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Cholera continues to be poorly controlled in multiple epidemic and endemic areas across the globe, with estimated annual incidence of 1.3–4.0 million cases, resulting in 21,000 to 143,000 deaths worldwide in 2015. The usual approach for patient diagnosis and cholera surveillance is clinical examination of cases of acute watery diarrhea (AWD), confirmed by positive culture or polymerase chain reaction tests. Rapid diagnostic tests (RDTs) are used in regions with limited laboratory capacities but have been found to demonstrate large variations in performance, ranging in sensitivity from 58% to 100% and in specificity from 60% to 100%. Most countries rely on hospital-based surveillance of diarrheal disease to compute the cholera burden. The World Health Organization (WHO) recommends that countries assess public health events involving cholera against the International Health Regulations 2005 criteria and determine need for official notification using the standard case definition. Cholera is an often under-recognized and under reported problem because of differences in case definitions, reluctance by authorities to acknowledge and report cholera, inadequacies in hospital surveillance systems, lack of effective diagnostic tests and commonalities in clinical presentation of cholera with other AWD etiologies. The resulting gap in burden data impairs economic analysis of disease impact and identification of areas for targeted control interventions. There is an urgent need to strengthen surveillance data by supplementing reported numbers with estimates from literature reviews and data from modelling studies, developing better-performing RDTs, enhancing monitoring and evaluation processes of in-country surveillance systems, and encouraging countries to report cholera cases by "rewarding" better reporting with technical support and improved access to vaccines. It is imperative that immediate steps are taken towards strengthening surveillance and reporting systems globally, especially in cholera-prone and resource-limited areas, where it will enable countries to articulate their demand for resources more accurately. [ABSTRACT FROM AUTHOR]

Graphical abstract Abstract Diabetic nephropathy (DN) is considered as one of the major microvascular complications of diabetes mellitus (DM) which leads to end stage renal disease (ESRD). Even though existing therapeutic options are effective in decreasing albuminuria, drugs targeting the preservation of GFR and prevention of ESRD may provide better strategy for the treatment. Since metabolic disorders are multifactorial, poly-herbal medications, and drug-herbal combination are in demand. Therefore, the present work is focused on the combinatorial renoprotective effect of rutin and ramipril on alloxan induced DN in experimental rats. Male Wistar rats were divided into five groups, group I-control, group II-diabetic rats, group III-diabetic rats treated with ramipril, group IV-diabetic rats treated with rutin, group V-diabetic rats treated with ramipril and rutin for a period of six weeks. Results revealed administration of alloxan induced hyperglycemia and alteration in antioxidant profile. However, combination of a bioflavonoid with an Angiotensin converting enzyme (ACE) inhibitor administration restored the antioxidant status in experimental DN rats. Over-expression of ACE, TGF-β1 and decreased podocin expression in diabetic rats was significantly reversed in rats administered with both ramipril and rutin. In addition to attentuating oxidative stress and fibrosis, combinatorial therapy significantly down-regulated endoplasmic reticulum stress markers GRP78 and CHOP. Notably, combination of both ramipril and rutin in low doses reduced the side effects than the administration of monotherapy alone. Histopathological results revealed that combinatorial therapy was associated with a reduction in tubulointerstitial injury. The current study contributes the understanding of the multifactorial nature of DN and implies combinatorial treatment of ACE inhibitor with an antioxidant will be a promising therapeutic strategy for DN by their mechanism of action targeting various pathophysiological changes and stress pathways. [ABSTRACT FROM AUTHOR]

Background and aim Insulin resistance plays a crucial role in the pathogenesis of type 2 diabetes and cardiovascular diseases. Recently, paraoxonase-1(PON1) is reported to have an ability to reduce insulin resistance by promoting glucose transporter-4 (GLUT-4) expression in vitro. Single nucleotide polymorphism (SNP) in PON1 is associated with variability in enzyme activity and concentration. Based on this we aimed to investigate the association of PON1 (Q192R and L55M) polymorphisms with the risk of developing insulin resistance in adult South Indian population. Methods Two hundred and eighty seven (287) Type 2 diabetes patients and 293 healthy controls were enrolled in this study. All the study subjects were genotyped for PON1 (Q192R and L55M) missense polymorphisms using polymerase chain reaction-restriction fragment length polymorphism (PCRRFLP) method. Fasting serum insulin level was measured by ELISA. Results The distribution of QR/RR and LM/MM genotypes were significantly higher in type 2 diabetes patients compared with healthy controls. Moreover, the R and M alleles were significantly associated with type 2 diabetes with an Odds Ratio of 1.68 (P < 0.005) and 2.24 (P < 0.005) respectively. SNP 192 Q > R genotypes were found to be significantly associated with higher BMI, cholesterol, triglycerides, LDL, fasting serum insulin and HOMA-IR. Further, the mutant allele or genotypes of PON1 L55M were associated with higher BMI, triglycerides, VLDL, fasting serum insulin and HOMA-IR among adult type 2 diabetes patients. Conclusion PON1 (Q192R and L55M) polymorphisms may play a crucial role in pathogenesis and susceptibility of insulin resistance thus leads to the development of type 2 diabetes in South Indian population. [ABSTRACT FROM AUTHOR]