Electroweak measurements in electron–positron collisions at w-boson-pair energies at lep

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Search for Charged Higgs bosons: Combined Results Using LEP Data

The four LEP collaborations, ALEPH, DELPHI, L3 and OPAL, have searched for pair-produced charged Higgs bosons in the framework of Two Higgs Doublet Models (2HDMs). The data of the four experiments are statistically combined. The results are interpreted within the 2HDM for Type I and Type II benchmark scenarios. No statistically significant excess has been observed when compared to the Standard Model background prediction, and the combined LEP data exclude large regions of the model parameter space. Charged Higgs bosons with mass below 80 GeV/c^2 (Type II scenario) or 72.5 GeV/c^2 (Type I scenario, for pseudo-scalar masses above 12 GeV/c^2) are excluded at the 95% confidence level

Advanced glycation end products (AGEs) in diabetic complications

Hyperglycemic condition in diabetes accelerates formation of advanced glycation end products (AGEs) that are formed as a result of series of reaction between reducing sugars and proteins. Accumulation of AGEs has been implicated in development of insulin resistance as well as in the pathogenesis of diabetic complications. The principal mechanism by which AGEs render harmful effects is through interaction with cell bound receptors. Certain receptors like AGE-R1 are involved in degradation of AGEs, while certain other receptors like receptor for AGE (RAGE) bring about counter effects exacerbating the situation. Accumulation of diverse AGEs, synergistically down regulate AGE-R1 while up regulate RAGE causing vicious cycle leading to enhanced formation and further accumulation of AGEs. In this article we discuss the formation of heterogeneous AGEs, importance of detection and quantification of AGEs, biological degradation of AGEs via different receptors, AGE-RAGE and its role in proinflammatory signaling, AGE mediated diabetic vascular complications such as nephropathy, retinopathy, neuropathy, cardiovascular and cerebrovascular diseases and finally the biological inhibition of AGEs is discussed along with chemical inhibitors for AGEs and natural products in AGE inhibition as a measure for the prevention of diabetic complications