attributed to nanoscale size of the particles. The dielectric measurements were carried in two frequencies for temperatures ranging from 40 to 150oC. The present study indicates that the polarization mechanism in the nano particles considered is mainly contributed by space charge polarization. It can be understood that the space charge contribution plays an important role in the charge transport and polarizability in all the systems considered in the present study. The dielectric constant, dielectric loss, AC conductivity and DC conductivity increases with increase in temperature.
EnglishNanoparticles, Microwave, AC conductivity, DC conductivity, Dielectric constant, Dielectric lossIntroduction
Semiconductor nano crystals have attracted impressive attention, because of their novel optical and electronic properties [1]. Varying the size of the particle and changes in the degree of confinement of the electron and affects the electronic structure of the solid in particular band edges, which are tunable with particle size. One of the most important II – VI group semiconductors and nano crystalline Wurtzite structured Cadmium Selenide has attracted great interest in their various promising optoelectronic applications owing to its excellent optical conductivity such as photoelectron chemicals, photo-conductors , thin film transistor [2-4]. Blue shift in the band gap of this material, with decreasing grain size has led to many applied investigations. Many strategies have been utilized to prepare 1-D nano structural materials, where wet chemical method is considered as a practical and effective method for the synthesis of 1-D nano materials because it is more convenient and facile to be compared with most physical methods and need little expensive equipment by which CdSe nanorods, nanowires and nano tubes have been prepared successfully.
CdSe has been considered in many applications such as optoelectronic devices [5], light sensors [6], biological labels [7], chemical libraries [8], etc. The nanopowder of CdSe provides excellent and unique properties which depend upon the shape and size of the nanostructures [8-12]. Various methods such as hydrothermal, sol–gel approach, surfactant-assisted approach, etc. had been utilized for the synthesis of nanoparticles [13,14]. Synthesis, structural, and optical properties of CdSe nanoparticles have been reported [15]. In the present study, the main focus is on the electrical properties of pellets of nanoparticles of CdSeO3 at different temperatures. The temperature dependence of dielectric constant, dielectric loss ac conductivity and dc conductivity was also investigated.
Experimental
The chemicals such as cadmium acetate dehydrate and sodium selinite were used as precursor materials to prepare CdSeO3 nano particles. Cadmium acetate dihydrate and sodium selinite in 1:3 ratio were dissolved in Ethylene glycol solvent and water and stirred well using a magnetic stirrer and this solution mixture is kept in a microwave oven till the solvent evaporates completely, then the colloidal precipitate is filtered and washed by water and acetone several times. The precipitate thus formed is collected and dried.
AC conductivity measurements
The prepared cadmium selenite samples were palletized using a hydraulic press (with a pressure of about 5 tons) and used for the AC electrical measurements. The flat surfaces of the cylindrical pellets were coated with good quality graphite to obtain a good conductive surface layer. Using a traveling microscope the dimensions of the pellets were measured. The capacitance (Cc ) and the dielectric loss factor (tan δ) were measured using the conventional parallel plate capacitor method [16-19] using an LCR meter (APLAB MODEL 4912) for all the samples with two frequencies 100 Hz and 1 kHz at various temperatures in the range 30 – 150°C. The observations were made while cooling the sample. The temperature was controlled to an accuracy of ±1°C. Air capacitance (Ca) was also measured for the thickness equal to that of the pellet. The area of the pellet in contact with the electrode was same as that of the electrode. The air capacitance was measured only at room temperature because the variation of air capacitance with temperature was found to be negligible. The dielectric constant of the pellet sample was calculated using the relation,
εr = Cc / Ca.
where Cc is the capacitance of the crystal and Ca is the capacitance of the air medium of the same dimension as the crystal. As the crystal area was smaller than the plate area of the cell, parallel capacitance of the portion of the cell not filled with the crystal was taken into account and, consequently, the above equation becomes
where Ccrys is the capacitance with crystal (including air), Cair is the capacitance of air, Acrys is the area of the crystal touching the electrode and Aair is the area of the electrode. From these measurements, er and tan δ (dielectric loss factor) are available for the evaluation of AC conductivity.
The AC electrical conductivity (σac) was calculated using the relation,
σac = ε 0 εr ω tan δ.
Here, ε0 is the permittivity of free space (8.85 x 10-12 C2 N-1 m-2) and ω is the angular frequency (ω= 2πf, where f is the frequency).
DC Conductivity Measurements
The DC electrical conductivity measurements were carried out to an accuracy of ±3% using the conventional two-probe (parallel plate capacitor) technique at various temperatures in the range 40–150 ºC [20-22]. The sample was prepared as done for the AC conductivity measurement. The resistance of the sample was measured using a million megohmmeter. The observations were made while cooling the sample. Temperature was controlled to an accuracy of ±1 ºC. The dimensions of the sample were measured using a traveling microscope (least count = 0.001 cm). The DC conductivity, σdc, of the crystal was calculated using the relation
σdc = d/(RA)
where R is the measured resistance, d is the thickness of the sample, and A is the area of the face in contact with the electrode.
Results and Discussion:
Powder XRD analysis
The powder XRD pattern for the as prepared sample was done using Bruker AXS D8 Advance Diffractometer with monochromatic Cu (λ=1.5406 A0) radiation. The XRD pattern of as prepared CdSe nanoparticles are shown in Fig.1. The diffraction peaks indicates the nanocrystalline nature. The intensity of the peaks shows that the CdSe nanoparticles are highly crystalline. The diffracted peaks (100),(002), (101),(102),(110), (103), (112),(004), (202), (210), (211), (105) and (300)are corresponding to Hexagonal phase with Wurtzite structure which are in very good agreement with hexagonal (P63mc) structure in (Join Committee on Powder Diffraction Standards) JCPDS CAS No. 08-0459 .The corresponding lattice constants are a = 4.299 Å and c =7.010 Å. The size of the nanocrystallites was estimated using the Debye-Scherrer formula (Sagirani et al. 2015)
where, A is coherence length, β is the full-widths-at-half maximum (FWHM) of the diffraction peak, λ (1.5418 Å) is the wavelength of X-ray radiation, and θ is the angle of diffraction. From different θ values, the calculated average particle size is about 28 nm.
The dielectric parameters viz. εr, tan δ and σac observed are shown in Figures 2-4. All the parameters increase with increase in temperature. The dielectric constant is attributed to four types of polarization which are space charge, dipolar, ionic and electronic [23]. At lower frequencies at which all four types of polarizations contribute, the rapid increase in dielectric constant is mainly due to space charge and dielectric polarizations, which are strongly temperature dependent [24]. In the case of space charge polarization which is due to the accumulation of charges at the grain boundary, an increase in polarization results as more and more charges accumulate at the grain boundary with the increase in temperature. Beyond a certain temperature, the charges acquire adequate thermal energy to overcome the resistive barrier at the grain boundary and conduction takes place resulting in decreasing of polarization. This interfacial polarization occurs up to frequency of 1 kHz with possibly some contribution from the dipolar polarization also as the temperature increases. The grain size observed for the system considered in the present study is significantly small (not more than 26 nm). So, it can be understood that the polarization mechanism is mainly contributed by the space charge polarization[25-29].
The observed DC electrical conductivities of cadmium nanocomposite are shown in Fig 5. Nanoparticles lie between the infinite solid state and molecule. The electrical resistivity of nanocrystalline material is higher than that of both conventional coarse grained polycrystalline material alloys. The magnitude of electrical resistivity and hence the conductivity in composites can be changed by altering the size of the electrically conducting component. The σac values observed in the present study are very small. When the grain size is smaller than the electron mean free path, grain boundary scattering dominates and hence electrical resistivity is increased [30]. Thus the space charge contribution plays an important role in the charge transport process and polarizability for the system considered in the present study.
Conclusion
Semiconductor nanoparticles of cadmium selenite were successfully prepared bysimple microwave assisted solvothermal process. The powder XRD result shows that particles are purely crystallized in hexagonal phase with the broadening of diffraction peaks attributed to nanoscale size of the particles. The dielectric parameters, viz. dielectric constant (εr), dielectric loss (tan δ) and AC electrical conductivity (σac) and DC conductivity (σdc) measurements were also carried out at various temperatures in the range 40-150ºC and these electrical parameters are found to increase with the increase in temperature.
Englishhttp://ijcrr.com/abstract.php?article_id=2400http://ijcrr.com/article_html.php?did=2400[1] D. Mohanta, G.A. Ahmed, F. Singh, D. K. Avasthi and A. Choud-hury, “Properties of MeV oxygen ion irradiated Zns:Mn nanoparticle and exploitation in nanophotonics”, Journal of nanoparticle Research, vol. 8, pp. 645-652, 2006.
[2] S. J. Lade, M. D. Uplane and C. D. Lokhande, “Photoelectro chemical properties of CdX (X=S, Se, Te) films electrodeposited from aqueous and non aqueous baths”, Materials chemistry and physics, vol. 68, no.1, pp. 36-41,2001.
[3] M. T. S. Nair, P. K. Nair, R. A. Zingaro, and E. A. Meyers, “Enhancement of Photosensitivity in Chemically Deposited CdSe Thin Films by Air Annealing”, Journal of Applied Physics, vol. 74, no.3, pp. 1879-1884,1993.
[4] Ganganagappa, Nagaraju and Gujjarahalli Thimmanna Chandrap-pa, “Surfactant assisted hydrothermal synthesis of CdSe nanostructural materials” J. Mater. Sci. Technol., vol. 28, no. 6, pp. 495-499, 2012.
[5]. Nazzal AY, Qu L, Peng X, Xiao M (2003) Photoactivated CdSe nanocrystals as nanosensors for gases. Nano Lett 3:819–822
[6]. Bruchez M, Moronne M, Gin P, Weiss S, Alivisatos AP (1998)Semiconductor nanocrystals as fluorescent biological labels. Science 281:2013–2016
[7]. Colvin VL, Schlamp MC, Alivisatos AP (1994) Light-emitting diodes made from cadmium selenide nanocrystals and a semiconducting polymer. Nature 370:354–357
[8]. Gaponik N, Radtchenko IL, Sukhorukov GB, Rogach AL (2002) Toward encoding combinational libraries: charge-driven microencapsulation of semiconductor nanocrystals luminescing in the visible and near IR. Adv Mater 12:879–882
[9]. Haram SK, Quinn BM, Bard AJ (2001) Electrochemistry of CdS nanoparticles: a correlation between optical and electrochemical band gaps. J Am Chem Soc 123:8860–8861
[10]. Wang ZL, Kong XY, Ding Y, Gao P, Hughes WL, Yang R, Zhang Y (2004) Semiconducting and piezoelectric oxide nanostructures induced by polar surfaces. Adv Funct Mater 14:943–956
[11]. Hench, L, C. and West, J, K. Principles of Electronic Ceramics 1990, [John Wiley and Sons, NewYork] ISBN10 0471618217
[12] Peng XG, Manna L, Yang WD, Wickham J, Scher E, Kadavanich A, Alivisatos AP (2000) Shape control of CdSe nanocrystals. Nature 404:59–61
[13]. Tang KB, Qian YT, Zeng JH, Yang XG (2003) Solvothermal route to semiconductor nanowires. Adv Mater 15:448–450
[14] Busbee BD, Obare SO, Murphy CJ (2003) An improved synthesis of high-aspect-ratio gold nanorods. Adv Mater 15:414–416
[15]. Dwivedi DK, Kumar V, Dubey M, Pathak HP (2011) Structural, electrical and optical investigations of CdSe nanoparticles. Chalcogenide Lett 8:521–527
[16]. Joseph John, Selvarajan P, Benita Jeba Silviya S., Mahadevan C. K, Growth and
Characterization of Disodium Hydrogen Orthophosphate (DSHP) Single Crystals, Materials and
Manufacturing Processes, 22:3, 379 – 383.
[17]. Joseph John, N. Mahadevan, C, K. Studies on NaCl Added ADP Single Crystals. Materials and Manufacturing Processes 2008, 23, 809-815.
[18] Joseph John N, Selvarajan P, Mahadevan C K, Growth, Structural, Optical, Mechanical and Dielectric Characterization of Diammonium Hydrogen Phosphate (DAHP) single Crystals, Journal of Minerals and Material characterization and Engineering, 10, 15, 1379 (2011).
[19] Joseph John N. “Growth and Studies on Ferroelectric Material L-proline doped TGS single crystals for IR detectors” , Int. J. Current Sci. 8,11, 2016, 41068-41074
[20] Jayaprakash Manoharan J A, Joseph John N , Andavan P, Effect of amino acid doping on the dielectric properties of triglycine sulphate (TGS) single crystals , Ind. J. of Sci. and Tech., 4,6, 688, (2011).
[21] Jayaprakash Manoharan A J, Joseph John N, Andavan P, Journal of Experimental Sciences, 2(2) (2011), 33.
[22] Sivaka P, Joseph John N, Perumal S, Int. Journal of Engineering Research and Applications, 4, 7 (2014), 145.
[23] Sivaka P, Joseph John N., Perumal S, Int. res. J. Eng. And Tech., 3, 2 (2016), 1273.
[24]. Joseph John N. “Dielectric properties of ferroelectric L-proline triglycine sulphate (LPTGS) crystal” Int. J. Innov. Sci. and Res. 5,11, 2016, 890-893
[25]. Ajin Sundar S., Joseph John N. “ Dielectric properties of Mn doped ZnO nanostructures”, Int. J. of Eng. and App. Sci.3, 3, 2016, 26-29.
[26]. Ajin Sundar S., Joseph John N., Investigation on the effect of Mn on structural and optical properties of ZnO nanoparticles, Int. J. current Research, 2016, 8, 4, 29398-29402
[27]. Ajin Sundar S. , Joseph John N., Synthesis and studies on structural and optical properties of zinc oxide and manganese doped zinc oxide nanoparticles, Nano systems : Physics, Chemistry and Mathematics , 2016, 7(6)P.1-7
[28]. Ajin Sundar S., Joseph John N., “Carbon dot – Graphene oxide - Zinc oxide nanocomplex: Synthesis, characterization and properties” Materials Science-Poland, In press
[29]. Ajin Sundar S., Joseph John N., “Synthesis, Structural, Optical and Dielectric Studies on Carbon dot-Zinc oxide (CDZO) nanocomplexes” – Int. J. nanoscience, 2017, 16, 3, 1750021 – 1750030
[30] Sagi Rani C., Athira P., Joseph John N. “Investigations on tri manganese tetra oxide nano particles prepared by thermal decomposition “, Nanosystems: Physics, Chemistry, Mathematics, 2016, 7 (4), P. 0–2
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26General SciencesEffects of Electromagnetic Radiation Emitted from Mobile Phones on Different Physiological Systems and Possible Remedies
English0613Debajyoti BhattacharyaEnglish Somnath GangopadhyayEnglish Mausumi Sikdar (nee Bhakta)EnglishAim: In this paper, we aim to provide a review of some of the studies which investigated the possible negative biological effects of mobile phone radiation on different mammalian systems. This review will provide answers to public concerns about the risks of using mobile phone.
Background: Mobile phone has become an indispensable gadget for all. The growth in the use of mobile phones has raised concerns about the possible interaction between the electromagnetic field (EMF) radiation and the biological effects on mammalian systems, particularly the nervous, haematological, endocrine and reproductive systems.
Conclusion: Our conclusion shows that long term exposure to EMF radiation may cause permanent damage to different mammalian systems. Finally, some studies have also showed no effects due to exposure to EMF. More long term studies and analysis are needed.
EnglishSAR (Specific absorption rate), Radio frequency, Electromagnetic radiation, GSM (Global System for mobile communications), CDMA (Code Division Multiple Access), Nutritional supplementINTRODUCTION
It is nowadays impossible to imagine a modern, socially active person who does not use mobile devices. During the last two decades there has been a significant increase in the use of mobile phones throughout the world.(1) These mobile phones radiate harmful radiation which may cause harmful effects on the different physiological systems.
The transfer of energy to electrons when they fall back to ground state is unique to each element, as it depends upon the electronic configuration of the orbital. The energy transfer is inversely proportional to the wavelength of electromagnetic radiation.
E = hc/?λ [Where, h = Planck’s constant
c = velocity of light
λ = wavelength](2)
The initial safety guidelines for radio frequency and microwave radiation (RFR and MWR) were set by American National Standards Institute (ANSI) in 1982 and the US Federal Communications Commission (FCC) on Feb 26, 1985 based on “ thermal effects.(3)
ANSI (1982) published the first exposure standard, incorporating a 10 fold safety factor for humans exposed to electromagnetic fields between 300 KHz and 100 GHz frequencies.
As per estimated figures released by Telecom Regulatory Authority of India (TRAI), there were 936 million active mobile connections in India as on March 2016. There are almost 5 billion mobile phone users all over the world. Out of them, more than 900 million are Indians, which accounts for more than 80% of the total Indian population.
Electromagnetic emissions from mobile towers (Base transceiver stations, BTS) emanate at 900 MHz, 1800 MHz, 2100 MHz and 2300 MHz frequencies and from mobile handsets at 900 MHz and 1800 MHz for GSM (Global System for mobile communications) and at 1800 MHz for CDMA (Code Division Multiple Access).(4)
Good nutrition may ameliorate the harmful effects of mobile phone radiation. Especially, high quality protein having good biological value can protect the mammalian systems from the harmful effects of radiation.
The Specific Absorption Rate (SAR) value and various regulatory agencies:
The SAR value defines the amount of energy deposited per kilogram of body weight and is a measure for assessing the thermal effects. International Commission for Non-ionising Radiation Protection (ICNIRP) and the FDA (Food and Drug Administration) safety standards of USA limit the spatial peak microwave exposure to 2W/Kg and 1.6W/Kg SAR values respectively, averaging over 10g tissue for 6 minutes.(5)
Legislations implemented by various Indian regulatory agencies regarding microwave radiation exposure:
In India also, there are several laws and regulations regarding the radiation emitted from different mobile base stations as well as mobile handsets.
Department of Telecommunications (DoT) monitors radiation emitted from 10% of the randomly selected base stations, as or and when, on a complaint basis. In this regard, an international committee was set up with members from Indian Council of Medical research (ICMR), DoT, Department of Biotechnology (DBT) and Ministry of Environment and Forest and in its meeting on 24/08/2010, the members expressed their concern that “Indians are at higher risk due to tropical climate, low body mass index, low fat content and high environmental EMR”. Based on their recommendations, DoT further lowered the safety standards with effect from 01/09/2012, i.e. frequency/2000W/Sq.m at the above mentioned frequencies. For the mobile handsets, the new standard is 1.6W/Kg averaged over 1 g of tissue, 6 minutes. These safety standards are stringent as compared to many western countries. Since 01/09/2013, it has become mandatory to display the SAR values on handsets and EMR (Electromagnetic radiation) should be monitored like noise and air-pollution through monitoring devices. (5)
DISCUSSIONS:
The effects of mobile phone radiation on different physiological systems and their possible remedies are discussed in this review article.
Carcinogenic effects of mobile phone radiation:
The International Agency for Research on Cancer (IARC) of the World Health Organisation (WHO) issued a press release on May 31, 2011,labelling cell phone radiation as “possibly carcinogenic to humans” and added it to the list of other group 2B agents.(6)
According to the data base of the National Cancer Institute, December 2014, it was suggested that the increasing cell phone usage in humans enhanced the risk of tumour formation. They also tried to establish whether there is any direct relation between cell phone radiation and formation of malignant tumours. In this context, a study was conducted in May, 2016, called the case control study. In this study, data regarding the incidence of cancer occurring in a large group of population using cell phones was analysed over time. The results of the study showed that the probability of formation of malignant tumours is increased among the people who used cell phones.(7)
In America the use of cell phone started since 1991. A large study was done by the US National Toxicology Program (NTP) where a large group of laboratory rats and mice were exposed to RF (radio frequency) energy over their entire bodies for about 9 hours a day, starting before birth and continuing for up to 2 years. They found a probability to get damaged the of gliomas and schwannomas of the hearts in the rats exposed to RF radiation.(8)
According to the American Cancer Society, as cell phones are held near the head when being used, they might cause tumours in the following are as:
Malignant brain tumours such as gliomas.
