Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30General SciencesEnvironmental Determinants of Phytoplankton Assemblages of a Lentic Water Body of Burdwan, West Bengal, India
English0107Debjyoti DasEnglish Sudin PalEnglish Jai Prakash KeshriEnglishThe present investigation concerns the seasonal changes of phytoplankton diversity and physico-chemical characteristic of water in a lentic water body. Diversity indices of 58 phytoplankton species and the regulatory effects of the 10 physico-chemical parameters of water on the phytoplankton diversity were assessed. The phytoplankton diversity, richness and dominance were high in winter but the evenness was high in the months of pre-summer. From the Euclidean distance of seasonal variation of phytoplankton diversity and physico-chemical parameters of water it was revealed that the phytoplankton diversity were changed with the seasonal i.e. pre-monsoon, monsoon and post-monsoon changes of physico-chemical parameters.
EnglishDiversity indices, Euclidean distance, Khan-pukur, Physico-chemical characteristic, PhytoplanktonINTRODUCTION
Algae are the major primary producers in the aquatic systems and are an important food source for other organisms like zooplanktons, rotifers and fishes etc. They include planktonic and benthic forms. Species composition and the seasonal variations of phytoplankton in fresh water bodies are dependent on interactions between physical and chemical factors in the tropical regions. Works on phytoplankton diversity in India were carried out by several workers. Several works have been done on the seasonal variations of phytoplankton from lakes and small water bodies in relations to the physiochemical parameters from India including West Bengal also (Roy, 1955; Jana, 1973; Jana et al., 1981; Mukhopadhyay et al., 1997; Ali et al., 1999; Chakraborty and Das, 2004; Chakraborty et al., 2004; Balasingh and Shamal, 2007; Chattopadhyay and Banerjee, 2007; Senthilkumar and Sivakumar, 2008; Goswami and Palit, 2010; Ghosh and Keshri, 2011; Das et al., 2011; Das and Keshri, 2012; Das and Keshri, 2013). India is among the countries of tropical region. Burdwan district is situated in the eastern part of the country. It is an agriculture based region and greater portion of this district is covered with fertile cultivated field and local people basically depend on this. Many small and large water bodies are there in this district and a large part of agriculture depend on the water of these water bodies. The chemical and biological manures directly leach out from this field into the water bodies and thus water chemistry become changed and therefore variable throughout the year depending on the nature of the leachates and time of leaching. This varied water chemistry directly affects the availability of the water micro-planktons of the water and have a great impact on the water kingdom also.
STUDY SITE
The district of Burdwan geographically forms part of the Gangetic plains of West Bengal and tropical region of India. This man-made, perennial wetland “Khan-Pukur”, is situated near the Korjona Village, 30 km away from Burdwan town and lies between the parallels 23° 20´ 34.50″ N to 23° 20´ 37.84″ N and 87° 53´ 17.99″ E to 87° 53´ 26.28″ E. It covers an area of 30 hectares, surround ed by cultivated land. The bank of the pond is covered by several big trees with semi aquatic wetland plants. It receives run-off water from the adjacent land. The average annual depth of water is 11ft. The water of this wetland is mainly used for agriculture.
MATERIAL AND METHODS
Measurement of Phytoplankton diversity
In the present investigation 30 hectares area was studied by choosing sites at random and the water samples were collected once in a month during the time period of January 2010 to December 2010 between 9-11 a.m. 1% Lugols’ Iodine solution and 10% Formalin solution were used to preserve the phytoplankton (PHYTO) samples. The identification and quantitative analysis were done by using Carl Zeiss Axiostar microscope with photo micrometry Nikon camera attachment.
Collection and Analysis of Water Samples
Water samples were collected in air tight Polyvinyl chloride (PVC) bottles. The pH, Temperature (TEMP), Conductivity (COND), Total Dissolved Solids (TDS), Salinity (SAL) were measured by PCS Testr- 35 and the other parameters such as dissolve oxygen (DO), Biological Oxygen Demand (BOD), Phosphate (PO4 +) Nitrate (NO3 - ) and Potassium (K+) were tested by following standard methods of American Public Health Association (APHA, 1995; Jadav and Jogdand, 1993; C.P.C.B. Publication, 1978).
Statistical Methods
The statistical analysis like measurement of Shannon’s index, Simpson’s index, Pielou’s index, Margalef’s index were done using PAST 2.07software, the correlation matrix and single linkage Eucladian distance of different variables were performed by STATISTICAw 580 software.
RESULTS
The species wise diversity represented in the Table 1. Total 73 phytoplankton species were found and identified by several monographs (Turner, 1892; Hustedt, 1930; Philipose, 1967; Pal and Mukhopadhyay, 2013; Wehr and Sheath, 2003). Among the 73 taxa recorded class Chlorophyceae represented by maximum number of 46 genera, Cyanophyceae by 10 genera, Euglenophyceae about 9 genera, Bacillariophyceae 7 genera and Dinophyceae only one genus. Seasonal variations of different diversity indices of phytoplankton species in pond are depicted in Table-2. The highest richness of phytoplankton were shown in December followed by January, November, and February that means in the winter the species richness was highest and lowest in July and August at the time of monsoon. The Simpson’s dominance index was also highest in winter seasons including the conjugative months December, January, and November. From the different physico-chemical parameters point of view (Table III) average water temperature was 31.25°C in summer, 26°C in monsoon and 24.75°C in winter. The water pH was always below 7 i.e. acidic throughout the year. The case wise correlation matrix (Table IV) of all parameters with phytoplankton diversity the number of phytoplankton were significantly positively correlated (pEnglishhttp://ijcrr.com/abstract.php?article_id=614http://ijcrr.com/article_html.php?did=614Ali MB, Tripathi RD, Rai UN, Pal A, Singh SP. Physico-chemical characteristics and pollution level of lake Nainital (U.P., India): Role of macrophytes and phytoplankton in biomonitoring and phytoremediation of toxic metal ions. Chemosphere 1999; 39(12): 2171-2182. American Public Health Association. Standard Methods for the Examination of water and waste water, 19th edition, APHA: Washington DC; 1995. Balasingh GSR, Shamal VPS. Phytoplankton Diversity of a Perennial Pond in Kanyakumari District. Journal of Basic and Applied Biology 2007; 1(1): 23-26. Central Pollution Control Board. Scheme of Zoing and classification of India Rivers, Estuaries and Coastal water (partI. Sweet water): ADSORBS/3/1978-79, Central Pollution Control Board Publication: Delhi; 1978. Chakraborty D, Das SK. Seasonal cycle of phytoplanktons and macrophytes in the river Jalangi. Environment and Ecology 2004; 22(2): 480-481. Chakraborty I, Dutta S, Chakraborty C. Limnology and plankton abundance in selected beels of Nadia district of West Bengal. Environment and Ecology 2004; 22: 576-578. Chattopadhyay C, Banerjee TC. Temporal changes in environmental characteristics and diversity of net phytoplankton in a freshwater lake. Turkish Journal of Botany 2007; 31(4): 287-296. Das D Keshri JP. Desmids of Khechiperi Lake, Sikkim Eastern Himalaya. Algological Studies 2013; 143: 27-42. Das D Keshri JP. Coccal Green algae from Bitang-cho Lake (a high altitude lake in Eastern Himalaya). Indian Hydrobiology 2012; 15(2): 171-182. Das D, Mustafa G, Keshri JP. Contributions to our knowledge of unicellular and colonial green algae belonging to the orders Volvocales and Tetrasporales (Chlorophyta) of Burdwan, West Bengal, India. Journal of Economic and Taxonomic Botany 2011; 35(1):218-223. Ghosh S, Keshri JP. Assessment of phytoplankton diversity and dynamics of a lentic water body of Belur rail station area, with reference to pollution status. Environment and Ecology 2011; 29(1): 232-234.Goswami G, Pal S, Palit D. Studies on the Physico-Chemical characteristics, Macrophyte Diversity and their Economic Prospect in Rajmata Dighi: A wetland in Cooch Behar District, West Bengal, India. NeBIO 2010; 1(3): 21-26. Hustedt F. Bacillariophyta (Diatomeae). In Die SüsswasserFlora Mitteleuropas, Pascher, A. Heft 10, Gustav Fischer, Jena; 1930. Jadav HV, Jogdand SN. Environmental, Chemical and Biological analysis, Himalayan Publishing House, New Delhi; 1993. Jana BB. Seasonal periodicity of plankton in a freshwater pond in West Bengal, India. International Revue gesamten Hydrobiologie Hydrography 1973; 58(1), 127-143. Jana BB, De UK, Das RN. Environmental-factors affecting the seasonal-changes of net phytoplankton in 2 tropical fish ponds in India. Swiss Journal of Hydrology 1981; 42(2): 225-246. Moitra SK, Bhattacharya BK.. Some hydrological factors affecting plankton production in a fresh pond in Kalyani, West Bengal, India. Ichthyologica 1965; (4): 8-12. Mukhopadhyay SK, Ghosh A, Roy S. Primary productivity of phytoplankton in two freshwater bodies at Chinsurah in summer. Geobios 1997; 24(1): 47-50. Pal S, Chattopadhyay B, Mukhopadhyay SK. Variability of carbon content in water and sediment in relation with physico-chemical parameters of East Kolkata Wetland Ecosystem: A Ramsar Site. NeBIO 2013; 4(6): 70-75. Philipose MT. Chlorococcales. Indian Council for Agricultural Research: New Delhi; 1967. Roy HK. Plankton ecology of the river Hooghly at Palta, West Bengal. Ecology 1955; 169-175. Senthilkumar R, Sivakumar K. Studies on phytoplankton diversity in response to abiotic factors in Veeranam lake in the Cuddalore district of Tamil Nadu. Journal of Environmental Biology 2008; 29(5): 747-752. Turner WB. The fresh-water algae (Principally Desmidieae) of East India. K. Sv. Vetensk. Acad. Handl 1892; 25(5): 1-187 pls. 1-23. Wehr JD, Sheath RG. Freshwater algae of North America, Academic Press: San Diego, CA; 2003.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareAwareness regarding child care and sanitation: A generation dependent comparison among mothers of Purba
and Paschim Medinipur districts, West Bengal
English0813Madhumita GuriaEnglish Kausik ChatterjeeEnglish Sabyasachi RayEnglish Debidas GhoshEnglishObjectives: The study focuses the awareness level of mothers of previous and present generations about child care and sanitation in families of remote villages of Purba Medinipur and Paschim Medinipur with low socio-economic condition.
Methods and materials: The study was completed by pre-tested structured questionnaire method. In this study 1330 mothers were randomly selected out of which 430 mothers from previous generation and 900 mothers from present generation were included. The remote villages of Purba and Paschim Medinipur districts of West Bengal were selected as study areas.
Results: The result shows that there are not so much awareness about child care and sanitation in these remote villages. Mothers of present generation are found with more awareness than mothers of previous generation in all respect. Educational level, cast and occupational variation as well as exposure to the mass media plays a vital role for awareness generation about child care and sanitation among mothers.
Conclusion: Government authority should take proper steps for the improvement of child care and sanitation through campaigning among family members as children are the backbone of the nation.
EnglishSanitation, Low socio-economic groups, Hygiene, Educational level, Mass mediaINTRODUCTION
Health care is one of the important interventions in the process of economic and social development and improved their quality of life in different socio-economic families1 . The successful sanitation program in West Bengal first started in 1991 is now serving as a global model for developing countries2 . Water and sanitation related diseases became one of the most significant child health problems worldwide3 . In some cases these diseases cause premature death, but more frequently resulted in fatal chronic conditions such as diarrhea, worm infections, cholera, malaria, trachoma and schistosomiasis4 . Children who suffer constantly from water borne diseases are in disadvantages in school as poor health directly reduces cognitive potential and indirectly undermines schooling through absentees, attention deficits and early drop out 5 . With support from NGO’s (Non-Government Organization), UNICEF and local Government these programs play a major role in empowering workers. Midnapore has inspired the other districts of the state with 100% coverage where the overall sanitation coverage in West Bengal state is 65% and the national coverage of 32% 6 . Holistic development of needy children is projected to be achieved through empowerment of the community. There are some programmes initiated namely Aakar, Parivertan, Lakshya, Aahar Apurti, Uphaar for child care and development with a motto to make a bridge between the gap of under privileged street children and their counterparts 7 .
With the growing inflation in the pricing policies of companies, common people are forced to cut short their comers and limit the area of designs. However, when it comes to the safety and betterment of child, no parents would like to sacrifice with the quality8 . For working parents it becomes necessary to join some child care programme, working parents can adopt different ways from which they can gain benefits for child care health and development 9 . It is essential to find desiring child care assistance which selecting child care programme for the baby10. Education and communication are important components of a hygiene promotion programme. All people have a right to know about the relationship between water, sanitation, hygiene and the health of themselves and their families 11.
METHODOLOGY
The survey covered ten remote villages where five (5) villages (Mayna, Shilaberia, Bararankua, Gonara Gangadharbar) from Purba Medinipur district and 5 villages (Binpur, Pingla, Mandar, Kulasini, Chhatra) from Paschim Medinipur district under taken from June, 2007 to December, 2009. From these villages 430 mothers of previous generation (age group >20 to ≤ 55 yrs) and 900 mothers of present generation (age group >55 to ≤ 75 yrs) were randomly selected to include a total of 1330 mothers out of 150 families. They were dependent principally on agriculture and the rests were engaged with daily basis labour, private company and other type of jobs with average monthly income of Rs. 4000 to 5000 per month. Maximum couples had more than two children. This study framed with five questionnaire domains and each domain contains 10 marks. So, this was a total of 50 point of questions about child sanitation and hygiene. These domains were on
(i) Food Sanitation and Kitchen Sanitation- Cleaning of utensils before and after cooking; Washing hands at the time of cooking; Covering and preservation of storage food, Washing of hands of the elder family members at the time of serving; Serving of warm or cold food items.
(ii) Personal hygiene – Using of separate water container for washing, bathroom, latrine, kitchen; Washing of hands of mother or family members after blowing their noses, diapering of children; Hand washing of children during toileting; Use of sandals at the time of going to toilet or latrine.
(iii)Hygiene of Latrine/Toilet/Waste matter – Hygienic status of Latrine; Availability of water facility near the latrine or toilet; Using of hand-wash or soap after using latrine or toilet; Disposal of waste matters (vegetable skins after pilling, used diaper, excretory products of domestic pet animals) with a safe distance or not from the house.
(iv)Child and infant sanitation- Cleaning and washing of body parts after diapering of children; Regularity of bathing with proper cleaning with bathing soap, using any soap, detergent or sanitizer for cleaning their clothes.
(v) Bed room hygiene- Proper dustering of bed; Washing of bed cover or pillow cover, mosquito net with detergent and warm water; Cleaning and moping of floor of bed room on daily basis. These results were transferred into percentage and grade as per following gradation system
RESULTS
From two tail Chi-square test of independence, it was found that there was a significant (P0.05). These were strengthened here from the data expressed in percentage where in previous generation and present generation of mothers the awareness level becomes increased due to advancement of their educational level. In uneducated group, awareness level in maximum cases was ‘very poor grade’ in mothers of both the generations. But in above secondary group, awareness level in maximum cases was in excellent grade in present generation of mother (Table 2). From Chi-square test of independence, it was noted that there was a significant association between awareness level of child care and sanitation of previous and present generation of mothers with their caste profile. This result indicated here by the comparative analysis in percentage which focused that in general caste of both generation of mothers there maximum awareness was in excellent grade. In SC, ST and other caste, maximum grade of their awareness was in excellent in present generations, whereas in previous generations of mothers, these were in poor and very poor (Table 3). Analysis of collected data using two tail Chi-square test of independence, it was found that there was a significant (PEnglishhttp://ijcrr.com/abstract.php?article_id=615http://ijcrr.com/article_html.php?did=6151. Hawe P, Shiell A, RileyT, Gold L. Methods for exploring implementation variation and local context within a cluster randomised community intervention trial. Journal of Epidemiology and Community Health. 2004; 58: 788-793.
2. UNCF (United Nations Children’s Fund).Towards Better Programming: A Sanitation Handbook. Water, Environment and Sanitation Technical Guidelines Series No-3. A Sanitation Handbook. UNICEF’s Water, Environment and Sanitation Section, Programme Division and USAID’s Environmental Health Project. Environmental Health Project, Contract No. HRN-5994-C-00-3036-00, Project No. 936- 5994:1-81. UN Plaza, New York, USA, 1997.
3. Das, K. Rural Drinking Water Supply in India: Issues and Strategies, 207-277. In: Sebastian Morris (ed.), India Infrastructure Report 2001: Issues in Regulation and Market Structure, Oxford University Press, New Delhi, 2001.
4. WHO (World Health Organization). Tools for assessing the operation and maintenance status of water supply and sanitation in developing countries. Document WHO/SDE/ WSH/00.3. Water Supply and Sanitation Collaborative Council and Operation/Maintenance Network, WHO, Geneva, 2000
. 5. UNDP. Human Development Report 2006-Beyond Scarcity: Power, Poverty, and the Global Water Crisis, 2006, Pp. 45.
6. Narayanan R, Norden HV, Gosling L, Patkar A. Equity and Inclusion in Sanitation and Hygiene in South Asia: A Regional Synthesis Paper. UNICEF, Water Aid, Water Supply and Sanitation Collaborative Council Report, 2011, Pp.1- 17.
7. French G. Children’s early learning and development: A research paper. National Council for Curriculum and Assessment (NCCA), 2007, Pp.4-30.
8. AECDHB (Arizona Early Childhood Development and Health Board). High-quality child care and early education: what arizona’s parents want (First Things First). N Central Ave, Phoenix, AZ, 2012, Pp:1-88.
9. RIC. Getting the right start: National Service Framework for Children Standard for Hospital Services. Department of Health, RIC, United Kingdome, 2003, Pp.1-50.
10. Crosson-Tower C. The role of educators in preventing and responding to child abuse and neglect. Child abuse and neglect user manual series. U.S. Department of Health and Human Services, Administration for Children and Families, Administration on Children, Youth and Families, Children’s Bureau, Office on Child Abuse and Neglect, 2003, Pp.1-79.
11. Child Action Inc. High quality child care, your guide to finding and selecting the best care for our child. Sacramento, CA, USA, 2013, Pp.31-42.
12. Cairncross S. Health Impacts in Developing Countries: New Evidence and New Prospects. Journal of the Institution of Water and Environmental Management. 1990; 4:571-577.
13. Ezzati M. Complexity and Rigour in Assessing the Health Dimensions of Sectoral Policies and Programmes. Bulletin of the World Health Organization. 2003; 81:458-459.
