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Photochemical glycosylation has attracted considerable attention in carbohydrate chemistry. However, to the best of our knowledge, visible-light-promoted glycosylation via photoactive glycosyl donor has not been reported. In the study, we report a photosensitizer-free visible-light-mediated glycosylation approach using a photoactive 2-glycosyloxy tropone as the donor. This glycosylation reaction proceeds at ambient temperature to give a wide range of O -glycosides or oligosaccharides with yields up to 99%. This method is further applied in the stereoselective preparation of various functional glycosyl phosphates/phosphosaccharides, the construction of N -glycosides/nucleosides, and the late-stage glycosylation of natural products or pharmaceuticals on gram scales, and the iterative synthesis of hexasaccharide. The protocol features uncomplicated conditions, operational simplicity, wide substrate scope (58 examples), excellent compatibility with functional groups, scalability of products (7 examples), and high yields. It provides an efficient glycosylation method for accessing O / N -glycosides and glycans. Visible light-induced glycosylation reactions are achieved by either photoactivating a photosensitizer or using a stoichiometric activator, while glycosylation via a photoactive glycosyl donor was so far not reported. In this study, the authors develop a photosensitizer free visible-light-mediated glycosylation approach using photoactive 2-glycosyloxy tropone as the donor, obtaining a wide range of O -glycosides or oligosaccharides.

Background： Previous studies suggested that zinc level was related to relationship between zinc level and all the microvascular complications in a certain diabetic microvascular complication. However, the type 2 diabetic patients remains unknown. The purpose of this study was to analyze the relationship between zinc level and each diabetic microvascular complication and identify the features related to low serum zinc level. Methods： We included the hospitalized patients with type 2 diabetes （T2D） at our department from May 30, 2013 to March 31,2014. We initially compared the serum zinc levels between patients with specific microvascular complications and those without. We then analyzed the association between zinc level and each microvascular complication. Furthermore, we identified the unique features of patients with high and low serum zinc levels and analyzed the risk factors related to low zinc level. Results： The 412 patients included 271 with microvascular complications and 141 without any microvascular complications. Serum zinc level was significantly lower in patients with diabetic retinopathy （P 〈 0.001）, diabetic nephropathy （DN, P 〈 0.001 ）, or diabetic peripheral neuropathy （P = 0.002） compared with patients without that specific complication. Lower zinc level was an independent risk factor for DN （odds ratio = 0.869, 95% confidence interval = 0.765-0.987, P 〈 0.05）. The subjects with lower serum zinc level had manifested a longer duration of diabetes, higher level of hemoglobin A I c, higher prevalence of hypertension and microvascular complications, and lower fasting and 2-h C-peptide levels. Conclusions： Lower serum zinc level in T2D patients was related to higher prevalence of diabetic microvascular complications, and represented as an independent risk factor for DN. Patients with lower zinc level were more likely to have a longer duration of diabetes, poorer glucose control, and worse β-cell function.

Terahertz (THz=1012Hz) radiation has attracted wide attention for its unprecedented sensing ability and its noninvasive and nonionizing properties. Tremendous strides in THz instrumentation have prompted impressive breakthroughs in THz biomedical research. Here, we review the current state of THz spectroscopy and imaging in various biomedical applications ranging from biomolecules, including DNA/RNA, amino acids/peptides, proteins, and carbohydrates, to cells and tissues. We also address the potential biological effects of THz radiation during its biological applications and propose future prospects for this cutting-edge technology. THz spectroscopy has proven to be an innovative tool for providing new insights into the hydration shell in the solvation dynamics of protein solutions. THz in-line digital holography, THz near-field imaging modality, and THz endoscope prototypes have been utilized to identify abnormal tissues faster and more accurately. Increasing applications of artificial modeling and numerical computation are becoming essential supplements for THz biological effect studies.

