Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors of nuclear hormone receptor superfamily comprising of the following three subtypes: PPARα, PPARγ, and PPARβ/δ. Activation of PPAR-α reduces triglyceride level and is involved in regulation of energy homeostasis. Activation of PPAR-γ causes insulin sensitization and enhances glucose metabolism, whereas activation of PPAR-β/δ enhances fatty acids metabolism. Thus, PPAR family of nuclear receptors plays a major regulatory role in energy homeostasis and metabolic function. The present review critically analyzes the protective and detrimental effect of PPAR agonists in dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, fertility or reproduction, pain, and obesity.

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Red mud, an aluminum industry waste, has been converted into an inexpensive and efficient adsorbent. The product obtained has been characterized and utilized in batch and column operations for the removal of cadmium and zinc from aqueous solutions over a wide range of initial metal ion concentrations (1.78 x 10(-5) to 1.78 x 10(-3) M for Cd2+ and 3.06 x 10(-5) to 3.06 x 10(-3) M for Zn2+; contact time, 24 h) adsorbent dose (5-20 g/L), and pH (1.0-6.0). The removal of Cd2+ and Zn2+ was almost complete at low concentrations, while it was 60-65% at higher concentrations at optimum pH's of 4.0 and 5.0, respectively, with 10 g/L of adsorbent in an 8-10 h equilibration time. The adsorption decreased with increase in temperature. Kinetic studies have been used to describe the mechanism of adsorption. Chemical regeneration of the columns has been achieved with 1% HNO3.

While injured persons demonstrate dissimilar levels of harm and every case is novel with specific recovery profiles, this article strengthens the recent pathophysiological sight of TBI mainly attention on oxidative stress, excitotoxicity, cerebral oxygenation and cerebral blood flow (CBF), development of edema, and inflammatory activities. For initial research acknowledgment of these recurring factors could permit clarification of possible beneficial targets.

Thus, the cellular and molecular mechanisms underlying diabetes mellitus, hyperhomocysteinemia, hypercholesterolemia hypertension and hyperuricemia leads to an imbalance of phosphorylation and dephosphorylation status of lipid and protein kinase that cause modulation of vascular endothelial L-arginine/nitric oxide synthetase (eNOS), to produce vascular endothelium dysfunction.

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