Non-cancerous tumours of the brain such as meningiomas.
Non-cancerous tumours in the nerves connecting the brain to the ear (vestibular schwannomas, also known as acoustic neuromas).
Non-cancerous tumours of the salivary glands.
Brain cancer rates in USA have increased by 25% since 1975. In 2001, 185,000 Americans were diagnosed with some form of brain cancer. A grade forebrain tumour can grow from the size of a grape to tennis ball size in just 4 months. Although no specific cause has been reported, but interestingly, a dramatic increase in the rate of RF exposure had been reported in these patients. This radiation exposure may thus be considered to be the causative factor for tumour formation in those brain tumour patients.(9)
An epidemiological study conducted by Dr. Lennart Hardell found a higher incidence of brain tumours on the sides of heads used by mobile phone subscribers to make and receive calls.(10)
In 2009, the Jennie Zoline foundation of the University of Pittsburgh Medical Centre and the Osaka Medical Research Foundation published an article which concluded that the correlation between cell phones and cancer is inconclusive. However, the article did lead to the circulation of a hospital-wide memo warning about the “growing body of literature linking long term cell phone use to possible adverse health effects including cancer” (UPCI Memo, 2009).(11)
Effect of mobile phone radiation on the nervous system:
Human beings have dual sensitivity i.e. to microwave carrier frequency and the low frequency pulsing at 8.34 Hz of TDMA technology (Time Division Multiple Access, where multiple users can communicate simultaneously with the base station) and 2 Hz of DTX mode (Discontinuous Transmission mode, when the user is only listening) that are similar to alpha and delta rhythms of human brain. These emissions can interfere with brain’s signal processing activity due to their oscillatory similitude to the above inherent rhythms of the brain. This phenomenon is akin to “Electromagnetic interference” (EMI) that occurs while using mobile phones in aeroplanes.(12)
A study was done in Zhejiang University School of Medicine, China by Y. Zhu et al. in 2008, where in vitro cultured cortical neuronal cells and in vivo rat’s brain were exposed to the electromagnetic waves emitted by mobile phone. The result showed that microwave radiation emitted from mobile phones is harmful for both the in vitro cultured cortical neuronal cells and in vivo brain neuronal cells from rat with cranial defect.(13)
Another study was done by Y.A Khadrawy et al. in National Research Centre, Giza, Egypt, 2009, where adult young rats were exposed to EMR for 1hour/day. Amino acid neurotransmitters - glutamate, aspartate, GABA (Gama Amino Butyric Acid), glycine and taurine in the cortex were measured. The data showed that, in the adult rats EMR induced significant changes in the cortical levels of some of the studied amino acids throughout the exposure period. However in the young rats, EMR induced significant changes were seen even after stopping of the exposure.(14)
A study was done by M. Jadidi et al., where animals were exposed to mobile phone radiation and their anxiety levels were observed. No behavioural changes were observed in animals exposed to different levels of electromagnetic radiation emitted from mobile phones.(15)
An update of reports on the neurological effects of non-ionising electromagnetic fields published, between 2007-2014 by Henry Lai, suggests the presence of neurological effects in 68% of the publications and absence of effects in 32% publications.(16)
The neurological effects described in the review are changes in brain electrical activities after acute exposure to mobile phone radiation like- event related potentials, changes of the alpha-wave power of EEG after exposure to 2G, but not 3G mobile phone radiation. However, some authors reported no significant effects on EEG and event related potentials recorded in awake and conscious human beings after exposure to mobile phone EMR. Electromagnetic hypersensitivity is reported in many individuals who are sensitive to mobile phone radiation. Headaches, dizziness, memory and sleep problems are experienced.
Effect of EMR on the cardio vascular systems:
A study was done in Electrical Engineering Department, National Institute of Technology, Calicut, Kerala, India by V.T. Ahamed et al. The study dealt with the effect of electromagnetic fields radiated from mobile phones on heart rate variability (HRV) of 14 male volunteers. The result indicated that HRV was increased when the mobile phone was kept near the chest and decreased when it is kept close to the head. Mobile phone radiation is thus not only responsible for causing variations in heart rates, but such variability is also dependent on the position in which the mobile phone is held.(17)
Saini and Pandey investigated the effects of wireless Network Radiations (WNR) on Heart Rate Variability (HRV). They chose two non-linear indices namely i) Approximate Entropy (ApEn), ii) De trented Fluctual Analysis (DFA) for deciphering the hidden dynamics of HRV. The study comprised of 19 healthy male subjects in the age group (23 + 4.3) years. The ECG of each subject obtained under three different exposure modes. The result showed that there were a significant increase of DFA scaling exponent when WNR level changed from minimum to maximum value.(18)
Role of mobile phone radiation on oxidative stress and liver damage:
Free radicals are atoms or molecules that have unpaired electrons; these are unstable and highly reactive. According to their source, free radicals are divided into two categories:
a) Reactive Oxygen Species (ROS), such as superoxide, hydroxyl radicals.
b) Reactive Nitrogen Species (RNS), such as nitrogen di-oxide, nitric oxide radicals and peroxynitrite.(19)
The liver is the main biochemical organ in the body. It represents the body’s major detoxification system. Liver detoxifies the different toxic materials which have entered into the body or are produced by the various spontaneous biochemical reactions in the body. Such detoxified materials are excreted by the kidney and the intestine. Thus the liver and the kidney continuously detoxify and excrete many toxic materials including metabolic wastes.(20) Parenchymal cells are primary cells subjected to oxidative stress injury in the liver. The mitochondria, microsomes and peroxisomes in liver parenchymal cells can produce ROS, regulating on PPARα (Peroxisome-proliferator activated receptor), it is mainly related to the liver fatty acid oxidation and gene expression. Moreover, Kupffer cells, hepatic stellate cells and endothelial cells are potentially more exposed or sensitive to oxidative stress related molecules. A variety of cytokines like TNFα can be produced in Kupffer cells induced by oxidative stress which might increase inflammation and apoptosis.(21) The general mechanism of production of oxidative stress induced by various factors on liver disease may also be explained by Fig 1.
Various research studies indicate that microwave radiation emitted from mobile phones may cause oxidative stress through its thermal effect on liver damage. In 1996, Cleary et al. suggested that mobile phone exposure to 900 MHz RF-EMW (Electromagnetic wave) was associated with a significant increase in the mitochondrial membrane potential. Very recently, Friedman et al. reported that RF-EMW stimulates plasma membrane NADH oxidase can lead to oxidative stress and subsequent carcinogens.(22)
A research was done by M. Asgari et al. in Islamic Azad University, Department of Hematology, Tehran, Iran. Male Wistar rats were exposed to mobile phone radiation for 1, 3 and 6 hour/day. After 8 weeks their blood were drawn for assay. The result showed that there was a significant increase in serum creatinine level in the group of rats exposed to mobile phone radiation.(23)
A study was done by M. Baleci et al. in Ankara Oncology hospital, Turkey. Forty Wistar Albino rats were exposed to mobile phone radiation (GSM frequency 900MHz with SAR value 1.2 W/Kg). After 4 weeks animals were sacrificed and their cornea and lens tissues were dissected. Tissues were homogenised and MDA (Malondialdehyde), SOD (Superoxide dismutase), GSH-Px (Glutathione peroxidase) and CAT (Catalase) enzyme activities in the supernatants were measured. Results indicated that the MDA and CAT enzyme activity were increased significantly in the animals exposed to mobile phone radiation while the SOD activity was decreased significantly in the same group.(24)
Mobile phone radiation on reproductive and foetal health:
Male reproduction:
A number of recent reports suggested a possible link between mobile phone use and male infertility.
An initial study was done by Desai et al. involving 361 men who had attended an infertility clinic suggested that the use of cell phones adversely affects semen quality by decreasing sperm count, motility, viability and morphology, which might be responsible for male infertility.(25) Why should electromagnetic radiation affects the movement of sperm? One study points to a possible explanation. Lishko (2010) showed the human sperm move to the egg in an electrically created pathway, which might be affected by the electromagnetic field created by mobile phone radiation.(26)
Similarly, Fejes et al. studied 371 men undergoing infertility evaluations and reported that the duration of possession and transmission time of cell phones correlated negatively with the proportion of rapidly progressive motile spermatozoa, suggesting that prolonged use of cell phones might have negative effects on sperm motility.(27)
Davoudi et al., in a small prospective study involving 13 men with normal semen analysis, also found that using mobile phones for 6 hour/day for 5 days decreased the rapid progressive motility of spermatozoa.(28)
Thus recent epidemiological studies have highlighted the role of mobile phone exposure on sperm motility, morphology and viability, thus proposing a reduction in the fertilizing potential of males.
In addition to the epidemiological studies, the effect of mobile phone radiation is well studied in animal models and in vitro studies on human semen. Many studies have indicated that EMW decreases the size of the testicular organs. A decrease in the diameter of the seminiferous tubules had been reported after exposure to mobile phone radiation. Ozyguner et al. demonstrated a decrease in seminiferous tubular diameter and epithelium thickness after applying RF-EMW of 869 to 894 MHz.(29)
These results support the study done by Saunders and Kowalczuk that microwave radiation of 50 mW / cm2at a frequency of 2.45 GHz for 30–40 minutes resulted in a significant degeneration of the seminiferous epithelium in mice. Wang et al. suggested that mobile phone radiation might change the permeability of blood testis barrier.(30) The radiofrequency emitted from mobile phone mediated ROS formation can lead to phosphorylation of heat shock protein (hsp), which can alter the secretion of growth factors. This in turn can increase the permeability of blood brain barrier as suggested in figure 2.(25)
Female reproduction:
The female genital system is composed of the uterus, ovaries, fallopian tubules, the released oocytes and germ somatic cells in their tissues. According to many researchers, neuro-endocrine changes caused by mobile phone radiation is a key factor in changing hormone function and causing infertility symptoms in females.(31) A number of other researchers have focused on the estrous cycle. One of the differences between women’s and female rodents’ sexual cycle is that the womens’ cycles are completed, and the peak of estrogen-progesterone level in the blood can be separated. In case of female rodents, the peak of these two hormones is concurrent.(32)
Besides, a lot of research has focused on the harmful effects of radiation on the granulosa cells of the oocytes. Apoptosis of these cells is another issue in many articles.(33)
In this paragraph, several reports regarding this fact are discussed. Spontaneous abortion and fetal abnormalities are two interrelated issues that have attracted the attention of many researchers.(34) Although the negative effects on fetal development are controversial, Williams and Fletcher (2010) concluded that “The fetus is most susceptible to radiation during organogenesis (2-7 week after conception) and in the early fetal period (8-15 weeks after conception)”.(35) The male offsprings of female rats after their exposure to 60 Hz frequency showed reduction in number, height and volume of seminiferous tubules and in the number and diameter of Leydig cells. However, serum levels of testosterone, gonadosomatic index, and number of Sertoli cells remained unchanged.(36).
Another study done to determine the relationship between electromagnetic radiation and ovulation in rats showed that the waves inhibited ovulation and reduced the number of corpora leutea.(37) Radiation exposures caused reproductive and developmental toxicity effect that degenerates oocytes in mice.(38) Another research showed that exposure to 33-50 Hz frequency for 3 days prevented the formation of antral follicles in vitro.(39) When female rats were exposed to 900 MHz frequency for 30 days, endometrial apoptosis and oxidative stress increased.
During mating, mice exposed to 50 Hz frequency for 4 h/day for 2 weeks had significant reduction in the number of blastocytes and increased DNA fragmentation.(40) This study suggested that exposure to electromagnetic radiations in the implantation period, may have deleterious effects on the development of embryos. Radiation for 4 h before ovulation showed negative effects on the early development of the embryo.(41)
A study done by Rozavinia A. et al. in Chennai where female rats were exposed to mobile phone radiation for 1, 3, 6 h/day. After 8 weeks serum level of progesterone was assayed. Results indicated that long term exposure increased serum progesterone level in female rats, which might seriously influence the endocrine system.(42)
Effects on haematological parameters:
Most significant studies were done by using GSM frequencies or the microwave frequencies and their effect on haematological parameters in animals.
Experiments were done by K. Nageswari et al. where rabbits were exposed to microwave radiation at 5mW/cm2, 2.1 GHz, 3h daily, 6 days / week for 3 months. The result speculated that the T-lymphocytes were sequestered to various lymphoid agents under the influence of microwaves. It is clear from the experiment that chronic microwave exposure leads to suppression of T-lymphocyte numbers.(43)
Liburdi R.P. et al. stated in their study that RF EMF was capable due to their thermal effects to increase the number of neutrophils and decreased the level of lymphocytes.(44)
An experiment was done by P. Kumari et al. in Manipal. They collected the blood from 37 volunteers, from the department of Physiology, Kasturba Medical College, Manipal. The blood samples were exposed to the mobile phone radiation. The total R.B.C. and W.B.C. count changed significantly. But there was no significant change in osmotic fragility of R.B.C. in mobile phone radiation exposed group.(45)
Md. F. Assasa from Al-Azhar University studied adult male Albino rats exposed to 900 MHz electromagnetic radiation emitted from mobile phones. Their total R.B.C. and W.B.C. count, packed cell volume and haemoglobin content were measured. From the result it was noted that there were significantly increase the total count of W.B.C., MCHC (Mean corpuscular haemoglobin content) and platelet count in the rats exposed to mobile phone radiation than the control group and R.B.C. total count, haemoglobin content, PCV (Packed cell volume) were decreased significantly in the same group than the control group.(46)
Another study was done by M. Sikdar et al. in Presidency University, Department of Biological Sciences, Kolkata. Male Swiss Albino Mice were exposed to electromagnetic radiation emitted from mobile phone and supplemented with High Protein diet (Fortified with 20% Casein) and the haematological parameters were studied. The total count of R.B.C., W.B.C., differential count of W.B.C. and total haemoglobin content were measured in the blood. The surface structures of R.B.C. were also studied under scanning electron microscope. It was observed that the animals exposed to mobile phone radiation, the total number of R.B.C. was decreased and the total number of W.B.C. was increased in comparison to control group. The haemoglobin concentration in the blood in animals exposed to mobile phone radiation was also decreased. The distorted R.B.C. structures were also seen under the electron microscope. Sign of recovery were seen in the group of animals supplemented with high protein diet.(47)
Usman et al. in 2012 investigated the effect of long term RF EMF (Electromagnetic field) exposures due to GSM frequencies. Blood samples and tissues were taken for hematology and histopathology tests. The complete blood count result showed that the hematological parameters both of sham exposed and exposed mice were within the normal range. A statistical analysis was also conducted to determine whether differences observed between the experimental groups were significant or not. The histopathology examination on some internal organs showed that spleen and bone marrow of the mice were normal for all three experimental groups, while a sign of tissue degeneration and inflammations were observed after 8 weeks of exposure on the brain, liver and lungs of the mice in the exposed groups. These signs increased in severity with prolonged exposure.(48)
Otitoloju A et al. had studied the levels of radiofrequency radiations around two GSM base stations located in the vicinity of residential quarter and workplace complex. The haematological studies revealed an elevation of W.B.C. counts in mice exposed to RF (Radio frequency) radiations compared to control group in both workplaces and residential complex area. The R.B.C count was not changed significantly in mice exposed to mobile phone radiation in residential areas compared to control group, but the animals exposed to RF radiation in work place area showed significantly a marked increase value.(49)
According to the study done by Sikdar et al. and Otitoloju et al. it is seen that the W.B.C. count increased significantly in the mice exposed to mobile phone radiation in both cases. From these studies it may be said that it is related to the induction of protective mechanism in the exposed mice to the effect of the RF radiation and other activities around the GSM base stations. Therefore, it could be deduced that exposure to radiofrequency radiations induces stress in exposed animals which led to the synthesis of abnormally high levels of white blood cells.
Role of various nutritional supplements preventing the damage caused by electromagnetic radiation:
Good nutrition, specially fortified with first class proteins have good biological values and rich in antioxidants can ameliorate these harmful effects of electromagnetic radiation in the body. Various studies are being conducted to search remedies to people make safe from the bad effects of radiations.
Mice were exposed to 10 GHz microwaves with the power density of 0.25 m W/ cm2. One group of mice supplemented with alcoholic extract of Prunus domestica. The blood samples were collected for the assay. This study was done by R. Sisodia et al. at Department of Zoology, University of Rajasthan. Microwave exposure resulted in significant decrease in haemoglobin, monocytes, packed cell volume, red blood cells, mean corpuscular haemoglobin concentration whereas, the number of white blood cells, lymphocytes, erythrocyte sedimentation rate and mean corpuscular volume increased significantly compared to the sham exposed animals. Signs of improvements in the haemoglobin and other haematological parameters were observed where the mice were supplemented with P. domestica extract.(50)
Casein is a first class milk protein, fortified with almost all essential amino acids. It is also fortified with various antioxidant agents. It has antioxidant properties studied in vitro. Experiments were done by M. Sikdar et al. where male Swiss Albino mice were exposed to 0.9 GHz electromagnetic radiation emitted from GSM mobile phone for 3 hour / day. One group of mice were supplemented with 20% casein diet. Various blood parameters were altered due to the exposure of electromagnetic radiation. Signs of recovery were noticed in the group supplemented with casein diet.(47)
B. Hajiuon from Islamic Azad University, Iran did an experiment with female rats, they were exposed to 900 MHz electromagnetic radiation emitted from mobile phone. The animals were treated with 400 mg and 200 mg/kg body weight garlic extract. The serum estrogen and progesterone level were assayed. The hormone level was altered due to mobile phone radiation. The changes were restored by the application of garlic extract.(51)
Protective action of vitamin E against the harmful effects of mobile phone radiation were studied by A. Ghanbari et al. Rats were exposed to electromagnetic radiation along with and treated with 200 mg / kg body weight vitamin E. After exposed to the radiation antioxidant stress enzymes like MDA, Glutathione peroxidise (GSH-Px) in the cells of substantianigra were increased significantly. But SOD activity was decreased significantly. Vitamin E treatment significantly prevented the level of increased MDA levels and GSHPx activity and also prevented the decreased SOD activity.(52)
From the studies on the effect of nutritional supplements on animals exposed to electromagnetic radiation, it could be attributed that electromagnetic radiation is considered as a stress factor acts on the different physiological systems of mammals. Supplements have good antioxidant properties can ameliorate these harmful effects of radiation.
CONCLUSION
Many studies are being done to assess the effect of electromagnetic radiation on different physiological systems. It has been proved that EMF has a negative role in the body. Different mobile phone companies always do not obey the rules and regulations regarding SAR values of the mobile phones for giving better service to their customers. It is also an unavoidable fact that the use of mobile phones cannot be stopped or lessens in this 21st century. So, it is needed to search a strong remedy which can ameliorate the harmful effects of mobile phone radiation in the body. Various researches are being carried out in search of the remedy. But further studies are needed to be carried out.
Englishhttp://ijcrr.com/abstract.php?article_id=2401http://ijcrr.com/article_html.php?did=2401
Harvey C, French PW. Effects on protein kinase c and gene expression in a human mast cell line, hmc?1, following microwave exposure. Cell Biol Int 1999 Nov 1;23(11):739-48.
Pathak C, Srivastava VK, Singh DN. Optimization of zeolite synthesis using microwave assisted acid digestion method. Int J Curr Res Rev 2012 May 4;9: 83-6.
