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An experimental technique was developed for two-dimensional Particle Image Velocimetry (PIV) measurement of wall shear flow around a bubble growing under dissolved gas supersaturation. Carbonated water was used as dissolved-gas-supersaturated liquid, and its flow was created in a small container with a tube pump. An isolated CO2 bubble nucleated from an intentionally created scratch on the glass surface was placed in the flow. The mass-diffusion-driven growth of the bubble (from nucleation to detachment from the surface) was recorded using a video camera with backlighting; the radius of the detached bubble was below 1 mm in the present experimental conditions. The velocity field without and with the wall-attached bubble was obtained through PIV with the water (seeded with fluorescent particles) and with a planar laser sheet, which enables one to obtain local shear flow. With the measured liquid velocity at the bubble center, the particle Reynolds number was found to be below 1. The proposed PIV measurement technique allows for careful examination of bubble detachment dynamics and convective mass transfer around attached bubbles.

The conserved long noncoding RNA MeXis has anti-atherosclerotic effects in mice by acting with the nuclear hormone receptor LXR in macrophages to promote cholesterol efflux. Nuclear receptors regulate gene expression in response to environmental cues, but the molecular events governing the cell type specificity of nuclear receptors remain poorly understood. Here we outline a role for a long noncoding RNA (lncRNA) in modulating the cell type–specific actions of liver X receptors (LXRs), sterol-activated nuclear receptors that regulate the expression of genes involved in cholesterol homeostasis and that have been causally linked to the pathogenesis of atherosclerosis. We identify the lncRNA MeXis as an amplifier of LXR-dependent transcription of the gene Abca1 , which is critical for regulation of cholesterol efflux. Mice lacking the MeXis gene show reduced Abca1 expression in a tissue-selective manner. Furthermore, loss of MeXis in mouse bone marrow cells alters chromosome architecture at the Abca1 locus, impairs cellular responses to cholesterol overload, and accelerates the development of atherosclerosis. Mechanistic studies reveal that MeXis interacts with and guides promoter binding of the transcriptional coactivator DDX17. The identification of MeXis as a lncRNA modulator of LXR-dependent gene expression expands understanding of the mechanisms underlying cell type–selective actions of nuclear receptors in physiology and disease.

Strand-selection is the final step of microRNA biogenesis in which functional mature miRNAs are generated from one or both arms of precursor. The preference of strand-selection is diverse during development and tissue formation, however, its pathological effect is still unknown. Here we find that two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, are inversely expressed and play exactly opposite roles in gastric cancer progression. Higher-5p with lower-3p expression pattern is significantly correlated with higher TNM stages and poor prognosis of gastric cancer patients. The increase of miR-574-5p/-3p ratio, named miR-574 arm-imbalance is partially due to the dynamic expression of their highly complementary targets in gastric carcinogenesis, moreover, the arm-imbalance of miR-574 is in turn involved and further promotes gastric cancer progression. Our results indicate that miR-574 arm-imbalance contribute to gastric cancer progression and re-modification of the miR-574-targets homeostasis may represent a promising strategy for gastric cancer therapy. Functional miRNAs derived from the 5p or 3p arm of some miRNA duplexes have opposite roles in cancer progression. Here, the authors show that oncogenic miR-574-5p has greater preference in aggressive gastric cancer as compared with miR-574-3p and this arm preference is partly dependent on complementary targets mediated miRNA decay.

Neuronal mitochondrial oxidative stress induced by β-amyloid (Aβ) is an early event of Alzheimer’s disease (AD). Emerging evidence has shown that antioxidant therapy represents a promising therapeutic strategy for the treatment of AD. In this study, we investigated the antioxidant activity of rhein against Aβ 1-42 oligomer-induced mitochondrial oxidative stress in primary neurons and proposed a potential antioxidant pathway involved. The results suggested that rhein significantly reduced reactive oxygen species (ROS) level, reversed the depletion of mitochondrial membrane potential, and protected neurons from oxidative stress-associated apoptosis. Moreover, further study indicated that rhein activated mitochondrial biogenesis accompanied by increased cytochrome C oxidase (CytOx) and superoxide dismutase (SOD) activities. CytOx on the respiratory chain inhibited the production of ROS from electron leakage and SOD helped to eliminate excess ROS. Finally, western blot analysis confirmed that rhein remarkedly increased the protein expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) together with its upstream deacetylase sirtuin 1 (SIRT1), and activated downstream transcription factor nuclear respiratory factor 1, promoting mitochondrial biogenesis. In conclusion, our results demonstrate that rhein activates mitochondrial biogenesis regulated by the SIRT1/PGC-1α pathway as an antioxidant defense system against Aβ 1-42 oligomer-induced oxidative stress. These findings broaden our knowledge of improving mitochondrial biogenesis as an approach for relieving neuronal oxidative stress in AD.

Background Conflicting results on the prognostic value of blood adiponectin level in patients with coronary artery disease (CAD) have been reported. This meta-analysis aimed to investigate the prognostic value of elevated adiponectin level in CAD patients. Methods A comprehensive literature search was conducted in PubMed and Embase databases up to May 10, 2019. Studies evaluating the association between adiponectin level and major adverse cardiovascular events (death, stroke, acute coronary syndrome or coronary revascularisation), cardiovascular mortality, and all-cause mortality in CAD patients were included. Pooled multivariable adjusted risk ratios (RR) and 95% confidence intervals (CI) was calculated for the highest vs the lowest category of adiponectin level. Results Twelve studies including 10,974 CAD patients were included. Elevated adiponectin level was independently associated with higher risk of cardiovascular (RR 1.93; 95% CI 1.55–2.42; p  < 0.001) and all-cause mortality (RR 1.96; 95% CI 1.64–2.34; p  < 0.001) in CAD patients. However, CAD patients with higher adiponectin level did not significantly increase major cardiovascular events risk (RR 1.12; 95% CI 0.86–1.45; p  = 0.407) after adjustment for potential confounders. Conclusions This meta-analysis indicates that elevated adiponectin level is an independent predictor of cardiovascular and all-cause mortality in CAD patients. Measurement of blood adiponectin level has potential to identify CAD patients who have high risk of death.

