Detecting Visually Observable Disease Symptoms from Faces

Recent years have witnessed an increasing interest in the application of machine learning to clinical informatics and healthcare systems. A significant amount of research has been done on healthcare systems based on supervised learning. In this study, we present a generalized solution to detect visually observable symptoms on faces using semi-supervised anomaly detection combined with machine vision algorithms. We rely on the disease-related statistical facts to detect abnormalities and classify them into multiple categories to narrow down the possible medical reasons of detecting. Our method is in contrast with most existing approaches, which are limited by the availability of labeled training data required for supervised learning, and therefore offers the major advantage of flagging any unusual and visually observable symptoms.     

氰酸盐诱导氧化应激促进肾小管上皮细胞上皮–间充质转化

该研究探讨氰酸盐(cyanate)诱导肾小管上皮细胞氧化应激损伤和促进肾纤维化的作用。氰酸盐作用HK-2肾小管上皮细胞后, CCK8法检测其对细胞活力的影响;倒置显微镜观察细胞形态的改变; DCFH-DA法检测细胞ROS水平;细胞免疫荧光和Western blot分别检测E-cadherin、Fibronectin、α-SMA的表达; Western blot检测TGF-β的表达水平。结果显示, 2 mmol/L氰酸盐明显下调HK-2细胞的活力(P<0.05),细胞形态变为长梭形。氰酸盐作用24 h后, HK-2细胞内ROS水平呈浓度依赖性升高。免疫荧光和Western blot结果均显示,氰酸盐作用24 h后, HK-2的Fibronectin、α-SMA表达升高, E-cadherin表达下降; TGF-β的表达水平随氰酸盐浓度升高而上调(P<0.05)。以上结果表明,氰酸盐诱导肾小管上皮细胞产生过量ROS,上调TGF-β水平促进细胞上皮–间充质细胞转化(epithelia-mesenchymal transition, EMT)。     

The roles of autophagy in cerebral ischemia

Recent studies indicate the existence of autophagy in cerebral ischemia, but the functions of autophagy in this setting remain unclear. Here we discuss the role of autophagy in cerebral ischemia based on our own publication and the literature on this subject. We propose that oxidative and endoplasmic reticulum (ER) stresses n cerebral ischemia-hypoxia are potent stimuli of autophagy in neurons. We also reviewed evidence suggesting autophagosomes may have a shorter half-life in neurons and that a fraction of LC3 protein is degraded within autolysosomes, leading to a smaller detectable amount of LC3-II in the brain while there are clear indications of on-going autophagy. Finally, we suggest autophagy is an important modifier of cell death and survival, interacting with necrosis and apoptosis in determining the outcomes and final morphology of deceased neurons.     

Mechanical analysis of deep tissue injury during sitting in patients with spinal cord injury via parametric finite element model

Biomechanics and Modeling in Mechanobiology - Spinal cord injury patients are prone to develop deep tissue injury because of long-term mechanical load. However, there is a lack of statistical...     

Biological mechanisms of aging predict age‐related disease co‐occurrence in patients

Genetic, environmental, and pharmacological interventions into the aging process can confer resistance to multiple age‐related diseases in laboratory animals, including rhesus monkeys. These findings imply that individual mechanisms of aging might contribute to the co‐occurrence of age‐related diseases in humans and could be targeted to prevent these conditions simultaneously. To address this question, we text mined 917,645 literature abstracts followed by manual curation and found strong, non‐random associations between age‐related diseases and aging mechanisms in humans, confirmed by gene set enrichment analysis of GWAS data. Integration of these associations with clinical data from 3.01 million patients showed that age‐related diseases associated with each of five aging mechanisms were more likely than chance to be present together in patients. Genetic evidence revealed that innate and adaptive immunity, the intrinsic apoptotic signaling pathway and activity of the ERK1/2 pathway were associated with multiple aging mechanisms and diverse age‐related diseases. Mechanisms of aging hence contribute both together and individually to age‐related disease co‐occurrence in humans and could potentially be targeted accordingly to prevent multimorbidity.