Abstract:

Background: Obesity is a well recognised as a state of chronic low grade inflammation and the main source of complement factors is the adipose tissue which is associated with Insulin Resistance, altered glucose and lipid metabolism, all of which promote the development of metabolic & cardiovascular disorders. Objective: Till date no study has been conducted in Indian ethnic population exploring the relationship of serum complement C3 with obesity and disorders like diabetes, dylipidemia and hypertension so our objective was to study the effect obesity & associated disorders on serum C3 levels. Material & Methods: The present study included 290 subjects (121 men & 169 women) out of which 203 (70 %) were overweight 61 (21 %) were obese class I and 26 (9 %) were Class II obese according to International Diabetes Federation (IDF) - Modified ATP III criteria. Biochemical parameters like Serum C3, Fasting sugar levels, serum Insulin levels and lipid profile were measured. Homeostasis model of assessment for insulin resistance (HOMA-IR) was calculated. Statistical analysis was done by Medcalc.v11.5.0.0.software. Results: Mean C3 levels in total no. patients were 148.61± 38.82 mg/dl. As BMI increased, there was significant increase in serum levels of C3. When the distribution of variables were studied in both sexes, no statistically significant differences were found for all variables except Age, BMI, blood pressure & C3 levels. Serum C3 also correlated significantly with BMI (r = 0.812, P< 0.0001), insulin resistance (r= 0.262, P <0.001), Triglyceride (r = 0.338, P < 0.001) & LDL (r= 0.431, P < 0.001). As associated disorders with obesity increased, there was significant increase in levels of C3 than only obese patients with no other associated disorders. (ANOVA, P< 0.001). Conclusion: In this study, association of serum C3 with increase in BMI was established & also relationship of C3 with Insulin levels, Insulin resistance and cardiovascular risk factors was found. Our study concluded that obesity associated with dyslipidemia, diabetes & hypertension have a significant effect in increasing the levels of serum C3 concentration. 

References:

[1]. Odum E.P., Asekomeh E.G., Ntuen N.A., Young E.E. Cardio metabolic Risk Factors in Obese Subjects. Journal of Dental and Medical Sciences. 2014; 13 (4): 63-67.

[2]. PW Peake, AD Kriketos, LV Campbell and JA Charlesworth. Response of the alternative complement pathway to an oral fat load in first-degree relatives of subjects with Type II diabetes. International Journal of Obesity 2005; 29: 429–435.

[3]. Setareh Dehdashtihaghighat, Abolfazl Mehdizadehkashi, Amirmohsen Arbabi, Mohadeseh Pishgahroudsari, Shahla Chaichian. Assessment of C-reactive Protein and C3 as Inflammatory Markers of Insulin Resistance in Women with Polycystic Ovary Syndrome: A Case-Control Study. J Reprod Infertil. 2013; 14(4):197-201.

[4]. M.M.J. van Greevenbroek, C.G. Schalkwijk, C.D.A. Stehouwer. Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences. The journal of medicine 2 0 13; 71(4): 174-187.

[5]. Riyaz somani, victoria r. Richardson, kristina f. Standeven, PETER J et al. Elevated Properdin and Enhanced Complement Activation in First-Degree Relatives of South Asian Subjects With Type 2 Diabetes. Diabetes care 2102; 35: 894-899.

[6]. Muscari A, Sbano D, Bastagli L, Poggiopollini G, Tomassetti V, Forti P et al. Effects of weight loss and risk factor treatment in subjects with elevated serum C3, an inflammatory predictor of myocardial infarction. Int J Cardiol 2005;100: 217–223.

[7]. Engstrom G, Hedblad B, Janzon L, Lindgarde F. Weight gain in relation to plasma levels of complement factor 3: results from a population-based cohort study. Diabetologia 2005; 48: 2525–2531.

[8]. Halkes CJ, Van Dijk H, de Jaegere PP, Plokker HW, van Der Helm Y, Erkelens DW et al. Postprandial increase of complement component 3 in normolipidemic patients with coronary artery disease: effects of expanded-dose simvastatin. Arterioscler Thromb Vasc Biol 2001; 21: 1526–1530.

[9]. Onat A, Uzunlar B, Hergenc G, Yazici M, Sari I, Uyarel H et al. Cross-sectional study of complement C3 as a coronary risk factor among men and women. Clin Sci (London) 2005; 108, 129–135.

[10]. Van Oostrom AJ, Alipour A, Plokker TW, Sniderman AD, Cabezas MC. The metabolic syndrome in relation to complement component 3 and postprandial lipemia in patients from an outpatient lipid clinic and healthy volunteers. Atherosclerosis 2007; 190: 167–173.

[11]. Standards of Medical Care in Diabetes. American Diabetes Association. Diabetes Care 2005; 28 (Suppl 1): S4–S36.

[12]. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance ad b-cell function from fasting plasma glucose ad insulin concentration in man. Diabetologia 1985; 28: 412–419.

[13]. Friedewald WT, Levy RI, Fredricson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of preparative ultracentrifuge. Clin Chem 1972; 18: 499–502.

[14]. Mohammed-Ali V, Pinkey JH, Coppack SW. Adipose tissue as an endocrine and paracrine organ. Int J Obes 1998; 22: 1145–1158.

[15]. A Hernandez-Mijares, MM Jarabo-Bueno, A Lopez-Ruiz, E Sola-Izquierdo, C Morillas-Arin, ML Martínez-Triguero. Levels of C3 in patients with severe, morbid and extreme obesity: its relationship to insulin resistance and different cardiovascular risk factors. International Journal of Obesity 2007; 31: 927–932.

[16]. Cianflone K. Acylation stimulating protein and the adipocyte. J Endocrinol 1997; 155: 203–206.

[17]. Weyer C, Tataranni PA, Pratley RE. Insulin action and insulinemia are closely related to the fasting complement C3, but not acylation stimulating protein concentration. Diabetes Care 2000; 23: 779–785.

[18]. Ylitalo K, Porkka KV, Meri S, Nuotio I, Suurinkeroinen L, Vakkilainen J et al. Serum complement and familial combined hyperlipidemia. Atherosclerosis 1997; 129: 271–277.

[19]. Hansson GK, Jonasson L, Seifert PS, Stemme S. Immune mechanisms in atherosclerosis. Arteriosclerosis 1989; 9: 567–578.

[20]. Koistinen HA, Vidal H, Karonen SL, Dusserre E, Vallier P, Koivisto VA et al. Plasma acylation stimulating protein concentration and subcutaneous adipose tissue C3 mRNA expression in nondiabetic and type 2 diabetic men. Arterioscler Thromb Vasc Biol 2001; 21: 1034–1039.

[21]. Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS et al. Subcutaneous adipose tissue release IL6 but no TNF-a in vivo. J Clin Endo Metab 1997; 82: 4196–4200.

[22]. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for

cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999; 19: 972–978.

[23]. Sniderman AD, Maslowska M, Cianflone K. of mice and men (and women) and the acylation-stimulating protein pathway. Curr Opin Lipidol 2000; 11: 291–296.

[24]. Bhavita Patel, Dilip Taviad, Brahmareddy Malapati, Rita Shah. Complement Component C3: Relationship with Obesity, Insulin resistance and Cardiovascular Risk markers. International Journal of Medical and Health Sciences 2015; 4(3): 351-356.

