Perturbed microRNA Expression by Promotes Macrophage Polarization Leading to Pro-survival Foam Cell.

Tuberculosis (TB) is one of the prevalent causes of death worldwide, with 95% of these deaths occurring in developing countries, like India. The causative agent, (MTb) has the tenacious ability to circumvent the host's immune system for its own advantage. Macrophages are one of the phagocytic cells that are central to immunity against MTb.

M235T polymorphism in the AGT gene and A/G(I8-83) substitution in the REN gene correlate with end-stage renal disease.

Background/aims: This study aimed at investigating if M235T polymorphism in the AGT gene and A/G(I8-83) polymorphism in the REN gene correlate with end-stage renal disease (ESRD).

Methods: We analyzed 173 ESRD patients and 329 individuals with normal kidney function for differences in the genotype distribution of AGT-M235T and REN-A/G(I8-83) polymorphisms between the two groups. The data for cases and controls were compared using the χ(2) test.

An improved method for the isolation of hepatitis B virus DNA from human serum.

Studies show that hepatitis B virus (HBV) DNA isolation methods vary in their efficiency to extract DNA from serum samples. The purpose of the present study was to develop an improved method for isolation of HBV DNA and compare it with commonly used HBV DNA isolation protocols. In order to develop HBV DNA isolation protocol, serum samples were collected from patients and screened for the presence of hepatitis B surface antigen, hepatitis B e antigen and HBV DNA.

Depleted TGF-β₁ levels in end stage renal disease patients from North India.

End stage renal disease is a clinical state that extends from chronic renal failure and is marked by an irreversible loss of renal function. TGF-β1 mediated renal fibrosis is a common pathology implicated in this form of kidney disease. In this study circulating protein and mRNA levels of TGF-β1 cytokine were investigated among ESRD patients and respective controls from North India.

Angiotensin-converting enzyme gene polymorphism in hypertensive rural population of Haryana, India.

Background: Essential hypertension is a complex genetic disorder influenced by diverse environmental factors. Of the various physiological pathways affecting the homeostasis of blood pressure, the renin-angiotensin system (RAS) is known to play a critical role. Angiotensin-I converting enzyme (ACE) is a significant component of RAS and an insertion/deletion (I/D) polymorphism in its gene has been implicated in predisposition to hypertension.

Spirulina protects against rosiglitazone induced osteoporosis in insulin resistance rats.

Aim: The study was undertaken to assess the protective effect of Spirulina fusiformis extract against Rosiglitazone induced osteoporosis and pharmacodynamic effects of Rosiglitazone with Spirulina in treating hyperglycemia and hyperlipidemia of insulin resistance rat.

Method: For this aim, 30 Wistar albino rats were equally divided into five groups as control (C), diabetes mellitus (DM), diabetes mellitus+Rosiglitazone (DM+R), diabetes mellitus+Spirulina (DM+S), and diabetes mellitus+Rosiglitazone+Spirulina (DM+R+S). Serum glucose, triglyceride, HDL, LDL and insulin concentrations were estimated by routine standard methods in blood samples collected on 21th day.

Tumor necrosis factor--alpha and transforming growth factor--beta1 polymorphisms in bronchial asthma.

Background: Bronchial asthma is a complex genetic disorder regulated by the release of cytokines and inflammatory mediators. Tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta1) cytokines play pivotal roles in the inflammatory response of the airways. Differential production of these two cytokines is associated with allelic variations in the transcriptional regulatory region of these genes.

Nitric oxide activates Rap1 and Ral in a Ras-independent manner.

Rap1 and Ral, the small GTPases belonging to the Ras superfamily, have recently attracted much attention; Ral because of Ral-specific guanine nucleotide exchange factors which are regulated by direct binding to Ras and Rap1 because of its proposed role as an antagonist of Ras signaling. We have previously demonstrated that nitric oxide (NO) activates Ras and proposed the structural basis of interaction between NO and Ras. In the present study we have shown that NO activates Rap1 and Ral in a time- and concentration-dependent manner.