Abstract-The mechanisms of sodium-induced myocardial hypertrophy and vascular hypertrophy are poorly understood.We tested the hypothesis that a high sodium concentration can directly induce cellular hypertrophy. Neonatal rat myocardial myoblasts (MMbs) and vascular smooth muscle cells (VSMCs) were cultured in a 50:50 mixture of DMEM and M199 supplemented with 10% fetal bovine serum. Key Words: sodium Ⅲ hypertrophy Ⅲ myocardial myoblasts Ⅲ muscle, smooth, vascular S odium homeostasis profoundly influences the cardiovascular system in normotensive and hypertensive subjects and is a major risk factor for cardiovascular morbidity and mortality independent of other cardiovascular risk factors (for review, see Reference 1). Mounting evidence from animal, epidemiological, and clinical studies suggests that a high dietary salt intake is associated with myocardial hypertrophy. [2][3][4][5][6] Although the mechanism of salt-induced myocardial hypertrophy is poorly understood, dietary salt intake is thought to modify the process of myocardial hypertrophy by hemodynamic and/or nonhemodynamic mechanisms. 7The development of cardiac hypertrophy in response to pressure and/or volume overload is generally considered to be an adaptive mechanism to normalize ventricular wall stress. High blood pressure is one of the most powerful determinants of LVH, 8 and several studies 5,9 -11 have shown that a high dietary salt intake is associated with increased blood pressure. Therefore, many investigators consider an increased pressure load on the myocardium to be a major cause of LVH in subjects with salt-induced hypertension.More recent evidence points to a close relationship between the development and persistence of LVH and sodium intake, which may be independent of blood pressure. 2,4,6,[12][13][14] Frohlich and associates 12 reported that a high sodium diet not only caused further cardiac enlargement in spontaneously hypertensive rats but also increased cardiac mass in normotensive Wistar-Kyoto rats in the absence of increased blood pressure. Studies in humans have shown that the intracellular sodium concentration of red blood cells is positively correlated with the degree of LVH. 15 Together these results suggest that sodium-induced cardiac hypertrophy may be partially mediated by a direct action of sodium on the myocardium, independent of hemodynamic factors.The present study sought to determine whether sodium can directly induce hypertrophy of individual cells that are not exposed to many of the in vivo factors, such as high blood pressure or increased cardiac output, commonly associated with a high salt diet. The results indicate that increasing the concentration of sodium in cell culture medium can induce hypertrophy of neonatal rat MMbs and VSMCs. The hypertrophy

We tested whether adenosine has differential effects on vascular endothelial growth factor (VEGF) expression under normoxic and hypoxic conditions, and whether A1 or A2 receptors (A1R; A2R) mediate these effects. Myocardial vascular smooth muscle cells (MVSMCs) from dog coronary artery were exposed to hypoxia (1% O2) or normoxia (20% O2) in the absence and presence of adenosine agonists or antagonists for 18 h. VEGF protein levels were measured in media with ELISA. VEGF mRNA expression was determined with Northern blot analysis. Under normoxic conditions, the adenosine A1R agonists, N 6-cyclopentyladenosine and R(-)- N 6-(2-phenylisopropyl)adenosine did not increase VEGF protein levels at A1R stimulatory concentrations. However, adenosine (5 μM) and the adenosine A2R agonist N 6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)]ethyl adenosine (DPMA; 100 nM) increased VEGF protein levels by 51 and 132% and increased VEGF mRNA expression by 44 and 90%, respectively, in cultured MVSMCs under normoxic conditions. Hypoxia caused an approximately fourfold increase in VEGF protein and mRNA expression, which could not be augmented with exogenous adenosine, A2R agonist (DPMA), or A1R agonist [1,3-diethyl-8-phenylxanthine (DPX)]. The A2R antagonist 8-(3-chlorostyryl)-caffeine completely blocked adenosine-induced VEGF protein and mRNA expression and decreased baseline VEGF protein levels by up to ∼60% under normoxic conditions but only by ∼25% under hypoxic conditions. The A1R antagonist DPX had no effect. These results are consistent with the hypothesis that 1) adenosine increases VEGF protein and mRNA expression by way of A2R. 2) Adenosine plays a major role as an autocrine factor regulating VEGF expression during normoxic conditions but has a relatively minor role during hypoxic conditions. 3) Endogenous adenosine can account for the majority of basal VEGF secretion by MVSMCs under normoxic conditions and could therefore be a maintenance factor for the vasculature.