Federal Communications Commission (FCC). In the matter of responsibility of the Federal Communications Commission to consider biological effects of radiofrequency radiation when authorizing the use of radiofrequency devices. www.fcc.gov,Feb.26,1985.http://cellphones.procon.org/sourcefiles/FCC_1985_RF_Regulations.pdf. (Accessed on 2/11/2014).
Telecom Regulatory Authority of India, Information paper No. 01/2014-QoS. On Effects of Electromagnetic Field Radiation from Mobile Towers and Handsets, 30th July2014;http://www.auspi.in/news/EMF-Information-Paper_30-72014.pdf. (Accessed on 2/11/2014 ).
Kumar G. Report on cell tower radiation submitted to Secretary, DOT, Delhi. December 2010;https://www.ee.iitb.ac.in/~mwave/gk-cell-tower-rad-report-dotdec2010. pdf.(Accessed on 31/10/2014).
International Agency for Research on Cancer (IARC). IARC Classifies Radio frequency Electromagnetic Fields as Possibly Carcinogenic to Humans.www.iarc.fr, May 31, 2011; (Accessed on 31/10/2014).
Praveenkumar GD, Sathishkumar G. Application of cancer data using topsis methods. IntJ Advnc Trnds in Comp Sci and Eng 2016 Jul;5(4): 17-20.
Morgan LL, Miller AB, Sasco A, Davis DL. Mobile Phone Radiation causes brain tumors and should be classified as a probable human carcinogen (2A) review. Int J Oncol 2015 May; 46(5): 1885-71.
Jemal A, Murray T, Ward E, Samuels A, Tiwari RC, Ghafoor A, Feuer EJ, Thun MJ. Cancer statistics, 2005.CA Cancer J Clin 2005 Jan ;55(1):10-30.
Morales-Suárez-Varela MM, Olsen J, Johansen P, Kaerlev L, Guénel P, Arveux P, Wingren G, Hardell L, Ahrens W, Stang A, Llopis A. Occupational risk factors for mycosis fungoides: a European multicenter case-control study. J Occup Environ Med 2004 Mar 1;46(3):205-11.
Ledford B. Cell phones, electromagnetic radiation, and cancer: a study of author affiliation, funding, bias, and results. Polit Policy 2010 Dec 1;38(6):1274-303.
Freude G, Ullsperger P, Eggert S, Ruppe I. Effects of microwaves emitted by cellular phones on human slow brain potentials. Bioelectromagnetics 1998 Jan 1;19(6):384-7.
Zhu Y, Gao F, Yang X, Shen H, Liu W, Chen H, Jiang X. The effect of microwave emmision from mobile phones on neuron survival in rat central nervous system. Prog Electromagn Res B Pier B 2008;82:287-98.
Khadrawy YA, Ahmed NA, Ezz HS, Radwan N. Effect of electromagnetic radiation from mobile phone on the levels of cortical amino acid neurotransmitters in adult and young rats. Romanian J Biophys 2009;19(4):295-5.
Esmaili MH, Masoumi H, Jadidi M, Miladi-Gorji H, Nazari H. The Effects of Acute Mobile Phone Radiation on the Anxiety Level of Male Rats. Middle East J Rehabil Health Stud 2017 Jan 23; 4 (2):
Lai H. Neurological effects of non-ionizing electromagnetic fields. BioInitiative Working Group:" A Rationale for Biologically-Based Exposure Standards for Low-Intensity Electromagnetic Radiation. 2012 Oct.
Ahamed VT, Karthick NG, Joseph PK. Effect of mobile phone radiation on heart rate variability. Comput Biol Med 2008 Jun 30;38(6):709-12.
Saini BS, Pandey A. Effect of wireless network radiation on heart rate variability. Int J Eng Res Appl 2014 Jan 1;4(1):70-3.
Lobo V, Patil A, Phatak A, Chandra N. Free radicals, antioxidants and functional foods: Impact on human health. Pharmacogn Rev 2010 Jul 1;4(8):118-26.
Bhattacharya D, Sikdar M. Renal and hepato protective effects of green tea (Camellia sinensis) extract on Wistar rats treated with sodium oxalate. Int J Pharma Bio Sci 2016 Oct;7(4): 740-6.
Grattagliano I, Bonfrate L, Diogo CV, Wang HH, Wang DQ, Portincasa P. Biochemical mechanisms in drug-induced liver injury: certainties and doubts. World J Gastroenterol. 2009 Oct 21;15(39):4865-76.
Cleary SF, Du ZH, Cao GU, Liu LM, McCrady CA. Effect of isothermal radiofrequency radiation on cytolytic T lymphocytes. FASEB J. 1996 Jun 1;10(8):913-9.
Asgari M, Ahmadi R, Gohari A. The effect of mobile phone radiation on serum levels of creatinine in male rats. Proceedings of the International conference on Earth, Environment and Life Sciences (EELS-2014), 2014 Dec 23-24; Dubai (UAE).
Balci M, Devrim E, Durak I. Effects of mobile phones on oxidant/antioxidant balance in cornea and lens of rats. Curr Eye Res 2007 Jan 1;32(1):21-5.
Desai NR, Kesari KK, Agarwal A. Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male reproductive system. Reprod Biol Endocrinol 2009 Oct 22;7(1):1-9.
Lishko PV, Kirichok Y. The role of Hv1 and CatSper channels in sperm activation. J Physiol 2010 Dec 1;588(23):4667-72.
Fejes I, Závaczki Z, Szöll?si J, Koloszár S, Daru J, Kovacs L, Pal A. Is there a relationship between cell phone use and semen quality?. Arch Androl 2005 Jan 1;51(5):385-93.
Davoudi M, Brossner C, Kuber W. The influence of electromagnetic waves on sperm motility. Urol Urogynecol 2002;19:18–32.
Ozguner M, Koyu A, Cesur G, Ural M, Ozguner F, Gokcimen A, Delibas N. Biological and morphological effects on the reproductive organ of rats after exposure to electromagnetic field. Saudi Med J 2005 Mar;26(3):405-10.
Saunders RD, Kowalczuk CI. Effects of 2· 45 GHz Microwave Radiation and Heat on Mouse Spermatogenic Epithelium. Int J RadiatBiolRelat Stud PhysChem Med1981 Jan 1;40(6):623-32.
Moore KL, Persaud TV, Torchia MG. O sistemanervoso. Desenvolvimento da medulaespinhal. Formação das meninges, da medulaespinhal. In: Moore KL, Persaud TV, Torchia MG, eds. Embriologiaclínica. 8th ed. Rio de Janeiro: Elsevier; 2008:391–93
Terner JM, De Wit H. Menstrual cycle phase and responses to drugs of abuse in humans. Drug Alcohol Depend 2006 Sep 1;84(1):1-3.
Smitz J, Dolmans MM, Donnez J, Fortune JE, Hovatta O, Jewgenow K, Picton HM, Plancha C, Shea LD, Stouffer RL, Telfer EE. Current achievements and future research directions in ovarian tissue culture, in vitro follicle development and transplantation: implications for fertility preservation. Hum Reprod Update 2010 Jul 1;16(4):395-414.
Baldwin VJ. Pathology of multiple pregnancy. Springer Science and Business Media; 2012 Dec 6.
Williams PM, Fletcher S. Health effects of prenatal radiation exposure. Am Fam Physician 2010 Sep;82(5):488-93.
Asghari A, Khaki AA, Rajabzadeh A, Khaki A. A review on Electromagnetic fields (EMFs) and the reproductive system. Electronic Physician. 2016 Jul;8(7):2655.
Khaki AA, Khaki A, Ranjbar M, Rahimi F, Ghahramanian A. P30. 11: The effects of electromagnetic field (EMF) on ovary in rat. Ultrasound Obstet Gynecol 2011 Oct 1;38(S1):269-.269.
Hamdi BA, Soleimani RJ, Khaki A, Roshangar L. Developmental exposure to emf and its effect on spermatogenesis in adulthood in mice. Iran J Reprod Med 2011;9(S1):67-67.
Jung KA, Ahn HS, Lee YS, Gye MC. Effect of a 20 kHz sawtooth magnetic field exposure on the estrous cycle in mice. J Microbiol Biotechnol 2007 Mar;17(3):398-402.
Borhani N, Rajaei F, Salehi Z, Javadi A. Analysis of DNA fragmentation in mouse embryos exposed to an extremely low-frequency electromagnetic field. Electromagn Biol Med 2011 Dec 1;30(4):246-52.
Gye MC, Park CJ. Effect of electromagnetic field exposure on the reproductive system. Clin Exp Reprod Med 2012 Mar 1;39(1):1-9.
Razavinia A, Ahmadi R, Gohari A. The effect of mobile phone radiation on serum levels of progesterone level in female rats. Proceedings of the International conference on Agricultural and Medical Sciences (CAMS-2014), 2014 May 2-3; Antalya (Turkey).
Nageswari KS, Sarma KR, Rajvanshi VS, Sharan R, Sharma M, Barathwal V, Singh V. Effect of chronic microwave radiation on T cell-mediated immunity in the rabbit. Int J Biometeorol 1991 Jun 1;35(2):92-7.
Liburdy RP. Radiofrequency radiation alters the immune system: II. Modulation of in vivo lymphocyte circulation. Radiat Res 1980 Jul 1;83(1):66-73.
Kumari P, Manjula SD, Gautham K. In vitro study of effect of radiation emitted by mobile phone on osmotic fragility and other blood parameters. Res J Pharm BiolChem Sci. 2016 July 7 (4): 1283-92.
Assasa MF. Effect Of Cellular Phone Field On Body Weight, Liver Enzymes Blood Indoces And Role Of Some Antioxidant In Albino Rats. AAMJ. 2010 Sep;8(3) 68-83.
Bhattacharya D, Ghosh N, Sikdar M. Effect of electromagnetic radiation exposure on haematological parameters of Swiss Albino mice and their modulation by high protein diet. Biomedicine. 2016 March 36 (1) : 121 – 27.
Usman AD, Ahmad WW, AbKadir MZ, Mokhtar M, Ariffin R. Effect of radiofrequency electromagnetic field exposure on hematological parameters of mice. World Appl Sci J. 2012;16(5):656-64.
Otitoloju AA, Osunkalu VO, Obe IA, Adewale OA, Akinde OR. Level of radiofrequency (rf) radiations from GSM base stations and its biological effects on albino mice, Musmusculus. J. Appl. Sci. Environ. Manage. 2010;14(3):87-93.
Sisodia R, Rifat F, Sharma A, Srivastava P, Sharma KV. Effects of 10-GHz microwaves on hematological parameters in Swiss albino mice and their modulation by Prunusavium. J Environ PatholToxicolOncol. 2013;32(3):205-17.
Hajiuon B. Effects of cell phone radiation on estrogen and progesterone levels and ovarian changes in rats treated with garlic (Allium sativum L.) hydro-alcoholic extract. Phytomedicine. 2013 Aug 23;4(2):81-8.
Ghanbari AA, Shabani K, Nejad DM. Protective Effects of Vitamin E Consumption against 3MT Electromagnetic Field Effects on Oxidative Parameters in Substantia Nigra in Rats. Basic Clin Neurosci. 2016 Oct 7(4):315-22.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26General SciencesStatistical Modelling for Job Satisfaction of Maharashtra State Road Transport Corporation Key Members
English1419Avinash S. JagtapEnglish Nilambari A. JagtapEnglish Pooja S. ZanjurneEnglishMobility is one of the characteristics of human beings; movement is the feature of human nature which simply means mere movement of persons from one place to another for getting comfort journey. Bus conductors and Drivers of MSRTC are serving to society. Moreover they can be considered as face of MSRTC as they are having direct contact with passengers. In this paper we study various factors affecting on the job satisfaction of conductors and drivers. Bus conductors and drivers are randomly selected as a sample. Their job satisfaction is analyzed through structured questionnaire. The first part of the questionnaire is focused on the personal information like age, education, number of family members, earning members etc. and second part is focused on the official information of the respondents like number of charge sheet, presentism and abstentism. The statistical analysis is done by using the statistical tools like Chi square test, linear discriminant analysis, multiple logistic regression. It is clear from this study that the working environmental factor affects the job satisfaction. The accuracy of fitted model is 67%. Linear Discriminant model has 96% accuracy.
EnglishJob satisfaction, Health problem, Stepwise regressionIntroduction: Traffic staff is one of the important factors for operating functions. Traffic staff includes drivers, conductors, traffic controllers, line checking staff, traffic inspectors and other traffic staff. The drivers and conductors are appointed with their services based on the sanctioned schedules, their work norms are set according to the provisions of Motor Transport Workers Act 1961 (MTW Act) which prescribes a daily steering duty of 8 hours and spread over duty of 12 hours.
Maharashtra State Road Transport Corporation(MSRTC) is a leading passenger road transport organization in India having fleet of over 18,000 buses and operating over 1,05,000 bus trips daily covering 58 lacks of Kms. MSRTC is aimed to provide punctual, safe, comfortable and economical services to the passengers. It spread in all over Maharashtra nearly 88% villages. MSRTC not only working in the area of providing transport facility to passengers but also it provide service carriage of parcels currier and Allied material by using the carriage of buses with consideration of given information MSRTC obviously need competent, motivated, trained ,satisfied and alert Human Resource for running one of the biggest public transport organizations of India. The following are two personnel who constitute the subject matter of study. As we know the conductors and drivers are Crew members (Conductors and Drivers) of MSRTC.
A bus conductor has to deal with thousands of passengers every day. Buses are two most important forms of public transport the other being trains. The burden of dealing with increasing number of commuters is very heavy. He has to behave well with the passenger and see to it that everyone is issued a right ticket, and thus increase passenger satisfaction, and in the process earn maximum revenue for the organization.
Job satisfaction is most important thing in any job. If the key members satisfy with their job then it tends to high quality of work they do. But they do not satisfy with their job it may be a serious issue because the key members have direct contact with public so that if they are unsatisfied with their job their behaviour is rood about passenger and this is one kind of the loss to MSRTC so that the checking crew member satisfaction with their job is important thing. With the help of this paper we will find which factor are strongly affecting on job satisfaction of key members. Also we find the association between variables.
Material and Methods:
The present study is undertaken on the employees (Drivers and conductors) of selected MIDC ST Depot, Baramati, Dist. Pune of MSRTC. The study is mainly based on primary data collected from the respondent the drivers, conductors, driver cum conductors of MSRTC by way of structured questionnaire, to be precise, pre-coded. This interview schedule has been organised in two parts. The first part of the questionnaire is focused on the personal information like Age, Education, No. of family Members, Earning Members etc. and second part is focused on the official information of the respondents like number of charge sheet, presentism and abstentism. Here we use the variable like Ts/TTS/DW is the permanent, temporary, and contract basis.
Multiple logistic regression: This is one type of generalized linear model (GLM). Multiple Logistic Regression is used when response variable is binary. It is utilized for predicting the outcome of a categorical variable based on one or more independent variables. Specific form of logistic regression model
Π(x)=exp^(g(x))/[1+exp^g(x)]
Generalized linear model: In a GLM the response variable distribution must only be a member of the exponential family which includes the normal, Poisson, binomial, exponential and gamma distribution as members. Distribution that the members of the exponential family have the general form
g(x)=β0+β1X1+…………….+βp Xp
We are interested in determining the future event, our response is binary for that purpose we use the GLM after getting the significant variable from cluster analysis we able to fit generalized linear model for our data. From the fitted model we can predict the future event.
Stepwise regression: Stepwise regression includes regression models in which the choice of predictive variables is carried out by an automatic procedure. Forward Selection, which involves starting with no variables in the model, testing the addition of each variable using a chosen model comparison criterion, adding the variable (if any) that improves the model the most and repeating this process until none improves the model. AIC –Akien’s Information Criteria: The general for calculating AIC is
AIC= -2*ln (likelihood) +2*k
AIC can also be calculated using residual sum of squares from regression,
AIC=n*ln (RSS/n) +2*k
Where, n is the number of data points, RSS is the residual sum of squares, AIC requires a bias-adjustment small sample size. From the stepwise regression we get the significant variables for regression models for our data. The model which has smallest value of AIC as compare to the other models it gives the best regression model for our data.
Confusion Matrix: A Confusion Matrix is a visual performance assessment of a classification algorithm in the form of a table layout or matrix. Each column of the matrix represents predicted classifications and each row represents actual defined classifications. This representation is a useful way to help evaluate a classifier model. A well behaved model should produce a balanced matrix and have consisted percent correctness numbers for accuracy, recall, precision and F measure. Accuracy= (True positive + false positive)/ (total)
Precision=True positives / (true positives + false positives).
To determine the accuracy of the fitted model we use the confusion matrix for the response variable.
Linear Discriminant Analysis(LDA): Linear Discriminant analysis and the related fisher’s linear discriminant are methods used in statistics, pattern reorganization and machine learning to find a linear combination of features which characterizes or separate two or more class of objects or events.LDA is a closely related to analysis of variance and regression analysis, which also attempt to express one dependent variable as a linear combination of other features or measurements.
Data Analysis: The analysis includes chi-square test of independence to examine the nature of relationship between variables. The collected data will be analysed by using Multiple Logistic Regression Analysis.
Abbreviations : Faci: Facilities, San: Sanitary, Clean : Cleanness, Spac: Space, Rest : Rest house facility, Guest: Guest house facility, df : Degrees of freedom, Dist :Distance, SY: Service years, Pay: Payment, EM: Earning members , HP: Health problem, Ts: Time skill, famliym: Family members, JS : Job satisfaction, TPM : Transition probability matrix.
Association between job satisfaction and various environmental factors
Logistic regression
Model 1:
The regression equation is,
Job satisfaction ~Age+Space+Distance+Serviceyears+Payment+Earningmembers+Healthproblem+Timeskill+ status+Guest house
Start: AIC=130.5
Coefficients:
(Intercept) Age spac Dist
-1.169e+00 2.422e-02 1.408e+00 1.175e-03
SY familym Pay EM
-4.508e-02 -1.361e-02 3.914e-05 3.110e-01
HP Ts status Guest
-9.731e-01 -5.486e-01 -7.272e-01 4.700e-01
Degrees of Freedom: 91 Total (i.e. Null); 80 Residual
Null Deviance: 126
Residual Deviance: 106.5 AIC: 130.5
>summary(model)
Call:
glm(formula = JS ~ Age + spac + Dist + SY + familym + Pay + EM +
HP + Ts + status + Guest, family = "binomial", data = mydata)
Model 2:
> X=step(model)
Start: AIC=130.46
JS ~ Age + spac + Dist + SY + familym + Pay + EM + HP + Ts +
status + Guest
Model 3:
Step: AIC=126.67
JS ~ spac + Dist + SY + Pay + EM + HP + Ts + status +
Guest
Model 4:
Step: AIC=124.96
JS ~ spac + Dist + SY + Pay + EM + HP + Ts + Guest
Model 5:
Step: AIC=123.37
JS ~ spac + SY + Pay + EM + HP + Ts + Guest
Model 6:
Step: AIC=121.93
JS ~ spac + SY + EM + HP + Ts + Guest
Model 7:
Step: AIC=120.01
JS ~ spac + EM + HP + Ts + Guest
Model 8:
Step: AIC=118.56
JS ~ spac + HP + Ts + Guest
Model 9:
JS ~ spac + HP + Ts
Deviance Residuals:
Min 1Q Median 3Q Max
-1.4745 -0.8385 -0.5272 0.9069 2.0210
Degrees of Freedom: 91 Total (i.e. Null); 88 Residual
Null Deviance: 126
Residual Deviance: 109.5 AIC: 117.5
Pridictor
Estimate
Std.Error
Zvalue
Pr(>|Z|)
Intercept
-0.08131
0.65692
-0.124
0.9015
Spac
1.5404
0.47891
3.216
0.0013
HP
-1.0388
0.65307
-1.591
0.1117
Ts
-0.78322
0.49801
-1.573
Englishhttp://ijcrr.com/abstract.php?article_id=2402http://ijcrr.com/article_html.php?did=2402
Andries du Plessis, Andrew Hobbs, Rebecca Marshall and Sherrol Paalvast, Human Resource Functions and Activities In The 21st Century To Attain Competitive Advantage, International Review of Business Research Papers, 2008, Vol. 4 No.3 Pp- 35-44.
