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Electrochemical nitrate reduction (NITRR) offers a promising alternative toward nitrogen recycling and ammonia production under ambient conditions, for which highly active and selective electrocatalyst is desired. In this study, metallic cobalt nanoarrays as facilely prepared from the electrochemical reduction of Co(OH)2 nanoarrays (NAs) are demonstrated to exhibit unprecedented NH3 producing capability from catalyzing NITRR. Benefitting from the high intrinsic activity of Co0, intimate contact between active species and conductive substrate and the nanostructure which exposes large number of active sites, the Co‐NAs electrode exhibits current density of −2.2 A cm−2 and NH3 production rate of 10.4 mmol h−1 cm−2 at −0.24 V versus RHE under alkaline condition and significantly surpasses reported counterparts. Moreover, the close‐to‐unity (≥96%) Faradaic efficiency (FE) toward NH3 is achieved over wide application range (potential, NO3− concentration and pH). Density function theory calculation reveals the optimized adsorption energy of NITRR intermediates on Co surface over Co(OH)2. Furthermore, it is proposed that despite the sluggish kinetics of Volmer step (H2O → *H + *OH) which provides protons in conventional hydrogenation mechanism, the proton‐supplying water dissociation process on Co surface is drastically facilitated following a concerted water dissociation–hydrogenation pathway. Metallic Co‐NAs that are electrochemically reduced from Co(OH)2‐NAs exhibit record‐high electrocatalytic activity and close‐to‐unity Faradaic efficiency toward ammonia production from nitrate reduction. DFT calculations reveal that different from the common hydrogenation pathway, fast water dissociation assisted by intermediates with unsaturated N atoms and their concurrent hydrogenation contribute to the superior NITRR activity.

Hydrotreating renewable oils over sulfided metal catalysts is commercially applied to produce green diesel, but it requires a continuous sulfur replenishment to maintain catalyst activity, which inevitably results in sulfur contamination and increases production costs. We report a robust P-doped NiAl-oxide catalyst with frustrated Lewis pairs (i.e., P atom bonded with the O atom acts as an electron donor, while the spatially separated Ni atom acts as an electron acceptor) that allows efficient green diesel production without sulfur replenishment. The catalyst runs more than 500 h at a weight hourly space velocity (WHSV) of 28.3 h −1 without deactivation (methyl laurate as a model compound), and is able to completely convert a real feedstock of soybean oil to diesel-range hydrocarbons with selectivity >90% during 500 h of operation. This work is expected to open up a new avenue for designing non-sulfur catalysts that can make the green diesel production greener. The commercial production of green diesel suffers from the requirement for continuous sulfur replenishment to maintain catalytic activity. Here, the authors report a sulfur-free catalytic system that can efficiently produce green diesel from various feedstocks over long periods of operation.

Human umbilical cord mesenchymal stem cells (huMSCs) can treat primary ovarian insufficiency (POI) related to ovarian granulosa cell (OGC) apoptosis caused by cisplatin chemotherapy. Exosomes are a class of membranous vesicles with diameters of 30–200 nm that are constitutively released by eukaryotic cells. Exosomes mediate local cell-to-cell communication by transferring microRNAs and proteins. In the present study, we demonstrated the effects of exosomes derived from huMSCs (huMSC-EXOs) on a cisplatin-induced OGC model in vitro and discussed the preliminary mechanisms involved in these effects. We successfully extracted huMSC-EXOs from huMSC culture supernatant and observed the effective uptake of exosomes by cells with fluorescent staining. Using flow cytometry (with annexin-V/PI labelling), we found that huMSC-EXOs increased the number of living cells. Western blotting showed that the expression of Bcl-2 and caspase-3 were upregulated, whilst the expression of Bax, cleaved caspase-3 and cleaved PARP were downregulated to protect OGCs. These results suggest that huMSC-EXOs can be used to prevent and treat chemotherapy-induced OGC apoptosis in vitro . Therefore, this work provides insight and further evidence of stem cell function and indicates that huMSC-EXOs protect OGCs from cisplatin-induced injury in vitro .

Polyvinylidene fluoride (PVDF) is widely used as a kind of water treatment membrane material, but its high hydrophobicity leads to easily being polluted by oily wastewater, which limits further development in the field of water treatment. In this paper, a simple and green strategy based on chitosan (CS) and tannic acid (TA) was taken to transform the hydrophobic PVDF membrane into superhydrophilic one. CS possessed excellent capability of antifouling but its surface binding affinity was relatively poor, while TA enjoyed wonderful surface adhesion and certain ability of absorbing water. Herein, combining the advantages of CS and TA, a special partially sacrificial coating was designed. (3-cholropropyl)trimethoxysilane (CTS) was used as a chain connecting the PVDF substrate with CS to form the first coating layer, and then TA was introduced as the second coating layer. Because of the unstable characteristic of CS coating, part of the polluted coating can be washed away by pure water with the contaminants. The modified membrane showed superhydrophilicity (the water contact angle was 17°) and underwater superoleophobicity (the underwater oil contact angle was 158°). Moreover, the initial pure water flux of modified membrane was 8579 L m −2  h −1 , which was more than twice than that of pristine membrane (3057 L m −2  h −1 ). After the membrane was contaminated by toluene emulsion and rinsed thoroughly with pure water, the water flux recovery rate of the modified membrane reached about 98%, meaning the modified membrane possessed excellent anti-fouling and self-recovery ability. Besides, the rejection rate of toluene emulsion was 99.1%, showing the modified membrane could be used to efficiently handle the oil/water separation. During six cycles of being polluted and rinsed, the water flux recovery rate would decrease a little after each cycle, from 98% to 94.3% in the end, which demonstrated that the sacrificial layer did exist. This facile approach has great potential in practical water remediation. Graphical abstract