Abstract:

Obesity is linked with the growth of white adipose tissue and associated chronic hyperleptinemia. Leptin is a hormone-like cytokine or adipokine secreted mainly from adipose tissue. High leptin state in obesity rapidly causes selective resistance, focused in the arcuate nucleus of the hypothalamus, and centered round leptin’s role in food intake and satiety. This resistance lowers the body’s reaction to food intake and prevents the anorexigenic effects of leptin. As this resistance builds up, the intake of food increases causing an enhancement in body adiposity and leptin levels. However, some pathways do not build resistance to leptin and continue to exhibit the stimulatory effects, which cause a persistent stimulation of sympathetic nervous system (SNS), particularly in the kidneys and skeletal muscles. The increase in SNS activity in the kidney, along with the endothelial dysfunction and oxidative stress, lead to an increase in blood pressure. Apart from leptin's effects on SNS and renal function, this adipokine influences vascular health and hypertension through several phenomena or mechanisms such as baroreflex sensitivity, release of nitric oxide and cardiac hormones. In this review, an attempt has been made to highlight different aspects of leptin biology, which are relevant to hypertension.

References:

[1]. Arnold, A. C., & Diz, D. I. (2014). Endogenous leptin contributes to baroreflex suppression within the solitary tract nucleus of aged rats. American Journal of Physiology - Heart and Circulatory Physiology, 307(11), H1539-1546.

[2]. Banks, W. A. (2008). The blood-brain barrier as a cause of obesity. Current Pharmaceutical Design, 14(16), 1606-1614.

[3]. Beltowski, J. (2012). Leptin and the regulation of endothelial function in physiological and pathological conditions. Clinical and Experimental Pharmacology and Physiology, 39(2), 168-178.

[4]. da Silva, A. A., Carmo, J. D., Dubinion, J., & Hall, J. E. (2009). The role of the sympathetic nervous system in obesity-related hypertension. Current Hypertension Reports, 11(3), 206-211.

[5]. da Silva, A. A., Do Carmo, J. M., & Hall, J. E. (2013). Role of leptin and CNS melanocortins in obesity hypertension. Current Opinion in Nephrology and Hypertension, 22(2), 135-140.

[6]. Fernandez-Riejos, P., Najib, S., Santos-Alvarez, J., Martin-Romero, C., Perez-Perez, A., Gonzalez-Yanes, C., & Sanchez-Margalet, V. (2010). Role of leptin in the activation of immune cells. Mediators of Inflammation, 2010, 568343.

[7]. Freeman, R. H., Go, O., Reams, G. P., Spear, R., Liu, K., & Villarreal, D. (2014). Obesity hypertension: pathophysiological role of leptin in neuroendocrine dysregulation. American Journal of the Medical Sciences, 347(6), 485-489.

[8]. Frühbeck, G. (2006). Intracellular signalling pathways activated by leptin. Biochemical Journal, 393(Pt 1), 7-20.

[9]. Hall, J. E., do Carmo, J. M., da Silva, A. A., Wang, Z., & Hall, M. E. (2015). Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms. Circulation Research, 116(6), 991-1006.

[10]. Haynes, W. G. (2005). Role of leptin in obesity-related hypertension. Experimental Physiology, 90(5), 683-688.

[11]. Humphreys, M. H. (2011). The brain splits obesity and hypertension. Nature Medicine, 17(7), 782-783.

[12]. Kalil, G. Z., & Haynes, W. G. (2012). Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications. Hypertension Research, 35(1), 4-16.

[13]. Korda, M., Kubant, R., Patton, S., & Malinski, T. (2008). Leptin-induced endothelial dysfunction in obesity. American Journal of Physiology - Heart and Circulatory Physiology, 295(4), H1514-1521.

[14]. Lane, M. L., & Vesely, D. L. (2013). Reduction of leptin levels by four cardiac hormones: Implications for hypertension in obesity. Experimental and Therapeutic Medicine, 6(2), 611-615.

[15]. Mantzoros, C. S., Magkos, F., Brinkoetter, M., Sienkiewicz, E., Dardeno, T. A., Kim, S. Y., Hamnvik, O. R., Koniaris, A. (2011). Leptin in human physiology and pathophysiology. American Journal of Physiology Endocrinology and Metabolism, 301(4), E567-584.

[16]. Martin, S. S., Qasim, A., & Reilly, M. P. (2008). Leptin resistance: a possible interface of inflammation and metabolism in obesity-related cardiovascular disease. Journal of the American College of Cardiology, 52(15), 1201-1210.

[17]. Mattu, H. S., & Randeva, H. S. (2013). Role of adipokines in cardiovascular disease. Journal of Endocrinology, 216(1), T17-T36.

[18]. Nakamura, K., Fuster, J. J., & Walsh, K. (2014). Adipokines: A link between obesity and cardiovascular disease. Journal of Cardiology, 63(4), 250-259.

[19]. Olofsson, L. E., Unger, E. K., Cheung, C. C., & Ku, A. W. (2013). Modulation of AgRP-neuronal function by SOCS3 as an intiating event in diet-induced hypothalamic leptin resistance. Proceeding of the National Academy of Sciences, 110(8), E697-E706.

[20]. Purkayastha, S., Zhang, G., & Cai, D. (2011). Uncoupling the mechanisms of obesity and hypertension by targeting hypothalamic IKK-β and NF-κB. Nature Medicine, 17(7), 883-887.

[21]. Pedroso, J. A., Buonfiglio, D. C., Cardinali, L. I., Furigo, I. C., Ramos-Lobo, A. M., Tirapegui, J., Elias, C. F., Donato J. Jr. (2014). Inactivation of SOCS3 in leptin receptor-expressing cells protects mice from diet-induced insulin resistance but does not prevent obesity. Molecular Metabolism, 3(6), 608-618.

[22]. Ray, A., & Cleary, M. P. (2010). Leptin as a potential therapeutic target for breast cancer prevention and treatment. Expert Opinion on Therapeutic Targets, 14(4), 443-451.

[23]. Reed, A. S., Unger, E. K., Olofsson, L. E., Piper, M. L., Myers, M. G., & Xu, A. W. (2010). Functional role of suppressor of cytokine signaling 3 upregulation in hypothalamic leptin resistance and long-term energy homeostasis. Diabetes, 59(4), 894-906.

[24]. Rivest, S. (2002). Does circulating leptin have the ability to cross the blood-brain barrier and target neurons directly? Endocrinology, 143(9), 3211-3213.

[25]. Simonds, S. E., & Cowley, M. A. (2013). Hypertension in obesity: is leptin the culprit? Trends in Neurosciences, 36(2), 121-132.

[26]. Skrapari, I., Tentolouris, N., Perrea, D., Bakoyiannis, C., Papazafiropoulou, A., Katsilambros, N., & Ioanna, S. (2007). Baroreflex sensitivity in obesity: relationship with cardiac autonomic nervous system activity. Obesity (Silver Spring), 15(7), 1685-1693.

[27]. Voulgari, C., Pagoni, S., Vinik, A., & Poirier, P. (2013). Exercise improves cardiac autonomic unction in obesity and diabetes. Metabolism, 62(5), 609-621.

[28]. Wang, J., Wang, H., Luo, W., Guo, C., Wang, J., Chen, Y. E., & Chang, L. (2013). Leptin-induced endothelial dysfunction is mediated by sympathetic nervous system activity. Journal of American Heart Association, 2(5), e000299.

[29]. Yang, R., & Barouch, L. A. (2007). Leptin signaling and obesity: Cardiovascular consequences. Circulation Research, 101(6), 545-559.

[30]. Zhang, X., Zhang, G., Zhang, H., Karin, M., Bai, H., & Cai, D. (2008). Hypothalamic IKKb/Nf-kB and ER stress link overnutrition to energy imbalance and obesity. Cell, 135(1), 61-73.