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The prolyl hydroxylation of hypoxia-inducible factor 1α (HIF-1α) mediated by the EGLN–pVHL pathway represents a classic signalling mechanism that mediates cellular adaptation under hypoxia. Here we identify RIPK1, a known regulator of cell death mediated by tumour necrosis factor receptor 1 (TNFR1), as a target of EGLN1–pVHL. Prolyl hydroxylation of RIPK1 mediated by EGLN1 promotes the binding of RIPK1 with pVHL to suppress its activation under normoxic conditions. Prolonged hypoxia promotes the activation of RIPK1 kinase by modulating its proline hydroxylation, independent of the TNFα–TNFR1 pathway. As such, inhibiting proline hydroxylation of RIPK1 promotes RIPK1 activation to trigger cell death and inflammation. Hepatocyte-specific Vhl deficiency promoted RIPK1-dependent apoptosis to mediate liver pathology. Our findings illustrate a key role of the EGLN–pVHL pathway in suppressing RIPK1 activation under normoxic conditions to promote cell survival and a model by which hypoxia promotes RIPK1 activation through modulating its proline hydroxylation to mediate cell death and inflammation in human diseases, independent of TNFR1. Zhang, Xu, Liu, Wang et al. identify an inhibitory mechanism for RIPK1 kinase through EGLN1/pVHL-mediated proline hydroxylation, which is disrupted upon prolonged hypoxia that activates RIPK1 activity to promote cell death and inflammation.

Interplay between energy-storing white adipose cells and thermogenic beige adipocytes contributes to obesity and insulin resistance. Irrespective of specialized niche, adipocytes require the activity of the nuclear receptor PPARγ for proper function. Exposure to cold or adrenergic signaling enriches thermogenic cells though multiple pathways that act synergistically with PPARγ; however, the molecular mechanisms by which PPARγ licenses white adipose tissue to preferentially adopt a thermogenic or white adipose fate in response to dietary cues or thermoneutral conditions are not fully elucidated. Here, we show that a PPARγ/long noncoding RNA (lncRNA) axis integrates canonical and noncanonical thermogenesis to restrain white adipose tissue heat dissipation during thermoneutrality and diet-induced obesity. Pharmacologic inhibition or genetic deletion of the lncRNA Lexis enhances uncoupling protein 1-dependent (UCP1-dependent) and -independent thermogenesis. Adipose-specific deletion of Lexis counteracted diet-induced obesity, improved insulin sensitivity, and enhanced energy expenditure. Single-nuclei transcriptomics revealed that Lexis regulates a distinct population of thermogenic adipocytes. We systematically map Lexis motif preferences and show that it regulates the thermogenic program through the activity of the metabolic GWAS gene and WNT modulator TCF7L2. Collectively, our studies uncover a new mode of crosstalk between PPARγ and WNT that preserves white adipose tissue plasticity.

Huangshui is a typical organic wastewater in Chinese Baijiu production, with high pollution and valuable ingredients. Conventional wastewater treatment leads to resource-wasting and environmental pollution. It is urgent that the demand for effective Huangshui treatment with the development of the Baijiu-making industry. This review systematically summarizes recent studies, revealing the main characteristics and application of Huangshui, focusing on the application of the rich microbial resources and flavor substances, which provides a practical approach to cascade and full use of Huangshui in medicine, cosmetic, functional food, fertilizer, and wastewater treatment fields. Further research suggested that Huangshui can also be used as an external carbon source for the denitrification system or as an organic liquid water-soluble fertilizer for more fruits and grains. The applications favor improving production efficiency and lowering pollutant emissions and introduce novel concepts for the sustainable development of related industries. Thus, Chinese Baijiu plants can achieve the near-zero emissions of wastewater and cleaner production.

Microbial foods include microbial biomass, naturally fermented foods, and heterologously synthesized food ingredients derived from microbial fermentation. Terpenoids, using isoprene as the basic structure, possess various skeletons and functional groups. They exhibit diverse physicochemical properties and physiological activities, such as unique flavor, anti-bacterial, anti-oxidant, anti-cancer, and hypolipemic, making them extensively used in the food industry, such as flavor, fragrance, preservatives, dietary supplements, and medicinal health food. Compared to traditional strategies like direct extraction from natural species and chemical synthesis, microbial cell factories for edible terpenoids have higher titers and yields. They can utilize low-cost raw materials and are easily scaling-up, representing a novel green and sustainable production mode. In this review, we briefly introduce the synthetic pathway of terpenoids and the applications of microbial cell factories producing edible terpenoids. Secondly, we highlight several typical and non-typical microbial chassis in edible terpenoid-producing cell factories. In addition, we reviewed the recent advances of representative terpenoid microbial cell factories with a gram-scale titer in food flavor, food preservation, nutritional enhancers, and medicinal health foods. Finally, we predict the future directions of microbial cell factories for edible terpenoids and their commercialization process.