COVID-19 is identified as a zoonotic disease caused by SARS-CoV-2, which also can cross-transmit to many animals but not mice. Genetic modifications of SARS-CoV-2 or mice enable the mice susceptible to viral infection. Although neither is the natural situation, they are currently utilized to establish mouse infection models. Here we report a direct contact transmission of SARS-CoV-2 variant B.1.351 in wild-type mice. The SARS-CoV-2 (B.1.351) replicated efficiently and induced significant pathological changes in lungs and tracheas, accompanied by elevated proinflammatory cytokines in the lungs and sera. Mechanistically, the receptor-binding domain (RBD) of SARS-CoV-2 (B.1.351) spike protein turned to a high binding affinity to mouse angiotensin-converting enzyme 2 (mACE2), allowing the mice highly susceptible to SARS-CoV-2 (B.1.351) infection. Our work suggests that SARS-CoV-2 (B.1.351) expands the host range and therefore increases its transmission route without adapted mutation. As the wild house mice live with human populations quite closely, this possible transmission route could be potentially risky. In addition, because SARS-CoV-2 (B.1.351) is one of the major epidemic strains and the mACE2 in laboratory-used mice is naturally expressed and regulated, the SARS-CoV-2 (B.1.351)/mice could be a much convenient animal model system to study COVID-19 pathogenesis and evaluate antiviral inhibitors and vaccines.

Human umbilical cord mesenchymal stem cell (HUMSC)-exosome gel played a significant role in promoting thin endometrial receptivity and improving the pregnancy rate by inhibiting endometrial fibrosis and accelerating subendometrial microangiogenesis. High-quality HUMSC-exosome were obtained by pretreating HUMSC with transforming growth factor-β1 (TGF-β1). Exosome gel mixture has good biocompatibility and physical rheological properties, stabilizing the structure of exosomes and prolonging the action of exosomes in the uterine cavity. HUMSC or HUMSC-derived exosomes were used to treat rat model of thin endometrium. In animal experiments, four groups, including the HUMSC, HUMSC-exosome, model (negative control), and sham operation groups, were designed. The therapeutic effects were evaluated by the thickness of the endometrium, the number of glands, the subendometrial vessel density, the markers of endometrial receptivity, and the pregnancy rate. In an in vivo study, three groups, involving HUMSC-coculture, HUMSC-exosome, and the control, were explored. The proliferation and migration of the human endometrial stromal cells (HESCs) were further determined by cell scratch and 5-ethynyl-2′-deoxyuridine (EdU) assays. The protein expression of the TGF-β1/smad2/3 signaling pathway was determined by Western blot. After treatment, the thickness of the endometrium, the number of glands, and the subendometrial microangiogenesis were obviously increased, and the level of inhibition of endometrial fibrosis, molecular markers of endometrial receptivity, and the pregnancy rate were also significantly improved. HUMSC-exosome and HUMSC significantly promoted the migration and proliferation of HESCs. And it was confirmed that HUMSC-exosome were superior to HUMSC in inhibiting HESCs fibrosis through TGF-β1/smad2/3 signaling pathway at the protein expression level.

Objectives To investigate whether breast edema characteristics at preoperative T2-weighted imaging (T2WI) could help evaluate axillary lymph node (ALN) burden in patients with early-stage breast cancer. Methods This retrospective study included women with clinical T1 and T2 stage breast cancer and preoperative MRI examination in two independent cohorts from May 2014 to December 2020. Low (< 3 LNs+) and high (≥ 3 LNs+) pathological ALN (pALN) burden were recorded as endpoint. Breast edema score (BES) was evaluated at T2WI. Univariable and multivariable analyses were performed by the logistic regression model. The added predictive value of BES was examined utilizing the area under the curve (AUC), net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Results A total of 1092 patients were included in this study. BES was identified as the independent predictor of pALN burden in primary ( n = 677) and validation ( n = 415) cohorts. The analysis using MRI-ALN status showed that BES significantly improved the predictive performance of pALN burden (AUC: 0.65 vs 0.71, p < 0.001; IDI = 0.045, p < 0.001; continuous NRI = 0.159, p = 0.050). These results were confirmed in the validation cohort (AUC: 0.64 vs 0.69, p = 0.009; IDI = 0.050, p < 0.001; continuous NRI = 0.213, p = 0.047). Furthermore, BES was positively correlated with biologically invasive clinicopathological factors ( p < 0.05). Conclusions In individuals with early-stage breast cancer, preoperative MRI characteristics of breast edema could be a promising predictor for pALN burden, which may aid in treatment planning. Key Points • In this retrospective study of 1092 patients with early-stage breast cancer from two cohorts, the MRI characteristic of breast edema has independent and additive predictive value for assessing axillary lymph node burden . • Breast edema characteristics at T2WI positively correlated with biologically invasive clinicopathological factors, which may be useful for preoperative diagnosis and treatment planning for individual patients with breast cancer.