The incidence of metabolic syndrome is significantly higher in patients with irritable bowel syndrome (IBS), but the mechanisms involved remain unclear. Gut microbiota is causatively linked with the development of both metabolic dysfunctions and gastrointestinal disorders, thus gut dysbiosis in IBS may contribute to the development of metabolic syndrome. Here, we show that human gut bacterium Ruminococcus gnavus -derived tryptamine and phenethylamine play a pathogenic role in gut dysbiosis-induced insulin resistance in type 2 diabetes (T2D) and IBS. We show levels of R. gnavus , tryptamine, and phenethylamine are positively associated with insulin resistance in T2D patients and IBS patients. Monoassociation of R. gnavus impairs insulin sensitivity and glucose control in germ-free mice. Mechanistically, treatment of R. gnavus -derived metabolites tryptamine and phenethylamine directly impair insulin signaling in major metabolic tissues of healthy mice and monkeys and this effect is mediated by the trace amine-associated receptor 1 (TAAR1)-extracellular signal-regulated kinase (ERK) signaling axis. Our findings suggest a causal role for tryptamine/phenethylamine-producers in the development of insulin resistance, provide molecular mechanisms for the increased prevalence of metabolic syndrome in IBS, and highlight the TAAR1 signaling axis as a potential therapeutic target for the management of metabolic syndrome induced by gut dysbiosis. Here, the authors show a causal role for gut bacteria-derived metabolites tryptamine and phenethylamine in contributing to insulin resistance and the development of metabolic syndrome in patients with irritable bowel syndrome and type 2 diabetes.

The rice–crayfish co-culture system, a representative of Agri-aqua food systems, has emerged worldwide as an effective strategy for enhancing agricultural land use efficiency and boosting sustainability, particularly in China and Southeast Asia. Despite its widespread adoption in China’s Jianghan Plain, the exact spatiotemporal dynamics and factors influencing this practice in this region are yet to be clarified. Therefore, understanding the spatiotemporal dynamics and influencing factors of the rice–crayfish fields (RCFs) is crucial for promoting the rice–crayfish co-culture system, and optimizing land use policies. In this study, we identified the spatial distribution of RCF using Sentinel-2 images and land use spatiotemporal data to analyze its spatiotemporal dynamics during the period of 2016–2020. Additionally, we used the Multiscale Geographically Weighted Regression model to explore the key factors influencing RCF’s spatiotemporal changes. Our findings reveal that (1). the RCF area in Jianghan Plain expanded from 1216.04 km2 to 2429.76 km2 between 2016 and 2020, marking a 99.81% increase. (2). RCF in Jianghan Plain evolved toward a more contiguous and clustered spatial pattern, suggesting a clear industrial agglomeration in this area. (3). The expansion of the RCFs was majorly influenced by its landscape and local agricultural conditions. Significantly, the Aggregation and Landscape Shape Indexes positively impacted this expansion, whereas proximity to rural areas and towns had a negative impact. This study provides a solid foundation for promoting the rice–crayfish co-culture system and sustainably developing related industries. To ensure the sustainable development of rice–crayfish co-culture industries in Jianghan Plain, we recommend that local governments optimize the spatial layout of rural settlements, improve transportation infrastructure, and enhance regional agricultural water sources and irrigation system construction, all in line with the national strategy of rural revitalization and village planning. Additionally, promoting the concentration and contiguity of RCF through land consolidation can achieve efficient development of these industries.

