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The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation.sup.1,2. The molecular basis of this bi-directional communication remains to be fully determined. Here we use thermogenic adipose tissue from mice as a model system to show that T cells, specifically [gamma][delta] T cells, have a crucial role in promoting sympathetic innervation, at least in part by driving the expression of TGF[beta]1 in parenchymal cells via the IL-17 receptor C (IL-17RC). Ablation of IL-17RC specifically in adipose tissue reduces expression of TGF[beta]1 in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes that are consistent with defective thermogenesis; innervation can be fully rescued by restoring TGF[beta]1 expression. Ablating [gamma][delta] [TAU] cells and the IL-17RC signalling pathway also impairs sympathetic innervation in other tissues such as salivary glands. These findings demonstrate coordination between T cells and parenchymal cells to regulate sympathetic innervation. V[gamma]6.sup.+ V[delta]1.sup.+ [gamma][delta] T cells control tolerance to cold by activating adipocyte IL-17RC and promoting sympathetic innervation of thermogenic adipose tissue in mice., Author(s): Bo Hu [sup.1] [sup.2] , Chengcheng Jin [sup.3] [sup.6] , Xing Zeng [sup.1] [sup.2] , Jon M. Resch [sup.4] , Mark P. Jedrychowski [sup.1] [sup.2] , Zongfang Yang [sup.4] [...]

Purpose: The purpose of the study was to investigate the changes of choroidal blood perfusion in different layers and quadrants and its possible related factors after 1 h visual task by augmented reality (AR) device in two‐dimensional (2D) and three‐dimensional (3D) mode, respectively. Methods: Thirty healthy subjects aged 22–37 years watched the same video source in 2D and 3D mode separately using AR glasses for 1 h with a one‐week interval. Swept‐source optical coherence tomography angiography (SS‐OCTA) was performed before and immediately after watching to acquire choroidal thickness (ChT), three‐dimensional choroidal vascularity index (CVI) of large‐ and middle‐sized choroidal vessels and choriocapillaris flow voids (FV%) at macular and peripapillary area. Near point of accommodation (NPA) and accommodative facility (AF) were examined to evaluate the accommodative ability. Pupil diameters by infrared‐automated pupillometer under scotopic, mesopic and photopic condition were also obtained. Results: Compared with pre‐visual task, the subfoveal CVI decreased from 0.406 ± 0.097 to 0.360 ± 0.102 after 2D watching (p < 0.001) and to 0.368 ± 0.102 after 3D watching (p = 0.002). Pupil sizes under different illuminance conditions became smaller after both 2D and 3D watching (all p < 0.001). AF increased after both 2D and 3D watching (both p < 0.05). NPA receded in post‐3D watching (p = 0.017) while a not significant tendency was observed in post‐2D. Conclusion: A reduction in subfoveal choroidal blood flow accompanied with pupil constriction was observed immediately after 1 h visual task using AR glasses in 2D and 3D mode. Accommodative facility improved after 2D and 3D watching with AR glasses, whereas decrease in the maximum accommodation power was only found in 3D mode. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and the leading cause of chronic liver disease in the Western world. Twenty per cent of NAFLD individuals develop chronic hepatic inflammation (non-alcoholic steatohepatitis, NASH) associated with cirrhosis, portal hypertension and hepatocellular carcinoma, yet the causes of progression from NAFLD to NASH remain obscure. Here, we show that the NLRP6 and NLRP3 inflammasomes and the effector protein IL-18 negatively regulate NAFLD/NASH progression, as well as multiple aspects of metabolic syndrome via modulation of the gut microbiota. Different mouse models reveal that inflammasome-deficiency-associated changes in the configuration of the gut microbiota are associated with exacerbated hepatic steatosis and inflammation through influx of TLR4 and TLR9 agonists into the portal circulation, leading to enhanced hepatic tumour-necrosis factor (TNF)-α expression that drives NASH progression. Furthermore, co-housing of inflammasome-deficient mice with wild-type mice results in exacerbation of hepatic steatosis and obesity. Thus, altered interactions between the gut microbiota and the host, produced by defective NLRP3 and NLRP6 inflammasome sensing, may govern the rate of progression of multiple metabolic syndrome-associated abnormalities, highlighting the central role of the microbiota in the pathogenesis of heretofore seemingly unrelated systemic auto-inflammatory and metabolic disorders., The prevalence of non-alcoholic fatty liver disease (NAFLD) ranges from 20-30% in the general population and up to 75-100% in obese individuals (1,2). NAFLD is considered one of the manifestations [...]