Blood urea and serum creatinine, used as markers of renal function, improved in patients requiring multiple doses of HES solutions during TPE. Further studies using novel renal biomarkers are required to examine whether HES induces any structural damage to kidneys.

Aim: India is a high burden tuberculosis country. Past BCG vaccination could cause sensitisation against TB antigens. Patients with systemic inflammatory rheumatic diseases (SIRDs) have inherent anergy. Also, they are often treated with glucocorticoids and other immunomodulatory drugs. These two confounders may affect TST, which is otherwise a robust screening method for studying TB epidemiology. Possibly for these reasons Indian Rheumatology Association did not recommend TST for the screening of TB infection (latent or disease) before initiating TNFi treatment. The present work examined TST results in SIRDs with the objective of whether it could be used for the screening of latent TB infection among SIRD patients in the Indian context. Method: 60 adult rheumatoid arthritis (RA) and 191 axial Spondyloarthritis (axSpA) patients were Mantoux tested using a higher PPD strength of 10 TU to offset inherent disease anergy. The test was read after 48 to 72 hours. It was interpreted according to the nationally recommended cutoffs that takes into account sensitisation to BCG or environmental mycobacteria. Thus, in this study, an induration of >10 mm was considered as 'latent TB infection'. Results: The positivity among RA and axSpA patients was 31.66% and 40.31% respectively, similar to that seen in adult Indians. Conclusion: Based upon these results use of modified TST with 10 TUPPD using >10 mm induration as the cutoff point is recommended for diagnosing TB infection; the test may be appropriate for the screening of latent TB infection in the Indian setting. IRA may consider revising its policy for latent TB screening accordingly.

Background & Objectives: Dengue is probably the most important arthropod-borne viral disease worldwide. Dengue is caused by flavi virus types 1-4. Liver involvement is one of the common features in dengue fever. Various studies have shown that in all those patients who develop complications like dengue hemorrhagic fever, dengue shock syndrome the levels of SGOT and SGPT were significantly raised. The severity of liver involvement can be a major predictor of morbidity and mortality of such patients with Dengue fever. So LFT can be a used to assess the severity of the disease which can thereby lead to early recognition of high risk cases. Materials & Methods: This study was conducted in Kanyakumari Government Medical College in the department of general medicine. 100 patients were included in the study over a period from August 2017 -July 2018 for a period of 1 year. Detailed history, a complete general physical and systemic examination, with relevant investigations were done on hundred patients. Results: Of 100 patients, 35% had less than 2-fold increase in SGOT levels, 31% had 2-10-fold increase and 12% had more than 10-fold increase. Overall 22% had normal values and 78% had values of SGOT above normal. With regard to SGPT 24% had normal values, 32% had less than 2-fold of normal, 26% had 2-10-fold increase and 18% had more than 10 fold increase from normal. Vomiting and pain abdomen in the early stage suggested hepatic involvement. AST and ALT were statistically higher in these patients and in those developing complications like DHF, DSS, hepatic failure, ARDS, AKI and encephalopathy. Conclusion: Liver involvement is common in adult patients with dengue. Hepatic involvement prolongs the clinical course of this self limiting disease and can be a major predictor of morbidity and mortality of such patients with Dengue fever. So AST and ALT can be a useful early marker to assess the severity of the disease which can thus lead to early recognition of high risk cases.

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