Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia:A minireview

Recently,specific immunometabolic profiles have been postulated in patients with schizophrenia,even before full-blown disease and independent of antipsychotic treatment.Proteomic profiling studies offer a promising potential for elucidating the cellular and molecular pathways that may be involved in the onset and progression of schizophrenia symptoms,and co-occurrent metabolic changes.In view of all this,we were intrigued to explore galectin-3(Gal-3)as a glycan,and in our previous study,we measured its elevated levels in remission of schizophrenia.The finding may be a consequence of antipsychotic treatment and may have an impact on the onset of inflammation,the development of obesity,and the presumed cognitive changes in schizophrenia.In the animal study,it was shown that downregulation of Gal-3 was beneficial in insulin regulation of obesity and cognitive preservation.Strategies involving plasma exchange are discussed in this review,particularly in the context of Gal-3 elimination.

Specifc inflammatory osteoclast precursors induced during chronic inflammation give rise to highly active osteoclasts associated with inflammatory bone loss

Elevated osteoclast(OC)activity is a major contributor to inflammatory bone loss(IBL)during chronic inflammatory diseases.However,the specific OC precursors(OCPs)responding to inflammatory cues and the underlying mechanisms leading to IBL are poorly understood.We identified two distinct OCP subsets:Ly6C^(hi)CD11b^(hi) inflammatory OCPs(iOCPs)induced during chronic inflammation,and homeostatic Ly6C^(hi)CD11b^(lo)OCPs(hOCPs)which remained unchanged.Functional and proteomic characterization revealed that while iOCPs were rare and displayed low osteoclastogenic potential under normal conditions,they expanded during chronic inflammation and generated OCs with enhanced activity.In contrast,hOCPs were abundant and manifested high osteoclastogenic potential under normal conditions but generated OCs with low activity and were unresponsive to the inflammatory environment.Osteoclasts derived from iOCPs expressed higher levels of resorptive and metabolic proteins than those generated from hOCPs,highlighting that different osteoclast populations are formed by distinct precursors.We further identified the TNF-αand S100A8/A9 proteins as key regulators that control the iOCP response during chronic inflammation.Furthermore,we demonstrated that the response of iOCPs but not that of hOCPs was abrogated in tnf-α^(-/-)mice,in correlation with attenuated IBL.Our findings suggest a central role for iOCPs in IBL induction.iOCPs can serve as potential biomarkers for IBL detection and possibly as new therapeutic targets to combat IBL in a wide range of inflammatory conditions.

分析泄漏功率攻击采用90nm CMOS技术的加密器件

在电子商务与电子银行等应用中，安全要求越来越严格。虽然加密技术提供了强健的算法，但这些算法的物理实现一般会通过器件电气运行中的物理现象，泄漏一些信息，攻击者会利用它来探测密钥。这些“旁路”（side-channel）攻击利用加密实现硬件模块所泄漏的信息。该信息可能包含数据与功耗或时序之间的相互关系（参考文献1）。一种广为报道的强大旁路攻击方法是微分功率分析（differential—power analysis），因为它能让攻击者用现售元件做出的测量设置探测出密钥（参考文献2）。攻击者依据的事实是，标准CMOS逻辑的动态功耗主要依赖于输入数据。例如，考虑一个简化的CMOS反相器模型，它以一只接地电容作为自己的负载。