14. RCP (Royal College of Psychiatrists). London Physical health in mental health; Final report of a scoping group. Occasional Paper OP67, 2009, Pp.5-68.
15. Baran S, Chase L, Courtright J. Television drama as a facilitator of positive social behavior. The Waltons. Journal of Broadcasting. 1979; 23: 277-284.
16. Pendley C. A Demand-based Approach to Rural Water Supply and Sanitation. In: K. Pushpangadan (ed.), National Seminar on Rural Water Supply and Sanitation, Centre for Development Studies, Trivandrum, 1997.
17. Ponthiere G. Mortality, Family and Lifestyles. Journal of Family and Economic Issues. 2011; 32:175-190.
18. Andrews AB, McLeese DG, Curran S. The impact of a media campaign on public action to help maltreated children in Addictive families. Child Abuse and Neglect. 1995; 19: 921-932.
19. Maiti S, Ali KM, Dash SS, Ghosh D. Impact of ‘Child-toFamily’ Strategy for Health Awareness Improvement at Rural Sectors of Paschim Medinipur District, West Bengal. Online Journal of Health and Allied Sciences. 2010, 9: l-3.
20. Guria M, De D, Bera TK, Ghosh D. Awareness Level of Family Planning Practices in School Going Adolescent Girls of Different Socio-economic Groups in Rural Sectors, West Bengal. Journal of Human Ecology. 2009; 27:101-104.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareA MORPHOMETRIC STUDY OF FORAMEN MAGNUM IN DRY ADULT HUMAN SKULL
English1419Kopal SainiEnglishAim: To study the morphology and morphometry of foramen magnum in dry adult human skull.
Materials and method: Ninety eight skulls were investigated for foramen magnum. The shape of foramen magnum was noted and classified into oval, round, tetragonal and asymmetrical. The length (antero-posterior) and width (transverse) of foramen magnum was measured using pair of dividers and ruler.
Results: 44 foramina magna were observed to be oval, 20 were tetragonal, 18 were round and 13 were found to be asymmetrical. The average length was 34.8 ± 2.45 (29-42) mm and average width was 30 ± 2.29 (26-36) mm. 3 skull showed occipitalization of atlas vertebra.
Conclusion: These data may be of use as a morphometric database for description of “normal” variants of foramen magnum morphology.
EnglishForamen magnum, Craniovertebral junctionINTRODUCTION
Foramen magnum is a Latin word meaning the largest aperture in skull. The foramen magnum is an important landmark for surgeries as it lies at the transition zone between spine and skull. The foramen magnum is a fundamental component in the complex interaction of bony, ligamentous and muscular structures composing the craniovertebral junction. Shape and size of the foramen are critical parameters for the manifestation of clinical signs and symptoms in craniocervical pathologies. Diseases associated with anomalies of the foramen magnum include occipital vertebra, basilar invagination, condylar hypoplasia, and atlas assimilation. The transcondylar approach is being increasingly used to access lesions ventral to the brainstem and cervicomedullary junction. Understanding the bony anatomy of this region is important for this approach. Focusing on forensic dentistry and medicine, the morphometric analysis of the skull can be used as part of an investigative process prior to more sophisticated and expensive analyses such as the DNA examination.1 Among developmental and acquired craniocervical junction disorders, achondroplasia is the commonly reported. Achondroplasia, the most common form of dwarfism, resulting in abnormal enchondral bone formation at the cranial base, leads to a narrow cervical spinal canal and a stenotic foramen magnum. Clinical manifestations of chronic brainstem compression by stenosis of the foramen magnum and related structures are respiratory complications, lower cranial nerve dysfunctions, upper and lower extremity paresis, hypo- or hypertonia, hyperreflexia or clonus, and general motor development delay.2 The configuration of the foramen magnum in patients with Chiari I and Chiari II malformations has been found to be different than in the normal population. Furthermore, development of symptoms has been found in patients with shorter anteroposterior diameters of the foramen magnum. Other diseases associated with stenosis of the craniovertebral junction include craniometaphyseal dysplasia, Jeune’s asphyxiating thoracic dystrophy, and spherophakia-brachymorphism (Marchesani’s syndrome). Stenosis of the foramen magnum has also been reported for Beare-Stevenson syndrome, a craniofacial syndrome characterized by hypertrophy of the bony margins. A wide foramen magnum has also been appreciated in patients with diastrophic dysplasia. The decisionmaking process for the diagnosis and treatment of such disorders with bony abnormalities resulting in changes of the anatomy of the foramen magnum demands a good understanding of the normal anatomy of this structure.2
Materials and methods
Ninety eight dry adult human skulls of indetermined gender were collected from the bone library of medical teaching institutes of Mumbai. The adult status of the skull was determined by the synostosis between the basiocciput and basi-sphenoid at the cranial base. Data were collected using a pair of dividers, ruler and digital camera. The pair of dividers was spanned across the distances to be measured. Distances were transferred to a ruler to record the readings. Data so collected were statistically analysed for descriptive statistics and using Microsoft excel software. Following parameters were considered-
• The shape of foramen magnum was noted and classified as oval, round, tetragonal and asymmetrical (figure 1)
• The length of foramen magnum was measured from the anterior border (basion) through the centre of the foramen magnum until the posterior border (opistio) in the sagittal plane (figure 2)
• The width of foramen magnum was measured perpendicular to length in the coronal plane at a point where it was maximum (figure 2)
Results
Out of the ninety eight skulls investigated, 95 foramina magna were considered for measurements and 3 foramina showed variations where measurements could not be taken. In the 95 foramina magna, 44 foramina magna were observed to be oval, 20 were tetragonal, 18 were round and 13 were found to be asymmetrical (graph 1). The average length of foramen magnum was 34.8 ± 2.45 mm within a range of 29 - 42 mm. The mean width of foramen magnum was 30 ± 2.29 mm within the range of 26 - 36 mm. 3 skull showed occipitalization of atlas vertebra as shown in figure 3.
Discussion
Configuration and size of the foramen magnum play an important role in the pathophysiology of various disorders of the craniovertebral junction. Thus, a fundamental knowledge of normal anatomy and basic craniometric measurements for assessing craniovertebral relations is important to the clinician who diagnose this region and the surgeon who operates on this anatomy. In the present study, oval shape of foramen magnum was commonly seen (46%). This was followed by tetragonal (21%), round (19%) and asymmetrical (14%). The findings of previous studies are presented in table 1. Muthukumar Net al.3 showed in their study in 2005 that, whenever the foramen magnum index was more than 1.2, the foramen was found to be ovoid. They calculated the index by dividing antero-posterior diameter by the transverse diameter. Forty six percent of the skulls studied exhibited an ovoid foramen magnum in their study. In the present study, the average length of foramen magnum was 34.8 ± 2.45 mm within a range of 29 - 42 mm. The average length in the present study is comparable with Sukumar S6 , Muthukumar N3 , AvcI E8 , Manoel C1 , Kanodia G10 and Radhakrishna SK11. The average lengths reported by these researchers are presented in table 2. The mean width of foramen magnum was 30 ± 2.29 mm within the range of 26 - 36 mm in this study which is comparable with values reported by Furtado SV4 , Gruber P5 , Osunwoke EA7 , AvcI E8 , Manoel C1 and RadhakrishnaSK11. Study average length of the foramen was greater than the width in the present study which is consistent with the oval shape of the foramen found commonly in the study sample. Vineeta Saini et al.12 found 2 skulls with assimilation of atlas vertebra in the anthropometric study of 126 skulls. Khamanarong K et al.14 reported 2 skulls with occipitalization of atlas vertebra in the 633 thai adult skulls. In the present study, 3 (3%) skulls showed occipitalization of the first vertebra. The percentage of this variation is higher in the study sample as the bones were collected from bone libraries of medical college. Knowledge of occipitalization of the atlas is of substantial importance to orthopaedicians, neurosurgeons, physiotherapists and radiologists dealing with abnormalities of the cervical spine. Occipitalization is a congenital synostosis of the atlas to the occiput. During the fourth week, sclerotome migrate around the spinal cord and the notochord to merge with cells from the opposing somite on the other side of the neural tube. As development continues, the sclerotome portion of each somite also undergoes a process called resegmentation. Resegmentation occurs when the caudal half of each sclerotome grows into and fuses with the cephalic half of each adjacent sclerotome. Thus each vertebra is formed from combination of the caudal half of one somite and the cranial half of its neighbour.13In a small number of cases, the disruption of this merging process may result in atlanto-occipital assimilation. This condition may be partial or complete. Occipitalization of atlas is associated with abnormalities as a result of narrowing of the foramen magnum, compressing the spinal cord or the brain stem. However, this anatomical variation may often go unnoticed but, incidentally, reveals its presence as a radiological, operative or autopsy finding.12
Conclusion
The average length and width of foramen magnum were 34.8 ± 2.45 mm and 30 ± 2.29 mm respectively. 3 skull showed occipitalization of atlas vertebra. This anatomic study elucidated the morphological and morphometric characteristics of foramen magnum and may serve as a future standard reference.
Acknowledgments
Authors are thankful to Head of Department of Anatomy, Seth G. S. Medical College and all staff members and colleagues from Department of Anatomy, Seth G. S. Medical College and K.E.M. Hospital, Mumbai. . 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=616http://ijcrr.com/article_html.php?did=6161. Manoel C, Prado FB, Caria PHF, Groppo FC. Morphometric analysis of the foramen magnum in human skulls of brazilian individuals: its relation to gender. Braz. J. Morphol. Sci 2009;26(2): 104-8. 2. Tubbs RS, Griessenauer C, Loukas M, Shoja MM, CohenGdol AA. Morphometric analysis of the foramen magnum: an anatomic study. Neurosurgery 2010; 66:385-8. 3. Muthukumar N, Swaminathan R, Venkatesh G, Bhanumathy SP. A morphometric analysis of the foramen magnum region as it relates to the transcondylar approach. Acta Neurochir. 2005 Aug;147(8):889-95. 4. Furtado SV, Thakre DJ, Venkatesh PK, Reddy K, Hegde AS. Morphometric analysis of foramen magnum dimensions and intracranial volume in pediatric Chiari I malformation. Acta Neurochir 2010;152:221–7. 5. Gruber P, Henneberg M, Boni T, Ruhli FJ. Variability of human foramen magnum size. The anatomical record 2009;292:1713–19. 6. Sukumar S, Yadav S, Manju HB. 3D Reconstruction Computer Tomography of foramen magnum and fronto nasal junction for sex determination in south Indian population. Int J Pharm Bio Sci 2012 Oct; 3(4):(B)615 – 9. 7. Osunwoke EA, Oladipo GS, Gwunireama IU, Ngaokere JO. Morphometric analysis of the foramen magnum and jugular foramen in adult skulls in southern Nigerian population. Am. J. Sci. Ind. Res, 2012; 3(6): 446-8. 8. AvcI E, Dagtekin A, Ozturk AH, Kara E, Ozturk NC, Uluc K et al. Anatomical variations of the foramen magnum, Occipital condyle and jugular tubercle. Turkish Neurosurgery 2011; 21(2): 181-90. 9. Murshed KA, Cicekcibasi AE, Tunker I. Morphometric evaluation of the foramen magnum and variations in its shape: a study on computerized tomographic images of normal adults. Turk J Med Sci 2003;33:301-6. 10. Kanodia G, Parihar V, Yadav YR, Bhatele PR, Sharma D. Morphometric analysis of posterior fossa and foramen magnum. J Neurosci Rural Pract 2012 Sep-Dec;3(3): 261– 6. 11. Radhakrishna SK, Shivarama CH, Ramakrishna A, Bhagya B. Morphometric analysis of foramen magnum for sex determination in south indian population. NUJHS 2012 mar;2(1):20-2. 12. Saini V, Singh R, Bandopadyay M, Tripathi SK, Shamal SN. Occipitalization of the atlas: its occurrence and embryological basis. International Journal of Anatomical Variations 2009; 2: 65–8. 13. Sadler TW. Langman’s Essential Medical Embryology. 12th ed. Baltimore:Lippincott William and Wilkins; 2007.p. 142. 14. Khamanarong K, Woraputtaporn W, Ratanasuwan S, Namking M, Chaijaroonkhanarak W, Sae-Jung S. Occipitalization of the atlas: Its incidence and clinical Implications. Acta Medica Academica 2013;42(1):41-5
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareAssociation of Serum Uric Acid with anthropometric, HbA1c and Lipid profile in Diabetic Retinopathy
English2026Munilakshmi U.English Prabhavathi K.English Shashidhar K. N.English Madhavi ReddyEnglish Lakshmaiah V.EnglishIntroduction: Diabetic Retinopathy (DR), one of the leading cause of visual impairment in adults, a kind of serious microvascular complication of Diabetes Mellitus. It is well known that purine metabolites are strongly associated with the development of diabetic microvascular complications. Uric acid, an end product of the purine metabolism, acts as a pro-oxidant and it may thus be a marker of oxidative stress.
Objectives:
1. To Estimate and Compare Anthropometric and Biochemical parameters in Diabetic Retinopathy patients, Diabetes without Retinopathy and clinically proven healthy controls.
2. To correlate Serum Uric acid levels with Anthropometric and Biochemical indices in Diabetic Retinopathy patients. Materials and Methods: Study group consisted total of 150 subjects divided into three groups- Group I (Clinically proven healthy controls), Group II (Type 2 Diabetes Mellitus without retinopathy) and Group III (Diabetic retinopathy), visiting RL Jalappa hospital and Research centre Kolar. Anthropometric & Biochemical parameters were estimated by standard methods.
Results: Comparison of Anthropometric & Biochemical parameters were done among the three Groups, we observed Age, Obesity index, Fasting Blood Sugar, HbA1c, Total Cholesterol, high density lipoproteins, low density lipoproteins & Uric acid were statistically significant with p value EnglishDiabetic Retinopathy, Diabetes Mellitus, Uric Acid, Obesity indexINTRODUCTION
Diabetes Mellitus a metabolic syndrome, characterized by hyperglycemia due to an absolute or a relative deficiency of insulin.Type 2 Diabetes Mellitus (T2DM) is undoubtedly one of the most challenging health problems in the 21st century and the number of diabetic patients diagnosed has reached 366 millions in 2011.Complications of diabetes areone of the major cause forreducing quality of life, disability and death. Approximately 25% of the people with newly detected diabetes already have microvascular disease, suggesting that they have had the disease for 4–7 years by the time of the diagnosis1 . In these patients, with earlier disease identification and the intensive treatment of hyperglycemia, the risk of developing microvascular complications can be reduced,particularly, diabetic retinopathy (DR)2 . Studies conducted by Klein. R et.al., stated that in age group of 30-65 years, Diabetic retinopathyis one of the leading cause for visual impairment is due to uncontrolled or long duration diabetes3 . Even today, the diagnosis of retinopathy depends on opthalmoscopy and fluorescein angiography. However, it is generally acknowledged that only the pathological changeswhich occur at the severe stages of the retinopathy canbe discovered using this diagnostic method. Thus, itis of tremendous importance to find a diagnostic marker thatcan be used for screening and prediction of retinopathy, especiallywith high precision and which should be easily measured3 . According to Ames BNet.al.,purine metabolites are strongly associated with the development of diabetic microvascular complications4 . Uric acid (UA), an end product of the purine metabolism, acts as a pro-oxidant and may thus thought to be a marker of oxidative stress. In diabetic patients, superoxide plays an important role in microvascular dysfunction and exerts direct tissue damage which leads to lipid and protein peroxidation.Uric acidhas also beenthought to have a therapeutic role as an antioxidant4 .Studies done by Nakagawa T et al., reported that hyperuricaemia has been added to the set of metabolic abnormalities which are associated with insulin resistance and/or hyperinsulinemia in the metabolic syndrome5 . UA was previously used to be thought as a predominant predictor of gouty diathesis6 . However, as a marker of metabolic syndrome (MetS), UA could worsen insulin resistance by disturbing insulin-stimulated glucose uptake and shows positive association between the serum uric acid levels and the development of T2DM7 . Studies conducted by Cirillo. P et al, Anwar M.M et al,andTanemoto M et al., reported that the high level of uric acid was associated with diabetic microvascular complications, such as nephropathy, retinopathy, and neuropathy 8,9,10, but it is usually considered a marker of tissue dysfunction rather than a risk factor for progression. Some researchers considered that uric acid might affect the function of vascular smooth muscle cells, which is related to diabetic retinopathy11. Therefore, the present study was designed to look for any association of serum uric acid with HbA1c andlipidprofile in T2DM, taking into consideration the relevant clinical, biochemical and the anthropometric data
Objectives
1. To Estimate and Compare Anthropometric and Biochemical parameters in Diabetic Retinopathy patients, Diabetes without Retinopathy and clinically proven healthy controls.
2. To correlate Serum Uric acid levels with Anthropometric and Biochemical indices in Diabetic Retinopathy.
Materials and Methods
The present study was conducted in R L Jalappa hospital attached to Sri Devaraj Urs Medical College, Kolar. Total 141individuals with the age group of 40-60 years of bothgenderswere selected in the Ophthalmology outpatient department during the year October 2011 to January 2012. These subjects were grouped into three categories Group I: Forty three clinically proven healthy controls. Group II: Forty eight T2DM subjects without retinopathy based on fundoscopic changes Group III: Fifty Diabetic retinopathy subjects based on fundoscopic examination. The study was approved by the institutional ethical clearance committee and a written informed consent was obtained from all the subjects who were enrolled in our study. Patients with hepatic disease, type 1 diabetes mellitus, peripheral vascular disease, acute or chronic infection, cancer and complications related to diabetes like ulcers, nephropathy and neuropathy, which might affect the estimation of various biochemical parameters, were excluded from the study. Clinical details such as anthropometric measurementsof all the subjects enrolled in the study were obtained from the hospital medical records. Venous blood sample was collected under strict aseptic conditions with a minimum of 8 hours of fasting.All the parameters were estimated using Johnson and Johnson vitros 250 dry chemistry auto analyzer which works on the principle of reflectance photometry. The blood glucose estimation was done by Glucose Oxidase Peroxidase method (GOD-POD)12, HbA1c was estimated by HPLC method12, Fasting Insulin by Chemilumuniscence assay12, uric acid was estimated by uricase method13 Total cholesterol (TC) was estimated by cholesterol oxidase method14, Triglycerides (TG) estimation was by Enzymatic colorimetric test- GPO PAP14, Highdensity lipoproteins (HDL) estimation was done by Direct Enzymatic method12, LDL-cholesterol, Non-HDL-cholesterol, were calculated14,15. Statistical analysis was carried out by one way analysis of variance (ANOVA) by using the SPSSversion 16.0, and p value < 0.05 wasconsidered significant and Pearsons Correlation Coefficient was used to rank different variables either positively or inversely correlated.