Gurav A.M. and Pralhad Krishna Mudalkar, A circle study of Human resource Practices in selected Sugar Factories /Journal-The lUP Joumal of Management Research, 2011, Vol. 10, No. 1. Page No.46-78.
Ashok Som , Innovative human resource management and corporate performance in the context of economic liberalization in India / journal The International Journal of Human Resource Management., 2008, Vol. 19. No. 7, 1278-1297.
Basraj Benni, Aniardeep. Jadhav, Bus transport Efficiency Measurement with Reference to MSRT ('Sus depots of Kolhapur division" 2012.
Carlos Sanchez- Runde, Richard Whittington, Javier quarilha, Human Resource Management implications of New Forms of Organizing., 2000.
Chatterjee, S. R. Human Resource Management in India: Where From' and Where To?’, Research and Practice in Human Resource Management, 2007, 15(2), 92-103.
Minbaeva, Dana B., HRM practices and MNC knowledge transfer /journal Personnel Review, 2005, Vol. 34 No. 1, pp. 125-144
Edel Conway, John McMackin, Developing a Culture for Innovation: What is the Role of the HR System?, DCU Business School Research Paper Series, 1997 Paper No 32, ISSN 1393-290X.
Mane Kiran Harish Chndra, A study of job satisfaction of Employees of Maharashtra state Road Transport Corporation (MSRTC) -A Field Study / Journal-Research Analysis and Evaluation, 2010, Vol. 1, Issue. 10. Page No.21 -23
Siiniannarayana M. Measuring Training and Development/Journal - The Indian journal of industrial Relations, 2011, Vol.47, No. I Page No. 117-125.
Mir Mohammed Nurul Absar, Recruitment & Selection practices in Manufacturing linen in Bangaladesh, Journal- the Indian journal of Industrial Relations, 2012, Vol-47. No-3. Page No. 436-449.
Manonnini M., Wage - Productivity Linkages in Indian Industries / Journal- The Indian journal of Industrial Relations. 2012, Vol-47,No-3. Page No. 450-458.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26General SciencesForecasting of Monthly Mean Rainfall in Rayalaseema
English2027J. C. Ramesh ReddyEnglish T. GaneshEnglish M. VenkateswaranEnglish PRS ReddyEnglishSeasonal Autoregressive Integrated Moving Average (SARIMA) model in analyzing the forecast of monthly mean rainfall in Rayalaseema (India) using R is discussed. We have checked the different ARIMA models according to the structure of the data, finally we found that the ARIMA (5,0,1)(2,0,0)[12] has been fitted to the data and the significance test has been made by using lowest AIC and BIC values.
EnglishINTRODUCTION
Andhra Pradesh is one of the states of Indian, in which we have taken the rainfall data of Rayalaseema which statistical reports called the drought area in the state. In this blog, we have done the analysis like forecasting of annual rainfall in Rayalaseema for coming years. For the experiment, we have taken data of Mean Annual Rainfall from www.data.gov.in. The data is having the information of mean annual rainfall from year 1901 to 2016. In this experiment we have taken the help of R programming that is now one of most useful software in the field of data science and statistics. For the analysis, first column of the dataset is chosen to do analysis that is having annual mean rainfall information in mm unit.
METHODOLOGY
ARIMA models are capable of modeling a wide range of seasonal data. A seasonal ARIMA model is formed by including additional seasonal terms in the ARIMA models we have seen so far. It is written as follows: ARIMA (p, d, q) (P, D, Q)m: the first parenthesis represents the non-seasonal part of the model and second represents the seasonal part of the model, where m= number of periods per season. We use uppercase notation for the seasonal parts of the model, and lowercase notation for the non-seasonal parts of the model. The additional seasonal terms are simply multiplied with the non-seasonal terms.
ACF/PACF The seasonal part of an AR or MA model will be seen in the seasonal lags of the PACF and ACF. For example, an ARIMA(0,0,0)(0,0,1)12 model will show: a spike at lag 12 in the ACF but no other significant spikes. The PACF will show exponential decay in the seasonal lags; that is, at lags 12, 24, 36,….etc. Similarly, an ARIMA(0,0,0)(1,0,0)12 model will show: exponential decay in the seasonal lags of the ACF a single significant spike at lag 12 in the PACF. In considering the appropriate seasonal orders for an ARIMA model, restrict attention to the seasonal lags. The modeling procedure is almost the same as for non-seasonal data, except that we need to select seasonal AR and MA terms as well as the non-seasonal components of the model. Seasonal autoregressive integrated moving average (SARIMA) model for any variable involves mainly four steps: Identification, Estimation, Diagnostic checking and Forecasting. The basic form of SARIMA model is denoted by SARIMA (p,d,q ) X (P, D, Q )s and the model is given by
involves four steps (Box et al., 1994): (i) identification (ii) estimation (iii) diagnostic checking and (iv) forecasting. First, the original series must be transformed to become stationary around its mean and its variance. Second, the appropriate order of p and q must be specified using autocorrelation and partial autocorrelation functions. Third, the value of the parameters must be estimated using some non-linear optimization procedure that minimizes the sum of squares of the errors or some other appropriate loss function. Diagnostic checking of the model adequacy is required in the fourth step. This procedure is continued until an adequate model is obtained. Finally, the future forecasts generate using minimum mean square error method (Box et al. 1994). SARIMA models are used as benchmark models to compare the performance of the other models developed on the same data set. The iterative procedure of SARIMA model building was explained by Kumari et al. (2013), Boiroju (2012), Rao (2011) and Box et al. (1994).
ARIMA ()
By default, the arima() command in R sets c=μ=0 when d>0 and provides an estimate of μ when d=0. The parameter μ is called the "intercept" in the R output. It will be close to the sample mean of the time series, but usually not identical to it as the sample mean is not the maximum likelihood estimate when p+q>0. The arima() command has an argument include. mean which only has an effect when d=0 and is TRUE by default. Setting include. mean+FALSE will force μ=0. The Arima() command from the forecast package provides more flexibility on the inclusion of a constant. It has an argument include.mean which has identical functionality to the corresponding argument for arima(). It also has an argument include.drift which allows μ#0μ#0 when d=1. For the d>1, no constant is allowed as a quadratic or higher order trend is particularly dangerous when forecasting. The parameter μ is called the “drift” in the R output when d=1. This is also an argument include.constant which, if TRUE will see include.mean=TRUE if d=0 and include.drift=TRUE when d=1. If include.constant=FALSE. Both include.mean and include.drift will be set to FALSE. If include.constant is used, the values of include.mean=TRUE and include. drift=TRUE are ignored. AUTO.ARIMA () The auto.arima() function automates the inclusion of a constant. By default, for d=0 or d=1, a constant will be included if it improves the AIC value; for d>1, the constant is always omitted. If allow drift+FALSE is specified, then the constant is only allowed when d=0. There is another function arima() in R which also fits an ARIMA model. However, it does not allow for the constant cc unless d=0, and it does not return everything required for the forecast() function. Finally, it does not allow the estimated model to be applied to new data (which is useful for checking forecast accuracy). Consequently, it is recommended that you use Arima() instead. Modeling Procedure When fitting an ARIMA model to a set of time series data, the following procedure provides a useful general approach. 1. Plot the data. Identify any unusual observations. 2. If necessary, transform the data (using a Box-Cox transformation) to stabilize the variance. 3. If the data are non-stationary: take first differences of the data until the data are stationary. 4. Examine the ACF/PACF: Is an AR(pp) or MA(qq) model appropriate? 5. Try your chosen model(s), and use the AICc to search for a better model. 6. Check the residuals from your chosen model by plotting the ACF of the residuals, and doing a portmanteau test of the residuals. If they do not look like white noise, try a modified model. 7. Once the residuals look like white noise, calculate forecasts. AIC and BIC are both penalized-likelihood criteria. They are sometimes used for choosing best predictor subsets in regression and often used for comparing non-nested models, which ordinary statistical tests cannot do. The AIC or BIC for a model is usually written in the form [-2logL + kp], where L is the likelihood function, p is the number of parameters in the model, and k is 2 for AIC and log(n) for BIC. AIC is an estimate of a constant plus the relative distance between the unknown true likelihood function of the data and the fitted likelihood function of the model, so that a lower AIC means a model is considered to be closer to the truth. BIC is an estimate of a function of the posterior probability of a model being true, under a certain Bayesian setup, so that a lower BIC means that a model is considered to be more likely to be the true model. Both criteria are based on various assumptions and asymptotic approximations. Each, despite its heuristic usefulness, has therefore been criticized as having questionable validity for real world data. But despite
AUTO.ARIMA ()
The auto.arima() function automates the inclusion of a constant. By default, for d=0 or d=1, a constant will be included if it improves the AIC value; for d>1, the constant is always omitted. If allow drift=FALSE is specified, then the constant is only allowed when d=0. There is another function arima() in R which also fits an ARIMA model. However, it does not allow for the constant cc unless d=0, and it does not return everything required for the forecast() function. Finally, it does not allow the estimated model to be applied to new data (which is useful for checking forecast accuracy). Consequently, it is recommended that you use Arima() instead.
Modeling Procedure
When fitting an ARIMA model to a set of time series data, the following procedure provides a useful general approach.
1. Plot the data. Identify any unusual observations.
2. If necessary, transform the data (using a Box-Cox transformation) to stabilize the variance.
3. If the data are non-stationary: take first differences of the data until the data are stationary.
4. Examine the ACF/PACF: Is an AR(pp) or MA(qq) model appropriate
5. Try your chosen model(s), and use the AICc to search for a better model.
6. Check the residuals from your chosen model by plotting the ACF of the residuals, and doing a portmanteau test of the residuals. If they do not look like white noise, try a modified model.
7. Once the residuals look like white noise, calculate forecasts.
AIC and BIC are both penalized-likelihood criteria. They are sometimes used for choosing best predictor subsets in regression and often used for comparing non-nested models, which ordinary statistical tests cannot do. The AIC or BIC for a model is usually written in the form [-2logL + kp], where L is the likelihood function, p is the number of parameters in the model, and k is 2 for AIC and log(n) for BIC.
AIC is an estimate of a constant plus the relative distance between the unknown true likelihood function of the data and the fitted likelihood function of the model, so that a lower AIC means a model is considered to be closer to the truth. BIC is an estimate of a function of the posterior probability of a model being true, under a certain Bayesian setup, so that a lower BIC means that a model is considered to be more likely to be the true model. Both criteria are based on various assumptions and asymptotic approximations. Each, despite its heuristic usefulness, has therefore been criticized as having questionable validity for real world data. But despite various subtle theoretical differences, their only difference in practice is the size of the penalty; BIC penalizes model complexity more heavily. The only way they should disagree is when AIC chooses a larger model than BIC. AIC and BIC are both approximately correct according to a different goal and a different set of asymptotic assumptions. Both sets of assumptions have been criticized as unrealistic. Understanding the difference in their practical behavior is easiest if we consider the simple case of comparing two nested models. In such a case, several authors have pointed out that IC’s become equivalent to likelihood ratio tests with different alpha levels. Checking a chi-squared table, we see that AIC becomes like a significance test at alpha=.16, and BIC becomes like a significance test with alpha depending on sample size, e.g., .13 for n = 10, .032 for n = 100, .0086 for n = 1000, .0024 for n = 10000. Remember that power for any given alpha is increasing in n. Thus, AIC always has a chance of choosing too big a model, regardless of n. BIC has very little chance of choosing too big a model if n is sufficient, but it has a larger chance than AIC, for any given n, of choosing too small a model. So what’s the bottom line? In general, it might be best to use AIC and BIC together in model selection. For example, in selecting the number of latent classes in a model, if BIC points to a three-class model and AIC points to a five-class model, it makes sense to select from models with 3, 4 and 5 latent classes. AIC is better in situations when a false negative finding would be considered more misleading than a false positive, and BIC is better in situations where a false positive is as misleading as, or more misleading than, a false negative.
Forecasting of rainfall in Rayalaseema
The data has been taken to predict the rain fall of Rayalaseema area of Andhra Pradesh from the year 1951 to 2016. The data has monthly rainfall for each year. In this section, we have to check forecasting model to this data using one of statistical tool R software. In R software majorly we need packages for forecasting model. Using these packages is predicting the model for the Rayalaseema data. The packages are ‘ggplot2’, ‘forecast’ and ‘tseries’. Install the above mentioned packages using install.packages() function and call that packages using library function as below:
Library (‘ggplot2’) # calls the packages using Library (). Library (‘forecast’) Library (‘tseries’) The data has been converted into “.csv” file and then read the data into the R programming.
CAEnglishhttp://ijcrr.com/abstract.php?article_id=2403http://ijcrr.com/article_html.php?did=2403
Alfaro, E. (2004). A Method for Prediction of California Summer Air Surface Temperature, Eos, Vol. 85, No. 51, 21 December 2004.
Anisimov O.A., (2001). Predicting Patterns of Near-Surface Air Temperature Using Empirical Data, Climatic Change, Vol. 50, No. 3, 297-315.
Box, G. E. P., Jenkins, G. M. and Reinsel, G. C. (1994). Time Series Analysis Forecasting and Control, 3rd ed., Englewood Cliffs, N.J. Prentice Hall.
Brunetti, M., Buffoni, L., Maugeri, M. and Nanni, T., (2000). Trends of minimum and maximum daily temperatures in Italy from 1865 to 1996. Theor. Appl. Climatol., 66, 49–60.
FAN Ke, (2009). Predicting Winter Surface Air Temperature in Northeast China, Atmospheric and Oceanic Science Letters, Vol. 2, NO. 1, 14−17.
Hejase, H.A.N. and Assi, A.H. (2012). Time-Series Regression Model for Prediction of Mean Daily Global Solar Radiation in Al-Ain, UAE, ISRN Renewable Energy, Vol. 2012, Article ID 412471, 11 pages.
J. C. Ramesh Reddy, T. Ganesh, M. Venkateswaran and P. R. S. Reddy (2017), “Rainfall Forecast of Andhra Pradesh Using Artificial Neural Networks”, International Journal of Current Research and Modern Education, Volume 2, Issue 2, Page Number 223-234. DOI: http://doi.org/10.5281/zenodo.1050435.
J. C. Ramesh Reddy, T. Ganesh, M. Venkateswaran, PRS Reddy (2017), Forecasting of Monthly Mean Rainfall in Coastal Andhra, International Journal of Statistics and Applications 2017, 7(4): 197-204. DOI: 10.5923/j.statistics.20170704.01.
Lee, J.H., Sohn, K. (2007). Prediction of monthly mean surface air temperature in a region of China, Advances in Atmospheric Sciences, Vol. 24, 3, 503-508.
Stein, M. and Lloret, J. (2001). Forecasting of Air and Water Temperatures for Fishery Purposes with Selected Examples from Northwest Atlantic, J. Northw. Atl. Fish. Sci., Vol. 29, 23-30.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26HealthcareSpectrum of Clinical Presentation of Intracranial Tuberculoma
English2831Rohit Kumar GargEnglish Rattilal MeenaEnglish Neera SamarEnglish Mayank SharmaEnglish Sourav ShristiEnglish Ankur MittalEnglishObjectives: To describe the clinical presentation, radiological findings in 15 patients with intracranial tuberculoma.
Design: Consecutive cases admitted with tuberculoma to the MBGH Hospital, Udaipur, Rajasthan, were included in the study. The diagnosis was based on clinical and neuro-imaging features.
Results and Conclusions: The commonest presenting features were generalized convulsion(86.66%) and altered consciousness (80%). Computerised axial tomography/magnetic resonance imaging (CT/MRI) revealed single or multiple lesions that
showed intense contrast enhancement and perilesional edema. After receiving 6 months of ATT all patients were symptom free. We advocate early empirical trial of anti-tuberculosis drugs for intracranial tuberculoma even after a presumptive diagnosis.
EnglishAnti-tuberculosis drugs, Intracranial tuberculomaINTRODUCTION
Tuberculosis (TB), which is caused by bacteria the Mycobacterium tuberculosis complex, is one of the oldest disease known to affect humans and is a major cause of death worldwide. This disease most often affects the lungs, although other organs are involved in up to one-third of cases.1
Central nervous system (CNS) tuberculosis is a serious form of TB, due to haematogenous spread of Mycobacterium tuberculosis, manifest as meningitis, cerebritis and tuberculous abscesses or tuberculomas.2
Intracranial tuberculomas are the least common presentation of CNS TB, found in 1% of these patients.3They are multiple in 15%-33% of the cases.4
Tuberculomas often present with symptoms and signs of focal neurological deficit without evidence of systemic disease.5 Our study highlights the spectrum of clinical presentations of intracranial tuberculomas with the role of magnetic resonance imaging, a noninvasive tool, in prompt diagnosis and thereby early clinical management of such cases with a positive outcome.
Study design
A retrospective cross sectional study was done in 15 patients in whom neuroimaging shows ring enhancing lesion and was suspected as tuberculoma lesion.
Material and methods
This study was done retrospectively by analyzing patients presenting with tubercular infection of the CNS in the form of tuberculoma under the author in last one and half years (July 2015-dec. 2016) in medicine department.
Inclusion criteria
Only adult patients (more than 16 year of age) were included
All patients with ring enhancing lesions on neuroimaging who were suspected as tuberculoma analyzed in the view of their clinical presentation.
Exclusion criteria
HIV positive patients
Methods
A detailed clinical history was noted as described in the study Performa in all patients in which neuroimaging study was suggestive of tuberculoma lesion. A detailed past, family and personal history was taken in all patients. A thorough general and systemic examination was done.
Laboratory tests done included a complete blood count with erythrocyte sedimentation rate(ESR), electrolytes and routine biochemical tests. Specific laboratory tests for establishing etiology were performed like screening for HIV-1 and 2, blood cultures, sputum microscopy and culture. Cerebrospinal fluid analysis for protein, sugar, cell count and morphology, Cerebrospinal fluid ADA, IgM toxoplasma antibodies, cryptococcal antigen were done when indicated. Imaging studies done included computed tomography (CT) brain or magnetic resonance imaging (MRI) brain with contrast as was indicated. Ancilliary investigation like X-ray chest and USG abdomen was done whenever the clinical situation demanded.
Results
Fifteen indoor patients admitted to medical ward satisfying the inclusion criteria were selected for the study, all of them from rural area near Udaipur. Table 1 showing the age and sex wise distribution of the patients. The age group of patients were ranged from 16-75 years. Majority of patients were in the age group of 46-60years. Out of 15 patients in the study group,9 patients were male (60%) and 6 were female (40%). The overall sex ratio was 1.5:1. All patients were laborers by occupation and nonvegeterian.
Clinical features of are summarized in Table 2.Seizure was the most common presenting feature. 13 patients (86.66%) out of 15 were presented with one or more episodes of seizure. The type of seizure was generalized tonic and clonic in all of them. History of altered consciousness was also present in 12 patients (80%). 11 patients (73.33%) were having complaint of headache.8 patients (53.33%) out of 11 who were having headache also have associated vomiting. History of fever was present in 9 patients (60%).
Past History
There was no previous history of pulmonary or extrapulmonary TB in any patient and none of them was diabetic.
