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Intracerebral hemorrhage, a common cause of stroke, has more dire consequences in diabetics than in nondiabetics. Using experimental rodent models, Jia Liu et al. find that the deleterious effects of diabetes on intracerebral hemorrhage may be due to the action of the protein plasma kallikrein, discovered to directly inhibit platelet aggregation through an osmolarity-sensitive mechanism.
Elevated triglyceride levels often occur in obesity and can contribute to cardiovascular disease. Brown adipose tissue (BAT) is known to burn fat, and now Joerg Heeren and his colleagues show that BAT actively takes up triglycerides in cold conditions, suggesting a possible therapy to lower triglyceride levels in states of obesity.
The authors show that miR-34a regulates progenitor and metastatic properties of prostate cancer cells, and they identify CD44 as a relevant target of the microRNA. The inhibition of metastasis observed after systemic delivery of miR-34a suggests that it could be used as a potential therapeutic agent in prostate cancer.
The current diagnosis of acute kidney injury involves the measurement of renal biomarkers, such as serum creatinine, which provide a crude means of detecting cellular stress and injury. To determine whether Ngal expression provides an alternate renal biomarker capable of detecting the initial phases of renal injury, Paragas et al. have developed an Ngal reporter mouse that offers a noninvasive and real-time method for the continuous and quantitative reporting of cell stress and injury at the injury site.
Tony Ko and his colleagues introduce a fluorescence microendoscopy imaging approach for time-lapse studies of deep brain tissue previously inaccessible to conventional optical imaging techniques. It can be used to study the cellular effects of brain disease over weeks to months with comparable resolution to light microscopy. They use the approach to monitor individual hippocampal neurons, neuronal dendrites and blood vessels and to follow the process of glioma angiogenesis.
Obesity is generally considered an inflammatory state. Vishwa Dixit and his colleagues have now shown that excess dietary lipids leads to the activation of the Nlrp3 inflammasome, a sensor of the innate immune system, and that its genetic deficiency results in decreased inflammation and improved insulin sensitivity. These results suggest a possible new therapeutic avenue to treat the effects of obesity.