Abstract:

Staphylococci represent the most commonly encountered blood culture isolates from ICU patients. Slime production is considered to be a significant virulence factor for some strains of Staphylococci. The importance of the role played by slime is further increased by its frequent association to reduced antibiotic susceptibility. This study was done to find out relationship of Bio-Film formation on the susceptibility pattern of the isolates. 27.6% of the isolates produced biofilm as detected by Congo Red Agar method; commonest being Staphylococcus epidermidis (53.9%). The percentage of resistance in the group which produces biofilm is always greater than the group which does not produce biofilm. Odds ratio for overall drug resistance was 2.10 (with 95% confidence interval as [1.6 – 2.6]) and with a p-value of 0.006.

References:

[1]. Morales Serrano T, Ramos S, Lara Gonzalez Y, Torres Colberg H, Vera Quiñones A, Miranda Santiago R, Amill S, Otero M, Cintron V, Villarreal Morales ML, ' Manatí Medical Center Sepsis Management Epidemiological Study', Bol Asoc Med P R (2015), Vol.107 No.2 pp.34-39.

[2]. Weinstein M P, Towns M L, Quartey S M, Mirrett S, Reimer L G, Parmigiani G, 'The clinical significance of positive blood cultures in the 1990s: a prospective comprehensive evaluation of the microbiology, epidemiology, and outcome of bacteremia and fungemia in adults', Clin Infect Dis. (1997), Vol.24 No.4 pp.584-602.

[3]. Bates D W, Sands K, Miller E, 'Predicting bacteremia in patients with sepsis syndrome. Academic Medical Center Consortium Sepsis Project Working Group', J Infect Dis (1997), Vol.176 pp.1538–1551.

[4]. Aygen B, Yoruk A, Yyldyz O, 'Bloodstream infections caused by Staphylococcus aureus in university hospital in Turkey: clinical and molecular epidemiology of methicillin-resistant Staphylococcus aureus', Clin Microbiol. Infect. (2004), Vol.10 pp.309–314.

[5]. Mathur P, Kapil A, Dan B, 'Nosocomial bacteremia in intensive care unit patients of a tertiary care center', Indian J Med Res. (2005), Vol.122 pp.305–308.

[6]. Ammendolia MG, Di Rosa R, Montanaro R, Arciola CR, Baldassarri L, 'Slime production and expression of the slime-associated antigen by Staphylococal clinical isolates', J Clin Microbiol (1999) Vol.37 pp.3235-3238.

[7]. Amorena B, Garcia E, Monzon M, Leiva J, Oteiza C, Perez M, 'Antibiotic susceptibility assay for Staphylococcus aureus in biofilms developed in-vitro', J. Antimicrob. Chemother. (1999), Vol.44 pp.43 – 55.

[8]. Kotulová D, Slobodníková L, 'Susceptibility of Staphylococcus aureus biofilms to Vancomycin, Gentamicin and Rifampin', Epidemiol Mikrobiol Imunol. (2010), Vol.59 No.2 pp.80-87.

Abstract:

The present ethno-medicinal study was carried out at 3 localities of Pechipparai hills of Southern Western Ghats of Tamilnadu, Kanyakumari district. Frequent field visits were made throughout the study period from 2012-2013. Data presented here are based on personal observations and interviews with informants like medicine men and village head men. In this context the Kani people has rich and abundant terminology. It is common that most of the medicinal plants have their own secret, for many safeguard their specialized knowledge. During the present course of investigation, a total 50 medicinal plant species were distributed across eighteen families and fifty genera. The result of the present study provide evidence that medicinal plants continue to play an important role in the health care system used by tribal community. Documentation of this knowledge is valuable for the communities and their future generations.

References:

[1]. Ayyanar M, Ignacimuthu S (2005). Traditional knowledge of Kanitribals in Kouthalai of Tirunelveli hills, Tamil Nadu, India. J.Ethanopharmacol.102:246-255.

[2]. Gamble J.S, (2008) (Rep.Ed) Flora of the Presidency of Madras 3 vols.

[3]. Gamble, J.S. (1996). The flora of the presidency of Madras (Adlard & Son LTD, London vol. I – III.

[4]. Ignacimuthu, S, Sankarasivaraman. K Kesavan.L (1998). Medico Ethnobotanical survey among Kanikar Tribal of Mundanthurai sanctuary. Fitoterapia 69. 409-414.

[5]. Janaki Ammal E.K, Prasad P.N (1984) . Ethno botanical findings on Costus Speciosus among the Kanikkars of Tamilnadu. J.Econ.Taxon. Bot .5:129-133.

[6]. Kala C.P (2005). Current status of medicinal plants used by Traditional vaidayas in Uttaranchal state of India, Ethnobot . Res. Appl. 3: 267-278.

[7]. Matthew K.M (1983).The Flora of the Tamilnadu Carnatic. The Rapinat Herbarium, St.Joseph’s college, Tiruchirapalli, India. vol: I – III.

[8]. Ngari E.W, Chiuri L.W Kariuki S.T Huckett S (2010). Ethnomedicine of Nakuru - Kenya. Ethnobot. Res. Appl 8:135-152.

[9]. Prasad P.N. Jabadhas.A.W Janaki Ammal E.K (1987). Medicinal plant used by the Kanikkars of south India. J.Econ. Taxon. Bot. 11:149-155.

[10]. Schultes, R.E (1962).The role of ethnobotanist in search for new medicinal plants. Lloydia 25:257-266.

[11]. Usha, M.(2012).Ethnomedicines used by Kani tribals of Pechipparai hills, Southern Western Ghats of Tamilnadu, India, Plant Sciences Feed 2(1): 5-10

Abstract:

Sacred groves exist in various parts of the country and are unique examples of ecological understanding and management. These are locked information sites. The Sacred grove concept is one of the strategies developed by many human societies to conserve biological resources using a traditional approach. In the present study deals with the floristic comparison and ethnobotanical practices of the two sacred groves, Punikkolkavu and Chirakkakavu, Kannur District, Kerala. Punikkolkavu is rich in plant diversity when compared to Chirakkakavu. A total of 70 plant species belonging to 36 families were located in Punikkolkavu and 41 plant species belonging to 22 families were located in Chirakkakavu were recorded. The mode of mythological and therapeutical uses and conservation practices of these plants by the local people have been recorded.

References:

[1]. Chandrashekara.U.M, and Sankar.S (1998) Ecology and management of Sacred groves in Kerala: Forest ecology and management.112; 165-177.

[2]. Divya. K.R and Manonmani. K (2013).Floristic composition and ethanobotanical practices of the Sacred Groves of Nenmmara, Palakkad District, Kerala: International Journal of Pharmaceutical Sciences and Business Management.Vol.1 Issue. 1, September- 2013, pg. 9-17

[3]. Freseet al., Frese, P. R. and Gray, S. J. M. Trees (1998). In The Encyclopaedia of Religion (ed. Eliade, M.), Macmillan Library Reference USA, IBH Publishing, New Delhi. 1998, 397 - 414.

[4]. Nayar, M.P (1996).Hot spots of endemic plants of India, Nepal and Butan.

[5]. Ramanujam. M.P. and Cyril, K.P.K. (2003).Woody species diversity of four sacred groves in the Pondicherry region of South India. Biodiversity and Conservation 12: 289 – 299.

[6]. Subrahmanyaprasad K. and Raveenran K.(2013);Floristic diversity in Niliarkottam Sacred Grove in Kannur District, Kerala, India. Life sciences leaflets1:64-73.

Abstract:

Introduction: Intra-Uterine Growth Retardation (IUGR) is failure to attain optimal intrauterine growth. Next to preterm birth, IUGR is the second leading cause of perinatal mortality. As many as 53% of preterm stillbirths and 26% of term stillbirths are growth restricted. Given the immediate and long-term implications of IUGR and its high prevalence in India, a focus on IUGR is both rational and strategic.