Examination
11 patients (73.33%) had pallor. There was no lymphadenopathy, icterus, pedal edema or clubbing.
On CNS examination 2 patients were having cranial nerve palsy but none of patient have papiloedema. Neck stiffness was present in 1 patient.
Investigations
Mean hemoglobin was 9.6 g/dl and ESR 68 mm at end of first hour. None of patient was HIV positive. chest x-ray was done in all the patients and there was no any patch except in one patient, in which it was showing milliary shadows in bilateral lung fields. Cerebrospinal fluid analysis for protein, sugar, cell count and morphology shows no abnormality in any of the patient. Cerebrospinal fluid ADA, IgM toxoplasmosis antibodies, cryptococcal antigen were negative.
MRI brain was done in all the patients which was showing tuberculoma lesion in all the patients at different locations.
DIAGNOSIS AND TREATMENT
Probable etiological diagnoses were based on the presence of supportive findings detected after clinical evaluation and above mentioned battery of investigations. The diagnosis remained probable be cause in none of the patients histopathological verification was obtained. Patients were provided appropriate symptomatic treatment (corticosteroids, mannitol, antiepileptic drugs and/or analgesics if required). Appropriate specific treatment according to the diagnosis was given. Some of above mentioned laboratory investigations were periodically repeated during hospitalization and on outdoor follow-up to monitor the disease activity on modifying the ongoing treatment.
DISCUSSION
The mean age of patients was 47.2 years with 53.33% of patients between 46-60 years of age. The mean age obtained in various studies is as shown in Table 3which is in accordance with our observation. Males predominated in all age groups. The sex wise incidence in various other studies is as shown in Table 3.
In our study Seizure was the most common presenting feature which was present in 13 patients (86.66%), loss of consciousness in 12 patients (80%),headache in 11 patients (73.33%),vomiting in 8 patients (53.33%) and fever was present in 9 patients (60%). Table 4 shows comparison of presenting clinical feature of previous studies and our study.
None of the patient was having history of tuberculosis. Chest X-ray shows milliary TB in only one patient. On neuroimaging, 60% shows multiple ring enhancing lesions. We use following criteria to differentiate tuberculoma from other causes of ring enhancing lesion in MRI10:-
ring enhancing lesion in neurocysticercosis usually shows multiple lesions in different stages of evolution.
ring enhancing lesions in abscesses are restrict on DWI.
ring enhancing lesions in neoplasm shows elevated choline peak on MRS.
The distribution of these lesions compared with other studies is shown in Table 5.
CONCLUSION
Brain tuberculoma is one of the neurological manifestation of tuberculosis, usually occur in immunocompromised individuals due to haematogenous spread from a primary focus, mainly from the lungs. In this study we studied 15 patients, all of them immunocompetent and none of them was having past history of tuberculosis. Only 1 out of 15 patients had chest x-ray suggestive of milliary tuberculosis.
We emphasize here that tuberculoma can be occur in immunocompetent patients without past history of TB and without any active lesion in lungs. In past various studies have been done on tuberculoma but only few of them was suggesting tuberculoma without any immunocompromised status and without any active lung lesion. So we should suspect brain tuberculosis in patients presenting with above mentioned clinical features despite good immune status, without any active lung lesion or negative tubercular history of patient.
Englishhttp://ijcrr.com/abstract.php?article_id=2404http://ijcrr.com/article_html.php?did=24041. Mario C. Raviglione chapter 202 page no.1102 Harrison 19th edition.
2. Rock RB, Olin M, Baker CA, Molitor TW, Peterson PK. Central nervous system tuberculosis: pathogenesis and clinical aspects. Clinical Microbiology Reviews2008;21(2):243e61.
3. Pimentel MLV, Alves SMV, Novis SAP, Brandão RZ, Neto EB. Intracranial tuberculomas developing during treatment of pulmonary tuberculosis: casereport. Arq Neuropsiquiatri 2000;58(2-B):572e7.
4. Hejazi N, Hassler W. Multiple intracranial tuberculomas with atypical responseto tuberculostatic chemotherapy: literature review and a case report. Infection1997;25(4):41e6.
5. Sahaiu-Srivastava S, Jones B. Brainstem tuberculoma in the immunocompetent: Case report and literature review. Clinical Neurology and Neurosurgery2008;110:302e4.
6. Enberg GM, Quezada B Mde L, de Toro VC, Fuenzalida LL. Tuberculous meningitis in adults: review of 53 cases. Rev Chilena Infectol 2006;23(2):134-9.
7. Cagatay AA, Ozsut H, Gulec L, Kucukoglu S, Berk H,Ince N, et al. Tuberculous meningitis in adults – experience from Turkey. Int J Clin Pract 2004;58(5):469-73.
8. Fan HW, Wang HY, Wang HL, Ma XJ, Liu ZY, Sheng RY.Tuberculous meningitis in Chinese adults: a report of 100cases. Zhonghua Nei KeZaZhi 2007;46(1):48-51.
9. Mahato PS, Dabhi AS, Thorat PB. Clinical and Investigative Profile of Ring-enhancing Lesions on Neuroimaging.
10. Osborn AG. Osborn's Brain: Imaging, Pathology and Anatomy. In: Tuberculosis Fungal, Parasitic and Other Infections, P.341.
11. Kumar N, Narayanaswamy AS, Singh KK. Ring enhancing CT lesions - a diagnostic dilemma. J Assoc Physicians India 1995;43(6):391-3.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26HealthcarePost Burn Ductal Carcinoma of Breast- A Rare Case Report
English3234Juhi KhannaEnglish Nandita P. MehtaEnglish Hansa M. GoswamiEnglishObjective: A 25 years old female presented to outpatient department of General Surgery of Civil Hospital with breast lump. The objective was to investigate and diagnose the case.
Material and Methods: The case was clinically examined in General surgery department. FNAC was done to diagnose swelling. The resected tissue was sent to histopathology for confirmation of the diagnosis. Histological analysis and Immunohistochemical staining was done in Pathology department.
Results: On FNAC-Infiltrating Ductal Carcinoma of breast. The patient was operated and tumor was resected. On gross examination, growth identified measures 4x3.5x2.5cm3, Cut surface
is whitish solid, well defined and firm to hard. On histological examination tumor was diagnosed to be Poorly Differentiated Ductal Carcinoma of Breast. Immuno-histo-chemical
staining revealed that the cells were positive for Estrogen receptor and Progesterone receptor. This case was to be Post burn Ductal Carcinoma of breast.
Conclusion: Malignancy arising from Burn scar is rare, Squamous cell Carcinoma is most common Burn scar neoplasia and adenocarcinoma is extremely rare. So such cases should be thoroughly examined and followed.
EnglishPost burn, Ductal CarcinomaINTRODUCTION:
Malignancy arising from burn scar is extremely rare. Squamous cell carcinoma is the most common, type, other types are basal cell carcinoma, malignant melanoma and rarely sacrcoma. Adenocarcinoma is extremely rare and only 4 cases have been reported till date and only one case of infiltrating Ductal carcinoma of breast has been reported. We report a care case of post burn carcinoma in a young woman.
Case Report:
A 25 years old female presented to outpatient department of General Surgery of Civil Hospital with breast lump. She had sustained thermal burns 14 years back, involving the right side of chest wall, arm and trunk. The burns where left to heal secondarily and no skin grafting was done. On examination, the burn scar was seen at right mammary area, axilla and arm. The right breast was deformed, nipple and areolar region was also unremarkable. Underneath the burn scar a large firm lump measuring4x3cm2 was seen in lower inner quadrant of right breast. The lump was adherent to chest wall but overlying skin was free. In the right axilla no lymph node where palpated. Left breast and axilla were unremarkable.
The patient was referred for fine needle aspiration (FNAC) from the lump which was performed as per standard technique. FNA from the lump yielded blood mixed aspirated which was processed as air-dried, hematoxylin and eosin stained smears where prepared.FNA smears show moderate cellularity with ductal cells arranged as irregular clusters and single cells(loss of cohesion). No myoepithelial cells seen. Ductal cells show moderated to severe nuclear atypia, enlargement, pleomorphism with evidence of occasional bizarre forms, irregular nuclear membrane and chromatin. The cytomorphology is of malignant breast lesion-Ductal carcinoma (DC)of breast-Robinsons cytological grade II.[Figure 1]
Patient underwent surgery and the specimen was received for histopathological examination.
Gross examination: Received specimen measured 22x15x2.5cm3.nipple areola was grossly not identified. One growth measuring 4x3.5x2.5cm3was identified. Cut section was whitish, solid, well defined and firm to hard in consistency. Growth is 3 cm away from superior margin,3 cm away from inferior argin,2 cm away from medial margin ,5 cm away from lateral margin,1.5 cm from base. Total 12 lymph nodes where resected size ranging from 0.3x0.2cm2 to 0.8x0.5cm2.
Microscopic examination: Sections showed histology of Poorly differentiated Ductal Carcinoma of Breast [Figure 2,3] with lymphovascular permeation by tumor cells. Stroma showed desmoplasia, lymphoplasmacytic infiltration, hemorrhage and necrosis. Surrounding breast showed fibrocystic changes. Section from all resected 12 lymph node does not show evidence of metastasis with histology of sinus histiocytosis. Section from resected surgical margin(superior, lateral, medial and inferior ) and base do not show evidence of tumor cells.
Conclusion: Poorly Differentiated infiltrating ductal carcinoma(IDC) of breast with tumor free resected surgical margins and base.
Modified BR grade III, TNM STAGING:T2NOMX,AJCC Stage grouping :stage IIA.[Figure 2 and 3].
Immunohistochemistry showed positivity for Estrogen receptor and progesterone receptor.
DISCUSSION:
Cancers arising in old burn scar is rare. 30years is the average latent period for development of malignancy. Most common cancer is Squamous cell carcinoma(71%),followed by basal cell carcinoma(6%),malignant melanoma(5%) and scarcomas(4%)[1]. Also rare case of malignant fibrous histocytoma, dermatofibrosarcoma protuberans, pleomorphic liposarcoma and verrucous carcinoma have been reported in post burn patient [1,2,3,4]. Adenocarcinoma in burn scar is extremely rare, total 5 cases have been reported and one case out of 5 was of IDC breast. This is the second case of IDC Breast developing in post burn.[5,6,7,8]
It has been seen that majority of burn scar carcinoma occur in burns that have not been grafted. It may also arise from chronic ulceration, but 50% patient had burn scar. The relatively avascular scar tissue with no lymphatic channels in scar may then act as immunological privileged site that allow the tumor to resist the body’s usual defenses[9,10].It is speculated that a carcinogenic toxin is produced from burned tissue and cicatrical tissue which prevents mechanism from checking the new tumor formation[11,12] .
As the breast is a modified sweat gland, DC post burn scar suggest that adnexal elements and adjacent subcutaneous tissue can also show malignant change.[7]
Promotion of rapid epithelisation and early grafting are the principles of treating initial burn.[9,10]
Conclusion:
Burn scar Malignancy is rare and Adenocarcinoma can occur in the burn scar although squamous cell carcinoma is most common. So patients need to be thoroughly examined and followed up. Skin grafting should be encouraged after burn as it might help in prevention of cancer.
Englishhttp://ijcrr.com/abstract.php?article_id=2405http://ijcrr.com/article_html.php?did=24051.Kowal-vern,criswell BK. Burn scar neoplasm: A literature and review and statistical analysis.
2.Tanaka A, HatokoM, Tada H, Kuwahara M, lioka H, Nitsuma K Dermatofibrosarcoma protuberans arising from a burn scar of axilla. Ann Plast Surg.2004:52:423-5
3.Nishimoto S ,Matsushita T, Matsumolo K, Adachi S . A rare case of burn scar malignancy. Burns 1996;22:497-9.
4. Hunag CY, Feng CH, HSIAO YC, Chuang SS, Yang JY. Burn Scar Carcinoma J Dermatology Treat 2010,21:350-6.
5.Losanoff JE, Konard A, Sauter ER. Breast Cancer after severe burn in injury co incidence or consequence? Breast J. 2008:14:87-9.
6.Balakrishnan C, Noorily MJ Prasad VK, Wilson RP. Metastatic adenocarcinoma in a recent in a recent burn scar. Burns 1994;20:371-2.
7.Vogelin E Feichler G, Luscher NJ .Breast cancer in previously burned skin:A Post Burn skin adenexal malignancy? Burns 1997;23:366-8.
8.Neha Singh, Seena Rao and Shyama Jain J.Cytol.2013 Apr-Jun;30(2):139-141.doi:10.4103/0970-9371.112660.
9.Futrell JW Myers GH Jr.The burn scar as an immunologically privlleged site .Surg forum 1972;23:129-131
10.Dellon AL, Potvin, Chretin PB, Rogentine CN. The immunobiology of skin cancer. Plast reconstruct surg.1975;55:341-354.
11.Kennawa EC Hieger J. Carcinogenic substances and their fluorescence BMJ 1930:I:1044-6.
12.Castillo JL, Goldsmith HS burn Scar malignancy in possible depressed immune setting. Surg forum 1968:19511.
13.Bostwich J. Pendergrast WJ, Vasconez LO. Marjolinsulcer: An immunologically privileged tumor? Plast Reconstruc surg. 1876:57:66-9
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26HealthcareAnalysis of Haemoglobin Variants and Oxygen Affinity in Indian and Kyrgyz Population Groups
English3539Supriya SainiEnglish Priya GaurEnglish Karan PalEnglish Alpesh K. SharmaEnglish Praveen VatsEnglish Akpay SarybaevEnglish Bhuvnesh KumarEnglish Shashi Bala SinghEnglishAim: The hemoglobin (Hb) variants can alter the structure and biochemical functions of Hb along with affecting physiological properties of the individual. In normal adult RBC, Hb variants that exist are HbA1, HbA2, HbS and HbF. Mutations in globin chains can change the Hb-O2 affinity which can alter the normal loading of oxygen in lungs and unloading in the tissues and also affect arterial oxygen saturation. Absence of abnormal Hbs rules out upto some extent presence of genetic or acquired facilitated oxygen affinity.
Methodology: The study was undertaken to compare haemoglobin variants using HPLC in Indians (n=10) and Kyrgyz population groups (n=10). We estimated oxygen affinity (P50) from PO2, SO2 and pH values using Lichtman equation and peripheral oxygen saturation (SpO2) using pulse oximetry at basal and upon acute HA exposure to 4111m in both the population groups.
Results: We obtained Hb fractions A1a, A1b, A1c and A2 within normal range and no HbF or HbS fractions were found in any volunteer from HPLC run. All the P50 values were well within normal range (22-28mmHg). No change in P50 was observed upon HA exposure in these two populations but Kyrgyz have been found to have a higher P50 compared to Indians at basal.
Discussion and Conclusion: Since our data rule-out the existence of abnormal Hb variant in either of the population, thus the significant decrease in SpO2 observed upon HA induction in both the groups is due to hypoxia at HA and higher P50 in Kyrgyz
compared to Indians is population specific.
EnglishHigh altitude, Haemoglobin variants, Kyrgyz, P50, SpO2Introduction
Haemoglobin (Hb) variants are structurally abnormal globin proteins and they are the mutant forms of Hb in a population and these defects are often inherited. Around 1000 Hb-variants exist and they are mostly missense or substitution mutations which may alter Hb-O2 affinity. In normal adult erythrocytes, Hb variants that exist are HbA1, HbA2, HbS (Sickle hemoglobin) and HbF (fetal haemoglobin). HbA1 (2α and 2β tetramer) is the major Hb which constitutes 95-98% of total haemoglobin. About 1.5-3.5% of all Hb molecules is constituted by HbA2 which contain 2α and 2δ tetramers. Fetal haemoglobin (HbF) constitutes ≤ 2.5% of total adult Hb (1). HbF has a slightly higher oxygen affinity then adult Hb. Greater than normal percentage of HbF in humans after 2 years of age may be due to occurrence of anemia (2). HbA0 is the non-glycated portion of HbA. HbA1a is glycated with fructose 1, 6 diphosphate and HbA1c is glycated with D-glucose at amino terminal of β-chain and is generally 6% of total Hb which may increase upto 12% in Diabetes mellitus. It’s a good indicator of long-term glycemic control. Hemoglobinopathies like thalassemia and sickle cell anaemia can be tested using High Performance Liquid Chromatography (HPLC), isoelectric focusing and spectroscopy and are the most commonly used routine tests to identify structurally abnormal haemoglobin variants (1, 3). HbA2 is increased in people with thalassemia. Absence of abnormal Hbs rules out upto some extent presence of genetic or acquired facilitated oxygen affinity (2, 4). Black Americans are at higher risk of sickle cell anaemia and Mediterranean ancestry individuals are at greater risk of β-thalassemia hemoglobinopathy (5). High altitude (HA) environment poses various stresses to individuals (6). Tibetan highlanders have higher oxygen affinity as part of their genetic adaptation which works as a beneficial factor to protect them from polycythemia and CMS vulnerability (2).
Understanding the Hb variants is useful in diagnosing hemoglobinopathies which can alter Hb function at high altitude and further affect HA adaptation in humans (5). The Hb variants can alter the structure and biochemical functions of Hb along with affecting physiological properties of the individual (7). Mutations that increase the Hb-O2 affinity basically activate erythropoeitic drive. Mutations that reduce Hb-O2 affinity leads to high deoxy-Hb levels (3), thus altering haemoglobin oxygen saturation. P50 is the oxygen partial pressure at which Hb is 50% saturated with oxygen (8). An abnormal Hb can alter P50 and arterial oxygen saturation. Occurrence of haemoglobin variants causes problems in oxygen delivery which may lead to altered P50 (2). This genetic effect may be population specific. We present here two different population groups, compared their Hb variants, P50 and peripheral oxygen saturation (SpO2) values to understand Hb-oxygen affinity, which may help in understanding HA adaptation.
Material and Methods
Blood collection and P50 estimation:
The study conformed to the ethical guidelines of the institute (Defence Institute of Physiology and Allied Sciences, Delhi) and is in accordance to 1964 Helsinki declaration and its later amendments or comparable ethical standards. After obtaining informed written consent, whole blood collected from 20 healthy male volunteers (10 Indian and 10 Kyrgyz) matched for age and height of age group 19 to 30 years. Blood was collected from an anticubital vein after approximately 12 hours of fasting at basal (Bishkek, Kyrgyzstan) and upon acute exposure to high altitude (Day3) at 4111 m. Measurements of pH, oxygen partial pressure (PO2), saturation of oxygen (SO2) were made from fresh blood using blood gas analyser (iSTAT systems, Abbott, USA). P50 calculation was done using following equation (9):
P50 =Log pO2 (7.4) = log pO2 (observed) - [0.5 (7.40-pH (observed)]
1/k = antilog (2.7 log pO2 (7.4) × [(100 - SO2 (observed) ÷SO2 (observed)]
Estimated P50 value = antilog [(log 1 / k) ÷ 2.7] (at pH=7.4, Temperature=37°C)
Peripheral oxygen saturation (SpO2) Measurement:
Saturation of peripheral oxygen was measured using finger pulse oximeter (Nonin Medical Inc. USA). It specifically measures percentage of oxygenated haemoglobin compared to total haemoglobin in blood giving an estimate of arterial oxygen saturation.
Hemolysate preparation:
Blood was centrifuged for 15min, at 3000 rpm, 4°C and supernatant was separated. Remaining packed cell volume of blood was washed three times with chilled isotonic potassium chloride (KCl) (1.15%), centrifuged (15 min, 3000 rpm, 4°C) and supernatant was removed each time to collect washed packed cells. 0.5 ml of these washed packed cells were lysed with 0.5 ml of saline (0.7% sodium chloride) and added 0.3 ml of carbon tetrachloride (HPLC grade). Centrifuged (3000 rpm, 30 min, 4ºC) and remove supernatant (hemolysate) and stored at -80°C until further analysis.
