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VPS9D1‐AS1 functions as an oncogene in many cancers. However, its role and potential mechanism in the progression of endometrial cancer (EC) are not fully understood. VPS9D1‐AS1 levels in EC and adjacent normal tissues were investigated using the TCGA‐UCEC cohort and 24 paired clinical samples. The roles of VPS9D1‐AS1 and miR‐187‐3p in cell cycle, proliferation, and apoptosis were evaluated by loss‐ and gain‐of‐function experiments. In addition, the effect of VPS9D1‐AS1 on tumor growth was further investigated in vivo. Rescue experiments were performed to investigate the involvement of the miR‐187‐3p/S100A4 axis in VPS9D1‐AS1 knockdown‐mediated antitumor effects. VPS9D1‐AS1 was highly expressed in EC tissues. VPS9D1‐AS1 knockdown, similar to miR‐187‐3p overexpression, significantly inhibited cell proliferation, inhibited colony formation, induced cell cycle arrest, and facilitated apoptosis of KLE cells. MiR‐187‐3p bound directly to VPS9D1‐AS1 and the 3′UTR of S100A4. Furthermore, VPS9D1‐AS1 negatively regulated miR‐187‐3p while positively regulating S100A4 expression in EC cells. MiR‐187‐3p knockdown or S100A4 overexpression partially reversed the tumor suppressive function of VPS9D1‐AS1 knockdown. The results suggest that VPS9D1‐AS1 affects EC progression by regulating the miR‐187‐3p/S100A4 axis. This may provide a promising therapeutic target to help treat EC. [ABSTRACT FROM AUTHOR]

Waste valorisation plays a crucial role in the sustainable production of valuable chemicals and materials. This study investigates the feasibility of green technology utilising food waste as a renewable substrate for lactic acid and the resulting residue for subsequent carbon dot production through microbial fermentation and hydrothermal reaction, respectively, while evaluating seashell waste as a replacement for commercial neutralisation reagents. The results demonstrated that seashell waste exhibited effective neutralisation performance during lactic acid fermentation. Within the five types of seashell waste studied, apart from abalone seashells, which led to a significant decrease in lactic acid productivity, all resulted in similar lactic acid fermentations. Additionally, fine powders of seashells were found to be optimal when combined with food waste hydrolysate for lactic acid fermentation. The highest lactic acid productivity of 1.48 g L−1 h−1 obtained in 2 L bioreactor batch fermentation using fine shell powder was 1.64-fold and 0.41-fold higher than those obtained using shell pieces and shell powder, respectively. The results of cell immobilisation fermentation exhibited a superior performance with 2.90 g L−1 h−1 glucose consumption rate and 1.89 g L−1 h−1 lactic acid productivity, which were 1.23-fold and 0.97-fold higher compared to those obtained using NaOH as the neutraliser, respectively. The results of life-cycle assessment also revealed lower environmental impacts associated with lactic acid production using food waste and seashell waste. Cell biomass derived from this study was further utilised to synthesise biomass-derived carbon quantum dots (Bio-CQDs), which demonstrated excellent water solubility, photophysical properties, and potential application as an antibiotic sensor. Overall, the study highlights the potential of seashell waste as an acid neutraliser in lactic acid fermentation and showcases the promising properties of fluorescent Bio-CQDs synthesised from cell biomass, providing valuable insights into the development and implementation of green and sustainable production from waste sources. [ABSTRACT FROM AUTHOR]