Objectives: 1) To study the Clinical pattern and outcome of IUGR babies and their Outcome during hospital stay. 2) To find out the Factors associated with Morbidity and Mortality of IUGR babies. 

Methodology: This Cross sectional Descriptive Study was carried out in the Department of Pediatrics, Sick Neonatal Nursery(SNN) ward, Department of Pediatrics, Tirunelveli Medical College Hospital. 120 babies were selected by systematic random sampling. The socio- demographic and antenatal characteristics were collected by interviewing the mother using a structured proforma. The outcome measures like morbidity pattern and condition at discharge were quantified.

Results:  Of 120 IUGR babies 22 (18.3%) are Preterm babies and 98 (81.7%) are Term babies. Hypoglycemia (63.3%) and Perinatal Asphyxia (45.0%), Sepsis (33.3%), Hypocalcaemia (30.0%), Hypothermia (28.3%) and Thrombocytopenia (25.0%) are the common complications.  22 (18.3%) have died at hospital and 98 (81.7%) have been discharged. Perinatal asphyxia and Meconium Aspiration are significantly associated with abnormal neurological examination at Discharge. Lower gestational age, Normal delivery and Lower weight of the baby are the statistically significant risk factors associated with mortality. 

Conclusion: Hypoglycemia  and Perinatal Asphyxia are the commonest complications of IUGR. Perinatal asphyxia, Meconium Aspiration, Gestational age, Delivery category and Weight of the baby are significant risk factors associated with morbidity and mortality.

References:

[1]. Barker, D. J. P. (1998), Mothers, Babies and Health in Later Life, Edinburgh, Churchill Livingstone.

[2]. Chard T, Yoong A, Macintosh M. (1993). The myth of fetal growth retardation at term. Br J Obstet Gynaecol; 100: 1076.

[3]. De Onis, M., Villar, J., Gulmezoglu, M. (1998), ‘Nutritional interventions to prevent intrauterine growth retardation: Evidence from randomized controlled trials’, European Journal of Clinical Nutrition, 52(1).

[4]. Erich Cosmi, Tiziana Fanelli, Silvia Visentin, Daniele Trevisanuto, Vincenzo Zanardo. (2011). Consequences in Infants That Were Intrauterine Growth Restricted. Journal of Pregnancy; Volume 2011, Article ID 364381, 6 pages: http://dx.doi.org/10.1155/2011 /364381

[5]. Garite TJ. (2004). Intrauterine growth restriction increases morbidity and mortality among premature neonates. Am J Obstet Gynecol; 191:481- 487.

[6]. Hack M, Fanaroff AA (2000). Outcomes of children of extremely low birth weight and gestational age in 1990s. Semin Neonataol; 5; 89-106.

[7]. Hawdon JM, Platt MPW. (1993). Metabolic adaptation in small for gestational age infants. Arch Dis Child; 68: 262.

[8]. Henry L. Galan. (2008). Introduction to IUGR. Seminars in Perinatology. Vol: 32, No: 3 June 2008; 139-40.

[9]. Kliegman RM. (1989). Alterations of fasting glucose and fat metabolism in intrauterine growth-retarded newborn dogs. Am J Physiol 1989; 256: E380.

[10]. Neelam Kle, Naveen Gupta. (2009).  Intrauterine Growth Retardation: Journey from conception to late adulthood. Indian Journal of Practical Pediatrics; 11(1) : 68- 81.

[11]. Pallotto EK1, Kilbride HW. (2006). Perinatal outcome and later implications of intrauterine growth restriction. Clin Obstet Gynecol. 2006 Jun;49(2):257-69.

[12]. Perez-Escamilla R, Pollitt E. (1992). Causes and consequences of intrauterine growth retardation in Latin America. Bull Pan Am Health Organ; 26(2):128-47.

Abstract:

The darkness of the night is broken by the brightness of the sun and people worship sun for this. Similarly, providing even a flicker of light to a person who has lost his/her sight is one of the greatest miracles a doctor can perform. Bionic Eye- visual prosthetic devices serve this purpose and helps to restore some kind of visual perception in patients with retinal pathologies like retinitis pigmentosa and age related macular degeneration. The inception of this idea dates back to the 18^th century but the recent advances in electronics, robotics and other technologies has helped in materializing the idea. The basic function of the device is to receive the images using a camera, convert it to electric signals and eventually stimulate the left-over healthier parts of the visual pathway. There are various kinds of devices based on the position of implants. Each of them have varied advantages. Understanding the existing systems would help in improvising them or in finding better systems to serve the same purpose.

References:

[1]. BBC (2015). Bionic Eye improves macular degeneration patient’s sight [News Article]. Retrieved from http://www.bbc.com/news/health-33612558.

[2]. Visual Prosthesis. (n.d.). In Wikipedia. Retrieved from http://en.wikipedia.org/wiki/ Visual Prosthesis.

[3]. Galvani, L. (1762) De ossibus. Theses physic-medical chirurgicae. Bononiae, St. Thomas Aquinatis. Repr. :(1996) Pantaleoni M. (Ed.) De ossibus. Lectiones quattuor. Bologna, Composers. Repr .:(1998) Bologna, Arnaldo Forni publisher.

[4]. Dobelle, W.H. (2000). Artificial vision for the blind by connecting a television camera to the visual cortex. ASAIO journal, 46(1), 3-9.

[5]. LeRoy C. (1755). Ou L’on rend compte de quelques tentative sue l’on a faites pour guerir plusieurs malaides par l’electricite. Hist Acad Roy Sciences (Paris). Memoire MathPhys 60:87-95

[6]. Cavallo, T. (1781). An essay on the theory and practice of medical electricity. The author.

[7]. Foerster O.(1929). Beitriige zur Pathophysiologie der Sehbahn und der Sehsphare. J Psychol Neuro, Lpz. 39: 463–85

[8]. Krause F, Schum H. (1931). Die epileptischen Erkrankungen. In: Kuttner H, ed. Neue Deutsche Chirurgie. Vol. 49a. Stuttgart: Enke. 482–6.

[9]. Tassicker GE. (1956). Preliminary report on a retinal stimulator. Br J Physiol Opt. 13: 102–5.

[10]. Joao Lobo Antunes.(n.d). Retreived from http://www.researchcafe.net/content/view/75/36.

[11]. Wyatt, Jr., J.L. (1998). The Retinal Implant Project. [PDF]. Research Laboratory of Electronics at MIT.

[12]. Zrenner E, Stett A, Weiss S et al. (1999) Can subretinal microphotodiodes successfully replace degenerated photoreceptors? Vision Res. 39: 2555–67.

[13]. Rizzo JF, Miller S, Denison T, Herndon T, Wyatt JL. (1996). Electrically evoked cortical potentials from stimulation of rabbit retina with a microfabricated electrode array. Invest Ophthalmol Vis Sci [ARVO Abstr] 37:5707

[14]. Grumet AE, Wyall JL Jr., Rizzo JF. (2000). Multi electrode stimulation and recording in the isolated retina. J neuroscimethods 101:31-42

[15]. Stett A, Barth W, Weiss S, Haemmerle h, Zrenner E. (2000). Electrical multisite stimulation of the isolated chicken retina. Vision Res 40:1785-1795

[16]. Veraart C, Raftopoulos C, Mortimer JT et al. Visual sensations produced by optic nerve stimulation using an implanted self-sizing spiral cuff electrode. Brain Res 1998; 813: 181–6.

[17]. Delbeke J, Oozeer M, Veraart C. Position, size and luminosity of phosphenes generated by direct optic nerve stimulation. Vision Res 2003; 43: 1091–102.