Quantification of Haemoglobin variant:
Sample preparation: Stored hemolysate was thawed and diluted in a ratio of 1:300 in a 1.5 ml sample vial with diluent solution provided with the HPLC system (D-10TM Dual Program HbA2/F/A1c diluent/calibrator set reference no. 220-0218)
Calibrator and Control: Calibrator and control were diluted as per manufacturer’s instructions. A1c and A2/F high and low controls run was performed to check the values followed by calibrator run. Two Calibrators (high and low) of HbA2/ F/ A1C were used. Calibration and control run was performed once in every 24 hours on the instrument.
HPLC Run: Prepared hemolysate samples were run on the HPLC system (Bio-Rad Variant II D-10) using D-10 Dual HbA2/F/A1C program and area % of HbA1a, HbA1b, HbA1c, HbA2 and P3 were assessed. Samples were also assessed for presence of HbF and HbS peak. Baseline characteristics and peak shape of HbA1c, HbA2 were analysed from chromatogram and recorded. Presence of any other variant or unknown peak was analysed from chromatogram.
Statistical Analysis: Graph pad Prism 6 was used for statistical analysis and graph construction. Student t-test was done for determining p-values. P-values less than 0.05 were considered significant. Values are mean±SEM.
Results:
Initially samples were screened for P3 peak values. Samples with P3 value less than 10 and total area between 10,0000 and 40,0000 were taken for further interpretation (Fig 1). The fractions HbA1a and HbA1b peak %area in Indian volunteers ranged from 1 to 1.5 and 0.7 to 1.1 respectively (Table 1). In case of Kyrgyz these peak %areas were in the range of 1.1 to 1.7 for HbA1a and 0.7 to 1 for HbA1b fraction (Table 2). These peak areas are within normal limit in all the volunteers of both the population groups. HbA0 is the non-glycated portion of the haemoglobin and occupies the maximum area on the chromatogram.
HbA1c values more than 6% of total area represents an Hb variant condition and is an indicator of poor diabetic control. In all 16 samples, none of the volunteer had such results. The data ranged from 4.7 to 5.1 representing no abnormality. Thalassemic hemoglobinopathies causes anemia and poses serious health problems in society (5). Thalassemia trait could alter the haemoglobin oxygen affinity which would change the high altitude response in man. In both the sample groups HbA2 values are normal and thus none of the volunteers possess the thalassemia trait. HbF and HbS are well known for causing hemoglobinopathies which alter the haemoglobin structure and function and can cause changes in affinity of oxygen to haemoglobin. None of the samples showed any HbF or HbS peak in the HPLC run. These results represent a normal haemoglobin fraction.
We also calculated the pressure at which 50% haemoglobin is saturated with oxygen (P50) from venous blood. A high P50 represents low oxygen affinity and vice-versa (10). The p50 values both at basal (24.4±1.5mmHg in Indians, 26.6±.15mmHg in Kyrgyz) and after induction to HA (24.5±0.64mmHg in Indians, 25.8±0.48mmHg in Kyrgyz) were well within permissible range. There was no change in P50 values upon HA exposure in any of the population group (Fig 2), but Kyrgyz had a higher mean P50 value at baseline compared to Indians. SpO2 reduced significantly in both the population groups upon HA exposure. In Indians, value decreased from 98.1±0.1% at basal to 88.1±0.94% at day 3. In Kyrgyz, value decreased from 98.1±0.18% at basal to 87.78±1.5% at day 3 (Fig 3).
Discussion
To the best of our knowledge, this is the first study which estimate and compare haemoglobin variants in Indians and Kyrgyz population groups. P50 was calculated using Litchman equation from PO2, SO2 and pH values of venous blood (9) .We observed no change in P50 values upon high altitude exposure in these two populations. Though the P50 values are well within normal range (22-28mmHg), but as compared to Indians, Kyrgyz had a higher mean P50 as compared to Indians representing a higher oxygen delivery. Additionally, our data rule-out the existence of abnormal Hb in either of the population group and the decrease in SpO2 observed upon HA induction is due to increase in altitude
Hb variants have been known to cause a reduction in oxygen supply to tissues (11). About 100 Hb variants are known in humans which can cause altered erythrocytosis (12). Impairment in β-globin protein production resulting in thalassemia is one of the most common hemoglobinopathy. (7). Another clinically important Hb variant is HbS (13). Mutations that alter α- or δ-globin are present at birth and mutations altering β-globin are expected few months after birth causing structurally abnormal haemoglobin (3). Thalassemia is characterised by abnormal Hb formation which can cause RBC destruction and also hinder oxygen transport (14). Hb variants can cause erythrocytosis and hemolysis in otherwise healthy individuals. Also they help in understanding RBC function. Mutations in hemoglobin fraction which leads to high Hb-O2 affinity increases hypoxic tolerance (15). Many Hb variants have modified oxygen binding site which may lead to altered Hb-O2 affinity. Mutations in globin chains can change the Hb-O2 affinity which can alter the normal loading of oxygen in lungs and unloading in the tissues (5). P3 fraction is for estimation of ‘degenerated hemoglobin’ and signifies the degraded haemoglobin in the sample (16). Normal acceptable cut off value of P3 fraction is Englishhttp://ijcrr.com/abstract.php?article_id=2406http://ijcrr.com/article_html.php?did=24061. Colah RB, Surve R, Sawant P, D'Souza E, Italia K, Phanasgaonkar S, et al. HPLC studies in hemoglobinopathies. Indian journal of pediatrics. 2007;74(7):657-62.
2. Tashi T, Feng T, Koul P, Amaru R, Hussey D, Lorenzo FR, et al. High altitude genetic adaptation in Tibetans: no role of increased hemoglobin-oxygen affinity. Blood cells, molecules and diseases. 2014;53(1-2):27-9.
3. Thom CS, Dickson CF, Gell DA, Weiss MJ. Hemoglobin variants: biochemical properties and clinical correlates. Cold Spring Harbor perspectives in medicine. 2013;3(3):a011858.
4. Huber FL, Latshang TD, Goede JS, Bloch KE. Does venous blood gas analysis provide accurate estimates of hemoglobin oxygen affinity? Annals of hematology. 2013;92(4):517-21.
5. Lorey FW, Arnopp J, Cunningham GC. Distribution of hemoglobinopathy variants by ethnicity in a multiethnic state. Genetic epidemiology. 1996;13(5):501-12.
6. Beall CM. Andean, Tibetan, and Ethiopian patterns of adaptation to high-altitude hypoxia. Integrative and comparative biology. 2006;46(1):18-24.
7. Forget BG, Bunn HF. Classification of the disorders of hemoglobin. Cold Spring Harbor perspectives in medicine. 2013;3(2):a011684.
8. Morgan TJ. The Significance of the P50. In: Vincent J-L, editor. Yearbook of Intensive Care and Emergency Medicine 1999. Yearbook of Intensive Care and Emergency Medicine. 1999: Springer Berlin Heidelberg; 1999. p. 433-47.
9. Lichtman MA, Murphy MS, Adamson JW. Detection of mutant hemoglobins with altered affinity for oxygen. A simplified technique. Annals of internal medicine. 1976;84(5):517-20.
10. Winslow RM, Monge CC, Statham NJ, Gibson CG, Charache S, Whittembury J, et al. Variability of oxygen affinity of blood: human subjects native to high altitude. J Appl Physiol Respir Environ Exerc Physiol. 1981;51(6):1411-6.
11. Percy MJ, Butt NN, Crotty GM, Drummond MW, Harrison C, Jones GL, et al. Identification of high oxygen affinity hemoglobin variants in the investigation of patients with erythrocytosis. Haematologica. 2009;94(9):1321-2.
12. Wajcman H, Galacteros F. Hemoglobins with high oxygen affinity leading to erythrocytosis. New variants and new concepts. Hemoglobin. 2005;29(2):91-106.
13. Cao A, Kan YW. The prevention of thalassemia. Cold Spring Harbor perspectives in medicine. 2013;3(2):a011775.
14. Weatherall DJ, Clegg JB. Inherited haemoglobin disorders: an increasing global health problem. Bulletin of the World Health Organization. 2001;79(8):704-12.
15. Soree P, Gupta RK, Singh K, Desiraju K, Agrawal A, Vats P, et al. Raised HIF1alpha during normoxia in high altitude pulmonary edema susceptible non-mountaineers. Scientific reports. 2016;6:26468.
16. Gupta M, Thalquotra M, Rao P. P3 Fraction: Effect on HbA1c Values by HPLC. Journal of clinical and diagnostic research : JCDR. 2016;10(9):BC12-BC4.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26HealthcareMediastinal Pancreatic Pseudocyst - A Rare Cause of Dysphagia (Case Report)
English4042Vipin MathurEnglish Rohit Kumar JainEnglishPseudocyst is a common complication of both acute & chronic pancreatitis due to any cause. It is a localised fluid collection, rich in pancreatic enzymes surrounded by a wall of non- epithelialized fibrous tissue. Mostly it presents in and around the pancreatic tissue but on rare occasions it may extend into mediastinum causing symptoms due to compression & invasion of adjacent structures. We report a rare presentation of a young patient with dysphagia due to pancreatic pseudocyst extending into posterior mediastinum and compressing esophagus.
Approximately 50 cases of mediastinal extension of the pancreatic pseudocyst in the world literature are reported. Successful drainage of a mediastinal pseudocyst using a transesophageal approach under endoscopic ultrasound guidance has been reported. The literature was reviewed for clinical presentation, complications, and available treatment options for mediastinal pancreatic pseudocysts.
EnglishMediastinal, Pancreatic pseudocyst, Dysphagia, Transesophageal drainageINTRODUCTION –
Pseudocysts are common complication of acute or chronic pancreatitis and pancreatic trauma. Most of them are located in and around pancreas but on rare occasions they can extend into mediastinum through anatomical openings in the diaphragm.
The mediastinal pseudocyst may present with symptoms like dysphagia, chest pain, dyspnoea, odynophagia, pseudoachalasia & cardiac tamponade.
CASE REPORT-
A 30 Years old male presented to us with complains of dysphagia of 3 months duration. Dysphagia was more to solids than liquids and nonprogressive. This young man had been consuming alcohol daily since last 8-10 years.
He was admitted 4-5 months earlier at a district hospital for severe pain abdomen, distention & vomiting. He was treated conservatively for 7-8 days and discharged in stable state. After 4-6 months of this episode he started feeling difficulty in swallowing.
His general physical examination, vitals signs and systemic examination did not reveal any significant abnormality. He was evaluated with basic lab investigations, gastroscopy and Contrast Enhanced-CT of abdomen.
Gastroscopy revealed a smooth bulge in lower esophagus with normal overlying mucosa. Contrast Enhanced-CT Abdomen revealed changes of chronic pancreatitis with multiple pseudocysts. A large cyst in the tail of the pancreas was found extending into thoracic cavity through esophageal hiatus, compressing the lower esophagus and adjacent left lung parenchyma.
The patient showed slight improvement in dysphagia during admission and was allowed semi solid food. Endoscopic ultrasound guided transesophageal drainage was planned but patient refused the procedure for time being. So he was advised to eat soft diet and review after 3 months, as spontaneous resolution is rare in these cases.
DISCUSSION-
Mediastinal pseudocyst was first described in 1951(1) and it remains a rare complication of pancreatitis. In general mediastinal pseudocyst occurs due to rupture of pancreatic duct posteriorly into retroperitoneal space & tracking of fluid through esophageal and aortic hiatus, hence posterior mediastinum is the most common location(2). Extension through foramen of Morgagni is less common while mid mediastinal extension have also been reported through direct erosion of diaphragm.
Mediastinal pancreatic pseudocyst can cause complications due to invasion or compression of mediastinal structure or rupture into surrounding structures(3). Rupture into pleural space can cause pancreatic pleural effusion. Pressure into cardiac chambers could lead to CHF or rarely cardiac tamponade.
Approximately 50 cases of mediastinal pancreatic pseudocyst have been reported in world literature till date(4). Spontaneous regression of mediastinal pseudocyst is rare. Treatment options depend on severity of symptoms, size of pseudocyst, the ductal anatomy and local expertise. Complete resolution of mediastinal pseudocyst with Octreotide infusion have been reported by Yasuda & colleagues(5). However it may take long time.
Before 2000, surgical drainage or percutaneous drainage was chosen option but these modalities had a recurrence rate of 20% & a complication rate of 15%. With advancement of endoscopic technique, endoscopic drainage has become the standard of care.
Endoscopic internal drainage options include ERCP (Endoscopic retrograde cholangiopancreatography) with transpapillary duct drainage combined with endoscopic stent placement or transmural drainage. All endoscopic procedures for the treatment of pancreatic pseudocysts have recurrence of less than 5% and complication rate of 10%(6)
Endoscopic retrograde cholangiopancreatography with transpapillar stent placement can be used only when the mediastinal pseudocyst communicates with the pancreatic duct. Endoscopic ultrasound is increasingly used to guide transesophageal internal drainage of mediastinal pancreatic pseudocyst. It helps to identify wall thickness, site to be punctured in a nonbulging cyst as well as help avoid major vessels.
CONCLUSION-
Mediastinal pancreatic pseudocyst should be suspected in a patient presenting with atypical chest pain, dyspnea, or dysphagia, in the setting of a clinical history of pancreatitis. The timely and accurate diagnosis is important for this unusual and potentially life-threatening presentation of a common complication of pancreatitis. The finding of a thin-walled low-attenuation cystic mass in the posterior or middle mediastinum in continuity with pancreas seen into radiological imaging and history suggestive of pancreatitis are required for diagnosis. With the limited experience so far transmural drainage using transesophageal or transgastric approach under endoscopic ultrasound guidance appears to be a technically feasible, minimally invasive, and safe procedure for drainage of such mediastinal pancreatic pseudocyst. Physicians should be aware of atypical presentations and treatment options available for such mediastinal extension of a pseudocyst in a patient with a history of acute or chronic pancreatitis.
Englishhttp://ijcrr.com/abstract.php?article_id=2407http://ijcrr.com/article_html.php?did=2407
Topa L, Laszlo F, Sahin P, PoszarJ ; Endoscopic transgastric drainage of a pancreatic pseudocyst with mediastinal and cervical extensions : Gastrointestendosc 2006, 64 : 460-63
Leung Mu, Grasser B, et al : Imaging of cystic masses of Mediastinum : Radiographics 2002
Komtong S, et al : Mediastinal pseudocyst with pericardial effusion and dysphagia treated by endoscopic drainage : IOP 2006-7 , 105-10
Rose EA ,Haider M, Yang SK. Medistinal extension of pancreatic pseudocyst. Am J. Gastroenterol, 2000 ; 95 : 3638-3639 [Pubmed]
Yasuda et al : A case of pancreatic pleural effusion and Mediastinal pancreatic pseudocyst. Eur I Gastroenterol Hepatol2002:14 , 1279-82.
BardiaA , Stokes N , Wilkinson NW : Mediastinal pancreatic pseudocyst with acute airway obstruction : J Gastroenterolsurg 2006 : 10, 146-50.
ACKNOWLEDGEMENT-
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
SOURCE OF FUNDING- NIL
CONFLICT OF INTEREST- None declared
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26HealthcareOvarian Neoplasms- Histopathological Patterns and Relative Frequencies in an Indian Tertiary Care Hospital
English4347Neeraja N. BarveEnglish Hansa M. GoswamiEnglish Urvi ParikhEnglishIntroduction: Ovarian neoplasms are tumors or cancer of the ovary. These neoplasms can be benign or malignant and are classified according to the tissue of origin, such as the surface epithelium, the stromal endocrine cells, and the totipotent germ cells.Ovarian neoplasms are one of the major causes of gynaecological problems in females and present with marked variation in their histological types. Western and Asian countries show a difference in relative frequency of these lesions. This study was conducted to find out frequency of various histological patterns of ovarian neoplasms received as surgical pathology specimens
at Histopathology department, Civil Hospital, Ahmedabad.
Material and Methods: The study was conducted on 186 cases of ovarian neoplasms, reported from July 2016 to June 2017.
Results: Mean age of the subjects was 35.6 years, ranging from 4 to 80 years. In a total of 186 cases of ovarian masses, 104(55.91%) were non-neoplastic and 82 (44.09%) were neoplastic. Among neoplastic lesions, 80.48% (66/82) were benign and 19.52% (16/82) were malignant. The commonest non-neoplastic lesion was Luteal cyst (43/104) followed by simple serous cyst
(25/104). The commonest benign tumor was serous cystadenoma (40/66) followed by dermoid cyst (12/66). The commonest malignant tumour was serous cystadenocarcinoma (5/16) followed by mucinous cystadenocarcinoma(3/16).
Conclusion: Non-Neoplastic lesions were more common than neoplastic lesions, while benign tumours outnumbered the malignant ones. The most common benign tumour was serous cystadenoma and malignant was serous cystadenocarcinoma. The most common non-neoplastic lesion was Luteal cyst. Among histological types of ovarian tumours, surface epithelial tumours dominated the other types.
EnglishLuteal cyst, Ovarian tumours, Cystadenocarcinoma, Serous cyst, Dermoid cystINTRODUCTION-The incidence of cancer is increasing in developing countries.[1,2] There are marked differences in distribution of different cancers in different regions of the world.[2,3] Ovarian cancer is the most frequent cause of death from gynaecological cancers and the fourth most frequent cause of death from cancer in women in Europe, United States[4] and Eastern India.[5] Exact incidence in India is not known, but ovarian cancer is the 4th most common cancer among females of India and continues to present at an advanced age.[6] The lifetime risk of ovarian cancer in women with no family history is 1.6%; with one affected first degree relative is 5%,[7] and 7% with two or more affected first degree relatives.[8] Ovarian neoplasms are insidious in onset and usually diagnosed at a late stage. They are rare in young age group.[9] They commonly present with abdominal pain, a lump or menstrual irregularities.[10] In addition to biopsy, various diagnostic modalities include transvaginal ultrasonography, MRI, positron emission tomography,[11] and markers like serum CA 125.[8] Diverse histopathologies are common in ovarian lesions. Relative frequency of different ovarian neoplasms is different for western world and Asian countries. For example surface epithelial tumors account for 50.0 – 55.0% of all ovarian tumors and their malignant counterpart for approximately 90.0% of all ovarian cancers in Western world whereas this figure is 46.0 – 50.0% and 70.0 – 75.0% respectively in Japan. Similarly mucinous tumors account for 12.0 – 15.0% of all ovarian tumors in Western world. This figure is 20.0 – 23.0% for Japan. Germ cell tumors account for 30.0% of primary ovarian tumors and malignant germ cell tumors account for 3.0% of all ovarian cancers in Western world.[12] Determination of these patterns is important for diagnosis, management and prognosis. This study was conducted to find out the histopathological patterns of ovarian neoplasmsreceived as surgical pathology specimens at Histopathology department, Civil Hospital, Ahmedabad.
MATERIALS AND METHODS: The study was carried out on 186 patients who had undergone surgical oophorectomy. Samples were analysed in the Pathology department of B.J.M.C.,Civil hospital, Ahmedabad. All Histopathological diagnosed cases of ovarian lesions referred to this department during July 2016 to June 2017were included in this study. These were mostly referred from gynaecology and obstetrics department of Civil Hospital, Ahmedabad, but a few were referred from other hospitals in the vicinity. Patients with abdominal-pelvic masses other than of ovarian tumours diagnosed on histopathology were excluded from the study. The histological characterisation of ovarian neoplasms was done according to the International Classification of Diseases, 9th ed. (ICD9) (WHO Classification, 1995).[13] The acquired data was analysed using the descriptive statistics.