Results
Table 1 shows the comparison of mean, standard deviation of anthropometric, physiological and biochemical indices between the three groups, age, obesity index, FBS, HbA1c, uric acid, TC, HDL and LDL-cholesterol levels were significantly higher in all the groups compared to controls. Table 2 shows the Post Hoc analysis using Bonferroni criterion for significance between Group I Vs Group II, age, OBI, FBS, HbA1c, uric acid, TC, HDL, LDL were significant (pEnglishhttp://ijcrr.com/abstract.php?article_id=617http://ijcrr.com/article_html.php?did=6171. Whiting DR, Guariguata L, Weil C, Shaw J. IDF diabetes atlas: global estimates of the prevalence of diabetes for 2011 and 2030. Diabetes Res ClinPract2011;94:311-321.
2. Harris MI, Klein R, Welborn TA, Knuiman MW. The onset of NIDDM occurs at least 4-7 years before its clinical diagnosis. Diabetes Care 1992; 15:815-819.
3. Klein, BE, Klein. K, Moss. SE, “The Wisconsin epidemiologic study of diabetic retinopathy. II. Prevalence and risk of diabetic retinopathy when age at diagnosis is less than 30 years,” Archives of Ophthalmology, 1984;102(4):520–526
4. Ames BN, Cathcart R, Schwiers E, Hochstein P. Uric acid provides an antioxidant defence mechanism in humans against oxidants and radicals which cause aging and cancer: a hypothesis. ProcNatlAcadSci USA 1981;78:6858- 6862.
5. Nakagawa T, Zharikov S, Tuttle KR, Short RA, Glushakova O. A causal role of uric acid in the fructose- induced metabolic syndrome. Am. J. Physiol. Renal. Physiol. 2005;290:625-631.
6. Murea M Advanced kidney failure and hyperuricemia. Adv Chronic Kidney Dis. 2012;19:419-424.
7. Tassone EJ, Presta I, Sciacqua A, Rotundo M. Uric acid promotes endothelial dysfunction: A new molecular model of insulin resistance. Eur J Clin Invest 2011;41: 81-82.
8. P. Cirillo, W. Sato, S. Reungjui. “Uric acid, the metabolic syndrome, and renal disease, Journal of the American Society of Nephrology 2006;17(3):S165–S168.
9. Anwar MM,Meki AM. “Oxidative stress in streptozotocininduced diabetic rats: effects of garlic oil and melatonin,” Comparative Biochemistry and Physiology A2003;135( 4):539–547.
10. Hsu SP, Pai MF, Peng YS, Chiang C, Ho T. “Serum uric acid levels show a “J-shaped” association with allcause mortality in haemodialysis patients,” Nephrology Dialysis Transplantation 2004;19(2):457–462.
11. David B Sacks MB. Estimation of Blood Glucose. In: Teitz, Burtis CA, eds. Clinical chemistry and Molecular Diagnostics. 4thed.New Delhi: Elsevier, 1999, pp 870-871.
12. Edmund Lamb, David J, Cristopher P. Creatinine estimation. In:Teitz, Burtis CA, eds. Clinical chemistry and Molecular Diagnostics. 4th ed. New Delhi: Elsevier, 1999, pp 798.
13. Nader Rifai, G. Russell Warnick. Friedewald Equation. In: Teitz, Burtis CA, eds. Clinical chemistry and Molecular Diagnostics. 4thed. New Delhi: Elsevier, 1999, pp 842-843.
14. Levy AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of diet in renal disease study group. Ann Intern Med 1990; 130:461- 470.
15. Roglic G, Unwin N, Bennett PH. “The burden of mortality attributable to diabetes: realistic estimates for the year 2000,” Diabetes Care 2005;28(9):2130–2135.
16. Flack JM, Peters R, Shafi T, Alrefai H, Nasser SA. “Prevention of hypertension and its complications: theoretical basis and guidelines for treatment,” Journal of the American Society of Nephrology 2003;14(2):S92–S98.
17. Kureja S, Malhotra N, Chhabra N. Correlation of the Serum Insulin and the Serum Uric Acid Levels with the Glycated Haemoglobin Levels in the Patients of Type 2 Diabetes Mellitus. Journal of Clinical and Diagnostic Research. 2013;7(7):1295-1297.
18. Oliveira E P, MoretoF, Arruda L V, Burini R C. Dietary, anthropometric, and biochemical determinants of uric acid in free-living adults Nutrition Journal 2013; 12:1-10.
19. Matthews D. R, Stratton I. M, Aldington S. J, Holman R. R, Kohner E. M, “Risks of progression of retinopathy and vision loss related to tight blood pressure control in type 2 diabetes mellitus: UKPDS 69,” Archives of Ophthalmology 2004;122(11):1631–1640
. 20. Schrier RW, Estacio RO,Mehler PS. “Appropriate blood pressure control in hypertensive and normotensive type 2 diabetes mellitus: a summary of the ABCD trial,” Nature Clinical Practice Nephrology 2007;3(8):428– 438.
21. Srinivasa NR, Gurumurthy P, Gururajan P, SarasaBarathi A, Krithivasan V, Saibabu R, et al. Comparison between Serum Insulin levels and its Resistance with Biochemical, Clinical and Anthropometric Parameters in South Indian Children and Adolescents. Indian Journal Clin. Biochem. 2011; 26(1): 22-27.
22. Pagano G, Pacini G, Musso G Non alcoholicsteatohepatitis, insulin resistance and metabolic syndrome: Hepatology. 2002; 35: 367-72
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25. Butturini U, Coscelli C, Zavaroni I. Insulin release in hyperuricemic patients. Harefuah. 1995;128:681-683.
26. Terrasa AM, Guajardo MH, Marra CA, Zapata G Alpha-Tocopherol protects against oxidative damage to lipids of the rod outer segments of the equine retina. 2009; 182: 463- 468.
27. Kowluru RA Diabetic retinopathy: mitochondrial dysfunction and retinal capillary cell death. Antioxid Redox Signal 2005;7: 1581-1587.
28. Plagemann PG. Transport and metabolism of adenosine in human erythrocytes: effect of transport inhibitors and regulation by phosphate, Journal of Cellular Physiology 1986;128,(3):491–500.
29. Ioachimescu AG, Hoogwerf BJ Comments on the letter by Pitocco et al. (Serumuric acid, mortality and glucose control in patients with type 2 diabetes mellitus: a PreCIS database study) Diabetic Medicine 2008;25(4):509.
30. Rema M, Srivastava BK, Anitha B, Deepa R , Mohan V. Association of serum lipids with diabetic retinopathy in urban South Indians-the Chennai Urban Rural Epidemiology Study (CURES) Eye Study-2. 2006;23(9):1029-1036.
31. Chew EY, Klein ML, Ferris FL III, Remaley NA, Murphy RP, Chantry K,Hoogwerf BJ, Miller D. Association of elevated serum lipid levels with retinal hard exudate in diabetic retinopathy. Early Treatment Diabetic Retinopathy Study (ETDRS) Report 22 Arch Opthalmol. 1996;114 (9):1079- 1084.
32. Sachdev N, Sahni A. Association of systemic risk factors with the severity of retinal hard exudates in a north Indian population with type 2 diabetes. 2010;56(1):3-6.
33. Idiculla J, Nithyanandam S, Joseph M, Mohan VA, Vasu U, SadiqM.Serum lipids and diabetic retinopathy: A cross-sectional study. 2012:16(Suppl 2):S492-494.
34. Benarous R, Sasongko MB, Qureshi S, Fenwick E, Dirani M, Wong TY, Lamoureux EL. Differential association of serum lipids with diabetic retinopathy and diabetic macular edema. Invest opthalmolvis sci. 2011; 52(10):7464-7469.
35. Valtuena S, Numeroso F, Ardigo D, Pedrazzoni M, Franzini L, Piatti PM, Monti L, Zavaroni I: Relationship between leptin, insulin, body composition and liver steatosis in non-diabetic moderate drinkers with normal transaminase levels. Eur J Endocrinol 2005; 153:283–290.
36. Larsson LI, Alm A, Lithner F, Dahlén G, Bergstrm R. The association of hyperlipidemia with retinopathy in diabetic patients aged 15-50 years in the county of Ume? ActaOpthalmolScand 1999;77(5):585-591.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareRENAL MANIFESTATIONS IN HEMATOLOGICAL MALIGNANCIES: A PROSPECTIVE STUDY
English2735Tafiq PanditEnglish Dar Maqsood AhmadEnglish Mustafa FarhatEnglish ShamimaEnglish Lone Shabir Ud DinEnglish Dar Owais HamiedEnglishBackground: The renal complications of cancer have become one of the important determinants of prognosis in patients with malignancies and combined efforts of the Hemato-Oncologist and the Nephrologist are required for care of these patients in view of the wide spectrum of syndromes that may occur. These renal complications of hematological malignancies are often preventable or reversible with prompt diagnosis and treatment.
Aims: To study the renal manifestations in haematological malignancies.
Material and Methods: The study entitled “Renal manifestations in hematological malignancies” was carried out in 60 patients with established diagnosis of a hematological malignancy admitted in different departments in Government Medical College, Jammu and associated Hospitals. This prospective study was conducted over a period of one year from 1st November 2008 to 31st October 2009. After confirmation of diagnosis all hematological malignancy patients were evaluated for clinical, biochemical, urinary, ultrasonographic and/or computed tomographic evidence of renal involvement, supported by histopathological confirmation (wherever feasible and indicated).This assessment was done at the time of admission, before institution of specific
treatment protocol for each patient, in the study group.
Observations: To summarize the important observations in the study, we found that significant renal enlargement of 1-4cms was observed in 19 cases and majority of these had bilateral enlargement. Commonest metabolic abnormality was hypokalemia (12 cases) followed by hypophoshatemia observed in 11 patients, 9 patients had hyperuricemia, 8 hypercalcemia and 8 patients had hypocalcemia The other metabolic abnormalities observed in the patients of hematological malignancies included hyponatremia in 7, hyperkalemia in 7, hypouricemia in 4 and hyperphoshatemia in 1 patient.
Conclusion: Renal involvement by tumor, although rare can sometimes be the sole manifestation of a hematological malignancy before it is detectable by routine methods. It can present as renal enlargement, obstructive uropathy, glomernlonephritis, tubular abnormalities or as paraneoplastic syndromes, so by keeping knowledge of these possibilities these tumor related catastrophes can be prevented from occurring or halted before these can endanger the life.
EnglishHypokalemia, Nephromegaly, Paraneoplastic, Hperphosphatemia, Glomernlonephritis, HematologicalINTRODUCTION
The renal complications of cancer have become one of the important determinants of prognosis in patients with malignancies and combined efforts of the Hemato-Oncologist and the Nephrologist are required for care of these patients in view of the wide spectrum of syndromes that may occur. The spectrum of diseases in hematological malignancies can be in various forms namely, acute renal failure (pre-renal, renal, post-renal), chronic renal failure, glomerulopathies, tubulointerstitial diseases, treatment related nephropathies, fluid and electrolyte abnormalities and acid-base disturbance s which can be tumor related or treatment related. These renal complications of hematological malignancies are often preventable or reversible with prompt diagnosis and treatment (1). The renal complications of malignancies in addition to paraneoplastic glomerulopathy can occur either due to: a) mechanical (direct) effect of tumor in the form of infiltration of renal parenchyma, obstructive uropathy, compression of renal vessels, b) metabolic (indirect) effects in the form of nephrocalcinosis, myeloma cast nephropathy, electrolyte disturbances, disseminated intravascular coagulation and thrombotic microangiopathy or c) treatment induced effects in the form of tumor lysis syndrome, lithiasis and uric acid nephropathy, radiation nephropathy, drug induced tubulointerstitial disease and thrombotic microangiopathy and mesangiolysis(2). The association of nephrotic syndrome and cancer is most striking in the patients with hematological neoplasias particularly in mixed cellularity type of hodgkins disease (3). Proteinuria tend to reappear with relapse of lymphoma, supporting the statement that nephrotic syndrome is a consequence of malignant disease and not a coincidence (4). Renal failure is the second most common cause of death in cases of multiple myeloma. Renal failure in multiple myeloma can be related to abnormal paraproteins, hypercalcemia, hyperuricemia, dehydration, the use of intravenous contrast agent, nephrotoxic drugs and many other factors(5). Considering the above facts, we conducted a prospective study to know the pattern of renal manifestations in patients with hematological malignancies like lymphomas, leukemias and multiple myeloma who were admitted in Government Medical College, Jammu and associated Hospitals.
AIMS AND OBJECTIVES
To study the renal manifestations in hematological malignancies
MATERIAL AND METHODS
The study entitled “Renal manifestations in haematological malignancies” was carried out in 60 patients with established diagnosis of a haematological malignancy admitted in different departments in Government Medical College, Jammu and associated Hospitals. This prospective study was conducted over a period of one year from 1st November 2008 to 31st October 2009. All the eligible patients were explained the purpose of study and were invited for participation. All leukemic patients were characterized as per FAB classification whereas lymphoma patients were subdivided on histological basis (working formulation). After confirmation of diagnosis all haematological malignancy patients were evaluated for clinical, biochemical, urinary, ultrasonographic and/or computed tomographic evidence of renal involvement, supported by histopathological confirmation (wherever feasible and indicated.) This assessment was done at the time of admission, before institution of specific treatment protocol for each patient, in the study group.
Definitions:
Leucocyturia, was defined if urine contained more than 3 leucocytes per high power field.
Hematuria, was defined when urine contained more than 3 erythrocytes per high power field
. Poteinuria, was taken when 24 hour urinary protein concentration was more than 150 mg/dl.
Urinary sodium was taken as low (hyponatremia) and high (hypernatremia) when the values were below 20 mmol/l and above 110 mmol/l respectively.
Urinary potassium was taken as low (Hypokalemia) and high (Hyperkalemia) when the values were below 12mmol/l and above 75mmol/l respectively .
Urinary creatinine below 30mg/dl and above 125mg/dl was taken as low and high respectively.
Urinary calcium was taken as low (Hypocalcemia) and high (Hypercalcemia) when the values were below 42mg/dl and above 353mg/dl respectively.
Urinary phosphorus values below (Hypophosphatemia) 20mg/dl and above (Hyperphosphatemia) 60mg/dl were taken as low and high respectively.
Similarly urinary uric acid values below 7.5mg/dl and above 49.5mg/dl were taken as low and high respectively.
Clinical evaluation
The study subjects were assessed for renal involvement by examining for pedal edema, facial puffiness , hypertension, renal enlargement / renal mass and renal angle tenderness.
Biochemical evaluation:
All patients in this study had undergone urea and creatinine estimation before treatment protocol was started. The estimations were done by using Diacetyl monoxime (DAM) method and alkaline picrate method respectively. Besides, all the patients were evaluated for hypo- and hyperkalemia, hypo-and hyperphosphatemia, hypo-and hypercalcemia, hypo-and hypernatremia and for hypo- and hyperuricemia. Serum electrolytes and other biochemical parameters, needed in the study, were estimated by Dade’s Behring Dimension AR automated analyzer. Arterial blood gas analysis was done by using AVL blood gas analyzer.
Urinary parameters: The patients in this study had undergone the analysis for the following urinary parameters:
1. Complete Urinalysis for Gross and microscopic examination, Urinary sugar by Benedict’s qualitative glucose test, Urinary proteins by heat and acetic acid test/ sulphosalicylic acid test.
2. 24 hour urinary protein estimation was done by using Esbach’s quantitative method. On the basis of proteinuria, patients were divided into two groups:- Group-a):- patients with non-nephrotic poteinuria with urinary proteins less than 50mg/kg body weight/day Group-B):- Patients with nephrotic proteinuria with urinary proteins more than 50mg/kg body weight/day.
3. Bence Jones protein detection was done by heat and sulphosalicylic acid.
4. Urinary sodium, potassium, calcium, phosphorus, uric acid and creatinine estimation was done by using Dade’s Behring Dimension AR automated analyzer.
In hyponatremic patients the fractional excretion of sodium (FENa+) was calculated from the equation:
All the investigations were done in the Nephrology, Biochemistry and Hemotology laboratories of Government Medical College, Hospital Jammu.
Ultrasonography (USG): All patients in the study underwent USG examination, before and after specific treatment, by an experienced sonologist who was unaware of the study, in order to determine the kidney size (normal 9-12cm X 3-5cm X 2-3cm) and extent of renal, para-renal and peri-renal involvement by the disease process. Renal enlargement in these patients was taken as per reference values given by Emamian SA et al in 1993 (9). Ultrasonography was done by using grey scale real-time ultrasound scanner. For adults transducer with a frequency of 3.5 MHZ and for children 5-7 MHZ transducer was used.
Computed tomography: Though highly sensitive than USG, in defining the renal lesions, size, extension and retroperitoneal involvement in hematological malignancies, was done only in few cases with suspicion or evidence of renal involvement.
Kidney biopsy: Percutaneous kidney biopsy was done in patients with kidney involvement where consant for such procedure was given by the patients and / or their attendants. Indication was nonnephrotic range proteinuria, nephrotic syndrome, unexplained renal failure and renal enlargement.
Ethical committee clearance: We undertook study after due clearance from the hospital ethical committee which composed of senior faculty members of the government medical college jammu. Regarding funding for the study, nothing was charged from the subjects as it was conducted in government hospital were all investigations charges were taken care of by the hospital. Only some medications were purchased by the patients in study which they had to buy otherwise also for their management and not related to nature of study itself.