Preterm premature rupture of membranes (PPROM) is a common pregnancy complication. Yet, the main cause of PPROM remains poorly understood. In this study, we used 16S rRNA gene sequencing technology to identify the differences in vaginal microbiota between pregnant women with PPROM and those who delivered at term. Vaginal samples were collected from 48 patients with PPROM and 54 age- and gestational age-matched pregnant women who delivered at term (controls). The vaginal microbiota of the two groups was compared using 16S rRNA gene sequencing of the V3-V4 regions. The vaginal microbial composition of the PPROM group was significantly different from that of the control group. Our results showed that the diversity of vaginal microbiota in patients with PPROM increased compared with controls. The relative abundance of sp. , and were more abundant in patients with PPROM, while and were more abundant in controls. sp. , and , could serve as biomarkers for PPROM. Finally, we proposed several metabolic pathways, including PWY-6339, PWY-6992, and PWY-7295. PPROM is characterized by vaginal microbial dysbiosis. The dysbiotic vaginal microbiota signatures in patients with PPROM include a higher bacterial diversity, decreased autochthonous bacteria, and increased pathogenic bacteria. These results may be beneficial for developing biomarkers for screening and early diagnosis of PPROM and may provide effective preventative treatments.

Pneumonia is one of the leading causes of death in patients with acute ischemic stroke (AIS). Antibiotics fail to improve prognosis of patients with post‐stroke pneumonia, albeit suppressing infection, due to adverse impacts on the immune system. The current study reports that bone marrow mesenchymal stem cells (BM‐MSC) downregulate bacterial load in the lungs of stroke mice models. RNA‐sequencing of the lung from BM‐MSC‐treated stroke models indicates that BM‐MSC modulates pulmonary macrophage activities after cerebral ischemia. Mechanistically, BM‐MSC promotes the bacterial phagocytosis of pulmonary macrophages through releasing migrasomes, which are migration‐dependent extracellular vesicles. With liquid chromatography‐tandem mass spectrometry (LC‐MS/MS), the result shows that BM‐MSC are found to load the antibacterial peptide dermcidin (DCD) in migrasomes upon bacterial stimulation. Besides the antibiotic effect, DCD enhances LC3‐associated phagocytosis (LAP) of macrophages, facilitating their bacterial clearance. The data demonstrate that BM‐MSC is a promising therapeutic candidate against post‐stroke pneumonia, with dual functions of anti‐infection and immunol modulation, which is more than a match for antibiotics treatment. Pneumonia is one of the leading causes of death after cerebral ischemia. The current study demonstrates that bone marrow mesenchymal stem cells (BM‐MSCs) produce migrasomes containing dermcidin, which enhances LC3‐associated phagocytosis (LAP) of macrophages, and thus facilitates bacterial clearance. It is proposed that BM‐MSC is a promising therapy against post‐stroke pneumonia, with dual functions of anti‐infection and immunol modulation.

The persistence of latent HIV-1 reservoirs remains a critical barrier to functional curing AIDS, as current latency-reversing agents (LRAs) exhibit limited clinical efficacy. While RNA modifications like N⁶-methyladenosine (m⁶A) regulate viral replication, their role in maintaining HIV-1 latency is poorly defined. Here, we identify the RNA-binding protein RBM39 as a scaffold organizing an m⁶A-dependent silencing complex that enforces viral latency. Through proteomic and functional analyses, we demonstrate that RBM39 recruits the m⁶A reader YTHDC1 and the RNA helicase DDX5, forming a tripartite complex that accelerates Tat RNA decay and enforces viral quiescence. Genetic or pharmacological degradation of RBM39 (using the clinically explored molecular glue indisulam ) potently reactivates latent HIV-1 in J-Lat cell models, primary CD4⁺ T cells from people living with HIV-1 (PLWH), and synergizes with established LRAs (Bryostatin-1, JQ-1, SAHA) to broadly activate proviral reservoirs. Our work reveals a previously unrecognized host pathway in which RBM39-organized RNA decay complexes silence HIV-1 through epitranscriptomic regulation of Tat. In addition to establishing RBM39 as a promising therapeutic target for addressing the limitations of current “shock and kill” strategies, our findings establish a novel mechanistic framework for m⁶A-dependent regulation of viral gene expression. This framework may serve as a valuable reference for investigating similar regulatory mechanisms in other latent viral infections or oncogenic processes where RNA methylation plays a pivotal role.