RESULTS- During the study period from July 2016 to June 2017, one hundred and eighty six consecutive cases of ovarian lesions were selected. Ages of the patients and their histopathology diagnoses were recorded. Patients were divided into eight age groups, with a difference of 10 years in each group. The commonest age group affected was from 21 to 30 years followed by age group from 31 to 40 years. The youngest patient was 4 years old and the oldest was 80 years old. Mean age was 35.6 years (Table 1).
In a total of 186 ovarian lesions, 104 (55.91%) were non-neoplastic and 82 (44.09%) were neoplastic. The neoplastic lesions comprised 66/82 (80.48%) benign and 16/82 (19.52%) malignant tumours (Fig. 1). In non-neoplastic lesions, Luteal cyst was the predominant category (43/104) followed by simple serous cyst (25/104) (Table 2).
The neoplastic tumours were divided in four groups, namely, epithelial tumours, germ cell tumours, sex cord stromal tumours and metastatic tumours. Epithelial tumours were maximum in number(62/ 82; 75.60%), followed by Germ cell tumours (14/82; 17.07%) (Table 3). Frequency pattern of different classes and subtypes of benign and malignant ovarian neoplasms (n = 82) is show in table 4.
The commonest histological class is surface epithelial tumours (62/82; 75.60%) followed by germ cell tumours (14/82; 17.07%). Among all the benign lesions (n = 82), serous cyst adenoma is the commonest (40/82), while dermoid cyst is at the second number (14/82).
Frequency pattern of different classes and subtypes of benign and malignant ovarian neoplasms (n = 82) is shown in table 4.
The commonest histological class is surface epithelial tumours (62/82; 75.60%) followed by germ cell tumours (14/82; 17.07%). Among all the benign lesions (n = 82), serous cyst adenoma is the commonest (40/82), while dermoid cyst is at the second number (14/82).
On the other hand, among all the malignant lesions (n = 16), serous cyst adenocarcinoma is at the top (05/45), followed with a little difference by mucinous cyst adenocarcinoma (03/45) and endometroid carcinoma (01/45) respectively.
DISCUSSION- Age range of our subjects was from 4 to 80 years and mean age was 35.6 years. Mean age observed in our study is lower than that observed in few other studies carried out in india. Our study shows the maximum incidence of ovarian masses between 21 and 40 years of age. This differs from the western data where it is between 50 and 70 years[16] but correlates with other studies conducted in India.
In our study non-neoplastic lesions were 55.91% (104/186) and neoplastic lesions were 44.09% (82/186).
Neoplastic lesions contained (66/82) benign and (16/82) malignant lesions.
Study by Tanwani[19] documented 31.4% non-neoplastic lesions, 46.4% benign tumours and 22.2% malignant tumours. Among non-neoplastic lesion, Luteal cyst was most common (43/104) followed by simple serous cysts (25/104) in our study. The pattern of distribution of non-neoplastic lesions is quite variable in other studies.Among the 82 neoplastic lesions in our study,80.48%were benign and 19.82% were malignant. The higher incidence of benign tumours is also documented in various other studies,[19,21,22] where it is 85%, 78%, 89.7% and 72.73% respectively and ratio of benign to malignant tumours is lower in these studies as compared to our study. No borderline tumor was found in our study. Among the major histological classes, the commonest type of ovarian neoplasm seen in our study was surface epithelial tumours, whether benign or malignant (62/82; 75.60%). Our finding is closer to the observations made in several other studies i.e. 64%, 66% and 70%[7,24,25] respectively.
However, Guppey et al[26] documented a higher incidence of epithelial tumours than in our study i.e. 90%. Germ cell tumours (GCT) in our study were 17.07%. This value is quite high as compared to Western data (370) [4] and data collected from other parts of india (1470)[16] and (27.13%).[7] This difference may be due to variations in sample size but genetic, socioeconomical and environmental factors may also be involved. The frequency of sex – cord – stromal tumours (SCST) in our study was 4.87%. This value is comparable with that of studies carried out in the west (5%)[27]and other parts of india (370).[16] Our study showed that serous tumours (whether benign or malignant) were more common than mucinous tumours (40/67 vs 16/67 cases). This finding correlates with other studies.[28,29]
The studies carried out by Khanum and Rehman[22] and Aziz et al[17] also observed serous cyst-adenomas to be the commonest tumours. The frequency of malignant tumours in our study was highest for serous cyst adenocarcinoma (5/16) followed by mucinous cyst adenocarcinoma (03/ 16). Similar pattern of distribution of malignant tumors are shown by many other studies.[7,20] However, Study conducted by Yasmeen et al shows endometrioid carcinoma to be more prevalent[21]. Germ cell tumours (GCTs) comprise the second largest group in our study in which benign tumours dominated the malignant ones (12/14 vs. 02/14). Among the benign GCTs our study showed the highest incidence of mature teratomas followed by dermoid cysts (08/14and 04/14 respectively).
A study of Thanikasalanm et al[30] conducted in India shows teratomas to be the predominant GCT,whereas study conducted by Ahmad et al[7]in Pakistan documents dermoid cysts to be the commonest GCT. Sex cord stromal tumours (SCSTs) were the least common in our study, next to metastatic tumours (4/82; 4.87%). The incidence of these tumours is variable in other studies.
Zohra[18] found only 1% SCSTs while Tanwani[19] documents 10.1% cases of SCST. Granulosa cell tumours were the commonest SCSTs in our study (2/4) while studies carried out by Yasmeen et al[21] and Ahmad et al[31] mentioned a variable incidence of 28.5% and 5.62% respectively. In conclusion according to this study ovarian tumours are common in age group of 21 to 40 years. Neoplastic lesions are more common than non-neoplastic lesions. Luteal cyst is the commonest nonneoplastic lesion. Among the histological classes of neoplastic lesions, surface epithelial tumours are predominant type, followed by germ cell tumors. The commonest benign tumour is serous cystadenoma and commonest malignant tumour is serous cystadenocarcinoma. This study is institutional – based, therefore the results obtained may or may not reflect the actual histological pattern of ovarian tumours in indian women. Therefore, multicentric study with larger sample size should be carried out.
CONCLUSION- Non-Neoplastic lesions were more common than neoplastic lesions, while benign tumours outnumbered the malignant ones. The most common benign tumour was serous cystadenoma and malignant was serous cystadenocarcinoma. The most common non-neoplastic lesion was Luteal cyst. Among histological types of ovarian tumours, surface epithelial tumours dominated the other types.
ACKNOWLEDGEMENTS
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed
Englishhttp://ijcrr.com/abstract.php?article_id=2408http://ijcrr.com/article_html.php?did=24081. Parkin DM, Muir CS, Whelan SL et al. eds. Cancer incidence in five countries. Lyon: IARC, 1997; 8: 1028-9.
2. Pisani P. Burden of cancer in developing countries. IARC Scientific Pub 1994; 129: 31-9.
3. Parkin DM, Pisani P, Farlay J. Estimates of worldwide incidence of 18 major cancers in 1985. Int J Cancer 1993; 54: 594-6.
4. Jacob IJ, Menon U. Progress and challenges in screening for early detection of ovarian cancer. Mol Cell Proteomics, 2004; 3: 355-66.
5. Sen U, Sankaranarayanan R, Mandal S, Romana AV, Parkin DM, Siddique M. Cancer pattern in eastern India: the first report of Kolkata cancer registry. Int J Cancer 2002; 100: 86-91.
6. Parveen S, Ilyas N, Asghar S. Patterns of care for ovarian cancer: patients at institute of Nuclear Medicine and Oncology (INMOL) india.
7. Ahmad Z, Kayani N, Hasan SH, Muzaffar S, Gill MS. Histopathological pattern of ovarian neoplasm. J Pak Med Assoc, 2000; 50: 416-9.
8. Kauff ND, Satagogan JM, Robson ME, Offit K. Risk reducing salpingo-oophorectomy in women with a BRCA1 or BRCA 2 mutation. N Engl J Med, 2002; 346: 1609-15.
9. Saadia Tariq, Rubina Sohail. Study of ovarian tumors in young girls. Professional Med J. 2011; 18 (1): 41-5.
10. Shahin R, Ghulam S, Abid A. A clinic – pathological study of ovarian cancer. Mother and Child 1998; 36: 117-25.
11. Rieber A, Nussle K. Preoperative diagnosis of ovarian tumors with MR imaging, comparison with transvaginal sonography, positron emission tomography and histological findings. AJR Am J Roentgenol 2001; 177: 123-9.
12. Tavassoli FA, Devilee P. WHO. Classification of Tumors. Pathology and Genetics. Tumors of breast and Female Genital Organs. IARC Press: Lyon 2003.
13. WHO Histologic Classification of Ovarian Tumors, Geneva, WHO, 1995.
14. Shahbaz Sarwar CM, Neelam Siddiqui, Rizwan Anwar Khokhar, Farhana Badar. Epithelial ovarian cancer at a cancer hospital in a developing country. Asian Pacific J Cancer Prevention, 2006; 7: 595-598.
15. Aria M, Utsunomiya, Miki Y. Familial breast and ovarian cancers. Int J Clin Oncol, 2004; 9: 270-82.
16. Mariam Malik, Farooq Aziz. Malignant ovarian tumors: a study of 75 patients. Pak J Obstetric Gynaecology May 1999; 12 (1,2): 83-6.
17. Aziz F., Mariam Malik, Nosheen Yousaf. The pattern of ovarian malignancies – a retrospective study over a period of three years. A retrospective study over a period of three years. Ann King Edward Coll Oct – Dec 1999; 5 (3,4): 276-8.
18. Zahra F. The pattern of ovarian masses. Ann King Edward med Coll Oct – Dec 2006; 12 (4): 480-2. 19. Tanwani A.K. Prevalence and pattern of ovarian lesions. Ann Pak Inst Med Sci Oct – Dec 2005; 1 (4): 211-4.
21. Yasmin S, Aiman yasmin, Mohammad Asif. Frequency of benign and malignant ovarian tumors in a tertiary care hospital. J postgrad Med Inst Oct – Dec 2006;20 (4): 393-7.
22. Khanum Z, Amanur Rehman. The prevalence and age distribution of ovarian cysts. Ann King Edward Med Coll Oct – Dec 2005; 11 (4): 392-3.
23. Naseem Junejo, Sheikh F, Mumtaz F. Clinical presentation and treatment outcome of ovarian tumors at gynaecology ward. J Liaquat Uni Med Health Sci. Jan – Apr 2010; 9 (1): 30-2.
24. Gatphol ED, Darnal HK. Pattern of ovarian neoplasm in Manipur. J Indian Med Assoc, 1990; 88: 338-9.
25. Tyagi SP, Maheswari V, Tyagi N, et al. Solid tumors of the ovary. J Indian.med assoc, 1993; 91: 227-30.
26. Guppy AE, Nathan PD, Rust n GJ. Epithelial Ovarian Cancer: A review of current management. Clin oncology (R coll Radiology), 2005; 17: 399-411.
27. Morrison J. Advances in the understanding and treatment of ovarian cancer. J Br Menopause Soc, 2005; 11: 66-71.
28. Yasmin S, Yasmin A, Asif M. Clinicopathological pattern of ovarian tumours in Punjab region. J Ayub Med Coll Abbottabaad 2008; 20 (4): 11-13.
29. Prabarker, Maingi K. ovarian tumors – prevalence in Punjab. Indian J Pathology Microbiology 1989; 32: 276-81.
30. Thanikasalam K, Ho CM, Adeed N, Shahida MN, Azizah WK. Links Pattern of ovarian tumors among Malaysian women at General Hospital, Kuala Lumpur. Med J Malaysia 1992; 47: 139-46.
31. Ahmad M, Malik TM, Afzal S, Mubarik A. Clinicopathological study of 762 ovarian neoplasms at Army Medical College india. ind J Pathology 2004; 15 (4): 147-52.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26HealthcareStudy of Breast Lesions with Special Reference to Rare Malignant Epithelial Tumors in a Tertiary Care Hospital with Brief Review of Litreature
English4854Sheema SheikhEnglish Rohi WaniEnglish Isma NiyazEnglish Farzana ManzoorEnglish Lateef Ahmed WaniEnglish Arshi BegEnglishBackground and Aim: Lesions of the breast vary from completely benign Fibroadenomas to Invasive Carcinomas No Special Type (NST) and rare malignant lesions. Breast cancer is ranked as number one cancer among females in India. A study was carried out to know about histopathological spectrum of breast lesions with particular emphasis on rare malignant breast tumors.
Methods: A total of 568 surgical specimens of breast tissue, subjected to histopathological examinations in our tertiary care hospital over a period of 2½ years were taken up for study and their clinical and microscopic details were noted. All the cases were tabulated as benign and malignant categories. Cases were stratified according to latest, 2012 WHO classification of tumors of breast. Among the tumors, 357(75.31%) were benign and 117(24.68%) were malignant. Out of the 357 benign tumors, 289 were fibroadenomas and 11 were benign phyllodes tumor. Among the various malignant tumors, Invasive carcinoma of no special
type (NST) was the commonest malignancy (79.48%). Almost all rare types of malignancies were encountered like, Carcinoma with neuroendocrine differentiation, Medullary carcinoma, Invasive lobular Carcinoma (ILC), Tubular carcinoma and Metaplastic Carcinoma with no special type. The incidence of these rare breast cancers in our study is almost same as many other studies. Future extensive studies and for longer time period are needed to confirm the exact incidence of these tumors since these tumors have different prognostic and therapeutic considerations when compared with the common breast epithelial malignancies.
EnglishBreast cancers, Invasive carcinomas no special typeIntroduction
Breast cancer is the most common female cancer in the world with an estimated 1.67 million cancer cases diagnosed in 2010¹. In India, also Breast cancer is ranked number one cancer among females² with age adjusted rate as high as 25.8 per 100,000 women with the mortality of 12.7 per 100,000 women³,4. The histopathological type is mainly Invasive carcinoma of no special type (NST) which is 70-80%, followed by Invasive lobular carcinoma (5-15%) 5. However, there are rare breast tumors (75% of tumor, absence of glandular structures, diffuse moderate to marked lymphoplasmacytic infiltrate, moderate to marked pleomorphism and complete histological circumscription. A tumor may be classified as atypical when upto 25% of it is composed of Invasive carcinoma and the rest is classical Medullary carcinoma. The 4th edition of WHO classification of Tumors of the breast recommend that Classic (Medullary carcinoma), Atypical (Medullary carcinoma) and Invasive carcinoma NST with Medullary features be grouped with the category of Carcinoma with Medullary features11. Medullary carcinomas occur at high frequency in patients with BRCA-1 gene mutation. These typically lack ER and PR expression as well as HER-2 amplification (triple negative) and are usually highly proliferative and apoptotic tumors12,13.
The prognosis of patients with small node-negative medullary carcinoma is particularily favourable with a disease free survival of 90% or better10,14. Several studies have confirmed the favourable prognosis of Medullary carcinoma7,10,15. Medullary carcinoma has been reported to have better prognosis than Invasive carcinoma NST9,10, but this has been questioned by some studies16,17. Differences in diagnostic criteria may account for disparity10,15,16. Strictly defined diagnostic criteria may account for disparity10,15,16. Strictly defined morphological criteria are necessary to preserve the entity of Medullary carcinoma characterised by relatively favourable prognosis which is not shared by Atypical Medullary carcinoma18,19.
Carcinoma with Neuroendocrine features: Five cases of Carcinoma with Neuroendocrine features were encountered in our study. The first case was a 55 years old female with lump in right breast for which mastectomy with axillary lymph node dissection was done. Grossly we received 19x17x5 cm specimen of right breast which on cut section showed a friable growth measuring 5.5x5 cm. All the eleven lymph nodes were free from tumor. The second case was a 35 year old female with lump on left breast reported as Atypical fibroadenoma on FNAC for which excision (lumpectomy) was done. Grossly it was a globular fibrofatty tissue measuring 4.5x3x2.5 cm which on cut section showed a necrotic 3.5x3 cm grey white growth. The third case was a review case submitted as wax blocks for review in our department, she was a 40 year old female with lump in right breast. The 4th case was a 40 years old female with lump in right upper quadrant for which wide local excision and axillary lymphnode dissection was done. Grossly we received a skin lined soft tissue with cut section showing 2.5x2.2x2 cm growth with haemorrhage. All the 37 lymhnodes dissected out were free from tumor. The fifth case was 32 years old female with left breast lump for which lumpectomy was done. Cut section showed a friable growth.
Breast carcinoma with neuroendocrine differentiation (NE-BC) are relatively uncommon representing 1-2% of all breast cancers. The diagnosis requires at least one Neuro-endocrine marker (Chromogranin A or Synaptophysin) positivity in at least 50% of tumor cells. Those tumors with positivity of Englishhttp://ijcrr.com/abstract.php?article_id=2409http://ijcrr.com/article_html.php?did=24091.Ferlay J, Soerjomataram I, Dikshit R, Eser S, Athers S et al: cancer incidence and mortality worldwide: sources, methods and major patterns in GOBOCAN 2012. Int J Cancer; 136, E359-E386 (2015).
2. Ghoncheh M, Momenimovahed Z, Salehiniya H. Epidemiology, incidence and mortality of breast cancer in Asia. Asian Pac J cancer Prev. 2016; 17: 47-52.
3. Malvia S, Bagdadi SA, Dubey US, Saxena S. Epidemiology of breast cancer in Indian women. Asia-Pac J Clin Oncol 2017;13: 289-295.
4. Gupta A, Shirdar k, Dhillow PK. A review of breast cancer awareness among women in India: Cancer literate or awareness deficit ? Enr J Cancer 2015; 51: 2058-66.
5. Yerushalmi R, Hayes MM, Gelmon KA. Breast carcinoma- rare types: review of literature. Ann Oncol 2009; 20: 1763-70.
6. Reimer T. Management of rare histological types of breast tumors. Breast care (Basel) 2008; 3: 190-6.
7. Ellis IO, Galea M, Broughton N et al. Pathological prognostic factors in breast cancer. Histological type: relationship with survival in a large study with long term follow up. Histopathology 1992; 20: 479-489.
8. Li CI, Uribe DJ, Darling JR. Clinical characteristics of different histological types of breast cancer. Br J Cancer 2005; 93:1046-1052.
9. Pederson L, Zedler K, Holk S, Schiodt T, Mouridsen HT (1995). Medullary carcinoma of breast, Prevalence and prognostic importance of clinical risk factors in breast cancers. Eur J Cancer 31A; 2289-2295.
10. Wargotz ES, Silverbery SG (1998). Medullary carcinoma of the breast. A clinicopathologic study with appraisal of current diagnostic criteria. Hum Pathol 1998; 19:1340-1346.
11. Jacquemier J, Reis-Filho JS, Lakhani SR, et al. Carcinoma with medullary features. In: Lakhani SR, Ellis Io, Schnitt SJ, et al; eds. WHO classification of Tumors, Vol 4, 4th edn. Lyson: World Health Organisation. IARC 2012.
12. Rakha EA, Aleskandarany M, El-Sayed ME, et al.2009. The prognostic significance of inflammation and medullary histological type in invasive carcinoma of breast. Eur J Cancer 2009;45:1780-1787.
13. Marginaean F, Rakha EA, Ho BC et al. 2010. Histological features of medullary carcinoma and prognosis in triple negative basal cell carcinomas of the breast. Mod Pathol 2010; 23:1357-1363.
14. Gamel JW, Meyer JS, Fever E, et al. The impact of stage and histology, the long term clinical course of 163,808 patients with breast carcinoma. Cancer, 1996; 77: 1459-1464.
15. Ridofi RL, Rosen PP, Port A, et al. Medullary carcinoma of the breast: a clinicopathologic study with 10 year follow up. Cancer 1977; 40: 1365-1385.