Observations:
Renal manifestations in hematological malignancies in 60 consanted patients were studied for a period of 1 year from Ist. November 2008 to 31st October 2009. There were 42 males and 18 females in the study population. The age of subjects ranged from 3 to 75 years (mean 43.12 years). All of these patients were admitted in Government Medical College, Jammu and associated Hospitals, in different departments. Of these 60 patients 14 had lymphoma, 36 leukemia and 10 had multiple myeloma Fig.1. In the lymphoma group 5 had Hodgkins disease and 9 had non-Hodgkin’s lymphoma, including 1 primary bone lymphoma. Out of 36 leukemic patients, 15 had acute myelocytic leukemia, 11 acute lymphoblastic leukemia, 8 chronic myelocytic leukemia and 2 had chronic lymphocytic leukemia Table 1. Our observations were diverse as the renal complications in hematological malignancies were concerned depending upon the type of hematological malignancy (Table 2). With respect to hodgkins lymphoma out of 5 patients, 1 patient had clinical evidence of anasarca and his urinalysis revealed nephrotic proteinuria, dysmorphic red blood cells and red cell casts. Renal histopathology of this patient was related to minimal change disease. One of the 5 patients had acute renal failure who on ultrasonography revealed bilateral renal enlargement with irregular contours but no evidence of dilated collecting system or retroperitoneal lymphadenopathy. Out of 9 patients of NHL, two patients had non-nephrotic proteinuria and 2 others had azotemia. Ultrasonography carried out in all these patients revealed bilateral nephromegaly in 2 patients and 1 more had unilateral enlargement of the kidney with a difference of more than 2 cms between the two sides. Renal size decreased significantly after appropriate treatment of the underlying disease and varied from 2 to 3.5 cms. Two Patients presented with oliguric renal failure and both of these patients revealed significant nephromegaly on ultrasound without any evidence of hydronephrosis. In case of multiple myeloma, out of 10 patients in the study, 1 patient had generalized edema, 3 others had evidence of pedal edema and peri- orbital puffiness. 1 patient had nephrotic proteinuria and 2 others had trace proteinuria. In addition urinalysis revealed leucocyturia in 3, hematuria in 2 and casts in 2 patients. Bence Jones proteinuria was demonstrated in 4 Patients. Ultrasonography revealed nephromegaly in one patient which did not regress significantly after treatment and 1 more had bilateral renal calculi without any hydronephrosis. Three of these patients had renal failure at presentation and 1 more developed it after chemotherapy. In one patient of renal failure there was frequent history of analgesic intake (NSAID-induced) and no other evident cause for renal failure. Three patients had significant hypercalcemia, with normal serum phosphorus. Other metabolic abnormalities found in this group were hyperkalemia in 2 patients with renal failure, hypophosphatemia in one and hyponatremia in one patient. Arterial blood gas analysis revealed metabolic acidosis in 3 patients of acute renal failure. In the CML group (8 patients) nephromegaly was found in 2 patients which reversed with treatment but renal biopsy couldn’t be done in these patients because of bleeding manifestations and severe nature of illness. Non-nephrotic proteinuria with pedal edema was present in one of these patients who was in blast crisis phase. Urinalysis, in addition to proteinuria, in this patient revealed hematuria and granular casts. Arterial blood gas analysis of this patient revealed respiratory alkalosis. Among two patients of chronic lymphocytic leukemia in the study one patient had nephromegaly with no features of obstructive uropathy. This patient also had hyperuricemia and his urinalysis revealed sterile leucocyturia and microscopic hematuria. In case of AML (15 patients) , we observed proteinuria in 6 patients, leucocyturia in 2, hematuria in 3, granuler casts in 3, Red blood cell casts in 1, and hyaline casts in 1 patient. One of the 15 patients had oliguria and 1 more had polyuria. Nephromegaly was observed in 4 patients which regressed in 3 patients after treatment by about 1.5- 2.5 cm. 2 patients had azotemia . Hypokalemia was the most frequent abnormality observed in 5 of 15 acute myeloid leukemic patients. Majority (4 of 6) of these hypokalemic patients were in AML-M4 subgroup. All these hypokalemic patients had fractional excretion of potassium more than 6.4%, suggestive of renal potassium wasting. Hypophosphatemia was observed in 4 patients and 3 of these had significant phosphaturia with fractional excretion of phosphorus more than 20 % while as one of these patients had phosphate excretion below normal range. Two patients had hyponatremia and one of these patients had fractional excretion of sodium (FENa) more than 3%, suggesting inappropriate natriuresis while as the other had FENa 6.4%). One of the 11 patients had kaliuresis but had no hypokalemia.
To summarise the important observations in the study, we found that significant renal enlargement of 1-4cms was observed in 19 cases and majority of these had bilateral enlargement. Nephromegaly was commonly observed in acute lymphoblastic leukemia group.Proteinuria was present in 18 cases and 2 of these had full blown nephrotic syndrome. Renal histopathology of 1 patient was suggestive of minimal change glomerulonephritis while as the other 1 had indirect evidence of amylodotic kidney. In rest of the 16 cases proteinuria was in nonnephrotic range. Commonest metabolic abnormality was hypokalemia (12 cases) followed by hypophoshatemia observed in 11 patients, 9 patients had hyperuricemia, 8 hypercalcemia and 8 patients had hypocalcemia. The other metabolic abnormalities observed in the patients of haematological malignancies included hyponatremia in 7, hyperkalemia in 7, hypouricemia in 4 and hyperphoshatemia in 1 patient. Azotemia was observed in 10 patients and majority (4) of these patients were in myeloma group . A total of 20 patients in this study had acid-base disturbance on arterial–blood gas analysis. The major acid– base disturbance observed was metabolic alkalosis, commonly observed in acute leukemia group.. In addition to proteinuria urinalysis of these malignancy patients revealed, urinary casts in 15, hematuria in 13 and leucocyturia in 12. These urinary abnormalities observed were most commonly in acute myeloid leukemia group. Three patients had tumor lysis syndrome in the study one of which was treatment related. All these renal complications of malignancies whether tumor or treatment related require care by a multidisciplinary team.
DISCUSSION
The renal complications of malignancy have become one of the important determinants of prognosis. Hence early diagnosis and effective management of these complications is necessary to improve survival and prognosis in these patients. In order to know the pattern of renal complications in hematological malignancies in our part of the world we conducted a study in different departments of GMC jammu. Out of total 60 patients included in the study, 19 (31.67%) patients showed enlarged kidneys on ultrasonography. None of these patients showed evidence of hydronephrosis. The renal enlargement was bilateral in majority of these patients (78.95%).The renal size regressed in the patients by 1 to 3.5 cms after appropriate treatment and this initial increase followed by decrease in size was related to renal infiltration of the kidneys by hematological neoplasias. Present study closely correlates with other reported series like Xiao JC (1997) and Martinez-Meldonado M (1966) (10) and (11), who reported renal infiltration in 34% and 42.3% cases respectively. Out of 36 patients with various leukemias in the study, 14 (38.89%) showed nephromegaly due to leukemic infiltration. Our study closely correlates with the study of Khanna UB et al, 1985 (12) who reported renal infiltration in 42.85% of leukemia cases. Autopsy data by Norris HJ et al (1961) and Shapiro JH et al (1962) (13) and (14) observed renal invasion in 47-61% and upto 60% cases respectively. Diffuse parenchymal infiltration is most frequent pattern of invasion in acute leukemias but can be seen in non-Hodgkin’s lymphoma also. The association of nephrotic syndrome and cancer is most striking in patients with hematological neoplasias. Though it may occur in various hematological neoplasias but nephrotic syndrome is most common in Hodgkin’s disease especially in mixed cellularity type (15). In a study by Eagen JW and Lewis EJ in 1977 (16) about 45% of cases of nephrotic syndrome occur concurrently with Hodgkin’s disease, 10% precede the lymphoma and in 40- 50% nephrotic syndrome is manifested after the tumor is diagnosed. However, in the present study only 1 out of 5 cases of Hodgkin’s lymphoma had nephrotic syndrome and renal biopsy was suggestive of minimal change glomerulonephritis. This case of nephrotic syndrome was diagnosed concurrently with the diagnosis of Hodgkin’s disease, although it might have preceded the lymphoma but history favoured concurrent occurrence. The disappearance of nephrotic proteinuria after chemotherapy most probably favours the paraneoplastic nature of nephrotic syndrome and not a coincidental phenomenon. Khanna UB et al in 1985 (17) reported that all of their patients with renal involvement had Bence Jones proteinuria. In our study, Bence-Jones proteinuria was present in 4 (40%) of 10 patients with multiple myeloma and in 3 of 4 patients it was associated with renal failure. A total of 10 patients had renal failure in our study. Two patients of acute myeloid leukemia, 1 patients of acute lymphoblastic leukemia, 1 patient of Hodgkin’s lymphoma and 4 patients of multiple myeloma were azotemic in the present study. Merrill D and Jackson H JR in 1943 (18) reported 2 cases of myelogenous leukemia associated with renal failure. In these, autopsy findings supported microvascular insufficiency from stasis and obstruction of blood vessels and glomeruli by masses of leukemic cells. One of our acute lymphoblastic leukemia (ALL-L3 FAB) patient had hyperuricemic renal failure due to Grade ‘0’ spontaneous tumor lysis syndrome, and precipitated by dehydration. Obrador GT et al in 1997 (19) reported a case who presented with acute renal failure secondary to massive lymphomatous infiltration of kidneys in whom chemotheraphy resulted in rapid improvement in renal function and regression of renal size. Gross hematuria from hemorrhagic necrosis of the kidney and tumor lysis syndrome from steroid induced lympholysis was additional features of this case. Of the 60 patients, a total of 8 (13.33%) patients had hypercalcemia which included 3 (30%) patients of myeloma, 3 (8.33%) patients of leukemia, and 2 (14.28%) patients of lymphoma. This study closely correlates with the study of Burt ME and Brennan MF, 1980 (20) who reported the incidence of hypercalcemia in haematological malignancies as 10.9% and relatively high incidence was found in multiple myeloma (28.1%) followed by non- Hodgkin’s lymphoma (13.0), leukemia (11.5%) and Hodgkin’s disease (5.4%). Two (22.22%) patients of non- Hodgkin’s lymphoma in our study had calcitriol-mediated hypercalcemia. Baechler R et al in 1985 (21) reported that incidence of hypercalcemia in high and intermediate grade non-Hodgkin’s lymphoma may be as high as 30%. This correlates well with our study. In the present study, 3 (37.5%) of 8 hypercalcemic patients were in leukemic group and the hypercalcemia in them was related to parathyroid hormone related peptide. This closely correlates with the study of Ratcliffe WA et al, 1992 (22) who reported that 33% of the hypercalcemic patients in haematological malignancies were related to production of parathyroid hormone related peptide. In our study, a total of 8 (13.33%) patients had hypocalcemia. Two (14.29%) patients of lymphoma and 6 (16.66%) of leukemia group had hypocalcemia while none of our multiple myeloma patients had hypocalcemia. Mckee L.C. JR in 1975 (23) reported hypocalcemia in 19 (10.4%) of the 182 patients of leukemia group. This was observed in 5 (9%) patients with acute leukemias, 5 (6%) patients with chronic lymphatic leukemia and in 9 (22%) patients with chronic myeloid leukemia. In 15 out of 19 cases hypocalcemia were related to poor renal function or to hypoalbuminemia. Out of 26 acute leukemic patients, a total of 10(38.46%) including 6(40%) of acute myeloid leukemia patients and 4(36.36%) of acute lymphatic leukemia patients had hypokalemia. This study closely correlates with the recent observations in a review article by Filippatos TD et al, 2005 (24) who reported hypokalemia in 43-64% of acute leukemic patients. In 10 (38.46) of our hypokalemic patients in acute leukemia group majority had it related to inappropriate kaliuresis, either due to lysozymuria-induced tubular injury or some leukemic factor induced renal potassium wasting. (25). One of our patients in chronic myeloid leukemia and 1 more in non-Hodgkin’s lymphoma group had hypokalemia related to inappropriate kaliuresis. This increased urinary potassium loss could be due to hypercalcemia induced tubular damage, which might impair sodium reabsorption and lead to increased flow of sodium and water to the collecting tubules and subsequent potassium wasting (26). A total of 7 (11.67%) i.e 2 (14.29) in leukemia, 2 (5.55) in lymphoma, and 3 (30%) in myeloma group had hyperkalemia. In 4 (57.14) of these patients hyperkalemia was related to renal failure while as 3(42.86%) others had hyperkalemia related to tumor lysis syndrome and associated urate nephropathy. Hyperkalemia could be due to the accumulation of electrolytes as a result of urate nephropathy or as a result of renal failure due to leukemic infiltration of the kidneys and/ or severe leukostasis with consequent microvascular insufficiency(27). Furthermore, hyperkalemia could be the result of potassium release from malignant cells following cytotoxic therapy due to tumor-lysis syndrome which typically occurs in patients with lympho proliferative malignancies who are exposed to chemotherapy, radiation or corticosteroids but can occur spontaneously in the absence of treatment (28) We reported hypophosphatemia in 11(18.33%) patients in this study . Out of these, 2 had lymphoma, 8 had leukemia and 1 more had multiple myeloma. Hypophosphatemia is a relatively common disturbance in patients with acute leukemias. Low serum phosphate levels have been reported in upto 30% of patients (29) .Young IS et al 1993 (30) described a case of severe hypophosphatemia due to both increased utilization of phosphate by rapidly growing tumor cells as well as tubular defectassociated excessive phosphate urinary losses. In our study only 1 patient had hyperphosphatemia that too was in multiple myeloma group. This patient of multiple myeloma had treatment induced tumor lysis syndrome In this study, a total of 4(6.67%) had hypouricemia. Three of the hypouricemic patients were in leukemic group and 1 more in lymphoma group. Out of 60 patients, 9 (15%) had hyperuricemia which comprised 5 (13.89%) patients of lymphoma, 4 (11.11%) patients of leukemia and 1(10%) patient of multiple myeloma. Hyperuricemia resulting in acute uric acid nephropathy is the most frequently recognized metabolic cause of renal insufficiency in acute tumor lysis syndrome (31). Hyperuricemic acute renal failure is usually a complication of high turnover tumors (spontaneous tumor lysis syndrome) or of their successful treatment with rapid tumor lysis (frequently complicated by hyperphosphatemia and hyperkalemia) (32). Seven (11.67%) of the 60 patients in our study had hyponatremia, 2 (14.29) of 14 patients of lymphoma, 4 (11.11%) of 36 patients of leukemia and 1 (10%) of 10 patients of multiple myeloma had hyponatremia. Three of our hyponatremic patients had it due to hypovolemic hyponatremia (gastrointestinal losses) and 1 more had it related to diuretic use. Whereas 2 other fulfilled the criteria for syndrome of inappropriate secretion of antidiuretic hormone (cytotoxic drugs related) and 1 more had inappropriate natriuresis probably due to leukemia induced tubular defect.Our study closely correlates with the study of Milionis HJ et al, 2005 (29) who reported hyponatremia in about 10% of their acute leukemia patients. We found acid-base disturbance in 20(33.33%) patients among which 6(10%) had metabolic acidosis, 9(15%) alkalosis and the rest 5(8.33%) patients had mixed acidbase disturbance. Metabolic alkalosis in our 7 patients was probably related to hypercalcemia, volume depletion and hypokalemia while as respiratory alkalosis in 2 patients was related to respiratory tract infection and hypoxemia. Metabolic acidosis however was related to renal failure. Filippatos TD in 2005 (24) reported metabolic alkalosis in 35%, metabolic acidosis in 10% and mixed acid-base disturbance in about 15% of the acute leukemic patients. In the present study 1 patient of multiple myeloma had treatment induced tumor lysis syndrome while 2 other patients (1 of ALL-L3 and 2nd in non-Hodgkin’s lymphoma) had grade ’o’ spontaneous tumor lysis syndrome as per Cairo-Bishop grading classification of tumor lysis syndrome (33)
CONCLUSION
In our study we found that majority of patients with haematological neoplasia had evidence of tumoral infiltration of Kidneys and metabolic derangements, which needed timely intervention to improve the survival and prognosis in these patients. Since these renal complications, whether tumor or treatment related, are often preventable and reversible, hence much can be done for these patients to improve their survival by decreasing or preventing these complications from occurring. Renal involvement by tumor, although rare can sometimes be the sole manifestation of a haematological malignancy before it is detectable by routine methods. It can present as renal enlargement, obstructive uropathy, glomernlonephritis, tubular abnormalities or as paraneoplastic syndromes, so by keeping knowledge of these possibilities these tumor related catastrophes can be prevented from occurring or halted before these can endanger the life.
Abbreviations: FAB: french American britain
Dam: diacetylmonoxime
FENa+ : fractional excretion of sodium
FEK+: fractional excretion of potassium
FEPo4 3- : fractional excretion of phosphorus
USG : ultrasonography
MHZ: megahertz NSAIDS: non steroidal anti inflammatory drugs
NHL: non hodgkins lymphoma
CML: chronic myeloid leukemia
AML: acute myeloid leukemia
ALL: acute lymphocytic leukemia
CLL: chronic lymphocytic leukemia
GMC: government medical college
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.
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7. Narins RG, Jones ER, Stom MC et al: Diagnostic strategies in disorders of fluid, electrolyte and acid base homeostasis. Am.J.Med :72 :496-520,1982.
8. Kelton J, Kelley WN, Holmes EW: A rapid method for the diagnosis of acute uric acid nephropathy. Arch intern. Med.138:612-615,1978.
9. Emamian SA, Nielsen MB, Pedersen JF, ytte L: Kidney Dimensions at Sonography: correlation with age, sex, and habitus in 665 adult volunteers AJR;160:83-86,1993.
10. Xiao JC, Walz –Mattmuller R, Ruck P, Horny HP, Kaiserling E: Renal involvement in myeloproliferative and lymphoproliferative disorders: A study of autopsy cases. Gen. Diagn. Pathol. 142(3-4):147-53,1997.
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareEFFECTS OF CHRONIC EXPOSURE TO 2G AND 3G CELL PHONE RADIATION ON MICE TESTIS
- A RANDOMIZED CONTROLLED TRIAL
English3647N. MugunthanEnglish J. AnbalaganEnglish A. Shanmuga SamyEnglish S. RajanarayananEnglish S. MeenachiEnglishObjective: The aim of our study is to evaluate possible effects of chronic exposure to 900 - 1800 MHz radiation emitted from 2G cell phone and 1900 -2200 MHz from 3G cell phone on the testis of mice and to compare the effects of 2G and 3G radiation on testis at the histological level.
Methods: Mice were exposed to 2G and 3G ultra-high frequency radiation, 48 minutes per day for a period of 30 to 180 days. The sham control mice were exposed to similar conditions without 2G or 3G exposure. Animal’s weight of 2G and 3G cell phone exposed group were recorded before sacrificing at the end of 30, 60, 90,120,150 and 180 days. Same numbers of control animals were sacrificed on the same period. Blood samples were collected to measure plasma testosterone. Both the testes were dissected and its size, weight and volume were measured. The testes were processed for histomorphometric study.