[18]. Duret FC, Delbeke J, Gerard B, Veraart C. (2004). Strategies of object recognition performed using a chronically implanted optic nerve prosthesis (Abstract). Annual Meeting of the Association for Research in Vision and Ophthalmology. Fort Lauderdale FL.

[19]. Duret F, Brelén ME, Lambert V, Gérard B, Delbeke J, Veraart C. (2006). Object localization, discrimination, and grasping with the optic nerve visual prosthesis. Restor Neurol Neurosci. 24: 31–40.

[20]. Veraart C, Wanet-Defalque MC, Gérard B, Vanlierde A, Delbeke J. (2003). Pattern recognition with the optic nerve visual prosthesis. Artif Organs. 27: 996–1004.

[21]. Chow AY, Chow VY, Packo KH, Pollack JS, Peyman GA, Schuchard R. (2004). The artificial silicon retina microchip for the treatment of vision loss from retinitis pigmentosa. Arch Ophthalmol. 122: 460–9.

[22]. Humayun MS, Weiland JD, Fujii GY et al. (2003). Visual perception in a blind subject with a chronic microelectronic retinal prosthesis. Vision Res. 43: 2573–81.

[23]. Weiland JD, Yanai D, Mahadevappa M et al. (2004) Visual task performance in blind humans with retinal prosthetic implants. Conf Proc IEEE Eng Med Biol Soc. 6: 4172–3.

[24]. Wilms M, Eger M, Schanze T, Eckhorn R (2003). Visual resolution with epi-retinal electrical stimulation estimated from activation profiles in cat visual cortex. Vis neurosci 20:543-555

[25]. Humayun MS, Dorn JD, Ahuja AK et al. (2009). Preliminary 6 month results from the Argus II epiretinal prosthesis feasibility study. Conf Proc IEEE Eng Med Biol Soc. 4566–8.

[26]. Sifferlin, A (2013). FDA approves first bionic eye (News Article). CNN-TIME

[27]. Javaheri M, Hahn DS, Lakhanpal RR, Weiland JD, Humayun MS. (2006). Retinal prostheses for the blind. Ann Acad Med Singapore. 35: 137–44.

[28]. Eckmiller R. (1997) Learning retina implants with epiretinal contacts [Review]. Ophthalmic Res. 29: 281–9.

[29]. Hornig R, Zehnder T, Velikay-Parel M, Laube T, Feucht M, Richard G. (2007). The IMI retinal implant system. In: Humayun MS, Chader G, Weiland JD, eds. Artificial Sight: Basic Reaserch, Biomedical Engineering, and Clinical Advances. New York: Springer-Verlag. 111–28.

[30]. Roessler G, Laube T, Brockmann C et al. (2009). Implantation and explantation of a wireless epiretinal retina implant device: observations during the EPIRET3 prospective clinical trial. Invest Ophthalmol Vis Sci. 50: 3003–8.

[31]. Rizzo JF 3rd,Wyatt J, Loewenstein J, Kelly S, Shire D. (2003). Methods and perceptual thresholds for short-term electrical stimulation of human retina with microelectrode arrays. Invest Ophthalmol Vis Sci. 44: 5355–61.

[32]. Rizzo JF 3rd,Wyatt J, Loewenstein J, Kelly S, Shire D. (2003). Perceptual efficacy of electrical stimulation of human retina with a microelectrode array during short-term surgical trials. Invest Ophthalmol Vis Sci. 44: 5362–9.

[33]. Bionic Vision Australia. Retrieved from: http://www.bionicvision.org.au.

[34]. Bionic Vision Australia. Our Approach. Retrieved from: http://bionicvision.org.au/about-us/ourapproach.html.

[35]. Lee SW, Seo JM, Ha S, Kim ET, Chung H, Kim SJ. (2009). Development of microelectrode arrays for artificial retinal implants using liquid crystal polymers. Invest Ophthalmol Vis Sci. 50: 5859–66.

[36]. Ong, J. M., Cruz, L., (2012). The bionic eye: a review. Clinical & Experimental Ophthalmology. 40: 6-17.

[37]. Chow AY, Chow VY, Packo KH, Pollack JS, Peyman GA, Schuchard R. (2004). The artificial silicon retina microchip for the treatment of vision loss from retinitis pigmentosa. Arch Ophthalmol. 122: 460–9.

[38]. Pardue MT, Phillips MJ, Hanzlicek B, Yin H, Chow AY, Ball SL. (2006). Neuroprotection of photoreceptors in the RCS rat after implantation of a subretinal implant in the superior or inferior retina. Adv Exp Med Biol. 572: 321–6.

[39]. Sachs HG, Gabel VP. (2004). Retinal replacement – the development of microelectronic retinal prostheses – experience with subretinal implants and new aspects. Graefes Arch Clin Exp Ophthalmol. 242: 717–23.

[40]. Sachs HG, Schanze T, Wilms M et al. (2005). Subretinal implantation and testing of polyimide film electrodes in cats. Graefes Arch Clin Exp Ophthalmol. 243: 464–8.

[41]. Gekeler F, Szurman P, Grisanti S et al. (2007) Compound subretinal prostheses with extra-ocular parts designed for human trials: successful long-term implantation in pigs. Graefes Arch Clin Exp Ophthalmol. 245: 230–41.

[42]. Sachs HG, Bartz-Schmidt KU, Gekeler F et al. (2010) Subretinal visual prosthetic devices in blind patients. Modifications in transchoroidal surgery and long term follow up in the first 12 patients. Annual Meeting of the Association for Research in Vision and Ophthalmology. Fort Lauderdale FL 2010 (Abstract).

[43]. Wilke R, Greppmaier U, Harscher A, Benav H, Zrenner E. (2010) Factors affecting perceptual thresholds of subretinal electric stimulation in blind volunteers. Annual Meeting of the Association for Research in Vision and Ophthalmology. Fort Lauderdale FL 2010 (Abstract).

[44]. Zrenner E. (2010). Recent developments in subretinal electronic implants: chances and limitations. Annual Meeting of the Association for Research in Vision and Ophthalmology. Fort Lauderdale FL 2010 (Abstract).

[45]. Zrenner E, Bartz-Schmidt KU, Benav H et al. (2011). Subretinal electronic chips allow blind patients to read letters and combine them to words. R.Proc Biol Sci. 278(1711): 1489–97.

[46]. Kelly SK, Shire DB, Chen J et al. (2009). Realization of a 15-channel, hermetically-encased wireless subretinal prosthesis for the blind. Conf Proc IEEE Eng Med Biol Soc 2009. 200–3.

[47]. Shire DB, Kelly SK, Chen J et al. (2009). Development an implantation of a minimally invasive wireless subretinal neurostimulator. IEEE Trans Biomed Eng. 56: 2502–11.

[48]. Mathieson, K., Loudin, J., et al. (2012). Photovoltaic retinal prosthesis with high pixel density. Nature Photonics. 6(6):391-397.

[49]. Loudin, J. D., Simanovskii, D. M., et al. (2007). Optoelectronic retinal prosthesis: system design and performance (PDF). J. Neural Engineering. 4(1):572-584.

[50]. Chowdhury V, Morley JW, Coroneo MT. (2005). Stimulation of the retina with a multielectrode extraocular visual prosthesis. ANZ J Surg. 75: 697–704.

[51]. Normann RA, Greger B, House P, Romero SF, Pelayo F, Fernandez E. (2009). Toward the development of a cortically based visual neuroprosthesis. J Neural Eng. 6: 035001.

[52]. Tehovnik EJ, Slocum WM, Smirnakis SM, Tolias AS. (2009). Microstimulation of visual cortex to restore vision. Prog Brain Res. 175: 347–75.