Angiogenesis plays a vital role in colon cancer growth and metastasis. The role of protein kinase N2 (PKN2) in colon cancer is rarely studied. In this study, we investigated the effect of PKN2 on angiogenesis in colon cancer. We evaluated the correlation between PKN2 expression and microvessel density (MVD) in tumor tissue of patients with colon cancer. The effect of PKN2 on tumor angiogenesis was investigated both in cultured colon cancer cells and in a mouse colon cancer model. PKN2 targeted vascular endothelial growth factor A (VEGFA) and basic fibroblast growth factor (bFGF) expression, and secretion were analyzed, and the specific regulatory role of PKN2 on HIF was explored. PKN2 expression was negatively correlated with tumor MVD in tumor tissue of patients with colon cancer. PKN2 inhibited angiogenesis in both in vitro and in vivo models of mouse tumors. Mechanistically, PKN2 suppressed the transcriptional activity of hypoxia‐inducible factor‐1α (HIF‐1α) and reduced its nuclear accumulation, leading to the inhibiting of VEGFA and bFGF transcription by preventing HIF‐1α binding to their promoters. Additionally, PKN2 directly interacted with HIF‐1α at the protein level and induced phosphorylation, resulting in ubiquitination‐dependent degradation of HIF‐1α in colon cancer cells. Our study demonstrated, for the first time, that PKN2 exerts inhibitory effects on tumor angiogenesis in colon cancer. We propose a novel mechanism by which PKN2 regulates VEGFA and bFGF expression through modulation of the dynamic equilibrium of HIF‐1α protein levels.

Radiation-induced skin injury (RISI) is an important challenge for clinical treatments. The main causes of RISI include hypoxia in the wound microenvironment, reactive oxygen species (ROS) activation, and downregulation of DNA repair proteins. Here, a multiple radioresistance strategy was designed for microRNA therapy and attenuating hypoxia. A novel mesoporous silica (MS) firmly anchored and dispersed cerium (IV) oxide (CeO 2 ) nanoparticles to form MS-CeO 2 nanocomposites, which exhibit superior activity in inhibiting radiation-induced ROS and HIF-1α activation and ultimately promote RISI wound healing. The miR129 serum concentrations in patients can promote radioresistance by directly targeting RAD17 and regulating the Chk2 pathway. Subsequently, MS-CeO 2 nanocomposites with miR129 were conjugated with iRGD-grafted polyoxyethylene glycol (short for nano-miR129), which increased the stability and antibacterial character, efficiently delivered miR129 to wound blood capillaries, and exhibited low toxicity. Notably, nano-miR129 promoted radioresistance and enhanced anti-ROS therapeutic efficacy in a subcutaneous RISI mouse model. Overall, this MS-CeO 2 nanozyme and miR129-based multiresistance radiotherapy protection strategy provided a promising therapeutic approach for RISI.

Diabetes is associated with an increased risk of coronavirus disease 2019 (COVID‐19)‐associated morbidity and mortality. COVID‐19 vaccines substantially reduce the risk of serious COVID‐19 outcomes, making them important for individuals with diabetes. However, the effects of the COVID‐19 vaccines on glucose control in patients with diabetes remain unclear. Here, we demonstrate that COVID‐19 vaccine boosters impair insulin sensitivity in both mice and patients with type 2 diabetes (T2D). In mice, the administration of four vaccine doses elevated the levels of SARS‐CoV‐2 spike protein and impaired glucose tolerance and insulin sensitivity. Mechanistically, we showed that the SARS‐CoV‐2 spike protein, guided by the mRNA COVID‐19 vaccine, interferes with insulin signaling by binding to angiotensin‐converting enzyme 2, TLR4, and ER. We found that 66% of T2D patients exhibited aggravated insulin resistance to booster shots of the mRNA COVID‐19 vaccine. Furthermore, treatment with metformin improved insulin signaling variations induced by COVID‐19 vaccine boosters in mice. These findings indicate that COVID‐19 vaccine boosters impair insulin sensitivity in T2D and that metformin may mitigate these effects. These results maintain the risk–benefit ratio in favor of COVID‐19 vaccination for the prevention of severe clinical outcomes, yet highlight the need for close glycemic monitoring of patients with diabetes after receiving mRNA COVID‐19. SARS Cov‐2 spike protein disrupts insulin signaling in type 2 diabetes as a target of the COVID‐19 vaccine in subject with type 2 diabetes (T2D), while metformin improved the insulin signaling variations induced by mRNA COVID‐19 vaccine boosters in mice.