Results: Following chronic exposure of 2G and 3G cell phone radiation in mice, there was significant reduction of animal weight at first, second and fourth month. The mean testis weight and volume of 2G and 3G radiation exposed mice were significantly reduced in the first three months. The comparison between 2G and 3G exposed groups, showed no significant changes in mean body weight, mean testis weight and mean testis volume. The mean density of seminiferous tubule, mean seminiferous tubule diameter, mean number of Sertoli and Leydig cells of 2G and 3G exposed groups had significantly lower value than the control. The following microscopic changes were observed in the 2G and 3G radiation exposed mice testis over control. 1. Wide interstitium
2. Detachment of Sertoli cells and spermatogonia from the basal lamina. 3. Vacuolar degeneration and desquamation of seminiferous epithelium. 4. Peripheral tubules showed reduced thickness of seminiferous epithelium and maturation arrest in the spermatogenesis. 5. Seminiferous tubules scored 7 to 9 using Johnson testicular biopsy score count. The mean total serum testosterone level of first, second, third, fourth and sixth month 2G and 3G exposed mice had significantly lower serum testosterone level than control. However, comparison between 2G and 3G showed no significant difference in the mean serum testosterone level.
Conclusion: Chronic exposure to ultra-high frequency radiation emitted from 2G and 3G cell phone could cause microscopic changes in the seminiferous epithelium, reduction of serum testosterone level, reduction in the number of Sertoli cells and Leydig cells.
English2G cell phone, 3G cell phone, Mice testis, Testosterone, Ultra-high frequency radiationINTRODUCTION
The increasing use of cell phone and handset devices emitting radiofrequency electromagnetic fields, particularly by children and teenagers, raises a great concern about the interactions of radiofrequency radiation on the male reproductive organs. Electromagnetic radiation emitted from the cell phone could be absorbed by testis when they are carried in belts. Most of the cellular phones work on the ultra-high frequency bandwidth of 900- 2200 MHz’s. Ultra high frequency (UHF) electromagnetic radiation or radiofrequency radiation (RFR) with a frequency range of 300- 3000 MHz is “non-ionizing”. The present inquest is concerned this form of radiation either to incriminate it as potentially hazardous or absolve it as absolutely harmless. The second generation cell phone (2G) network operates in the 900-1800 MHz frequency and third generation cell phone (3G) network operates in the 1900-2200 MHz frequency for GSM (Global System for Mobile Communications)1 . Mobile phone in operation emits a pulsed radiofrequency electromagnetic field (RF-EMF). Most of the energy is found to be absorbed into user’s body particularly in the head region, which can produce heat stress and non-thermal stress in the form of releasing free radicals, alter the enzyme reaction and thereby compromises immune system2 . Specific absorption rate (SAR) is a unit of Watt per kilogram to measure the amount of electromagnetic radiation absorbed by body tissue whilst using a mobile phone3, 4. The higher the SAR the more radiation is absorbed. International Commission on Non-Ionising Radiation Protection (ICNIRP Guidelines 1998) recommendations has set a SAR limit of 2.0 W/Kg in 10 grams of tissue. Whole body average SAR of 0.4W/Kg is widely adopted in most guidelines, which were based on the threshold of the observed effects due to whole-body heating to cause significant elevation of core temperature (>1°C)1 . Review of literature shown that exposure to mobile phone radiation could induce damage to tissues which include an increase in single and double strand DNA breakages5 , increased risk of acoustic neuroma associated with mobile phone use of at least ten years duration6 , genotoxic effects in human peripheral blood leukocytes7 , reduction of Purkinje cell number in the adult female rat cerebellum8 , and disturbance of short term memory in mice9 . Authors have reported that short term exposure to mobile phone radiation induced damage to kidney10-14. Keeping a cell phone on or close to the waist can decrease sperm concentration15, decrease in sperm viability and motility due to direct exposure of semen to cell phone radiation16. Long term exposure to mobile phone radiation could lead to reducing sperm motility, serum testosterone levels17-20, increased ROS (reactive oxygen species) 21-24, reduction in seminiferous tubule diameter and thickness of epithelium25 and vacuolisation in the cytoplasm of Sertoli cell 26 In contrary to above findings some researchers reported that no adverse biological effects of exposure to non-ionizing radiation emitted from the cell phone, such as no double stranded DNA breaks or effects on chromatin of rat brain27, no effect on mouse embryonic lens development28, psychomotor performance was not influenced by brief repeated exposures to mobile phones29.The lack of histological changes on rat testis30, 31 and no alterations in serum testosterone32 were cited. The present study is undertaken because of the contradictory findings on the effects of exposure to non-ionizing radiation emitted from the 2G and 3G cell phone on testis. The aim of our study is to evaluate possible effects of chronic exposure to 900 - 1800 MHz radiation emitted from 2G cell phone and 1900 -2200 MHz from 3G cell phone on the testis of mice; and to compare the effects of 2G and 3G radiation on testis at microstructure level.
MATERIALS AND METHODS
Our study was approved by the Institutional Animal Ethics Committee of Mahatma Gandhi Medical College and Research Institute, Puducherry.Fifty four male neonatal albino mice were obtained from the King Institute of Preventive Medicine and Research, animal section, Guindy, Chennai. New born mice (with the mother for twenty one days) were randomly divided into three independent groups; control, 2G exposed and 3G exposed. Animals were kept in mice cages at the temperature of 22 ± 1°C, 60% relative humidity and housed in the central animal house provided with adequate ventilation; twelve hours of illumination alternated with twelve hours of darkness. During the study, all the animals received appropriate animal care and were fed with laboratory diet and water ad libitum. Eighteen mice were exposed to 900-1800 MHz frequency radiation emitted from 2G cell phone and eighteen mice were exposed to 1900-2200 MHz frequency radiation emitted from 3G (video call) cell phone. Eighteen mice were sham control. The roof of the mice cage was designed to hang the 2G and 3G (video call) cell phone from the distance of five centimetres from the floor; which allow the mice to move freely and to avoid direct thermal injury in mice. 2G and 3G (video call) mobile phone in non-vibrating, silent, do not disturb (DND) and auto answer mode activated was kept hanging inside the mice cage. EMF emitted from a 2G and 3G standard handset with a frequency bandwidth of 900-1800 MHz and 1900 – 2200MHz respectively with the power of 2W/Kg. The highest specific absorption rate (SAR) value for this standard handset was 1.69 W/Kg (10gm).The mobile phone which was kept inside the mouse’s cage was rung upon from other 2G and 3G (video call) cell phone for every half an hour, each call lasting for two minutes. Mice were exposed forty eight minutes per day for a twelve hour periods (from 8.00AM to 8.00PM) and total duration of exposure was 30 to 180 days. RF meter was used to measure the amount of radiation exposed in 2G and 3G experimental groups. The sham control group of eighteen mice was kept under similar conditions without 2G or 3G exposure. Before sacrificing, we measured the body weights of mice in all three groups. Three mice each were sacrificed at the end of 30, 60, 90, 120, 150 and 180 days of exposures in the experimental groups after 24 hours of last exposure. Equal numbers of control mice were sacrificed on a similar time points. We sacrificed mice under anaesthesia and collected 1 ml of blood by cardiac puncture for total serum testosterone measurement and all samples were read in duplicate. Testes were dissected out and its weight and volume measured. We used Denver’s digital weighing machine (0.001gm) for measuring weight and water displacement method to calculate volume. After the morphometric analysis, testes were fixed by 4% formalin solutions for a period of twenty four hours and then tissues processed and embedded in paraffin. Tissues were sectioned at five microns, stained with Haematoxylin and Eosin. We analysed testis sections from random slide, random sections and random field under the light microscope; for histomorphometric parameters and structural changes. Diameters of 50 randomly selected essentially round seminiferous tubules from each testis were measured using calibrated ocular micrometre. We measured the seminiferous tubule diameter in both horizontal and vertical axis and the mean average was taken. The mean seminiferous tubule density per unit area was calculated by square graticule which was mounted on an eyepiece. All the testis sections were blindly reviewed by the same investigator. Each seminiferous tubule was analysed and classified into one of 10 different grades utilizing Johnson testicular biopsy score count33. The total serum testosterone measured by enzyme linked fluorescent immunoassay (ELFA) method.
Statistical analysis
We used ANOVA and Kruskal–Wallis test to compare all three groups; independent t test and Mann Whitney U test for comparing 2G and 3G groups. P value ≤ 0.05 was considered statistically significant.
RESULTS
Morphometric study: The mean body weight of mice sacrificed during first, second and fourth month was significantly differing amongst three groups by ANOVA (p value 0.05) (Table 1-3). Histomorphometric study: The mean density of seminiferous tubule (per unit area of 578µ2 ), mean seminiferous tubule diameter (in micron), mean number of Sertoli and Leydig cells of mice sacrificed every month were significantly differing amongst three groups by ANOVA (p value 0.05) (Table. 7). The following microscopic changes were seen in the 2G and 3G radiation exposed mice testis over control. 1. The interstitium between tubules appeared morewide 2. Sertoli and spermatogonial cells appeared detached from the basal lamina. 3. Vacuole degeneration and desquamation of seminiferous epithelium. 4. Most of the peripheral tubules showed reduced thickness of seminiferous epithelium and maturation arrest in the spermatogenesis 5. Seminiferous tubules scored 7 to 9 using Johnson testicular biopsy score count (Table. 8) (Figure. 4 and 5). Biochemical Study: Mean serum testosterone (ng/ml) of first, second, third, fourth and sixth month mice were significantly differed amongst three groups by ANOVA (p value 0.05) (Table.9) (Figure.6).
DISCUSSION
The present study has been undertaken to investigate the effects of chronic exposure of 2G and 3G cell phone radiations on mice testis; and to compare the effects of 2G and 3G radiations on testis at the histological level. Chronic exposure of 2G and 3G cell phone radiation to mice, resulted in reduction of animal weight at first, second and fourth month. The mean testis weight of 2G and 3G radiation exposed mice was significantly reduced in the first three months, however in fifth month mean testis weight was significantly increased. Similarly mean testis volume of 2G and 3G radiation exposed mice was significantly reduced in the first three months. The mean density of seminiferous tubule, mean seminiferous tubule diameter, mean number of Sertoli and Leydig cells of 2G and 3G exposed groups were significantly lower than control group. When compared to control group mean serum testosterone level of 2G and 3G exposed mice was significantly lower. Sections of 2G and 3G radiation exposed mice testis showed wide interstitium, detachment of Sertoli cells and spermatogonia from the basal lamina, vacuolar degeneration and desquamation of the seminiferous epithelium. Most of the peripheral tubules showed reduced thickness of seminiferous epithelium and maturation arrest in the spermatogenesis. Seminiferous tubules scored 7 to 9 in Johnson testicular biopsy score count. In earlier studies of Ozguner M et al (2005)34 and Hanci H et al (2013)25, rat was exposed to 900MHz cell phone radiation and found there was a significant decrease in seminiferous tubular diameter, mean height of the seminiferous epithelium and serum total testosterone level. Our study agreed with Ozguner M et al and Hanci H et al study with the above mentioned parameters in mice testis indicating that there was no species difference. Our study agreed with S Dasdag et al study (1999)35 on rat exposed to microwaves emitted by cell phone The author reported significant reduction of mean seminiferous tubular diameter and Johnson testicular biopsy score count was between 8 to 10. In the study of LatifaIshaqKhayyat (2011)12 and Pradeep Kumar (2014)36, the electromagnetic field of cell phones induced Leydig cell hypoplasia, wide interstitium, atrophied seminiferous tubules, maturation arrest in the spermatogenesis, decreased germ cell population, pyknotic nuclei in germ cell and vacuolisation in spermatogenic cells. They also observed detachment of spermatogonia and Sertoli cells from the basal lamina, shrinkage, residual cytoplasm and debris of degenerating cells in the seminiferous tubules. The present study conducted with mice was in agreement with Latifa Ishaq Khayyat12 and Pradeep Kumar study36. Our study agreed with the findings of Ali H.M.Omer et al (2009)37 who observed reduction of serum testosterone level inthe rat after exposure of 900MHz electromagnetic radiation. Similar reduction in serum testosterone level have been cited by Salem Amara et al (2006)38, Mugunthan et al (2014)39 and Wang S M et al (2003)20. H.OzlemNisbet et al (2011)40 found that exposure of the rat to 900 to 1800 MHz radiations produced severe vacuolar degeneration, necrosis and desquamation of the seminiferous epithelium; they also reported high level of mean plasma testosterone in experimental group than the sham control group. Our study showed significant reductions in mean serum total testosterone level in mice. Study conducted by ZsoltForgacs et al (2006)41 on mice exposed to 1800 MHz GSM like microwave observed significant increase in serum testosterone without any structural changes in testis. The present study showed structural changes in mice seminiferous epithelium and lower serum testosterone level.The present study disagreed with Ji Yoon Kim et al (2007)42 who observed long term exposure of rats to 2.45 GHz radiations induced increase in the number of Leydig cells and increased serum total testosterone level. Leydig cells are most susceptible to electromagnetic radiation. Radiation might be detrimental to the structure and function of Leydig cells and thereby reduce the serum testosterone level20. This could be responsible for the significant reduction in the mean number of Leydig cells and serum testosterone level of 2G and 3G exposed mice in our study. Cell phone radiation could cause increased vascular permeability and thereby interstitial oedema43. We observed wide interstitium in the sections of 2G and 3G radiation exposed mice testis and it could be the reason for the significantly low mean density of seminiferous tubules per unit area in 2G and 3G radiation exposed mice testis. The surface organ such as testis could be more affected by the radiation emitted from the cell phone. Even though mice testis movesto abdomen through the inguinal canal (abdomino-scrotal), energy absorbed (SAR) by testis could be more as it is predominantly surface organ. This could be probable reason for the predominant damages observed on the peripheral tubules of testis exposed to 2G and 3G cell phone radiations.
CONCLUSION
Chronic exposure of mice to ultra-high frequency radiation emitted from 2G and 3G cell phone could cause a reduction in body weight, testis weight and volume. Microscopic changes in the testis such as reduction in mean seminiferous tubule density, seminiferous tubule diameter, vacuolar degeneration and desquamation of the seminiferous epithelium; reduction in the thickness of seminiferous epithelium and maturation arrest in the spermatogenesis of the peripheral tubules could occur. Decreased serum testosterone level, reduction in the number of Sertoli and Leydig cells could also occur following chronic exposure to 2G and 3G cell phone radiation. Thus long term exposure of cell phone radiation could cause male infertility in mice.
ACKNOWLEDGEMENT
The authors sincerely thank the Professors and Heads of the Department of Anatomy, Pharmacology and Pathology of Mahatma Gandhi Medical College and Research Institute, Puducherry, for their whole hearted support to undertake this research work. Authors thank Dr.SaravananGanesan, Director, Laboratory Medicine, Nanolab, Nammakkal, Tamil Nadu, for his support to carry out this research work. Authors also thank Mr.Chandresekar, senior histology technician at Mahatma Gandhi Medical College and Research Institute, Puducherry, for his valuable support. 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 considered and discussed.
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareEFFECT OF INCREASED ADIPOSITY ON OCULAR PERFUSION PRESSURE IN YOUNG ADULTS
English4853Rajalakshmi R.English Gowd Aruna R.EnglishBackground: The objective of this study was to study the effect of increased adiposity on Ocular Perfusion Pressure (OPP) and its relation with obesity indices.
Methods: The study included 82 subjects grouped into two based on their Body Mass Index
(BMI) as obese group (n=41) and Normal group (n=41). Blood Pressure was measured using sphygmomanometer. Mean Arterial Pressure (MAP) was calculated. Intraocular Pressure (IOP) was recorded using Schiotz indentation tonometer after anaesthetizing the cornea with 2% paracaine solution. OPP was calculated as 2/3 the MAP minus IOP, Systolic Ocular Perfusion Pressure (SOPP) was calculated by Systolic Blood Pressure minus IOP and Diastolic Ocular Perfusion Pressure (DOPP) was calculated by Diastolic Blood Pressure minus IOP. Statistical analysis was performed using the SPSS version 19.
Results: Resting mean SBP, DBP, MAP, IOP, OPP, SOPP & DOPP were significantly higher (pEnglishObesity, Ocular perfusion pressure, Obesity indicesINTRODUCTION
Obesity is characterized by the accumulation of excess adipose tissue and can occur as a result of white adipose tissue enlargement, caused by adipocytes hyperplasia and/or hypertrophy1 . Obesity is a complex condition resulting from the interplay among genetics, environment, and lifestyle2 . The prevalence of obesity has increased dramatically as a result of our modern lifestyle and is one of the most important targets of public health programs and its associated pathological conditions3 . The normal functioning of tissues depends on the maintenance of an adequate perfusion, with sufficient blood flow. Presence of ample perfusion pressure is necessary to meet tissue needs and this requires a balance between arterial and venous blood pressure4 . Ocular Perfusion Pressure (OPP) is expressed as the difference between the arterial BP and the intraocular pressure (IOP), which is considered a substitute for the venous pressure. The perfusion pressure equals 2/3 the Mean Arterial Pressure (MAP) minus IOP 5 . Alterations in ocular perfusion could cause ischemia and thus reduced perfusion of tissues in the optic nerve can have deleterious effects4 . The relationship between obesity and hypertension is well established both in adults and children6, 7. Obese individuals exhibit higher blood pressure levels than non obese individuals even in the normotensive range. Thus the combination of obesity and hypertension increases the risk of cardiovascular diseases 8 . Obesity is characterized by increase intraorbital fat and episcleral venous pressure which may contribute to increase in IOP9, 10. High IOP is a major risk factor for glaucoma and is related to optic nerve damage even in case of normal pressure glaucoma 11. Hence we hypothesize that variation in MAP & IOP can lead to variation in OPP in obese persons. Thus this study was undertaken to know the effect of obesity on OPP and to evaluate the independent association of obesity indices with OPP in healthy young adults of Indian population.
MATERIALS AND METHODS
This is a comparative study done on the first year medical students (n = 150). Subjects were screened using a questionnaire which included inclusion and exclusion criteria’s and by physical examination for their age, history of hypertension, cardiac or pulmonary diseases, eye disorders, other factors affecting IOP, smoking and consumption of alcohols. The weight, height Waist Circumference (WC) and Hip Circumference were measured for each subject. BMI was calculated as weight (kg) / height (mt)2 and Waist Hip Ratio (WHR) was computed. Subjects fitting the inclusion and exclusion criteria’s (n = 115) were considered for the study. Overweight subjects (n=15) and subjects with refractive errors (n=20) were excluded. Subjects were divided into two groups depending on BMI cut off for Indian population. Study group was formed by obese subjects with BMI ≥ 25 Kg.m2 (n = 41) and Control group was formed by normal weight subjects with BMI 18.5 to 22.9 Kg.m2 ( n=41). Out of 74 normal weight subjects 41 were selected randomly by using random number table. Thus the study consisted of two group’s namely Normal Weight (NW) and obese groups. This sample size was estimated to be enough to detect a clinically relevant difference of 10% in the parameters under study at 5% level of significance with 80% power. The study was approved by the Ethical committee of Institution. Subjects were informed about the purpose of the study, the study protocol and the informed consent was obtained. Study was carried out in the research laboratory in the department between 3 to 5 PM by a single observer in a quiet room. Subjects were briefed again about the experiment protocol and were allowed to relax for 10 minutes. Systolic and Diastolic Blood Pressure were measured in sitting posture with a standard mercury sphygmomanometer. Pulse Pressure (PP) and Mean Arterial Pressure (MAP) were calculated. IOP was recorded using Schiotz indentation tonometer after anaesthetizing the cornea with 2% paracaine solution. OPP was calculated 2/3 the MAP minus IOP, Systolic Ocular Perfusion Pressure (SOPP) was calculated by SBP minus IOP and Diastolic Ocular Perfusion Pressure (DOPP) was calculated by DBP minus IOP. Descriptive statistics with mean and Standard Deviation (SD) were calculated. Inferential statistical analysis Independent sample t-test, Pearson’s correlation and regression analysis were performed using the SPSS version 19. p Value < 0.05 are considered to be significant.