[53]. Schmidt EM, Bak MJ, Hambrecht FT, Kufta CV, O’Rourke DK, Vallabhanath P. (1996). Feasibility of a visual prosthesis for the blind based on intracortical microstimulation of the visual cortex. Brain. 119: 507– 22.

[54]. Deep Brain Stimulation for Parkinson’s Disease Study Group. (2001). Deep-brain stimulation of the subthalamic nucleus or the parts interna of the globus pallidus in Parkinson’s disease. N Engl J Med. 435: 956–63.

[55]. Kumar R, Lozano AM, Kim YJ et al. (1998). Double-blind evaluation of subthalamic nucleus deep brain stimulation in advanced Parkinson’s disease. Neurology. 51: 850–5.

[56]. Limousin P, Pollak P, Benazzouz A et al. (1995). Bilateral subthalamic nucleus stimulation for severe Parkinson’s disease. Mov Disord.10: 672–4.

[57]. Pezaris JS, Reid RC. (2007). Demonstration of artificial visual percepts generated through thalamic microstimulation. Proc Natl Acad Sci U S A.104: 7670–5.

[58]. Pezaris JS, Reid RC. (2009). Simulations of electrode placement for a thalamic visual prosthesis. IEEE Trans Biomed Eng. 56: 172–8.

[59]. Pezaris JS, Eskandar EN. (2009). Getting signals into the brain: visual prosthetics through thalamic microstimulation. Neurosurg Focus. 27: E6.

[60]. Manasa, L., (2015). Obstacle Detection Technologies to Empower Visually Challenged: A Short Notes. International Journal of Science and Research. SUB159017

Abstract:

This article will look into how Research, Technology and Innovation have improved primary health care around the world through telemedicine. Telemedicine and tele health have revolutionised medical care across the globe.

Objective: The paper is an original manuscript which will go into the entire gamut of primary health care and how innovation and technological improvements have revolutionised the concept of telemedicine and how patients across the world have immensely benefitted from this.

Design: This article will be a narrative on the research and technological advances of telemedicine over the years. This will refer to several studies and research works undertaken by several luminaries in this field. The references will be duly documented at the end of this article.

Procedure: The procedure to be followed will be a chronological sequencing of telemedicine as it evolved over the years and how innovation and technology have improved the patient care at the primary health care setting.

Results: A review of the scholarly articles and other studies in this field have pointed to one palpable truth – Research Technology and Innovation have revolutionised way telemedicine and primary healthcare have evolved over the years. With technology driven telemedicine, primary health care has become easy, quick and very affordable.

Conclusion: The bedrock for global development is indeed Research Technology and Innovation. As a doctor, my focus on telemedicine reveals how, technology has touched the lives of millions of people worldwide and how telemedicine has revolutionised this niche market of healthcare. 

References:

[1]. Armstrong IJ, Haston WS. Medical decision support for remote general practitioners using telemedicine. J Telemed Telecare. 1997;3:27–34.[PubMed]

[2]. Benger J. A review of minor injuries telemedicine. J Telemed Telecare 1999;5(suppl 3):S5-13

[3]. Bergmo TS. An economic analysis of teleradiology versus a visiting radiologist service. J Telemed Telecare. 1996;2:136–142.[PubMed]

[4]. Chan WM, Woo J, Hui H, Hjelm NM. The role of telenursing in the provision of geriatric outreach services to residential homes in Hong Kong. J Telemed Telecare. 2001;7:38–46.[PubMed]

[5]. Currell R, Urquhart C, Wainwright P, Lewis R. Telemedicine versus face to face patient care: effects on professional practice and health care outcomes. Cochrane Database Syst Rev 2000;(2):CD002098. [PubMed]

[6]. Harrison R, Clayton W, Wallace P. Can telemedicine be used to improve communication between primary and secondary care? BMJ. 1996;313:1377–1380. [PMC free article][PubMed]

[7]. Haukipuro K, Ohinmaa A, Winblad I, Linden T, Vuolio S. The feasibility of telemedicine for orthopaedic outpatient clinics—a randomized controlled trial. J Telemed Telecare. 2000;6:193–198.[PubMed]

[8]. Hussain P, Melville D, Mannings R, Curry D, Kay D, Ford P. Evaluation of a training and diagnostic ultrasound service for general practitioners using narrowband ISDN. J Telemed Telecare. 1999;5(suppl 1):95–99.[PubMed]

[9]. Johnston B, Wheeler L, Deuser J, Sousa KH. Outcomes of the Kaiser Permanente Tele-Home Health Research Project. Arch Fam Med. 2000;9:40–45.[PubMed]

[10]. Keen J, Wyatt J. Back to basics on NHS networking. BMJ. 2000;321:875–878. [PMC free article][PubMed]

[11]. Larson A, Lynch DA, Zeligman B, Harlow C, Vanoni C, Thieme G, et al. Accuracy of diagnosis of subtle chest disease and subtle fractures with a teleradiology system. Am J Roentgenol. 1998;170:19–22.[PubMed]

[12]. Loane MA, Bloomer SE, Corbett R, Eedy DJ, Hicks N, Lotery HE, et al. A comparison of real-time and store-and-forward teledermatology: a cost-benefit study. Br J Dermatol. 2000;143:1241–1247.[PubMed]

[13]. Mair FS, Haycox A, May C, Williams T. A review of telemedicine cost-effectiveness studies. J Telemed Telecare 2000;6(suppl 1):S38-40

[14]. McLaren P, Mohammedali A, Riley A, Gaughran F. Integrating interactive television-based psychiatric consultation into an urban community mental health service. J Telemed Telecare. 1999;5(suppl 1):100–102.[PubMed]

[15]. Minor injuries telemedicine. Proceedings of a meeting held in Belfast, 16 October 1998. J Telemed Telecare. 1999;5(suppl 3):1–50.

[16]. Munro J, Nicholl J, O'Cathain A, Knowles E. Impact of NHS Direct on demand for immediate care: observational study. BMJ. 2000;321:150–153. [PMC free article][PubMed]

[17]. Melzer SM, Poole SR. Computerized pediatric telephone triage and advice programs at children's hospitals: operating and financial characteristics. Arch Pediatr Adolesc Med. 1999;153:858–863.[PubMed]

[18]. Oakley AM, Kerr P, Duffill M, Rademaker M, Fleischl P, Bradford N, et al. Patient cost-benefits of realtime teledermatology—a comparison of data from Northern Ireland and New Zealand. J Telemed Telecare. 2000;6:97–101.[PubMed]

[19]. Strode SW, Gustke S, Allen A. Technical and clinical progress in telemedicine. JAMA 1999;281:1066-8

[20]. Wootton R. Telemedicine: a cautious welcome. BMJ 1996;313:1375-7

[21]. Whitten P, Collins B. The diffusion of telemedicine. Sci Commun. 1997;19:21–40. 

Abstract:

Background Most new HIV infections are acquired from stable, long‐term partners. HIV serodiscordant relationships are among the most vulnerable to acquiring???? It is not uncommon getting exposed to body fluids of an HIV infected partner in a serodiscordant (magnetic couples) set ups. This is an interesting case scenario cutting across many issues about the transmissibility of HIV infection in. There may be queries from apprehensive people – seeking advice reg?? HIV’s probability of acquisition under some very uncommon conditions which may be helpful for training/teaching purposes

Objectives The scenario (A non‐HIV Patient getting exposed to semen of a HIV positive man with an undetectable viral load –VL at the hand having an open cut) is an interesting, educative and unique case scenario as it involves almost all issues related to HIV prevention i.e. scanty information ‐‐withholding his/her name and gender possibly due to stigma/discrimination issues forwarded by the questioner and issues involving responses to various situations in serodiscordant couples (‘magnetic couples ‘) exposure in an unique non‐occupational yet non‐sexual mode, counseling& testing issues, initiating nPEP (Non‐occupational Post Exposure Prophylaxis) and PrEP (Pre‐Exposure Prophylaxis), TasP (Treatment as Prevention) and HTPN 052 Study. The importance of answering this kind of scenarios lies in the fact that it would help many‐‐including the questioner itself.

