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β-phase polyvinylidene fluoride (PVDF)-BaTiO nanocomposite samples have been prepared by solution mixing method. XRD data represent that the crystallinity of PVDF decreases with increase in loading level of BaTiO nanoparticles. DSC curve represents that the melting point of PVDF is lightly affected by loading concentration of BaTiO. The morphology and microstructure of PVDF and PVDF embedded by BaTiO nanofillers were investigated by using inverted contrast microscopy (ICM) and scanning electron microscopy (SEM). FTIR interferrometry is proven that PVDF and BaTiO are not chemically interacting; therefore, interaction of BaTiO is van der Waals type of interaction. The thermally stimulated discharge current (TSDC) of PVDF and PVDF-BaTiO nanocomposites sample was characterized by single peak. The observed TSDC peak is discussed on the basis of dipolar and interfacial polarization. [ABSTRACT FROM AUTHOR]

Flavivirus vaccines based on ChimeriVax technology contain the nonstructural genes of the yellow fever vaccine and the premembrane and envelope genes of heterologous flaviviruses, such as Japanese encephalitis and West Nile viruses. These chimeric vaccines induce both humoral and cell-mediated immunity. Mice were vaccinated with yellow fever, chimeric Japanese encephalitis virus (YF/JE), or chimeric West Nile virus (YF/WN) vaccines, followed by a secondary homologous or heterologous vaccination; the hierarchy and function of CD8(+) T cell responses to a variable envelope epitope were then analyzed and compared with those directed against a conserved immunodominant yellow fever virus NS3 epitope. Sequential vaccination with heterologous chimeric flaviviruses generated a broadly cross-reactive CD8(+) T cell response dependent on both the sequence of infecting viruses and epitope variant. The enhanced responses to variant epitopes after heterologous vaccination were not related to preexisting antibody or to higher virus titers. These results demonstrate that the sequence of vaccination affects the expansion of cross-reactive CD8(+) T cells after heterologous chimeric flavivirus challenge. [ABSTRACT FROM AUTHOR]

Background/Aims: Reactive oxygen species, and especially superoxide (O2·–),have been implicated in diabetic nephropathy. O2·– accumulation in cells is dependent on O2·– production (by NADH/NADPH oxidase) as well as scavenging by superoxide dismutase (SOD) activity. This study was designed to investigate the effects of high glucose (HG) on O2·– accumulation and SOD activity in human mesangial cells (HMC) and to determine if these effects are mediated by angiotensin II (Ang II). Methods: HMC were incubated in media containing 10 mMglucose (control, C), 30 mM glucose (HG), 10 mM glucose + either 20 mM 2-deoxy-D-glucose (2-DG) or 20 mM mannitol (high mannitol, HM) (osmotic controls), or Ang II (10–5M). Ang II action was antagonized by employing 10–4M of Ang II receptor antagonists (losartan or irbesartan) or 10–4M of NADH/NADPH oxidase inhibitors [diphenyleneiodonium chloride (DPI) or apocynin]. Superoxide and total SOD activity were assayed using chemiluminescence of lucigenin. Results: Incubation of HMC in HG resulted in a 1.6-fold increase in Ang I (p < 0.05) and a 1.4-fold increase in Ang II levels (p < 0.05) in cell lysates. These changes were accompanied by a >2-fold increase in O2·– accumulation (p < 0.01), which was inhibited by losartan and irbesartan. Exogenous Ang II increased net O2·– accumulation by 2.7-fold (p < 0.01), which was normalized by losartan and irbesartan. DPI and apocynin blocked the HG and Ang II-induced increases in O2·– (p < 0.01). HG but not exogenous Ang II inhibited total SOD activity by 30%, which was not affected by losartan. Conclusion: High glucose increases O2–· accumulation in HMC primarily by increasing its production via the Ang II-NADH/NADPH oxidase system. Copyright © 2005 S. Karger AG. Basel. [ABSTRACT FROM AUTHOR]

Considerable evidence suggests that the intrarenal renin-angiotensin system plays an important role in diabetic nephropathy, Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) receptor blockers (ARBs) can attenuate progressive glomerulosclerosis in disease models and can slow disease progression in humans. Because agents that interfere with Ang II action may decrease glomerular injury without altering glomerular pressures, it has been suggested that Ang II has direct effects on glomerular cells to induce sclerosis in dependent of its hemodynamic actions. To study nonhemodynamic effects of Ang II on matrix metabolism, many investigators have used cell culture systems. Glucose and Ang II have been shown to produce similar effects on renal cells in culture. For instance, incubation of mesangial cells in high-glucose media or in the presence of Ang II stimulates matrix protein synthesis and inhibits degradative enzyme (e.g., collagenase, plasmin) activity. Glucose and Ang II also can inhibit proximal tubule proteinases. Glucose increases expression of the angiotensinogen gene in proximal tubule cells and Ang II production in primary mesangial cell culture, which indicates that high glucose itself can activate the renin-angiotensin system. The effects of glucose and Ang II on mesangial matrix metabolism may be mediated by transforming growth factor-β (TGF-β). Exposure of mesangial cells to glucose or Ang II increases TGF-β expression and secretion. Their effects on matrix metabolism can be blocked by ant-TGF-β antibody or ARBs such as losartan, which also prevents the glucose-induced increment in TGF-β secretion. Taken together, these findings support the hypothesis that the high-glucose milieu of diabetes increases Ang II production by renal and especially, mesangial cells, which results in stimulation of TGF-β1 secretion, leading to increased synthesis and decreased degradation of matrix proteins, thus... [ABSTRACT FROM AUTHOR]

Role of angiotensin II in diabetic nephropathy. Considerable evidence suggests that the intrarenal renin-angiotensin system plays an important role in diabetic nephropathy. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) receptor blockers (ARBs) can attenuate progressive glomerulosclerosis in disease models and can slow disease progression in humans. Because agents that interfere with Ang II action may decrease glomerular injury without altering glomerular pressures, it has been suggested that Ang II has direct effects on glomerular cells to induce sclerosis independent of its hemodynamic actions. To study nonhemodynamic effects of Ang II on matrix metabolism, many investigators have used cell culture systems. Glucose and Ang II have been shown to produce similar effects on renal cells in culture. For instance, incubation of mesangial cells in high-glucose media or in the presence of Ang II stimulates matrix protein synthesis and inhibits degradative enzyme (e.g., collagenase, plasmin) activity. Glucose and Ang II also can inhibit proximal tubule proteinases. Glucose increases expression of the angiotensinogen gene in proximal tubule cells and Ang II production in primary mesangial cell culture, which indicates that high glucose itself can activate the renin-angiotensin system. The effects of glucose and Ang II on mesangial matrix metabolism may be mediated by transforming growth factor-β (TGF-β). Exposure of mesangial cells to glucose or Ang II increases TGF-β expression and secretion. Their effects on matrix metabolism can be blocked by anti-TGF-β antibody or ARBs such as losartan, which also prevents the glucose-induced increment in TGF-β secretion. Taken together, these findings support the hypothesis that the high-glucose milieu of diabetes increases Ang II production by renal, and especially, mesangial cells, which results in stimulation of TGF-β1 secretion, leading to increased synthesis and decreased degradation of matrix proteins, thus producing matrix accumulation. This may be an important mechanism linking hyperglycemia and Ang II in the pathogenesis of diabetic nephropathy. [ABSTRACT FROM AUTHOR]