(2020) Therapeutic manipulation of gut microbiota by polysaccharides of Wolfiporiacocos reveals the contribution of the gut fungi-induced PGE 2 to alcoholic hepatic steatosis,

Fe3O4/VAN@MIL-101(Fe) with both mesoporous and mixed-valence Fe3+/Fe2+ structures was controllably synthesized in the synthesis of MIL-101(Fe), and it was used as a bifunctional photocatalyst in photocatalytic water splitting.

Highlights d A Ganoderma meroterpene derivative (GMD) reduces nonalcoholic hepatic steatosis in rats d Bacteroides spp. and folate are increased in the gut microbiota of GMD-treated rats d The Bacteroides-folate-liver axis is upregulated d Bacteroides xylanisolvens is a potential probiotic beneficial for NAFLD

Flexible solid-state zinc–air batteries (ZABs) with low cost, excellent safety, and high energy density has been considered as one of ideal power sources for portable and wearable electronic devices, while their practical applications are still hindered by the kinetically sluggish cathodic oxygen reduction and oxygen evolution reactions (ORR/OER). Herein, a Janus-structured flexible free-standing bifunctional oxygen electrocatalyst, with OER-active O, N co-coordinated Ni single atoms and ORR-active Co3O4@Co1–x S nanosheet arrays being separately integrated at the inner and outer walls of flexible hollow carbon nanofibers (Ni-SAs/HCNFs/Co-NAs), is reported. Benefiting from the sophisticated topological structure and atomic-level-designed chemical compositions, Ni-SAs/HCNFs/Co-NAs exhibits outstanding bifunctional catalytic activity with the ΔE index of 0.65 V, representing the current state-of-the-art flexible free-standing bifunctional ORR/OER electrocatalyst. Impressively, the Ni-SAs/HCNFs/Co-NAs-based liquid ZAB show a high open-circuit potential (1.45 V), high capacity (808 mAh g–1 Zn), and extremely long life (over 200 h at 10 mA cm–2), and the assembled flexible all-solid-state ZABs have excellent cycle stability (over 80 h). This work provides an efficient strategy for developing high-performance bifunctional ORR/OER electrocatalysts for commercial applications.

Rationale: Prior chronic treatment with statins has been shown to be associated with more favorable outcomes in patients with acute coronary syndrome (ACS). Specific changes in the gut microbiota and microbial metabolites have been shown to influence the progression of coronary artery disease. However, the critical microbial and metabolomic changes associated with the cardiovascular protective effects of statins in ACS remain elusive. Methods: In the present study, we performed 16S rRNA sequencing and serum metabolomic analysis in 36 ACS patients who had received chronic statin treatment, 67 ACS patients who had not, and 30 healthy volunteers. A follow-up study was conducted. Metagenomic functional prediction of important bacterial taxa was achieved using PICRUSt2. Results : Statins modulated the gut microbiome of ACS patients towards a healthier status, i.e., reducing potentially pathogenic bacteria such as Parabacteroides merdae but increasing beneficial bacteria such as Bifidobacterium longum subsp. longum , Anaerostipes hadrus and Ruminococcus obeum . Moreover, prior chronic statin therapy was associated with improved outcome in ACS patients. Multi-omics analysis revealed that specific changes in bacterial taxa were associated with disease severity or outcomes either directly or by mediating metabolites such as fatty acids and prenol lipids. Finally, we discovered that important taxa associated with statins were correlated with fatty acid- and isoprenoid-related pathways that were predicted by PICRUSt2. Conclusions: Our study suggests that statin treatment might benefit ACS patients by modulating the composition and function of the gut microbiome, which might result in improved circulating metabolites and reduced metabolic risk. Our findings provide new insights for understanding the heterogenic roles of statins in ACS patients through host gut microbiota metabolic interactions.

DDB2 (damage-specific DNA-binding protein 2) is the product of the xeroderma pigmentosum group E gene which is involved in the initiation of nucleotide excision repair via an ubiquitin ligase complex together with DDB1 and CUL4A (cullin 4A). PAQR3 (progestin and adipoQ receptor family member III) is a newly discovered tumour suppressor that is implicated in the development of many types of human cancers. In the present paper, we report that DDB2 is involved in ubiquitination and degradation of PAQR3. DDB2 is able to interact with PAQR3 in vivo and in vitro. Both overexpression and knockdown experiments reveal that the protein expression level, protein stability and polyubiquitination of PAQR3 are changed by DDB2. Negative regulation of EGF (epidermal growth factor)- and insulin-induced signalling by PAQR3 is also altered by DDB2. At the molecular level, Lys(61) of PAQR3 is targeted by DDB2 for ubiquitination. The cell proliferation rate and migration of gastric cancer cells are inhibited by DDB2 knockdown and such effects are abrogated by PAQR3 knockdown, indicating that the effect of DDB2 on the cancer cells is mediated by PAQR3. Collectively, our studies not only pinpoint that DDB2 is a post-translational regulator of PAQR3, but also indicate that DDB2 may play an active role in tumorigenesis via regulating PAQR3.

No abstract

Intracerebral hemorrhage is the most dangerous complication in tPA thrombolytic therapy for ischemic stroke, which occurs as a consequence of endothelial cell death at the blood–brain barrier (BBB) during thrombolytic reperfusion. We have previously shown that cerebral ischemia‐induced rapid occludin degradation and BBB disruption. Here we demonstrated an important role of occludin degradation in facilitating the evolution of ischemic endothelial cells toward death. Cultured brain microvascular endothelial cells (bEnd.3 cells) were exposed to oxygen‐glucose deprivation (OGD) or incubated with occludin siRNA or occludin AAV to achieve an occludin deficiency or over‐expression status before exposing to reoxygenation (R) or TNF‐α treatment. Cell death was assessed by measuring lactate dehydrogenase release, TUNEL staining, and flow cytometry analysis. Inhibition of OGD‐induced occludin degradation with SB‐3CT or over‐expression of occludin with occludin AAV both significantly attenuated OGD/R‐induced apoptosis and pyroptosis in bEnd.3 cells. Consistently, knockdown of occludin with siRNA potentiated TNF‐α‐induced apoptosis, supporting an important role of occludin integrity in endothelial cell survival. Similar results were observed for pyroptosis, in which occludin knockdown with siRNA led to a significant augmentation of cytokines secretion, inflammasome activation, and pyroptosis occurrence in TNF‐α‐treated bEnd.3 cells. Lastly, up‐regulation of c‐Yes, PI3K/AKT, and ERK concurrently occurred with occludin degradation after OGD/R or TNF‐α treatment, and the level of these proteins were further increased when inhibition of occludin degradation or over‐expression of occludin. These data indicate that occludin degradation inflicted during ischemia makes BBB endothelial cells more vulnerable to reperfusion‐associated stress stimuli.