Organophosphorus (OP), the commonest agent for poisoning in India due to its easy availability, acts by inhibiting acetylcholinesterase at muscarinic and nicotinic receptors. Erythrocyte cholinesterase (EchE) and plasma cholinesterase (PchE) are reduced in OP poisoning, but their estimation is costly and not regularly performed. There are emerging options for new cheaper biochemical markers in relation to OP poisoning. Serum level of creatine phosphokinase (CPK) is often found to be elevated in OP poisoning. This study was conducted to see if CPK may be used as an alternative of cholinesterase levels in blood to assess the severity of OP poisoning. This was a prospective and observational study. Sixty-three patients of OP poisoning without any prior treatment, presenting within 6 hours, were selected and their clinical severity was categorized according to Peradeniya organophosphorus poisoning (POP) scale. Level of serum CPK, blood EchE and pH were measured following admission, and total dose of atropine (mg) until the final clinical outcome (complete recovery or death) was calculated. Student's t-test and Pearson's correlation coefficient was used for the assessment of statistical significance. According to POP scale, clinical severity was mild (score 0–3) in 17 (27%), moderate (score 4–7) in 32 (50.8%) and severe (score 8–11) in 14 (22.2%) patients. Serum CPK, EchE level, blood pH and total atropine dose strongly correlated with clinical severity. Our study recommends serum CPK as an alternative marker.

Results. Leishmanial lipid inhibited the release of tumor necrosis factor ␣, interleukin-1␤, and NO in the culture, decreased their cytosolic protein levels, and decreased NF-B p65 levels in SFMCs, in a dosedependent manner. It had the reverse effect on interleukin-10 levels. Leishmanial lipid-induced apoptosis involved the activation of caspase 3, caspase 9, and Bax, the release of cytochrome c, the alteration of mitochondrial membrane potential, and the downregulation of Bcl-2.Conclusion. These results suggest that leishmanial lipid has strong antiinflammatory and apoptosisinducing effects on SFMCs from patients with RA, and that apoptosis occurs via the mitochondrial pathway.

BackgroundHuman immunodeficiency virus (HIV) infection is associated with an increased risk for human herpes viruses (HHVs) and their related diseases and they frequently cause disease deterioration and therapeutic failures. Methods for limiting the transmission of HHVs require a better understanding of the incidence and infectivity of oral HHVs in HIV-infected patients. This study was designed to determine the seroprevalence of human herpes viruses (CMV, HSV 2, EBV-1, VZV) antibodies and to evaluate their association with age, sex as well as other demographic and behavioral factors.ResultsA study of 200 HIV positive patients from Eastern India attending the Calcutta Medical College Hospital, Kolkata, West Bengal, Apex Clinic, Calcutta Medical College Hospital and ART Center, School of Tropical Medicine, Kolkata, West Bengal was done. Serum samples were screened for antibodies to the respective viruses using the indirect ELISA in triplicates.CytoMegalo virus (CMV), Herpes Simplex virus type 2 (HSV-2), Varicella Zoster virus (VZV), and Epstein Barr virus (EBV-1) were detected in 49%, 47%, 32.5%, and 26% respectively.ConclusionThis study has contributed baseline data and provided insights in viral OI and HIV co-infection in Eastern India. This would undoubtedly serve as a basis for further studies on this topic.

Background: Laryngoscopy and tracheal intubation after the induction of anesthesia are nearly always associated with a sympathetic hyperactivity. To attenuate the pressor response, various drugs have been tried, but studies to compare the effects of dexmedetomidine or clonidine on the hemodynamic response during laryngoscopy and tracheal intubation are anecdotal and sparse. This study aims to fi nd the drug, which was best suited for this purpose and to compare their effects on sedation and anesthetic requirements. Methods: This was a prospective study, which involved three groups of patients. Each group had 20 patients who presented for elective, non-cardiovascular surgeries. The patients in group I (control) were given normal saline and the groups II and III were given dexmedetomidine and clonidine, respectively. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and Ramsay sedation score were recorded at 1 and 2 min after completion of administration of study drug. Induction was done with propofol and required dose is noted. HR, SBP, and DBP were again assessed during intubation and at 1, 3, 5, and 10 min after intubation. The obtained clinical data were analyzed statistically with analysis of variance. Results: In our study, HR, SBP, and DBP all increased during intubation and thereafter in all three groups. Pretreatment with dexmedetomidine 1 μg/kg and clonidine 2 μg/kg signifi cantly attenuated the cardiovascular and catecholamine responses to tracheal intubation. However, attenuation was signifi cantly more with the dexmedetomidine group with a quicker return to baseline. Dexmedetomidine also fared in terms of anesthetic requirement (propofol) and sedative action. Conclusion: Preoperative administration of a single dose of dexmedetomidine blunted the hemodynamic responses more than clonidine or placebo during laryngoscopy, and reduced anesthetic requirements.

Background: The potential for PPAR agonists to positively affect risk of cardiovascular disease in patients with type 2 diabetes (T2DM) is of persistent attention. The PRESS XII study primarily aimed to evaluate the efficacy and safety of saroglitazar (2 mg and 4 mg) as compared to pioglitazone 30 mg on glycemic control in patients with type 2 diabetes mellitus. Methods: In this randomized double-blind study, patients with T2DM [glycosylated hemoglobin (HbA1c) ≥ 7.5%] were enrolled from 39 sites in India. Patients received once-daily doses of either saroglitazar or pioglitazone (1:1:1 allocation ratio) for a total of 24 weeks. Patients were continued in a double blind extension period for an additional 32 weeks. Efficacy evaluations of glycemic parameters [HbA1c (Primary endpoint at week 24), FPG and PPG] and other lipid parameters (TG, LDL-C, VLDL-C, HDL-C, TC, Non HDL-C, Apo A1 and Apo B) were conducted at week 12, 24 and 56 and compared to the baseline levels. The efficacy analyses were performed by using paired t-test and ANCOVA model. Results: A total of 1155 patients were enrolled in this study. The baseline characteristics were similar between the three treatment groups. The within group mean (± SD) change in HbA1c (%) from baseline of the saroglitazar (2 mg and 4 mg) and pioglitazone treatment groups at week 24 were: − 1.38 ± 1.99 for saroglitazar 2 mg; − 1.47 ± 1.92 for saroglitazar 4 mg and − 1.41 ± 1.86 for pioglitazone, respectively. Statistically significant reduction from baseline in HbA1c was observed in each treatment group at week 24 with p-value < 0.016. There was a significant reduction in TG, LDL-C, VLDL-C, TC and Non HDL-C with a significant increase in HDL-C from baseline levels (< 0.016). Most of the AE's were 'mild' to 'moderate' in severity and were resolved by the completion of the study.