Methods Descriptive study discussing the different aspects of HIV Prevention.

Results The questioner’s HIV‐acquisition risks are extremely low (theoretically) & unwarranted still we will try to put his/her fears to rest by examining the issues involved in this case critically and coming up with scientifically based explanations and accordingly advice him/her taking into the considerations of HIV Testing and Treatment policies and Guidelines of the land available.

Conclusions This scenario is a very interesting one, requiring many basic concepts of prevention of HIV/AIDS for answering and may be used for teaching/training even medical professionals. The questioner’s HIV‐acquisition risks are extremely low (theoretically) & unwarranted and we will try to put his/her fears to rest by examining the issues involved in this case critically and coming up with scientifically based explanations and accordingly advice him/her taking into the considerations of HIV Testing and Treatment Policies and Guidelines of the land available. The importance of answering this kind of scenarios lies in the fact that it would help other health professionals and questioners alike and may be useful in teaching/training settings.

References:

[1]. ART PEP after sexual, injection drug use or other non‐occupational exposure to HIV in US,MMWR – Recommendations and Report 2005, 54: 1‐20

[2]. CDC Guidelines for PrEP for MSM and heterosexual couples where one partner in infected with HIV, Smith et al MMWR 2012, 61: 588‐589

[3]. CD4 Counts and Viral Loads of Newly Diagnosed HIV‐Infected Individuals: Implications for Treatment as Prevention: Sarishen Govender, et al http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0090754 Accessed on 20^th.Oct 2015

[4]. Chemaitelly H et al. Distinct HIV discordancy patterns by epidemic size in stable sexual partnerships in sub‐Saharan Africa.

[5]. Demographic and Health Survey (DHS) 2000–2010. http://www.measuredhs.com/surveys/dhs/start.cfm

[6]. Effect of ART on the sheading of in seman, Vernazetal: AIDS: 1997 – 11: 1249‐1254.

[7]. EyawoO et al. HIV status in discordant couples in sub‐Saharan Africa: a systematic review and meta‐analysis. The Lancet infectious Diseases, 2011, 11(4):263–264.

[8]. Guidance on couples HiV Testing and counseling including anti‐retroViral Therapy for Treatment and prevention in serodiscordant couples Recommendations for a public health approach, April 2012, WHO

[9]. HAART does not completely suppress HIV in semen in sexually active HIV infected MSM, Politch JA et al, AIDS: 2012, 26: 1535‐1543

[10]. HIV and its Transmission sheet: http://www.cdc.gov/hiv/pubs/facts/transmission.htm.

[11]. Lingappa JR et al. Regional differences in prevalence of HIV‐1 discordance in Africa and enrollment of HIV‐1 discordant couples into an HIV‐1 prevention trial. PLoS One, 2008, 3(1):e1411.

[12]. Non‐occupational post exposure prophylaxis for HIV: a systematic review, J Bryant, L Baxter and S Hird Health Technology Assessment 2009; Vol. 13: 1‐82

[13]. Persistence of HIVRNA in semen despite Effective ART, Sheth P M et al: AIDS: 2009‐23 = 2050‐2054

[14]. Prevention of HIV ‐1 Infection with early ART Cohen et al, NEJM 2011, 365: 493‐505

[15]. Reduction of seminal shedding in receiving HAART: A 18 month longitudinal studies, Leruez – villa M et al: AIDS 2002 ‐16: 456‐488

[16]. Revised Recommendations for HIV Testing of Adults, Adolescents, and Pregnant Women in Health‐Care Settings (MMWR September 22, 2006 / 55(RR14);1‐17)

[17]. Sexually Transmitted Infections, 2012, 88:51–57. De Walque D. Sero‐discordant couples in five African countries: Implications for prevention strategies.

[18]. Understanding HIV Transmission Risk in Married, HIV Serodiscordant Couples in Gujarat, India: The Positive JeevanSathi Study By: Shilpa N. Patel http://www.cfar.emory.edu/downloads/news/DissAbstract_Patel.pdf

[19]. Vital Signs: HIV Prevention through Care and Treatment, Cohen et al US MMWR‐2011 60: 1618‐1623

[20]. VL and Hetero sexual transmission of HIV ‐1, Quinn et al, NEJM, 2000: 342: 921‐929

Abstract:

Based on traditional medicinal use Apium graveolens seed was selected to evaluate its anti-cancer property with special reference to apoptosis induction, if any. When the water, alcohol and hexane extracts of the dried powder of the plant seeds were tested for cytotoxicity to Dalton’s Lymphoma Acitic (DLA) cells in vitro using Tryphan blue method, only the n-hexane extract showed significant activity at 500 µg/ml level. The extract induced apoptosis as evidenced by morphological changes. The cytotoxicity of this extract was found to be more to cancer cells (DLA) compared to normal cells (thymocytes and macrophages). An active chloroform fraction was separated from this extract. The active fraction at a dose of 200 mg/kg protected 75 % of the mice challenged with 1 X 10⁶ DLA cells whereas all untreated control mice died of cancer. Thin Layer Chromatography (TLC) on silica gel further separated this anticancer fraction into 2 cytotoxic components. One of them was identified as a steroid positive component whereas the other was an alkaloid positive component. The steroid component induced apoptotic cell death while the other component induced necrotic cell death. These components are attractive materials for further studies leading to possible anti-cancer drug development.

References:

[1]. Pushpangadan P, Subramoniam A. Pharmacological investigations on Indian medicinal plants: a search for anti-cancer agents. Amala Research Bulletin 1998: 18:123-129

[2]. Subramoniam A. Defining molecular targets in the discovery of phytomedicines for cancer. Amala Res Bull 2001: 2: 82-87.

[3]. Bertram JS. Cancer prevention by carotenoids. Mechanistic studies in cultured cells. Ann N Y Acad Sci 1993: 691: 177-191.

[4]. Blot WJ, Li J-Y, Taylor PR, et al. Nutrition intervention trials in Linxin, China: Supplementation with specific vitamin/mineral combinations, cancer incidence, and disease specific mortality in the general population. J Natl Cancer Inst 1995: 85: 1483- 1492.

[5]. Menon LG, Kuttan R, Kuttan G. Inhibition of lung metastasis in mice induced by B16F-10 melanoma cells by polyphenolic compounds. Cancer Lett 1995: 95: 221-225.

[6]. Cardile V, Scifo C, Russo A, Falsaperla M, Morgia G, Motta M, Renis M, Imbriani E, Silvestre G. Involvement of HSP70 in resveratrol-induced apoptosis of human prostate cancer. Anticancer Res. 2003: 23: 4921-4926.

[7]. Crowell PL. Prevention and therapy of cancer by dietary monoterpenes. J Nutr 1999: 129: 775S-778S.

[8]. Jose JK, Joy KL, Kuttan R. Effect of Emblica officinalis, Phyllanthus amarus and Picrorrhiza kurroa on N-nitrosodiethylamine induced hepatocellular carcinogenesis. Cancer Letter 1999: 135: 1-6.

[9]. Joy KL, Kumar NV, Kuttan G, Kuttan R. Effect of Picrorrhiza kurroa extract on transplanted tumors and chemical carcinogenesis in mice. J Ethnopharmacol. 2000: 71: 261-267.