As a high-efficiency electrocatalyst for NH 3 production via NO 2 − reduction, Mo-doped Co 3 O 4 nanoarray exhibits an extremely high Faradaic efficiency of 96.9 % and a corresponding NH 3 yield of up to 651.5 μmol/h cm−2 at −0.5 V. [Display omitted] • Mo-doped Co 3 O 4 nanoarray on titanium mesh is synthesized as an effective catalyst for NO 2 −-to-NH 3 conversion. • Mo-Co 3 O 4 /TM exhibits a high NH 3 Faradaic efficiency of 96.9 % and a related yield of 651.5 μmol h−1 cm−2 with strong stability. • DFT calculations reveal the catalytic mechanism of NO 2 −RR on Mo-Co 3 O 4. • The fabricated Zn-NO 2 − battery achieves a peak power density of 3.6 mW cm−2 and a satisfactory NH 3 yield of 108.4 μmol h−1 cm−2. Electrochemical conversion of nitrite (NO 2 −) contaminant to green ammonia (NH 3) is a promising approach to achieve the nitrogen cycle. The slow kinetics of the complex multi-reaction process remains a serious issue, and there is still a need to design highly effective and selective catalysts. Herein, we report that molybdenum doped cobalt oxide nanoarray on titanium mesh (Mo-Co 3 O 4 /TM) acts as a catalyst to facilitate electroreduction of NO 2 − to NH 3. Such a catalyst delivers an extremely high Faradaic efficiency of 96.9 % and a corresponding NH 3 yield of 651.5 μmol h−1 cm−2 at −0.5 V with strong stability. Density functional theory calculations reveal that the introduction of Mo can induce the redistribution of electrons around Co atoms and further strengthen the adsorption of NO 2 −, which is the key to facilitating the catalytic performance. Furthermore, the assembled battery based on Mo-Co 3 O 4 /TM suggests its practical application value. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the contribution of the cleavage stage morphological parameters to the prediction of blastocyst transfer outcomes. Methods: A retrospective study was conducted on 8383 single-blastocyst transfer cycles including 2246 fresh and 6137 vitrified-warmed cycles. XGboost, LASSO, and GLM algorithms were employed to establish models for assessing the predictive value of the cleavage stage morphological parameters in transfer outcomes. Four models were developed using each algorithm: all-in model with or without day 3 morphology and embryo quality-only model with or without day 3 morphology. Results: The live birth rate was 48.04% in the overall cohort. The AUCs of the models with the algorithm of XGboost were 0.83, 0.82, 0.63, and 0.60; with LASSO were 0.66, 0.66, 0.61, and 0.60; and with GLM were 0.66, 0.66, 0.61, and 0.60 respectively. In models 1 and 2, female age, basal FSH, peak E2, endometrial thickness, and female BMI were the top five critical features for predicting live birth; In models 3 and 4, the most crucial factor was blastocyst formation on D5 rather than D6. In model 3, incorporating cleavage stage morphology, including early cleavage, D3 cell number, and fragmentation, was significantly associated with successful live birth. Additionally, the live birth rates for blastocysts derived from on-time, slow, and fast D3 embryos were 49.7%, 39.5%, and 52%, respectively. Conclusions: The value of cleavage stage morphological parameters in predicting the live birth outcome of single blastocyst transfer is limited. [ABSTRACT FROM AUTHOR]

Acquired aplastic anemia (AA) is a life-threatening disease associated with an imbalance in Th17/Treg cells. Regulating this balance may be an effective treatment approach for AA. Rhodiola rosea has shown efficacy in AA treatment, but its mechanisms remain unclear. We investigated salidroside's effect (a component of Rhodiola rosea) on Th17/Treg balance in adult AA patients and a mouse model. HIF-1α mRNA and protein levels were measured in AA patients' peripheral blood. Flow cytometry, qRT-PCR, and WB analyzed salidroside's impact on T cell differentiation, Th17 cells, Treg cells, STAT3, HIF-1α, and RORγt expression. ELISA measured hematopoietic growth factors in mouse serum. AA patients exhibited elevated HIF-1α levels. Salidroside improved hematopoietic function, increasing blood cell count and enhancing bone marrow. Salidroside induced SCF, TPO, and IL-3 expression while inhibiting IL-2 in mice. Salidroside reduced STAT3, HIF-1α, RORγt, and IL-17a, while increasing FoxP3 expression, correcting the Th17/Treg imbalance in vitro and in vivo. Salidroside has potential as a novel AA treatment by correcting the Th17/Treg imbalance through the STAT3/HIF-1α/RORγt pathway. [ABSTRACT FROM AUTHOR]

Aging promotes numerous intracellular changes in T cells that impact their effector function. Our data show that aging promotes an increase in the localization of STAT3 to the mitochondria (mitoSTAT3), which promotes changes in mitochondrial dynamics and function and T‐cell cytokine production. Mechanistically, mitoSTAT3 increased the activity of aging T‐cell mitochondria by increasing complex II. Limiting mitoSTAT3 using a mitochondria‐targeted STAT3 inhibitor, Mtcur‐1 lowered complex II activity, prevented age‐induced changes in mitochondrial dynamics and function, and reduced Th17 inflammation. Exogenous expression of a constitutively phosphorylated form of STAT3 in T cells from young adults mimicked changes in mitochondrial dynamics and function in T cells from older adults and partially recapitulated aging‐related cytokine profiles. Our data show the mechanistic link among mitoSTAT3, mitochondrial dynamics, function, and T‐cell cytokine production. [ABSTRACT FROM AUTHOR]