Learning Faces to Predict Matching Probability in an Online Matching Platform

With the increasing use of online matching platforms, predicting matching probability between users is crucial for efficient market design. Although previous studies have constructed various visual features to predict matching probability, facial features, which are important in online matching, have not been widely used. We find that deep learning-enabled facial features can significantly enhance the prediction accuracy of a user’s partner preferences from the individual rating prediction analysis in an online dating market. We also build prediction models for each gender and use prior theories to explain different contributing factors of the models. Furthermore, we propose a novel method to visually interpret facial features using the generative adversarial network (GAN). Our work contributes the literature by providing a framework to develop and interpret facial features to investigate underlying mechanisms in online matching markets. Moreover, matching platforms can predict matching probability more accurately for better market design and recommender systems

Tonicity response element binding protein associated with neuronal cell death in the experimental diabetic retinopathy

AIM: To study the contribution of tonicity response element binding protein (TonEBP) in retinal ganglion cell (RGC) death of diabetic retinopathy (DR). METHODS: Diabetes was induced in C57BL/6 mice by five consecutive intraperitoneal injections of 55 mg/kg streptozotocin (STZ). Control mice received vehicle (phosphate -buffered saline). All mice were killed 2mo after injections, and the extent of cell death and the protein expression levels of TonEBP and aldose reductase (AR) were examined. RESULTS: The TonEBP and AR protein levels and the death of RGC were significantly increased in the retinas of diabetic mice compared with controls 2mo after the induction of diabetes. Terminal deoxynucleotidyl transferase (TdT) -mediated dUTP nick end labeling (TUNEL) -positive signals co -localized with TonEBP immunoreactive RGC. These changes were increased in the diabetic retinas compared with controls. CONCLUSION: The present data show that AR and TonEBP are upregulated in the DR and TonEBP may contribute to apoptosis of RGC in the DR.close2

Transcriptional Regulator TonEBP Mediates Oxidative Damages in Ischemic Kidney Injury

TonEBP (tonicity-responsive enhancer binding protein) is a transcriptional regulator whose expression is elevated in response to various forms of stress including hyperglycemia, inflammation, and hypoxia. Here we investigated the role of TonEBP in acute kidney injury (AKI) using a line of TonEBP haplo-deficient mice subjected to bilateral renal ischemia followed by reperfusion (I/R). In the TonEBP haplo-deficient animals, induction of TonEBP, oxidative stress, inflammation, cell death, and functional injury in the kidney in response to I/R were all reduced. Analyses of renal transcriptome revealed that genes in several cellular pathways including peroxisome and mitochondrial inner membrane were suppressed in response to I/R, and the suppression was relieved in the TonEBP deficiency. Production of reactive oxygen species (ROS) and the cellular injury was reproduced in a renal epithelial cell line in response to hypoxia, ATP depletion, or hydrogen peroxide. The knockdown of TonEBP reduced ROS production and cellular injury in correlation with increased expression of the suppressed genes. The cellular injury was also blocked by inhibitors of necrosis. These results demonstrate that ischemic insult suppresses many genes involved in cellular metabolism leading to local oxidative stress by way of TonEBP induction. Thus, TonEBP is a promising target to prevent AKI

Adeno-Associated Virus-Mediated Gene Transfer to Renal Tubule Cells via a Retrograde Ureteral Approach

www.karger.com/nne This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License (www.karger.com/OA-license), applicable to the online version of the article only. Distribution for non-commercial purposes only

Childhood adversity and late-life depression: moderated mediation model of stress and social support

BackgroundAs life expectancy increases, understanding the mechanism for late-life depression and finding a crucial moderator becomes more important for mental health in older adults. Childhood adversity increases the risk of clinical depression even in old age. Based on the stress sensitivity theory and stress-buffering effects, stress would be a significant mediator, while social support can be a key moderator in the mediation pathways. However, few studies have tested this moderated mediation model with a sample of older adults. This study aims to reveal the association between childhood adversity and late-life depression in older adults, taking into consideration the effects of stress and social support.MethodsThis study used several path models to analyze the data from 622 elderly participants who were never diagnosed with clinical depression.ResultsWe found that childhood adversity increases the odds ratio of depression by approximately 20% in older adults. Path model with mediation demonstrates that stress fully mediates the pathway from childhood adversity to late-life depression. Path model with moderated mediation also illustrates that social support significantly weakens the association between childhood adversity and perceived stress.ConclusionThis study provides empirical evidence to reveal a more detailed mechanism for late-life depression. Specifically, this study identifies one crucial risk factor and one protective factor, stress and social support, respectively. This brings insight into prevention of late-life depression among those who have experienced childhood adversity

Shortening of primary cilia length is associated with urine concentration in the kidneys

Background The primary cilium, a microtubule-based cellular organelle present in certain kidney cells, functions as a mechano-sensor to monitor fluid flow in addition to various other biological functions. In kidneys, the primary cilia protrude into the tubular lumen and are directly exposed to pro-urine flow and components. However, their effects on urine concentration remain to be defined. Here, we investigated the association between primary cilia and urine concentration. Methods Mice either had free access to water (normal water intake, NWI) or were not allowed access to water (water deprivation, WD). Some mice received tubastatin, an inhibitor of histone deacetylase 6 (HDAC6), which regulates the acetylation of α-tubulin, a core protein of microtubules. Results WD decreased urine output and increased urine osmolality, concomitant with apical plasma membrane localization of aquaporin 2 (AQP2) in the kidney. After WD, compared with after NWI, the lengths of primary cilia in renal tubular epithelial cells were shortened and HDAC6 activity increased. WD induced deacetylation of α-tubulin without altering α-tubulin levels in the kidney. Tubastatin prevented the shortening of cilia through increasing HDAC6 activity and consequently increasing acetylated α-tubulin expression. Furthermore, tubastatin prevented the WD-induced reduction of urine output, urine osmolality increase, and apical plasma membrane localization of AQP2. Conclusions WD shortens primary cilia length through HDAC6 activation and α-tubulin deacetylation, while HDAC6 inhibition blocks the WD-induced changes in cilia length and urine output. This suggests that cilia length alterations are involved, at least in part, in the regulation of body water balance and urine concentration

Polyneuropathy Associated with IgA Paraproteinemia and Amyloidosis: A Case Report and Literature Review

Paraproteinemia potentially causes peripheral neuropathy via an unknown underlying pathogenetic mechanism. We report a case of pathologically proven amyloid neuropathy with AL amyloidosis with an IgA kappa light chain, which was initially diagnosed as neuropathy associated with monoclonal gammopathy of undetermined significance. This case indicates that in cases of neuropathy with paraproteinemia, the other potential causes should be excluded by appropriate means, especially pathological evaluations

Treatment of an Acute Mycotic Aneurysm of the Common Carotid Artery with a Covered Stent-Graft

We report herein a case successful endovascular treatment with a stent-graft of a rare case of rapidly growing mycotic aneurysm of the left common carotid artery due to acute bacterial endocarditis after eradication of the infection. Infected mycotic aneurysms of the peripheral vasculature have been considered as a contraindication for stent-graft implantation because of the possibility of microorganism spreading to the stent-graft; however, if there is evidence of complete eradication of microorganism and surgery is not an option, stent-graft implantation can be an effective and safe treatment modality for exclusion of the mycotic aneurysm