16. Fisher ER, Kenny JP, Cass R, et al. Medullary cancer of breast revisited. Breast Cancer Res Tract 1990;16:215-219.
17. Black CL, Morris DM, Goldman LI, McDonald JC. The significance of lymphnode involvement in patients with medullary carcinoma of breast. Surg Gynaecol Obstret 1983;157:497-499.
18. Rapin V, Contesso G, Mouriesse H, Bertin F, LaCombe MJ, Piekarski JD, Travalgi JP, Gadenne C, Friedmann S. Medullary breast carcinoma. A reevaluation of 95 cases of breast cancer with inflammatory stroma. Cancer 1998; 61: 2501-2510.
19. Rubens JR, Lewandrowski KB, Kopans DB, Koerner FC, Hall DA, McCarthy KA. Medullary carcinoma of breast. Overdiagnosis of a prognostically favourable neoplasm. Arch surg 1990;125: 601-604.
20. Tang F, Wei B, Tian Z et al. Invasve mammary carcinoma with neuroendocrine differentiation: histological features and diagnostic challenges. Histopathology 2011;59:106-115.
21. Righi L, Sapino A, Marchio C, et al. Neuroendocrine differentiation in breast cancers: established facts and unsolved problems. Semin Diagn Pathol 2010; 27: 69-76.
22. Zhang JY, Chen WJ. Bilateral primary breast neuroendocrine carcinoma in a young woman: report of a case. Surg Today. 2011; 41:1575-1578.
23. Kawasaki T, Mochizuhi K, Yamauchi H, et al. Neuroendocrine cells associated with neuroendocrine carcinoma of breast, nature and significance. J Clin Pathol 2012; 65: 699-703.
24. Sapino A, Papotti M, Righi L, et al. Clinical significance of neuroendocrine carcinoma of the breast. Ann Oncol 2012;12(Suppl-2): S115-117.
25. Wei B, Ding T, xing Y, et al. Invasive neuroendocrine tumors of breast: a distinctive subtype of aggressive mammary carcinoma. Cancer 2010;116:4463-4473.
26. Louwman MW, Virezen M, Van Beck MW, et al. Uncommon breast tumors in perspective: Incidence, treatment and survival in Netherlands. Int J cancer 2007;121: 127-35.
27. Scopsi L, Andreola S, Pilotti S, et al. Mucinous carcinoma of breast. A clinicopathological, histochemical and immunocytochemical study with special reference to neuroendocrine differentiation. Am J Surg Pathol 18, 702-711.
28. Rosen PP, Wang TY. Colloid carcinoma of breast. Analysis of 64 patients with long term follow up. Am J Pathol 1980;70:304.
29. Cao AY, He M, Liu ZB, et al. Outcome of pure mucinous carcinoma compared to infiltrating ductal carcinoma: a population based study from China: Ann Surg Oncol 2012; 19: 3019-3027.
30. Tokkanen and Kajuri H. Pure and mixed mucinous carcinoma of breast: a clinicopathological analysis of 61 cases along with long-term follow up. Hum Pathol 1989;20:758-764.
31. Li CI. Risk of mortality by histologic type of breast cancer in United states. Horm Cancer 2010; 758-764.
32. Komaki K, Sakamoto G, Sugano H, Morimoto T, Mondey Y. Mucinous carcinoma of the breast in Japan. A prognostic analysis based on morphologic features. Cancer 1988; 989-996.
33. Clinicopathological characteristics of Mucinous breast cancer: A retrospective analysis of a 10 year study. Lei L, Yu X, Chen B, Chen Z, Wang X (2016), PLOS ONE 11(5): e155132.
34. Khan HN, Wyld L, Dunne B et al. Spindle cell carcinoma of the breast: a case series of a rare histological type. Eur J Surg Oncol 2003; 29: 600-603.
35. Brogi E. Carcinoma with metaplasia and low grade adenocarcinoma. In: Hoda SA, Brogi E, Koener FC, Rosen PP, editors. Rosen’s Breast Pathology. 4th edn. LIPPINCOTT WILLIAMS and WILKINS, Wolter Kluwer; c-2014. p547-594.
36. Carter MR, Hornick JL, Lester S et al.2006. Spindle cell (sarcomatiod) carcinoma of breast: a clinicopathologic and immunohistochemical analysis of 29 cases. Am J Surg Pathol 30:300-309.
37. Okada N, Hasebe T, Iwasaki M, et al. 2010. Metaplastic carcinoma of the breast . Hum Pathol 2001;41:960-970.
38. Rosen PP. The pathological classification of human mammary carcinoma, Past, Present and Future. Ann Clin Lab Sci 1979; 9:144-156.
39. NHS Breast screening programme 2005. Pathology reporting of breast disease; 3rd edn. NHS Breast screening programme publication no 58. NHS cancer screening programme. Royal college of Pathologists, Sheffield, UK.
40. Diab SG, Clark GN, Osborne CK, Libby A, Allred DC, Ellede RM. Tumor characteristics and clinical outcome of tubular and mucinous breast carcinoma. J Clin Oncol 1999;17:1442-1448.
41. Peters GN, Wolff M, Hagensen CD (1981). Tubular carcinoma of the breast. Clinical pathological correlations based on 100 cases. Ann Surg 1981;193:138-149.
42. Rakh EA, Lee AH, Evan AJ et al. Tubular carcinoma of the breast, further evidence to support its excellent prognosis. J Clin Oncol 2010,28: 99-104
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241924EnglishN2017December26General SciencesSoret and Dufour Effects on MHD Casson Fluid Over a Vertical Plate in Presence of Chemical Reaction and Radiation
English5561N. Ananda ReddyEnglish K. JanardhanEnglishThe combined effects of chemical reaction, radiation, Dufour and Soret effects on Casson MHD fluid flow over a vertical plate with heat source/sink has been studied with constant velocity, variable temperature and concentration. The governing equations of the flow have been solved by using the finite difference method. The effects of various parameters on velocity, temperature and concentration fields are studied with the help of graphs. It is found that velocity decreased with the increase of Casson parameter, Hartmann number, thermal conductivity, Schmidt number, Chemical parameter and decrease of Soret effect, Thermal
Grashof number and Mass Grashof number. Concentration found to be decreasing with the decrease of Soret number and increasing chemical parameter. Temperature decreased when thermal radiation is increased and heat source is decreased.
EnglishCasson fluid, Dufour effect, Soret effect, MHD, Chemical reactionIntroduction
Casson fluid exhibits yield stress. It is well known that Casson fluid is a shear thinning liquid which is assumed to have an infinite viscosity at zero rate of shear, a yield stress below which no flow occurs, and a zero viscosity at an infinite rate of shear, i.e., if a shear stress less than the yield stress is applied to the fluid, it behaves like a solid, whereas if a shear stress greater than yield stress is applied, it starts to move. Casson fluids like Honey, human blood, jelly, sauces, etc., are having significant importance. Human blood can also be treated as Casson fluid.
In recent days, Casson fluids have occupied a prominence role in various fields like biological, chemical, medical and engineering applications. in industrial environment, Various researchers have carried out their research work in this direction enlightening the effects of various parameters on the flow of the Casson fluid.Mustafa and Khanstudied the MHD flow and heat transfer of Casson nanofluid over a non-linearly stretching sheetwith non-linear temperature distribution.The heat and mass transfer characteristics of a magneto hydrodynamic Casson fluid flow on a parallel plate channel having stretching walls, when subjected to a uniform transverse magnetic field are analyzed by Sarojamma et al. Swati et al numerically examined the boundary layer flow due to an exponentially stretching surface in the presence of an applied magnetic field. Casson fluid model is used to characterize the non-Newtonian fluid behavior. The flow issubjected to suction/blowing at the surface. Analysis is carried out in presence of thermal radiation and prescribed surfaceheat flux. Prakash et al studied the MHD two-dimensional boundary layer flow of a Casson fluid in the presence of chemical reaction and thermal radiationaccompanied by heat and mass transfer towards an exponentially stretching sheet.
Animasaun et al. studied the thermal conductivity and motion of temperature dependent plastic dynamic viscosityof steady incompressible laminar free convective MHD Casson fluid flow over an exponentially stretching surface with suction and exponentially decaying internal heat generation. The effects of thermal radiation, suction/blowing, viscous dissipation, heat source/sink and chemical reaction onboundary layer flow of a non-Newtonian Casson fluid in presence of heat and mass transfer towards a porous exponentially stretching sheet with velocity slip and thermal slipconditions were analyzed by Saidulu and Lakshmi. The steady flow and heat transfer of Casson fluid from a permeable horizontal cylinder in the presence of slip condition in a non-Darcy porous medium is analyzed by maintaining the cylinder surface at a constant temperatureis studied by Prasad et al. Shehzad et al derived a series solution for the effect of mass transfer in the MHD flow of a Casson fluid over a porous stretching sheet in the presence of a chemical reaction. Casson fluid flow over a vertical porous surface with chemical reaction in the presence of hydromagnetic field has been studied by Arthur et al. The heat and mass transfer effect in a boundary layer flow of an electrically conducting viscous fluid subject to transverse magnetic field past a moving vertical plate through porous medium in the presence of heat source and chemical reaction is analysed by Tripathy et al.
The aim of the present paper is to analyze the combined effects of chemical, radiation, Dufour and Soret parameters on Casson MHD fluid flow over a vertical plate with heat source/ sink has been studied with constant velocity, variable temperature and concentration. The governing equations of the flow have been solved by using the finite difference method. The effects of varies parameter on velocity, temperature and concentration fields are studied with the help of graphs.
Formulation of the problem:
Consider a two-dimensional steady Casson fluid of incompressible, viscous, electrically conducting fluid over a vertical plate moving with constant velocity with radiation and chemical reaction in the presence of Soret and Dufour is considered. Consider the flow of an incompressible viscous fluid passing a flat sheet coinciding with plane y = 0.We select the Cartesian coordinate system such that the x − axis be taken parallel to the surface and y is perpendicular to the surface. The fluid occupies a half space y>0. The flow is subjected to a constant applied magnetic field B0 in the y-direction. The magnetic Reynolds number is considered to be very small so that the induced magnetic field is negligible in comparison to the applied magnetic field. The surface temperature of the plate oscillates with small amplitude about a nonuniform mean temperature. The fluid is assumed to have constant properties except for the influence of the density variations with temperature and concentration which are considered only in the body force term. The temperature of the plate oscillates with little amplitude about a non-uniform temperature.
The rheological equation of state for an isotropic flow of a Casson fluid [000]can be expressed as:
In Equation (1), =ei j ei j, where ei jis the (i , j)th component of deformation rate. This means that is the product of the component of deformation rate with itself. Also, is a critical value of this product based on the non-Newtonian model, is the plastic dynamic viscosity of the non-Newtonian fluid and Py is the yield stress of the fluid. The equations governed the unstudied boundary layer flow of the Casson fluid is
Equations (2),(3) and (4) refers Momentum Equation, Energy Equation and Species Equation respectively where u is the velocity of the fluid, b is Casson parameter, Q0 is the heat source/sink parameter, D is the molecular diffusivity, k is thermal conductivity, C is mass concentration, t is time, υ is the kinematics viscosity, g is the gravitational constant, b and b* are the thermal expansions of fluid and concentration, ρ is density, cp is the specific heat capacity at constant pressure, Dm Coefficient of mass diffusivity, kt Thermal diffusion ratio, Tm Mean fluid temperature, T∞ Free stream temperature of the surrounding fluid, C∞ Free stream concentration, T Fluid temperature, C Fluid concentration y is distance, qr is the radiative flux, b is the magnetic field, kr is the chemical reaction rate constant.
R.H.S. of equation (2), second term is thermal heat effect,third term is thermal concentration effect, fourth term is magnetic effect, and second term is thermal buoyancy effect. R.H.S. of equation (3) second term is thermal radiation flux and third term is thermal radiation and fourth term is Dufour effect. R.H.S. of equation (4), second term is chemical reaction and third term Soret effect. Under the above assumptions the physical variables are functions of y and t. The boundary conditions for the velocity, temperature and concentration fields are:
Introducing the dimensionless quantities with thermal radiation flux gradient expressed and we assume that the temperature differences within the flow are sufficiently small so that can be expressed as a linear function of after using Taylor’s series to expand about the free stream temperature and neglecting higher-order terms. This results in the following approximation.
The following dimensionless quantities are introduced
The thermal radiation flux gradient may be expressed as follows
Considering the temperature difference by assumption within the flow are sufficiently small such that may be expressed as a linear function of the temperature. This is attained by expanding in Taylor’s series about and ignoring higher orders terms.
Substituting the dimensionless variables (7) into (2) to (4) and using equations (8) and (9), reduce to the following dimensionless form.
The corresponding boundary conditions are
Where Gr is thermal Grashof number, Pr is the prandtl number, kr is the chemical reaction parameter, R is the thermal radiation conduction number, M is Hartmann number, Gc is the mass Grashof number, Q is the heat source/sink parameter and Sr is the Soret number.
Method of Solution
Equations (10)-(12) are linear partial differential equations and are to be solved with the initial and boundary conditions (13). In fact the exact solution is not possible for this set of equations and hence we solve these equations by finite-difference method. The equivalent finite difference schemes of equations for (10)-(12) are as follows:
Here, the suffix ‘i’ refer to y and ‘j’ to time. The mesh system is divided by taking ?y = 0.1. From the initial condition in (13), we have the following equivalent:
The boundary conditions from (13) are expressed in finite-difference form as follows
The velocity at the end of time step viz, u(i, j+1)(i=1,200) is computed from (14) in terms of velocity, temperature and concentration at points on the earlier time-step. After that θ (i, j +1) is computed from (15) and then C (i, j +1) is computed from (16). The procedure is repeated until t = 0.5 (i.e. j = 500). During computation ?t was chosen as 0.001.
Skin-friction:
The skin-friction in non-dimensional form is given by the relation
Rate of heat transfer:
The dimensionless rate of heat transfer in terms of Nusselt number is given by
Rate of mass transfer:
The dimensionless rate of mass transfer in terms of Sherwood number is given by
Results and Discussion:
The effects of various parameters such as Casson Parameter “ ”, Thermal Grashof Number “Gr”, Mass Grashof Number “Gr”, Thermal Conductivity “K”, chemical reaction parameter kr, Prandtl Number “Pr” Schmidt Number “Sc” Thermal radiation conduction number “R”, Hartmann number M, Heat source/sink parameter Q and Soret number Sr on the velocity, temperature and concentration fields are studied numerically and represented the results through graphs. The influence of Casson parameter, Hartmann number, thermal conductivity, Schmidt number and chemical reaction parameter on velocity is shown in the figures 1,5,6,8,9. From these figures, it is recognized that the velocity decreases with the increasing of these parameters respectively. The influence of Soret number, thermal Grashof number, the mass Grashof number on velocity are shown in the figures 2,3,4. It is clear that the velocity decreases with the decrease of these parameters respectively. The effect of Prandtl number on the velocity is shown in the figure 7. It is observed that the velocity decreases near the plate and increases far away the plate with the falling of the Prandtl number. The effect of Soret number on the concentration field is illustrated in figure 10. As the Soret number decreases the concentration is found to be decreasing. The effect of chemical reaction parameter on the concentration field is illustrated in figure 12. It is clear that the concentration is decreasing for increasing chemical reaction parameter. The effect of thermal radiation conduction number on concentration field is shown in figure 11. It is noted that the concentration decreases near the plate and increases far away the plate with falling thermal radiation conduction number. Figure 13 shows the variations of thermal radiation conduction number on temperature. It is found that the temperature is decreased when R is increased. Figure 14 shows the variation of the heat source sink parameter on temperature. It is clear that the temperature decreases when Q decreases. In Figure 15, the skin friction decreases when thermal Grashof number increases and figure 16 shows that the skin friction decreases when Soret number increases.
CONCLUSION
In this paper, from the study of the combined effects of chemical reaction, radiation, Dufour and Soret effects on Casson MHD fluid flow over a vertical plate with heat source / sink, it is concluded that
Velocity decreased with the increase of Casson parameter, Hartmann number, thermal conductivity, Schmidt number, Chemical parameter and decrease of Soret effect, Thermal Grashof number and Mass Grashof number.
Concentration is found to be decreasing with the decrease of Soret number and increasing chemical parameter.
Temperature is decreased when thermal radiation is increased and heat source is decreased
Skin friction decreased when thermal Grashof number and Soret number are increased
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles
are cited and included in references of this manuscript. The authors are
also grateful to authors / editors / publishers of all those articles, journals
and books from where the literature for this article has been reviewed and
discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=2410http://ijcrr.com/article_html.php?did=2410M. Mustafa, and Junaid Ahmad Khan , Model for flow of Casson nanofluid past a non-linearly stretching sheet considering magnetic field effects, AIP Advances5, 077148 (2015); doi: 10.1063/1.4927449
G. Sarojamma, B.Vasundhara, K. Vendabai, MHD Casson Fluid Flow, Heat and Mass Transfer in a Vertical Channel with Stretching Walls , International Journal of Scientific and Innovative Mathematical Research (IJSIMR) Volume 2, Issue 10, October 2014, PP 800-810
Swati Mukhopadhyaya, Iswar Chandra Moindala, and Tasawar Hayat, MHD boundary layer flow of Casson fluid passing through an exponentially stretching permeable surface with thermal radiation, Chin. Phys. B Vol. 23, No. 10 (2014) 104701, DOI: 10.1088/1674-1056/23/10/104701
S. A. Shehzad, T. Hayat, M. Qasim and S. Asghar , Effects of mass transfer on mhd flow of casson fluid with chemical reaction and suction, Brazilian Journal of Chemical Engineering, Vol. 30, No. 01, pp. 187 - 195, March, 2013.
J. Prakash, P. Durga Prasad, G. Vinod Kumar, R. V. M. S. S. Kiran Kumar and S. V. K. Varma, Heat and Mass Transfer Hydromagnetic Radiative Casson Fluid Flow over an Exponentially Stretching Sheet with Heat Source/Sink, International Journal of Engineering Science Invention, Volume 5 Issue 7, July 2016, pp.12-23
I.L. Animasaun, E.A. Adebile, A.I. Fagbade, Casson fluid flow with variable thermo-physical property along exponentially stretching sheet with suction and exponentially decaying internal heat generation using the homotopy analysis method, Journal of the Nigerian Mathematical Society 35 (2016) 1–17, http://dx.doi.org/10.1016/j.jnnms.2015.02.001
N Saidulu and A Venkata Lakshmi, Slip Effects on MHD Flow of Casson Fluid over an Exponentially Stretching Sheet in Presence of Thermal Radiation, Heat Source/Sink and Chemical Reaction, European Journal of Advances in Engineering and Technology, 2016, 3(1): 47-55
Ramachandra Prasad V, Subba Rao A and Anwar Bég O, Flow and Heat Transfer of Casson Fluid from a horizontal Circular Cylinder with Partial Slip in non-Darcy porous Medium, J Appl Computat Math 2013, 2(2), http://dx.doi.org/10.4172/2168-9679.1000127
Emmanuel Maurice Arthur, Ibrahim Yakubu Seini, Letis Bortey Bortteir, , Analysis of Casson Fluid Flow over a Vertical Porous Surface with Chemical Reaction in the Presence of Magnetic Field. Journal of Applied Mathematics and Physics, (2015) 3, 713-723.
http://dx.doi.org/10.4236/jamp.2015.36085
R.S. Tripathy , G.C. Dash , S.R. Mishra , S. Baag, Chemical reaction effect on MHD free convective surface over a moving vertical plate through porous medium, Alexandria Engineering Journal (2015) 54, 673–679, http://dx.doi.org/10.1016/j.aej.2015.04.012