RESULTS
The study included 82 young adults in the age group of 18 to 21 yrs (obese group n=41 & NW group n=41). The physical characteristics of the two groups are represented in Table 1. There was significant difference in Weight, BMI, WC, HC & WHR between the two groups. Age and Height showed no significant difference between the two groups. Resting mean level of SBP, DBP & MAP among obese young adults was significantly higher (pEnglishhttp://ijcrr.com/abstract.php?article_id=620http://ijcrr.com/article_html.php?did=6201. Hid kuni Inadera.The usefulness of circulating adipokine levels for the assessment of obesity related health problems. Int J Med Sci 2008; 5(5): 248-262.
2. Jana V. van Vliet-Ostaptchouk, Harold Snieder, Vasiliki Lagou. Gene–Lifestyle Interactions in Obesity. Current Nutrition Reports. 2012; 1(3) : 184-196.
3. Mello MM, Studdert DM, Brennan TA. Obesity- the new frontier of public health law. New England Journal of medicine. 2006 ; 354 :2601-10.
4. Leske MC. Ocular perfusion pressure and glaucoma: clinical trial and epidemiologic findings. Curr Opin Ophthalmol. 2009 March; 20(2): 73–78.
5. Leske MC, Wu SY, Hennis A, Honkanen R, Nemesure B; BESs Study Group. Risk factors for incident open-angle glaucoma: the Barbados Eye Studies. Ophthalmology 2008;115(1):85–93.
6. Kotsis V, Stabouli S, Bouldin M, Low A, Toumanidis S, Zakopoulos N. Impact of obesity on 24-h ambulatory blood pressure and hypertension. Hypertension 2005; 45: 602– 607.
7. Stabouli S, Kotsis V, Papamichael C, Constantopoulos A, Zakopoulos N. Adolescent obesity is associated with high ambulatory blood pressure and increased carotid intimal medial thickness. Journal of Pediatrics 2005; 147: 651–656.
8. Mancia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, Germano G et al. Management of Arterial Hypertension of the European Society of Hypertension; European Society of Cardiology. Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007; 25: 1105–1187.
9. K Mori, F Ando, H Nomura, Y Sato, H Shimokata. Relationship between intraocular pressure and obesity in Japan. International Journal of Epidemiology. 2000; 29(4):661-666.
10. Akinci A, Cetinkaya E, Aycan Z, Oner O. Relationship between intraocular pressure and obesity in children. J Glaucoma. 2007 ; 16(7):627-630.
11. Douglas R Anderson. Normal-tension glaucoma (Low-tension glaucoma). Indian J Ophthalmol. 2011; 59(Suppl1): S97–S101.
12. Bonomi L, Marchini G, Marraffa M, et al. Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study. Ophthalmology. 2000;107:1287–1293.
13. Quigley HA, West SK, Rodriguez J, et al. The prevalence of glaucoma in a population-based study of Hispanic subjects: Proyecto VER. Arch Ophthalmol. 2001;119:1819–1826.
14. Leske MC, Connell AM, Wu SY, Hyman LG, Schachat AP. Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Ophthalmol. 1995 Jul; 113(7):918-924.
15. Mitchell P, Lee AJ, Rochtchina E, Wang JJ. Open-angle glaucoma and systemic hypertension: the blue mountains eye study. J Glaucoma. 2004 Aug;13(4):319-26.
16. Gasser P, Stumpfig D, Schotzau A, Ackermann-Liebrich U, Flammer J. Body mass index in glaucoma. J Glaucoma. 1999;8:8–11.
17. Pasquale LR, Willett WC, Rosner BA, Kang JH. Anthropometric measures and their relation to incident primary open-angle glaucoma. Ophthalmology. 2010;117:1521– 1529.
18. Yip JLY, Broadway DC, Luben R, Garway-Heath DF, Hayat S, Dalzell N. Physical activity and ocular perfusion pressure: the EPIC-Norfolk Eye Study. Invest Ophthalmol Vis Sci 2011;52:8186–92.
19. Remzi Karadag, Zeynel Arslanyilmaz, Bahri Aydin, Ibrahim F. Hepsen. Effects of body mass index on intraocular pressure and ocular pulse amplitude Int J Ophthalmol. 2012; 5(5): 605–608.
20. Zheng He, Christine T. O. Nguyen, James A. Armitage, Algis J. Vingrys, Bang V. Bui. Blood Pressure Modifies Retinal Susceptibility to Intraocular Pressure Elevation. PLoS One. 2012; 7(2): e31104. doi:10.1371/journal.pone.0031104.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcarePROTEIN ENERGY WASTING (PEW) / CACHEXIA IN CHRONIC KIDNEY DISEASE - ROLE OF LEPTIN AND INSULIN
English5459D. PonnudhaliEnglish P. NagarajanEnglish R. ShankarEnglishBackground: The prevalence of protein energy wasting (PEW)/ cachexia is very high among patients with chronic kidney disease (PEW), increasing in severity with the progression of the disease. Among other factors, increased serum Leptin levels and insulin resistance have been implicated in the pathogenesis of PEW/cachexia in CKD
Aim and objectives: To assess the serum leptin & insulin levels along with HOMA IR (Homeostasis model assessment-Insulin Resistance) in non diabetic chronic kidney disease patients and to study the correlation of these parameters with glomerular filtration rate (GFR) & body mass index (BMI).
Materials and methods: Non-diabetic CKD patients (group1; n=45) and healthy non-diabetic individuals (group 2; n=45) with normal renal function were recruited for the study. Serum leptin and Insulin levels were assessed using ELISA kits. Calculated values of HOMA IR & BMI were taken for the analyses.Statistical analysis: The statistical analysis was done using SPSS version 16. The parameters were compared among the 2 groups using Independent t test and correlation coefficient.
Results: Serum Leptin levels (24.15 ± 17.44 ng/ml) were increased significantly (p=.000) in group 1 patients compared to those in group 2 (7.50 ± 1.28 ng/ml). Serum insulin levels (p=.000) were increased in CKD patients (15.49 ± 9.39 μU/ml) from that of the healthy controls (7.50 ± 1.28μU/ml). The HOMA IR was also significantly high (p=0.000) in the CKD group ( 3.69 ± 2.26) than the controls (1.69 ± 0.35). Leptin, insulin & HOMA IR showed a highly significant negative correlation with GFR & BMI .The serum albumin and total cholesterol in the CKD group were 3.20 ± 0.19 g/dl & 127.47 ± 31.75 mg/dl respectively.
Conclusion: Hyperleptinemia and insulin resistance may be responsible for protein energy wasting/cachexia associated with CKD.
EnglishLeptin, protein energy wasting (PEW), Cachexia, Insulin resistanceINTRODUCTION
Protein energy wasting (PEW)/ cachexia is highly prevalent among patients with chronic kidney disease(CKD). PEW is a devastating complication of CKD, as it increases the incidence of cardiovascular outcomes as well as the morbidity & mortality associated with CKD, making it a major clinical problem. The International Society of Renal Nutrition and Metabolism (ISRNM) panel has described PEW as a state of decreased body stores of protein and energy fuels (body protein and fat masses). It describes a progressive loss of adipose tissue and lean body mass, with cachexia constituting the severe form of protein energy wasting (PEW) [1].The PEW/cachexia syndrome in CKD patients consists of anorexia, increased energy expenditure, decreased protein stores characterized by low serum albumin, loss of body weight and loss of muscle mass. The etiology of PEW in chronic kidney disease (CKD) is complex and includes inflammation, metabolic acidosis, insulin resistance, increase in serum leptin [2], transient catabolic illnesses, hyperparathyroidism and so many other conditions. CKD is associated with insulin resistance even from an early stage, when the GFR is normal [3]. Leptin is an adipocyte- derived hormone that has an inhibitory effect on food intake while it increases the energy expenditure. Elevated levels of serum leptin have been reported in CKD patients and has been linked with the pathogenesis of PEW/cachexia [4,5]. Hence we decided to assess the serum leptin & insulin levels along with HOMA- insulin resistance, in non diabetic CKD patients, graded to have PEW/ cachexia. We have also correlated the levels of these parameters with glomerular filtration rate(GFR) and body mass index(BMI). This study is an attempt to highlight the role played by leptin and insulin in the pathogenesis of PEW in non diabetic CKD and, its relation to the declining GFR & BMI.
MATERIALS AND METHODS
Our study has been conducted in patients with chronic kidney disease who were non diabetic and not on dialysis, recruited from the department of Nephrology, Government Mohan Kumaramangalam Medical College Hospital, Salem. Friends, family members and colleagues of the patients constituted the control group. Written consent was obtained from all the subjects, after clearly explaining to them about our study protocol. This study was approved by the ethical committee of Govt Mohan Kumaramangalam Medical College Hospital. Group 1 comprised of 45 non diabetic patients with Chronic Kidney Disease (CKD), diagnosed and staged, based on NKF K/DOQI guidelines [6]. Group 2 comprising of 45 healthy adults with normal renal function (GFR > 90 ml/min), formed the control group. The study group 1 included CKD patients, not on hemodialysis/ peritoneal dialysis. Patients with history of diabetes, metabolic syndrome, endocrine disorders, obesity, pregnancy, malignancy or any other terminal illness were excluded from the study. The control group 2 included healthy individuals, with normal renal function. Subjects with diabetes, hypertension, renal disease, chronic infections, pregnancy, systemic illness, endocrine disorders, malignancy or neuropsychiatric illness were excluded from the study. All subjects in both the control and study group were age and sex matched.
Laboratory analysis:
After an overnight fast of at least 8 hrs, fasting blood samples were collected from both the patients and controls. Plasma and serum were separated immediately after collection, and stored at -20°C , until further analysis. Complete blood count, urine routine , blood glucose, urea, creatinine, albumin & Total Cholesterol were estimated using the semi autoanalyzer- Microlab 300. These biochemical analyses were done, in the clinical Biochemistry Laboratory, VMKV Medical College, Salem. Serum Leptin was analyzed using DRG (sandwich) EIA 2395 ELISA kit [7]. Serum Insulin was analyzed using Monobind’s Insulin/ MAPS ELISA kit [8]. Homeostasis model assessment-Insulin Resistance (HOMA-IR) was calculated using the formula, HOMA-IR = fasting serum insulin (µIU/ml)* fasting plasma glucose (mg/ dl)/405 [9]. GFR was calculated using the MDRD (Modification of Diet in Renal Disease) formula available online [10].
PROTEIN ENERGY WASTING (PEW)/ CACHEXIA:
We have tried to assess the protein energy wasting (PEW) in the CKD patients based on the following criteria, proposed by The International Society of Renal Nutrition and Metabolism (ISRNM):
We have also calculated BMI using the formula: Weight in kilograms / (height in meters)2 Kg/m2 [12].The standard weight status categories associated with BMI ranges for adults are Herewith we have selected 4 parameters to diagnose the protein energy wasting (PEW) in CKD patients - serum albumin, serum cholesterol, BMI & Dietary Energy Intake- DEI. Nutritional diaries were provided to the CKD patients and they were taught to make entries, which will explain their complete dietary regimen through out the day. From the entries their dietary energy intake was calculated, for further analysis.
Statistical analysis
Statistical analysis was done using the software SPSS version 16. Data was expressed as mean ± 2SD and differences in mean between the 2 groups were analyzed using independent t test. Bivariate correlations of Leptin, Insulin & insulin resistance (IR) with BMI and GFR, were performed using Pearson’s correlation.
RESULTS
The present study was conducted in 45 non diabetic CKD patients (group1) not on dialysis and 45 healthy controls (group2), with normal renal function. Serum leptin, insulin, albumin and total cholesterol were analyzed in the blood samples. HOMA IR and BMI were the calculated parameters, taken for the study. The results are displayed in Table 1. Serum Leptin levels (24.15 ± 17.44 ng/ml) were increased significantly (p=.000) in group 1 patients compared to those in group 2 (7.50 ± 1.28 ng/ml). Serum insulin levels (p=.000) were increased in CKD patients (15.49 ± 9.39 µU/ml) compared to the healthy controls (7.50 ± 1.28µU/ml). The HOMA IR was also significantly high (p=0.000), in the CKD group. The correlations of serum Leptin, Insulin & HOMA-IR with BMI & GFR, were performed using Pearson’s correlation which is depicted in Table-2. Leptin, Insulin & HOMA IR were found to have a highly significant negative correlation with GFR & BMI . Indicators of protein energy wasting/ cachexia: Certain biochemical tests were done to assess the status of protein energy wasting/ cachexia. Serum albumin (3.20 ± 0.19g/dl) was found to be significantly decreased (p=.000) in the group 1 patients from that of the group2 (4.1 ± 0.30 mg/dl) subjects. Serum cholesterol levels (group1: 127.47 ± 31.75mg/dl, group2: 161.16 ± 39 mg/dl) showed a significant decrease in group1 patients (p=.000). The BMI levels were significantly decreased (p=.001) in the group1 (21.96 ± 3.46 kg/m2) patients compared to those in group 2 (25.50 ± 4.61 kg/m2). We have found that the serum albumin levels were below 3.8 g/dl in the CKD patients. The serum cholesterol levels though were decreased in CKD patients , their levels were not below 100mg/dl. The BMI levels were below 23 in the CKD patients. All these values are shown in Table 1. The dietary energy intake (DEI) of CKD patients was assessed from their nutritional dairies. Their mean DEI was found to be less than 24 kcal kg−1day−1 . The CKD patients in group 1 satisfy three of the four criteria stated by the ISRNM [11]. Hence the patients in group 1, can be placed under the category of protein energy wasting (PEW)/ cachexia syndrome.
DISCUSSION
We have conducted our study in 45 non diabetic predialysis CKD patients and 45 healthy controls. Serum leptin levels have been significantly increased in CKD patients (group1) compared to healthy controls (group 2). There is negative significant correlation of serum leptin levels with BMI & GFR. Leptin is a 167 amino acid peptide , an adipocytokine, produced abundantly by the adipose tissue and acts as a major regulator of food intake and energy homeostasis. It circulates as both free and protein- bound form and exerts inhibitory effects on food intake while increasing energy expenditure [13]. The leptin receptor belongs to class I cytokine receptor superfamily and possesses strong homology to the signal transducing subunits of the IL-6 receptors [14]. At least five isoforms of receptors (OBRa, OBRb, OBRc, OBRd, and OBRe) are known to exist and result from alternate gene splicing. Among these most biological effects of leptin are mediated by the leptin receptor OBRb, which is primarily present in the hypothalamus, where action of leptin is important in energy homeostasis. The OBRb receptors are also expressed in peripheral tissues including heart, skeletal muscle , adrenals, kidneys, adipocytes , smooth muscle cells, endothelial cells etc . An association of increased serum leptin levels with CKD, have been emphasized in certain studies, in different populations. [15,16,17]. Leptin is cleared from the circulation by kidney, by glomerular filtration followed by metabolic degradation in the renal tubules [17]. In CKD, due to reduced GFR, there is increased serum leptin levels. We have also found a negative significant correlation between serum leptin levels and GFR , which confirms that serum leptin is increased due to declining renal function in CKD. In CKD, inflammation is another important factor which contributes to hyperleptinemia [13]. The increased leptin levels may mediate protein energy wasting and cachexia, by regulating food intake and energy consumption via signalling through the hypothalamic melanocortin system [18]. Pro-opiomelanocortin (POMC) is a propeptide precursor that is produced in neurons found in the hypothalamic arcuate nucleus [19]. POMC neurons are thought to provide tonic inhibition of food intake and energy expenditure by production and release of α-melanocyte stimulating hormone (α- MSH) [4]. α- MSH in turn activates the hypothalamic type 4 melanocortin receptor (MC-4R), leading to suppressed food intake and increased energy expenditure. Leptin is able to activate the POMC neurons in the hypothalamus, triggering the production and release of α- MSH, which binds to MC3/MC4 receptors expressed on the hypothalamic nuclei, inducing a reduction of appetite and increase in energy consumption [20]. Leptin also suppresses the activity of Neuropeptide Y & Agoutirelated peptide (AGRP), which are endogenous antagonists of MC- 4R [21]. Hence increased serum leptin levels could be an important causal factor for protein energy wasting/ cachexia seen in CKD patients [4,5].This fact has been tested by Wai Cheung et al, who have identified that leptin causes MC-4R blockade and that it plays a significant role in transducing cachexic signals in CKD [4]. Pecoits- Filho et al suggest that free circulating leptin concentrations are elevated in patients with end stage renal disease and may be associated with inflammation associated cachexia [5]. As we have observed in our study, serum leptin increases as the BMI decreases, showing a probable relation between increasing leptin levels and PEW/ cachexic manifestations. Hence leptin may play an important role in anorexia/ cachexia syndrome seen in CKD patients. Some of the causes of protein energy wasting (PEW) in CKD patents are inflammation, metabolic acidosis and insulin resistance [21]. Leptin secretion have been found to be regulated by insulin, glucocorticoids and catecholamines [22]. In our study we have identified the occurrence of hyperinsulinemia and increased HOMA-IR, in CKD patients. Hyperinsulinemia may be due to reduced clearance of insulin by the kidneys / compensatory to insulin resistance. We have also obtained negative significant correlation between serum insulin levels & HOMA-IR with GFR and BMI. The insulin resistance in CKD, results in uremic myopathy due to increased muscle breakdown. Insulin has an anticatabolic effect, by activating protein synthesis and inhibiting proteolysis. In insulin resistance, there is decreased utilization of glucose as an energy source, by the skeletal muscles.CKD attenuated insulin stimulated protein synthesis and increased protein degradation in skeletal muscle [23]. Many studies have documented insulin resistance as an important complication of CKD, with varied metabolic changes [24,25,26]. In CKD, insulin resistance is due to a post-receptor signalling defect : reduced activity of PI3K (phoshpatidylinositol 3-kinase) in turn causing reduced levels of phoshorylated Akt (pAkt). This dysfunction of PI3K signalling pathway is a common initiator of muscle protein degradation by enhancing the activity of ubiquitin-proteosome pathway, in muscle [27]. Ubiquitin proteosome proteolytic (Ub-P’some) system consists of the 7- KDa protein ubiquitin, E3 ubiquitin ligases (atrogin-1, MAFbx & MuRF1) and proteosome (large multi-subunit complex found in all mammalian cells). Insulin resistance activates the Ub-P’some system through suppressing PI3 Kinase pathway & by activating MEK/ERK pathway [28]. This PI3K signalling defect activates FOXO group of transcription factors ,which in turn induces the expression of ubiquitin conjugating enzymes atrogin-1, MAFbx & MuRF1 [29]. Insulin resistance also results in the activation of MEK/ERK pathway, causing increased expression of ubiquitin (UbC) . Hence the Ubiquitin proteosome proteolytic (Ub-P’some) system is activated as shown in figure1. The suppression of PI3K signalling pathway also results in activation of Bax proteins which in turn activates the enzyme caspase 3. Caspase 3 plays an initial role in muscle protein degradation, by cleaving actomyosin and presenting them to the ATP dependent Ubiquitin proteosome proteolytic (Ub-P’some) system which in turn degrades the monomeric actin/myosin fragments but not the actomyosin complexes [30]. Hence increased insulin resistance seen in CKD patients may play an important role in muscle protein degradation causing a reduction in lean body mass. An important consequence of insulin resistance in CKD is the pathogenesis of PEW/ cachexia [31]. Leptin and insulin- Role in kidney damage: Serum leptin levels and insulin resistance increases in chronic kidney disease and both these parameters play an important role in the pathogenesis of PEW/ cachexia. Apart from this both leptin & insulin are known to activate the sympathetic nervous system, causes impairment of natriuresis
and inhibition of nitric oxide synthesis [32,33]. All these factors may contribute to the up regulation of blood pressure and hence worsening of renal function.
