This review addresses recent investigations and discussions of the following hypotheses behind diabetic hyperfiltration: Increased proximal tubular volume reabsorption results in a pressure drop in Bowman’s capsule which increases glomerular filtration rate (GFR). Proximal tubular hyperreabsorption induces an increase in GFR mediated by tubuloglomerular feedback. Dietary NaCl restriction results in a paradoxically increased GFR and increased urine volume in diabetic animals.”
“Background: Heart failure (HF) patients are at risk for influenza despite

widespread vaccination. Both humoral (antibody) and cytotoxic T-lymphocyte (CTL) responses are important for protection. We explored antibody- and CTL-mediated responses to the influenza vaccine in HF patients compared with healthy controls.

Methods and Results: We studied 29 AZD6738 HF patients (9 ischemic, 20 nonischemic) stable on HF therapies and 17 healthy Autophagy inhibitor controls. Participants had phlebotomy before and after influenza vaccination. Antibody production was measured in serum by hemagglutination inhibition assay and CTL responses (via interferon [IFN]-gamma and interleukin [IL]-10 production) were measured in isolated peripheral blood mononuclear cells with enzyme-linked immunosorbent assay. CTL responses demonstrated increased IL-10 production in HF patients after vaccination (P = .002), but similar IFN-gamma

responses to healthy controls. AZD1152 concentration All participants demonstrated antibody seroprotection; groups had similar rates of seroconversion (P = NS). Antibody-mediated response to the newest vaccine antigen, H3N2, was reduced in HF (P = .009).

Conclusions: Patients with HF had higher vaccine induced IL-10 concentrations, suggesting a different CTL phenotype for vaccine responses. HF patients did not mount as vigorous of an antibody immune response to the newest vaccine viral strain compared with healthy individuals. These data suggest

that immunologic memory may be important for vaccine protection in HF patients. (J Cardiac Fail 2009;15:368-373)”
“Oxidative stress is well known to play a pivotal role in cerebral ischemia-reperfusion injury. On the basis of this fact, antioxidative agents have been demonstrated to be neuroprotective. Neohesperidin (NH) is abundant in citrus flavonoids and possesses reactive oxygen species scavenging activity and neuroprotective effects in vitro. However, little is known about its effects on cerebral ischemia-reperfusion injury and the underlying mechanisms. In this study, we use a rat model of middle cerebral artery occlusion (MCAO) to investigate the neuroprotective effects of NH. NH significantly improved neurological functions and attenuated MCAO-induced infarct volume, pathological changes, and neuronal loss. Moreover, it enhanced antioxidant capacity and suppressed oxidative stress in the brain.