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Partner notification and testing could expand HIV testing and link infections to care. We performed a meta-analysis on HIV testing rate and prevalence among couples of people diagnosed with HIV in China.

Six electronic databases (PubMed, Cochrane Library, Embase, Web of Science, the China National Knowledge Internet, and WanFang) and abstracts of five HIV/sexually transmitted infections conferences were searched up to February 1, 2020. Meta-analysis was conducted using a random-effects model to assess HIV testing rate and prevalence among couples of Chinese people diagnosed with HIV.

Of 3,657 records retrieved, 42 studies were identified. Among them, three studies were conducted among pregnant women and 10 among men who have sex with men. The pooled uptake rate of couples HIV testing among Chinese people diagnosed with HIV was 65% (95% confidence interval, 57% -73%; 23 studies). API-2 inhibitor The pooled HIV prevalence among couples who had an HIV test was 28% [24%-32%] (38 studies). Subgroup analyses showed that the pooled couples HIV testing uptake rates among pregnant women and men who have sex with men were 76% [66%-86%] (3 studies) and 49% [30%-68%] (8 studies), and the pooled HIV prevalence in two populations was 53% [27%-78%] (3 studies) and 14% [10%-17%] (10 studies), respectively.

Nearly two-thirds of couples of people diagnosed with HIV have had an HIV test, of whom 28% were positive. Couples of MSM with a positive HIV diagnosis had a lower testing rate, which indicates more effective strategies need to be carried out to improve couples HIV testing among Chinese MSM.

Nearly two-thirds of couples of people diagnosed with HIV have had an HIV test, of whom 28% were positive. Couples of MSM with a positive HIV diagnosis had a lower testing rate, which indicates more effective strategies need to be carried out to improve couples HIV testing among Chinese MSM.How acute hyperglycaemia affects memory functions and functional brain responses in individuals with and without type 2 diabetes is unclear. Our aim was to study the association between acute hyperglycaemia and working, semantic, and episodic memory in participants with type 2 diabetes compared to a sex- and age-matched control group. We also assessed the effect of hyperglycaemia on working memory-related brain activity. A total of 36 participants with type 2 diabetes and 34 controls (mean age, 66 years) underwent hyperglycaemic clamp or placebo clamp in a blinded and randomised order. Working, episodic, and semantic memory were tested. Overall, the control group had higher working memory (mean z-score 33.15 ± 0.45) than the group with type 2 diabetes (mean z-score 31.8 ± 0.44, p = 0.042) considering both the placebo and hyperglycaemic clamps. Acute hyperglycaemia did not influence episodic, semantic, or working memory performance in either group. Twenty-two of the participants (10 cases, 12 controls, mean age 69 years) were randomly invited to undergo the same clamp procedures to challenge working memory, using 1-, 2-, and 3-back, while monitoring brain activity by blood oxygen level-dependent functional magnetic resonance imaging (fMRI). The participants with type 2 diabetes had reduced working memory during the 1- and 2-back tests. fMRI during placebo clamp revealed increased BOLD signal in the left lateral frontal cortex and the anterior cingulate cortex as a function of working memory load in both groups (3>2>1). During hyperglycaemia, controls showed a similar load-dependent fMRI response, whereas the type 2 diabetes group showed decreased BOLD response from 2- to 3-back. These results suggest that impaired glucose metabolism in the brain affects working memory, possibly by reducing activity in important frontal brain areas in persons with type 2 diabetes.Impaired formation of the intrahepatic biliary network leads to cholestatic liver diseases, which are frequently associated with autoimmune disorders. Using a chemical mutagenesis strategy in zebrafish combined with computational network analysis, we screened for novel genes involved in intrahepatic biliary network formation. We positionally cloned a mutation in the nckap1l gene, which encodes a cytoplasmic adaptor protein for the WAVE regulatory complex. The mutation is located in the last exon after the stop codon of the primary splice isoform, only disrupting a previously unannotated minor splice isoform, which indicates that the minor splice isoform is responsible for the intrahepatic biliary network phenotype. CRISPR/Cas9-mediated nckap1l deletion, which disrupts both the primary and minor isoforms, showed the same defects. In the liver of nckap1l mutant larvae, WAVE regulatory complex component proteins are degraded specifically in biliary epithelial cells, which line the intrahepatic biliary network, thus disrupting the actin organization of these cells. We further show that nckap1l genetically interacts with the Cdk5 pathway in biliary epithelial cells. These data together indicate that although nckap1l was previously considered to be a hematopoietic cell lineage-specific protein, its minor splice isoform acts in biliary epithelial cells to regulate intrahepatic biliary network formation.Spinal microglia are highly responsive to peripheral nerve injury and are known to be a key player in pain. However, there has not been direct evidence showing that selective microglial activation in vivo is sufficient to induce chronic pain. Here, we used optogenetic approaches in microglia to address this question employing CX3CR1creER/+ R26LSL-ReaChR/+ transgenic mice, in which red-activated channelrhodopsin (ReaChR) is inducibly and specifically expressed in microglia. We found that activation of ReaChR by red light in spinal microglia evoked reliable inward currents and membrane depolarization. In vivo optogenetic activation of microglial ReaChR in the spinal cord triggered chronic pain hypersensitivity in both male and female mice. In addition, activation of microglial ReaChR up-regulated neuronal c-Fos expression and enhanced C-fiber responses. Mechanistically, ReaChR activation led to a reactive microglial phenotype with increased interleukin (IL)-1β production, which is likely mediated by inflammasome activation and calcium elevation.