CONCLUSION
The present study shows an increase in serum leptin, insulin and HOMA-insulin resistance, showing a strong correlation with GFR & BMI. Increased leptin signalling and insulin resistance might significantly contribute to the development of protein energy wasting (PEW)/ cachexia syndrome in patients with chronic kidney disease. Understanding the role played by these parameters might help in early intervention of the wasting disorder, when the skeletal muscle complications might still be reversible. The emerging role of therapeutic agents like AGRP (agouti-related peptide- endogenous antagonist of MC-4R receptors) & orexigenic agents/appetite stimulants (neuropeptide Y, Ghrelin) and their appropriate use in maintaining the skeletal muscle homeostasis, should be further confirmed by well controlled studies.
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
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11. Yashpal P. Jadeja, Vijay Kher. Protein energy wasting in chronic kidney disease: An update with focus on nutritional interventions to improve outcomes Indian Journal of Endocrinology and Metabolism / Mar-Apr 2012 / Vol 16 | Issue.
12. Kronenberg. F et al. Lipoprotein(a) serum concentrations and apolipoprotein(a) phenotypes in mild and moderate renal failure. J Am Soc Nephrol. 2000;11: 105–1
13. RH Mak, W Cheung, RD Cone and DL Marks. Leptin and inflammation-associated cachexia in chronic kidney disease. Kidney International .2006; 69:794–797.
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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareCADAVERIC STUDY OF COMMUNICATION BETWEEN MEDIAN AND MUSCULOCUTANEOUS NERVE
English6062Soma Sekhar R.English Raju SugavasiEnglishBackground: Communications between the branches of brachial plexus is a common phenomenon and it has several clinical and surgical implications. The knowledge of communications between musculocutaneous and median nerves is also important in the anterior approach for the fracture of the humerus and regional nerve blocks
Methods: Cadaveric study was carried out on 100 upper limbs by using 50 embalmed cadavers to find out the communication between median and musculocutaneous nerve
Results: out of 100 upperlimbs, the variation was found in 2 specimens.
Conclusion: The occurrence of such type of communication is clinically important for surgeons and anesthetists to perform pain management Therapies in related to the upper limb.
EnglishMedian nerve, Musculocutaneous nerve, CommunicationINTRODUCTION
Variations like communication between the median nerve and musculocutaneous nerves are interest for anatomists and surgeons because these variations may be vulnerable to damage in surgical procedures .The median nerve, formed by the union of the terminal branch of the lateral (C5, C6, C7) and medial (C8, T1) cords of the brachial plexus, after the formation it enters the arm lateral to the brachial artery and to the forearm between the two heads of the pronator teres. The musculocutaneous nerve is the continuation of the lateral cord of the brachial plexus. It pierces the coracobrachialis muscle and descends laterally between the biceps and brachialis muscles and supplies all the muscles in the anterior compartment of the arm [1].
MATERIALS&METHODS
In the present cadaveric study, we dissected a Total numbers of 100 upper extremities of 50 cadavers. An incision was made longitudinally on the anterior surface of the arm, from the level of acromion process to the elbow joint and bilateral horizontal incision was made in both proximal and distal ends of the longitudinal incision. The skin, superficial fascia and deep fascia were incised, later various flexor muscles were retracted and searched for unusual communications of median and musculocutaneous nerves. The present study was conducted at Kurnool medical college, Andhra Pradesh, India.
RESULTS
Out of 100 upper limb specimens, the abnormal variations in the communication between the median nerve and the musculocutaneous nerve were found in 2 specimens. The two variations were identified in right side of upper limbs (FIGURE: 01 & 02).
DISCUSSION
According to Le Minor et al [2], variations of communication between median (MN) nerve and musculocutaneous nerves (MCN) are classified as 5 types, in type I there is no communication between the MN and MCN. In type II the fibres of medial root of MN pass through MCN and join the MN in the middle of the arm, in type III MN and MCN run together later that lateral root of MN separates from it. In type IV MCN arises from median nerve after joining to lateral root of the MN. In type V MCN is absent. Veinreratos & Anagnostopolou et al conducted studies on 79 cadavers and 22 cadavers found communications between MCN and MN in [3]. Prasada Rao and Chaudhary et al [4], observed 24 cases of such communications, but communication branch arising from the musculocutaneous nerve to the median nerve. Lovesh shukla et al [5] observed four communications between median and musculocutaneous nerve. According to Sharadkumar Pralhad Sawant et al [6] Out of 100 specimens the variations in the anastomosis between the median nerve and the musculocutaneous nerve were found in 30 specimens. Loukas & Aqueelah et al [7] found 63.5% of cadavers consist of abnormal communicating branch between the median and musculocutaneous nerves. According to Veinreratos& Anagnostopolou et al [8] out of 79 cadavers, 22 cases were found communications between MCN and MN. Chauhan et al [9] recommend the consideration of the phylogeny and the development of the nerves of the upper limb for the interpretation of the nerve anomalies of the arm. According to Chiarapattanakom et al. [10] limb muscles develop from the mesenchyme of local origin, while axons of spinal nerves grow distally to reach the muscles and or skin. They blamed the lack of coordination between the formation of the limb muscles and their innervations for appearance of a communicating branch.
CONCLUSION
Anatomical Knowledge of communications between the MCN and the MN may clinically important in related to axilla and upperlimb injuries, as well as in their repair operations. This kind of study may be useful to surgeons at the time of peripheral nerve repair and posttraumatic evaluations.
ACKNOWLEDGEMENTS
Authors wish to convey our sincere thanks to Dr. Haniman, MS Anatomy, Head of The Anatomy Department, Kurnool medical college, Andhra Pradesh, India, for his valuable help, support and inspiration. The authors are also grateful to previous publishers of all those articles, journals and books from where the present literature has gathered.
Englishhttp://ijcrr.com/abstract.php?article_id=622http://ijcrr.com/article_html.php?did=6221. Standring S. Gray’s anatomy. The anatomical basis of clinical practice. London: Elsevier Churchill Livingstone; 40 ed: 2008.821-822.
2. Le Minor JM. A rare variation of the median and musculocutaneous nerves in man. Arch Anat Histol Embryol 1990;73: 33-42.
3. Venieratos D, Anagnostopoulou S. Classification of communications between the musculocutaneous and median nerves. Clin Anat 1998; 11(5):327-31.
4. Prasada Rao PV, Chaudhary SC. Communication of the musculocutaneous nerve with the median nerve. East Afr Med J 2000; 77: 498-503.
5. Lovesh shukla, Gargi soni, Neha gaur. Four communications between median and musculocutaneous nerves. International Journal of Anatomical Variations (2010) 3: 186–187.
6. Sharadkumar Pralhad Sawant, Shaguphta T. Shaikh. Study of anastomosis between the musculocutaneous nerve and the median nerve. International Journal of Analytical, Pharmaceutical and Biomedical Sciences. ; 2012; 1(3): 37- 43.
7. Loukas M, Aqueelah H. Musculocutaneous and median nerve connections within, proximal and distal to the coracobrachialis muscle. Folia Morphol 2005; 64: 101-8.
8. Venieratos D, Anagnostopoulou S. Classification of communications between the musculocutaneous and median nerves. Clin Anat.1998; 11: 327-331.
9. Chauhan, R., Roy, TS. Communication between the median and musculocutaneous nerve: A case report. Journal of Anatomical Society of India, 2002, vol. 51, n. 1, p. 72-75.
10. Chiarapattanakom, P., Leechavengvons, S., Witoonchart, K., Uerpairojkit, C., Thuvasethakul, P. Anatomy and internal topography of the musculocutaneous nerve: The nerves to the biceps and brachials muscle. Journal of Hand Surgery, 1998, vol. 23A, p. 250-255.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareEFFECT OF TRIAZOPHOS-AN ORGANOPHOSPHATE INSECTICIDE ON MICROBIAL POPULATION IN PADDY SOILS
English6367B. Lakshmi KalyaniEnglish T. MadhuriEnglish V. IndraniEnglish P. Suvarnalatha DeviEnglishTriazophos is a Thiophosphoric and is the active ingradient of the insecticide Hostathion. The aim of the study is to determine the effects of triazophos at five different concentrations on soil bacterial and fungal count. The effect of triazophos on bacterial and fungal population by incubation in soil for 7 days was determined. Results revealed that triazophos caused significant reduction in the bacterial and fungal populations. By statistical analysis, the concentrations of the pesticides as well as the dilution of soil sample were analyzed by two way ANOVA. Study reveals that both bacterial and fungal population the concentration of triazophos vs sample dilution has been significantly affected. The change in concentration brought significant reduction in bacterial count. We conclude that triazophos insecticide is using in paddy soils highly toxic pollutant to the bacterial and fungal organisms.
EnglishTriazophos, Soil, Bacteria, Fungi, Two- way ANOVAINTRODUCTION
India is primarily an agriculture based country with more than 60-70 per cent of its population dependent on agriculture. It’s fast growing population is projected to cross 1.3 billion by 2020 (Kanekar et al., 2004).Organophosphates are a group of highly toxic pesticides widely used for increasing agricultural productivity in soil. Organophosphates are also reared as non persistent (Racke and Coats, 1988). The reduced persistence of organophosphate insecticides attributed to soil microorganisms has been described by (Chapman and Harris., 1982; Gorder et al., 1982; Sharmila et al., 1989). Triazophos (TAP, O,O-diethyl-O-1-phenyl-1H-1,2,4-triazol-3-ylphosphorothioate) is one of the broad-spectrum, toxic, nonsystemic contact organophosphorus pesticides (OPs). It has been used on various crops, including rice, cotton, okra and maize to contro pest insects, nematodes and acarids acarids some since the late 1970s (Aungpradit et al., 2007; Lin and Yuan., 2005). Pesticides in soil for longer period is undesirable and it leads to the accumulation of the chemicals in soil to highly toxic levels. In addition, these pesticide residues may be assimilated by the plants and get accumulated in edible plant products such as root crops (Babu et al., 2008). Microorganisms are found in large numbers in soil with bacteria and fungi being the most prevalent. It is stated that usually more than 109 microorganisms are present per gram of soil representing 4000 to 7000 different genomes and biomass of 300 to 3000 kg per hectare (Ranjard and Richaume, 2001).Soil bacsteria play a key role in the global recycling of carbon and other essential elements because of their outstanding range of 106 to 109 bacteria per gram of soil and metabolic activities to exploit many sources of energy and carbon (Alexander, 1977). The influence of these pesticides on soil bacteria is dependent on physical, chemical and biochemical conditions, in addition to the nature and concentration of the pesticides (Aurelia, 2009).Fungi form a large part of the total biomass of micro flora in soil. Microbial biomass in soil is considered to be agents of breakdown of organic matter, when organic materials are applied to soil (Jenkenson and Ladd, 1981). They are usually abundant in the upper layers of the soil, where aerobic conditions prevail. However, numerically much less abundant (between 104 and 106 fungal propagules per gram of soil) than bacteria (Alexander, 1977).The present paper deals with impact assessment of commonly used organophosphate insecticide triazophos (40%EC) on soil bacteria and fungal population dynamics.
MATERIALS AND METHODS
Pesticide
Triazophos was selected for the present investigation in view of it’s wide usage in Srikalahasti paddy cultivation for the control of aphids, thrips, midges, beetles, larvaes, cutworms and other soil insects. It is an organophosphorous insecticide as per the international union of pure and applied chemistry (IUPAC),chemical formula of the compound is diethyl o-(1-phenyl-1h-1,2,4-triazol-3-yl) phosphorothioate. It is also known as nicotinamide, and a common insecticide, was obtained from Sudarshan Chemical Industries Ltd., Pune, India.
Collection of Soil
The soil samples were collected from Srikalahasti, Chittoor district a semi-arid region in Andhra Pradesh, India. Samples of about 1 kg were taken from the first 15 cm of depth and then pooled and sieved. Samples were air dried and stored in polyethylene bags at 4 ?C. The texture of the soil was Black loam-sandy clay with a pH of about 7.6, maximum water holding capacity 0.224 ml/g, sand 50%, silt 20%, clay 29%, organic matter 0.9%.
Soil incubation studies
The effect of different concentrations of triazophos on microbial population was determined in soil sample.
Effect of Triazophos on soil population
Population of bacteria
The effect of different concentrations of triazophos on bacterial population in agricultural soil sample, in triplicate, was determined. Aliquots (0.05 ml) from stock solutions of the pesticides were applied to five-gram portions of soil contained in test tubes (15 X 150mm). The final concentrations (w/w) of each pesticide concentrations 5, 10, 25, 50 and 100 µg/g soil, which are equivalent to 0.5, 1.0, 2.5, 5.0 and 10.0 kg ha-1. The soil samples receiving only distilled water served as controls. According to Shukla and Mishra (1997), Soil samples were then homogenized to distribute the insecticide, and enough distilled water was added to maintain at 60% water holding capacity (WHC) and incubated at room temperature (28 ± 40 C). Seven days after incubation, triplicates of each treatment were withdrawn for estimation of bacterial population. Aliquots were prepared from 10-1 to 10-7 from treated and untreated soil samples by serial dilution plate method on nutrient agar medium and subsequently incubated for 24 hrs in an incubator at 300 C. The experiments were performed in triplicate.
Population of fungi
The effect of different concentrations of triazophos on fungal population(triplicates) in agricultural soil samples was determined, following the same procedure adopted as in the case of bacterial population. Soil plate method was used to asses fungal propagules developing on rose bengal agar medium and subsequently incubated for five days at 25ºC (Shukla and Mishra, 1996).
STATISTICAL ANALYSIS
The data on Triazophos impact on microbial bacterial and fungal populations was interpreted by two way Analysis of variance(ANOVA) and duncan multiple range test (DMR).
RESULTS AND DISCUSSION
Physico-chemical properties of soil
The physico-chemical properties of the experimental soil was shown in (Table 1).
Population of bacteria
The effects of triazophos on the number of bacteria cells per gram of soil was shown in (Table 2) and (Figure1). Results reveals that the reduction in the total bacterial count with increase in the insecticide concentrations when compared with control group. The results of the present study doesn’t agree with many studies used insecticides on soil microbial communities(Stanlake and Clark, 1975; Digrak and Kazanici 2001 ) who notice that the presence of pesticides led to an increase in the total number of soil bacteria, nevertheless, the present study shows that the presence of insecticides led to inhibition in the growth rate of soil bacteria. Bacterial population has been significantly affected by the concentration (F=536.37 ; df 5; pEnglishhttp://ijcrr.com/abstract.php?article_id=623http://ijcrr.com/article_html.php?did=6231. Ahmed S and Ahmed M S. Effect of Insecticides on the total number of soil bacteria under laboratory 2006.
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8. Digrak M and Kazanici F. Effect of some organophosphorus insecticides on soil microorganisms. Turkey Journal of Biology 2001; 25: 51-58.
9. Domsch K H. The effects of soil fungicides. III. Quantitative changes in soil microflora. Z.Planzendau Pflanzenschutz 1959; 66:17.
10. Gorder G W, Dahm P A and Tollefson J J. Carbofuran persistence in cornfield soils. Journal of Economic Entomology 1982; 75: 637-642.
11. Hashem F, Hafes H and El-Mohandes M A O. Isolation and identification of pyrethroid insecticides degrading bacteria from soil. Ann. Agric. Sci. Cairo., 1999; 44(1): 123-137.
12. Jenkinson D S and Ladd J N. Microbial biomass in soil: Measurement and turnover. In: Paul EA, Ladd JN (eds) Soil Biochemistry, vol 5. Marcel Dekker, New York, Basel 1981 ;415-471.
13. Kanekar P P, Bhadbhade B, Deshpande N M and Sarnaik S S. X Biodegradation of organophosphorus pesticides, IN : Proceedings of Indian National Science Academy 2004;70:57- 70.
14. Lin K D, Yuan D X. Degradation kinetics and products of triazophos intertidal sediment. Jounal of Environmental Sciences 2005;17(6):933–6.
15. Racke K D and Coats J R. Comparative degradation of organophosphorus insecticides in soil : Specificity of enhanced microbial degradation. Journal of Agriculture and Food Chemistry 1988; 36: 193- 199.
16. Ranjard L and Richaume A S. Quantitative and qualitative microscale distribution of bacteria in soil. Research in Microbiology 2001;152: 707-716.
17. Sharmila M, Ramanand K and Sethunathan N. Effect of yeast extract on the degradation of organophosphorus insecticides by soil enrichment and bacterial cultures. Canadian Journal of Microbiology 1989; 35: 1105-1110.
18. Shetty P K and Magu S P. Effect of metalaxyl on soil microbial population. Journal of Tropical Agriculture 2000 ; 38: 63-65.