[10]. Subramoniam A, Rajasekharan S, Latha PG, Evans DA and Pushpangadan P. Immunomodulatory and anti-tumor activities of Janakia arayalpathra. Fitoterapia 1996: 57: 140-144.

[11]. Subramoniam A. Role of cis unsaturated fatty acids in cell growth regulation. Amala Res Bull 1997:17: 27-31.

[12]. Subramoniam A, Rajasekharan S, Pushpangadan P, George V, Nair SG. A process to prepare an herbal formulation for cancer from Janakia arayalpathra root and Trichopus zeylanicus leaf. Inventors (Chennai/2001). Patent No: MAS/659/01(Patent obtained).

[13]. Mehta RG, Pezzuto, JM. Discovery of cancer preventive agents from natural products: From plants to prevention. Curr Oncol Rep 2002: 4: 478-486.

[14]. Shylesh BS, Ajikumaran Nair S, Subramoniam A. Induction of cell specific apoptosis and protection from Daltons’ Lymphoma challenge in mice by Emilia sonchifolia (active fraction) containing a terpene, active principle. Indian J Pharmacol 2005: 37:232-237.

[15]. Subramoniam, A, Subhisha S, Ajikumaran Nair S, Shylesh BS, Nair G.M. Bryophytes of Kerala: a potential source of anti-cancer agents. Amla Res. Bull.2003: 23: 78-83

[16]. Hanahan D, Weinberg RA. Resistance to apoptosis and cancer. Cell, 2000: 100: 57- 70.

[17]. Martin Z, Anne-Odile H, Wiebke B, Gerard E. Apoptosis regulators and their role in tumorigenesis. Biochem Biophys Acta, 2001: 1551:F1-F37.

[18]. Green DR, Kroemer G. The pathophysiology of mitochondrial cell death. Science, 2004: 305: 626-629.

[19]. Subramoniam A., Ajikumaran Nair S. Application of apoptosis in the search for plant-derived chemopreventive/therapeutic agents. Amala Research Bulletin, 2004: 24: 1-11.

[20]. Shaik Imam, Hussain SJ. Some important herbs used in the treatment of cancer: part-1. In: Role of biotechnology in medicinal and aromatic plants. I A Khan & A Khanum (eds) 2004: Volume 11, 1-50. Ukaaz Publications, Hyderabad.

[21]. Choochote W, Tuetun B, Kanjanapothi D, Rattanachanpichai E, Chaithong U, Chaiwong P, Jitpakdi A, Tippawangkosol P, Riyong D, Pitasawat B. Potential of crude seed extract of celery, Apium graveolens L., against the mosquito Aedes aegypti (L.) (Diptera:Culicidae). J Vector Ecol. 2004: 29: 340-346.

[22]. Seetharami Reddi TVV, Prasanthi S and Ramarao Naidu BVA. Medicinal and aromatic plants of India. In: Role of biotechnology in medicinal and aromatic plants. I A Khan & A Khanum (eds) 2005: Volume12,1-146. Ukaaz Publications, Hyderabad.

[23]. Mary KT, Kuttan G, Kuttan R. Partial purification of tumour reducing principles from Helianthes elastica. Cancer Lett. 1994: 81: 53-56.

[24]. Wagner H, Bladt S, Zgainski EM. Plant drug analysis. Berlin, Heidelberg, New York, Tokyo; Springer-Verlag, 1984.

Abstract:

Background: Injuries are the leading causes of death, hospitalizations and disabilities. Traumatic injuries, poisoning and burns are the major types of injuries reported in Sri Lanka, according to the National Health Statistics. Life style changes such as using alcohol and increasing of vehicle usages are believed to be having relation with the prevalence of injuries. Gender and age group also have effects on types of injuries.

Objective: To identify the prevalence of various types of acute injuries in Batticaloa, Teaching Hospital.

Method: It is a cross sectional descriptive study involving simple random sample of one hundred and ninety one (206) injured patients who were atmitted at Teaching Hospital, Batticaloa.Data was collected by using a pre designed structured interviewer administered questionnaire.

Results: Altogether, 206 patients with an age range of 01-80 years were studied. Males accounted for 62.8 % of the study sample. Majority of causes are dog bite (33.5 %), and RTA (24.2 %), fall injury (16 %), poisoning (6.3 %) and Cat bite (8.7 %).Among that, 50 % injuries are occur due to the animals in whole injuries. There was a significant relationship between age groups and causes of injuries and there was no relationship between habit of alcohol use and accidental injuries. Among body parts, upper limb (35 %) and lower limb (53 %) are most often affected by injuries. 11. 165 % of injured people get disabilities due to their injuries.

Conclusion: According to this study, majority of injuries are caused by dog bites, road traffic accidents (RTA), fall injuries, poisoning and cat bites respectively. Considering the affected body parts, injuries in upper extremities and lower extremities are more common. Around 11. 2 % of patients get disabilities as the consequences of their injuries.

References:

[1]. World Health Organization (WHO), NLM classification: WA 530.1, The world health report, 2006.

[2]. Lamawansa MD, Piyathilake A. Incidence of Physical Injuries in a Rural Community in Sri Lanka: Results of the First Community Survey in Sri Lanka. Indian J Community Med2008; 33(4): 238–242.

[3]. Ministry of Health, Sri Lanka, National Policy & Strategic Framework on Injury Prevention & Management in Sri Lanka, 2009.

[4]. Ministry of Health, Sri Lanka, Annual Health Bulletin, 2009.

[5]. Navaratne KV, Fonseka P, Rajapakshe L, Somatunga L, Ameratunga S, Ivers R, Dandona R. Population-based estimates of injuries in Sri Lanka, Inj Prev2009; 15:170-175.

[6]. World Health Organization (WHO), World Health Survey, 2002.

[7]. Bhalla K, Navaratne KV, Shahraz S, Bartels D, Abraham J, Dharmaratne S. Estimating the incidence of road traffic fatalities and injuries in Sri Lanka using multiple data sources, International Journal of Injury Control and Safety Promotion2010; 17(4): 239-246.

[8]. Alamode SB, Dharmaratne SD, Alamode TC. Incidence and predictors of onboard injuries among Sri Lankan flight attendants, BMC Public Health2009; 9:227.

[9]. Kobusingye O, Guwatudde D, Lett R. Injury patterns in rural and urban Uganda, Inj Prev 2001; 7:46-50.

[10]. Ekstrand J, Hägglund M, Waldén M. Injury incidence and injury patterns in professional football, Br J Sports Med 2011;45:553-558.

[11]. McManus A, Cross DS. Incidence of injury in elite junior Rugby Union, Journal of Science and Medicine in Sport 2004; 7(4):438-445.

[12]. Saadat S, Mafi M, Alhoseini MS. Population based estimates of non-fatal injuries in the capital of Iran, BMC Public Health 2011; 11:608.

[13]. Nilambar J, Srinivasa DK, Gautam R, Jagdish Epidemiological study of road traffic accident cases, Indian Journal of Community Medicine2004; 29(1):20-20.

[14]. Agarvval N, Reddaiah VP. Knowledge, attitude and practice following dog bite, Health and Population Perspective and Issues 2003; 26 (4):154-161.

[15]. Etman A, Wijlhuizen GJ, Heuvelen MJ, Chorus A, Hopman M. Falls incidence underestimates the risk of fall-related injuries in older age groups, Age and Ageing 2012; 41: 190–195.

[16]. Weerawardena WAK, Illanagasingha TDB1, Piyadasa IJ, Rathnayaka SM, Subaweera WTDUPL, Niroshana GAL. Analysis of patients admitted with history of road traffic accidents to surgical unit B Teaching Hospital Anuradhapura, Sri Lanka, Anuradhapura Medical Journal 2013; 7(1): 2-5.