19. Shukla P K and Mishra R R. Response of microbial population and enzyme activities to fungicides in potato field soil. Proceedings of Indian National Science Academy section B 1996; 62 (5): 435-438.
20. Stanlake G J and Clark J B. Effects of a commercial malathion preparation on Selected Soil Bacteria. Applied Microbiology 1975; 30(2) :335-336.
21. Tawfic M A, Ismail S M M and Mabrouk S S. Residues of some chlorinated hydrocarbon pesticides in rainwater, soil and ground water and their influence on some soil microorganisms. Environmental International 1998 ; 24(5-6): 665-670.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareTO EVALUATE THE EFFICACY OF ANTHRALIN WITH AND WITHOUT COALTAR IN SHORT CONTACT THERAPY OF MILD TO MODERATE PSORIASIS- A RANDOMIZED DOUBLE BLIND CONTROLLED STUDY
English6871Veena R. M.English Satheesh B. C.English Sumathy T. K.EnglishBackground: Anthralin and coal tar, since their introduction in the treatment of psoriasis have remained one of the main modalities of treatment despite fluctuation. The principle of giving both treatments together is of course not new as the Ingram regime includes both tar baths and anthralin. It has been shown that short contact therapy with the combination of anthralin and coal tar is effective in chronic plaque psoriasis.However, clinical evidence suggested that the addition of coal tar to reduce the irritation and pigmentaion due to anthralin resulted in a compromised efficacy of combinations. The antipsoriatic effect of coal tar itself is low but is boosted when combined with anthralin.
Objectives: To evaluate whether combining the coal tar with anthralin in short contact therapy in mild to moderate chronic plaque psoriasis compromises the efficacy of combination compared to anthralin alone.
Methods: Fifty cases having mild to moderate psoriasis were studied in a double blind randomized controlled study. Twenty five patients in group A were treated with anthralin ointment 0.5% and twenty five patients in group B were treated with combination of coal tar 5% and anthralin. Results were analyzed using PASI scores.
Results: P values at the end of 1st visit, 2nd visit in both the groups Group A and Group B were significant. There was also significant decrease in the PASI score in the patients treated with the combination of anthralin plus coal tar than anthralin alone (PEnglishPsoriasis, Anthralin, Dithranol, Coal tar, Short contact therapy, Combination therapyINTRODUCTION
Psoriasis is difficult to manage in general practice, mainly because the standard treatments produce side effects, or are ineffective in both the short and long term.1 Anthralin (Dithranol) though efficacious has a strong reducing methylene group that binds with oxygen from the skin. The auto-oxidation of anthralin results in the formation of anthraquinones causing irritation and burning of skin.2 Due to this many formulations have been developed to increase the efficacy and compliance. In recent years, the main topical therapies have included anthralin or extracts of crude coal tar (CCT). 3The exact mode of action of anthralin and CCT in the treatment ofpsoriasis is unknown.CCT, however, has been shown to have an atrophogenic effect on normal epidermis indicating that it can act as a cytostatic agent on normal human skin.3 The principle of giving both treatments together is of course not new as the Ingram regime includes both tar baths and anthralin.3 However, the clinical evidence suggested that the use of combination 5% coal tar to anthralin regimen (0.05%) in the clinic is limited as the addition of 5% coal tar to reduce the irritation and pigmentaion due to anthralin resulted in a compromised efficacy of combinations.It has been shown that short contact CCT therapy is effective in chronic plaque psoriasis. 3The antipsoriatic effect of tar itself is low but is boosted when combined with anthralin.4,5,6 The purpose of this study was to determine whether adding 5%coal tar to anthralin regimen (0.05%)in short contact therapy is more effective than anthralin alone. Clinical assessment was recorded using a severity score determination.
MATERIAL AND METHODS
The study was conducted in 50 patients attending the department of Dermatology of M.S.Ramaiah Medical Teaching Hospital, Bangalore. The duration of the study was for a period of one year from July 2003-June 2004.
Method of collection of data It is a randomized double blind comparative study of subjects with mild to moderate psoriasis. Patients were randomly allotted into two groups with 25 patients in each group.However the lesions did not exceed 20% of total body surface area. Patients in one group were treated with sample A which consisted of only anthralin ointment (0.5%) and patients in other group were treated with sample B which consisted of coal tar 5% added to anthralin (0.5%). All preparations were from single batch specially prepared to ensure uniformity.Patients were instructed to apply a thin layer of the given ointment over the lesions for about 10 minutes; wipe it off with cotton dipped in any vegetable oil. Patients were then asked to expose the affected parts to the sunlight for about 20 minutes. If at any stage, marked irritation or burning occurred patients were instructed to cease therapy and report the next day. Severity score for erythema, scaling and plaque thickness was graded using PASI (Psoriasis Area Severity Index) score.7 Lesions was scored using PASI score by a dermatologist in the Department of Dermatology, who was unaware of the treatment being used by the patient. The first visit was considered as baseline visit. There was a two week treatment phase with the baseline visit, week-2 and a follow up at week-4. During the patients initial visit medical history was obtained and body systems were reviewed. An informed consent from the patient was obtained. The data was entered in the questionnaire form and evaluated at the end of the study.
Inclusion Criteria
Patients aged above 15 years of either sex, patients withdrawn from previous antipsoriatic medications for three to four weeks and freshly diagnosed psoriatic cases were included in the study.
Exclusion criteria Patients who received investigational medication within four weeks before the study, pregnant women, lactating women, women of reproductive age not practicing conception, patients on concomitant use of other topical medications on the lesion were excluded. PASI Score was calculated in subjects having target lesions in one or more of the five anatomical regions mentioned - Trunk, Upper extremities, Lower extremities, elbows/knees, Palms/soles7 Clinical assessment was performed by dermatologist in the department of dermatology at the onset of the therapy and repeated at an interval of two weeks constituting baseline visit, first visit and second visit respectively. Fredriksson and Pettersson created the PASI in 1978 as a method to evaluate the clinical efficacy of a new treatment for psoriasis. 7 When using the PASI, psoriatic plaques are graded based on three criteria: redness(R), thickness (T) and scaliness (S). Severity is rated for each index on a 0-4 scale (0for no involvement up to 4 for severe involvement). The body is divided into four regions comprising the head(h), upper extremities (u), trunk(t) and lower extremities(l). In each of these areas, the fraction of total surface area affected on a 0-4 scale (0-for no involvement: up to 4 for severe involvement). The various body regions are weighted to reflect their respective proportion of body surface area (BSA). The composite PASI score can then be calculated by multiplying the sum of the individual severity scores for each region by the weighted area of involvement score for that respective regions and then summing the four resulting quantities7 The highest potential score is 72; the lowest is 0. PASI scores are nearly continuous, with 0.1 increments within these values. PASI 75 or a reduction in baseline PASI score of > 75% is the standard used by FDA to assess the efficacy of psoriasis agent. The PASI score and percentage body surface area were the only measures recommended by an American Academy of Dermatology (AAD) consensus group to assess extent of psoriasis when planning treatment.7 Perilesional irritation is graded using the scale. 0-Nil, 1-Mild, 2-Moderate, 3-Sever, 4- Very severe.7
Statistical analysis
The collected data were compiled and processed using Microsoft Excel 2005. Statistical analysis was carried out by statistical package SPSS 14.5. Students unpaired t test was used to evaluate the significant difference in the efficacy of Anthralin with and without coal tar in mild to moderate psoriasis. Significance repeated measures ANOVA was used to evaluate the efficacy of individual treatment at the end of the three follow up. A p- value less than 0.05 were considered to be statistically significant. RESULTS All the 50 patients completed the study. Out of 50 patients who received the therapy,28 were male and 22 were females.The age of the patients ranged between 18 to 60 years. In the present study mild to moderate itching was present in 82% of patients. It was severe in 4% of patients. It was a symptomatic in 14% of patients. None of the cases included in the present study showed nail or joint involvement. At the end of the study, PASI scores in patients treated with only anthralin (Sample A) were analyzed at baseline, 1st visit and 2nd visit and it was noted that there was a significant decrease(PEnglishhttp://ijcrr.com/abstract.php?article_id=624http://ijcrr.com/article_html.php?did=6241. Harrington CI. Low concentration dithranol and coal tar (Psorin) in psoriasis: a comparison with alcoholic coal tar extract and allantoin (Alphosyl). Br J ClinPract. 1989;43(1):27-9.
2. DominikPeus, Astrid Beyerle, et al. Anti-Psoriatic Drug Anthralin Activates JNK via Lipid Peroxidation: Mononuclear Cells are More Sensitive than Keratinocytes. Journal of Investigative Dermatology. 2000; 114: 688–692
3. Thami G, Sarkar R.Coal tar: past, present and future. ClinExpDermatol. 2002;7(2):99-103.
4. Statham BN, Ryatt KS, Rowell NR. Short-contact dithranol therapy--a comparison with the Ingram regime. Br J Dermatol. 1984;110(6):703-8.
5. Schulze HJ, Schauder S, Mahrle G, et al. Combined taranthralin versus anthralin treatment lowers irritancy with unchanged antipsoriatic efficacy. Modifications of shortcontact therapy and Ingram therapy. J Am AcadDermatol. 1987;17(1):19-24.
6. Swinehart JM1, Lowe NJ. UVABA therapy for psoriasis. Efficacy with shortened treatment times with the combined use of coal tar, anthralin, and metal halide ultraviolet machines. J Am AcadDermatol. 1991;24(4):594-7.
7. Fredriksson, T, Pettersson, U: Severe psoriasis–oral therapy with a new retinoid. Dermatologica. 1978:157: 238–244,
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524174EnglishN-0001November30HealthcareRELATIONSHIP OF LIMB GIRTH, SEGMENTAL LIMB LENGTH, HAMSTRING FLEXIBILITY WITH VERTICAL JUMP IN MALE SPORTS PLAYERS
English7275Mohemed Zubeir SaiyedEnglish Veena PaisEnglish Afshan ShaikhEnglish Arakkal Maniyat ShemjazEnglish Sudeep PaisEnglishObjective: To determine if upper and lower body segment length, girth and hamstring flexibility contributes to vertical jump (VJ)
displacement.
Methods: Two hundred male sports players aged between 18 to 25 years were recruited. Upper limb length (humerus, ulna, hand), lower limb length (femur, tibia, foot), upper limb girth (arm, forearm), lower limb girth (thigh, calf) and hamstring flexibility were assessed. The subjects were asked to perform VJ and the average of 3 readings was calculated.
Results: Data was analyzed using Pearson’s correlation. The results showed a moderate positive correlation of lengths of humerus, ulna, femur, tibia, foot with VJ (pEnglishVertical Jump, Limb length, Limb girth, Hamstring FlexibilityINTRODUCTION
Vertical jumping is an important aspect of various sports such as basketball, volleyball, and football. Performance of jumping has now become an important part in testing physical abilities in sports players1 . In particular, it has been shown that the height of various types of VJs could serve for assessment of muscular strength and power2 and muscle fiber composition3 .It has been found that a jump height can be affected by various factors, such as muscle mass4-7, flexibility, isometric muscle strength, age, height, weight8 , and level of expertise9 . During a VJ, muscle force is produced primarily from the back extensors, gluteus maximus, quadriceps, gastronemius, and soleus resulting in a powerful ground reaction force that propels the body upward against gravity. Greater muscle girth may lead to greater production of propulsive force and may have a beneficial influence on VJ. It is theorized that body segment length (trunk, femur, tibia, and foot) may influence vertical jump displacement. As in any lever system, the length of the lever arm affects joint torque, with longer lever arms possessing the ability to impart greater force10. Take-off velocity during a vertical jump was approximately 10% higher while a jump is performed with arms compared to when the arms are restricted11. Research has shown that 60% of the increased performance were due to an increase in take-off velocity12.It has been widely reported that takeoff velocity can be enhanced by 6–10% or more when using an arm swing11,13,14. The arms can be used while jumping to create a rotary force, or torque, which is the product of force and the perpendicular distance from the line of axis to the axis of rotation. There is increased torque at the hip and knee joints during the propulsive phase of jumping when using an arm swing12. A body segment length that improves the arm torque during initiation of a VJ could improve the height of the jump Flexibility of muscle is the ability of muscle to lengthen, allowing one joint or more than one joint in a series to move through a range of motion15. Good muscle flexibility will allow the muscle tissue to accommodate the imposed stress more easily and allow efficient movement. Enhancing the hamstring muscle flexibility may be another factor that can assist in improving VJ performance and may prevent or minimize injuries16,17 From the literatures reviewed there are conflicting results regarding the influence of above mentioned factors on VJ.21,23Very few studies have been done to find the correlation between hamstring flexibility and VJ. So this study aimed to find the relationship of hamstring flexibility, limb length and limb girth on VJ among sports players.
MATERIAL AND METHODS
This was a cross-sectional study conducted on 200 male sports players aged between 18 to 25 years who participated in at least one tournament of one or more sports such as basketball, football and cricket in the last one year. Subjects were excluded if they had any history of recent surgery, recent fracture, immediate post-operative status and pain, musculotendinous injury, joint pathologies (such as arthritis, bone bruise or chondral injury), ligament or tendon injury, any neurological deficits, any spinal pathology, joint instability, any type of acute or chronic pain which restricted movements of upper limb, lower limb and trunk. Institutional ethical committee approval was taken and verbal advertisement was done in the university. After screening informed consent was obtained. The subjects were asked to perform arm-reach height and VJ and the following variables were measured.
1. Length measurement of Aram, Forearm, Hand, Thigh, Leg, and Foot were measured using the length of Humerus, Ulna, Hand, Femur, Tibia and Foot respectively 18
a. Humerus - Humerus length was measured from the lateral lip of the greater tuberosity to the lateral epicondyle.
b. Ulna - The subject was asked to flex the elbow to 90 degrees and the ulna measurement was taken from the olecranon down the ulnar ridge to the ulnar styloid process.
c. Hand - The hand was held palm up and measurement was taken from the proximal palm at the level of lunate to the distal end of the third phalanx.
d. Femur – This was measured from the greater trochanter of the femur to the lateral joint line of the knee.
e. Tibia - Tibia length was measured as the distance from the medial joint line of the knee to the medial malleolus. f. Foot - Foot length was measured from the posterior heel to the longest toe.
2. Girth measurement18
a. Arm – Palm up, arm straight and extended in front of the body, measurement taken at the midpoint between the shoulder and elbow.
b. Forearm – Measurement was taken at maximum girth with the arm extended in front of the body and palm up.
c. Thigh – Measurement was taken at upper thigh just below the buttocks.
d. Calf – Measurement was taken at widest girth midway between the ankle and knee.
3. Test for hamstring flexibility19
Active knee extension test (AKE): The subjects had to lie supine on a bench with right hip and knee flexed to 90 degrees. They were then instructed to hold their femur by using their right hand and was asked to maintain this position throughout the test. The participants were then instructed to extend their right leg as far as possible, keeping their feet relaxed, and hold the position for five seconds. Each participant performed a single repetition of the movement to familiarize themselves with action. A second repetition was performed during which the angle of knee extension was measured at the end of 5 seconds hold period. The angle of knee extension was measured using a standard Perspex Goniometer (Physiomed, Manchester, UK). Center of the Goniometer was positioned over the axis point previously marked on the lateral joint line, and the Goniometer arms were positioned along the lines marked on the femur and fibula and the knee extension range in degrees was noted.
4. Vertical Jump Test (VJT)20
The VJT was done using a wall mounted inch tape. The subjects were asked to stand straight with dominant side next to the wall, both feet firmly on the ground. The subjects’ finger tips were marked with chalk powder and they were instructed to touch the wall as high as possible. Subjects performed a countermovement consisting of bending knees and hips while at the same time flexing the trunk. Each subject was instructed to lower themself to a most comfortable point at the same time moving their arms back into hyperextension. Then the subjects would leap vertically as high as possible using both arms and legs, assisting the body upwardsand the highest point reached was marked and recorded. Three readings were taken and an average was calculated.
STATISTICAL METHODS
The data collected was analyzed using SPSS version 17 software. Kolmogorov Smirnov test of normality was used. The mean of hamstring flexibility, limb length, and limb girth was calculated. Pearson’s correlation coefficient test was used to analyze the relation of hamstring flexibility, limb girth, limb length with VJ. Level of significance was set at pEnglishhttp://ijcrr.com/abstract.php?article_id=625http://ijcrr.com/article_html.php?did=6251. Ugarkovic D, Matavulj D, Kukolj M, and Jaric S. Standard anthropometric, body composition and strength variables as predictors of jumping performance in elite junior athletes. Journal of Strength and Conditioning Research, 2002; 16(2): 227–230.
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12. Feltner M.E., Frasceti D.J., Crisp R.J. Upper extremity augmentation of lower extremity kinetics during countermovement vertical jumps. Journal of Sports Sciences, 1999; 17:449–466.
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14. Shetty A.B. and Etnyre B.R. Contribution of arm movement to the force components of maximal vertical jump. Journal of Orthopaedic and Sports Physical Therapy, 1989; 11: 198–201.
15. Zachezewski JE. Improving flexibility. Physical Therapy. Philadelphia, Lippincott; 1989. pp. 698–699.
16. Cijullo JV, Zarins B. Biomechanics of the MusculotendinousUnit : Relation to Athletic Performance and Injury. Clinical Sports Medicine, 1983; 2(1):71-86.
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18. Hoppenfeld S. Physical examination of the spine and extremities. Appleton and Lange, East Norwalk,1976.
19. Nelson R.T., Bandy W.D. Static stretching improves hamstring flexibility of high school males. Journal of Athletic Training, 2004; 39(3):254–258.
20. Shankar R, Rajpal H. and Arora M. Effect of high intensity and low intensity plyometric on vertical jump height and maximum voluntary isometric contraction in football players.Journal of Exercise Science and Physiotherapy,2008; 4(2):81-87.
21. Davis DS et al. The relationship of body segment length and vertical jump displacement in recreational athletes. Journal of Strength and Conditioning Research, 2006; 20(1):136-40.
22. Fattahi A, Ameli M, Sadeghi H, Mahmoodi B. Relationship between anthropometric parameters with vertical jump in male elite volleyball players due to game’s position. Journal of Human Sports and Exercise, 2012; 7(3):714-726.
23. Crewther B, Cronin J, Keogh J. Possible stimuli for strength and power adaptation: Acute mechanical responses. Sports Medicine, 2005; 35(11):967-89. 2
4. Turki O. et al. Ten minutes of dynamic stretching is sufficient to potentiate vertical jump performance characteristics. Journal of Strength and Conditioning Research, 2011; 25(9): 2453–2463.
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