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Low‐level of chronic inflammation activation is characteristic of obesity. Nonalcoholic fatty liver disease (NAFLD) is closely linked to obesity and is an emerging health problem, it originates from abnormal accumulation of triglycerides in the liver, and sometimes causes inflammatory reactions that could contribute to cirrhosis and liver cancer, thus its pathogenesis needs to be clarified for more treatment options. Once NAFLD is established, it contributes to systemic inflammation, the low‐grade inflammation is continuously maintained during NAFLD causing impaired resolution of inflammation in obesity, which subsequently exacerbates its severity. This study focuses on the effects of obesity‐induced inflammations, which are the underlying causes of the disease progression and development of more severe inflammatory and fibrotic stages. Understanding the relationship between obesity and NAFLD could help in establishing attractive therapeutic targets or diagnostic markers in obesity‐induced inflammation response and provides new approaches for the prevention and treatment of NAFLD in obesity. Obesity plays a vital role in the development of associated nonalcoholic fatty liver disease by affecting several inflammatory reactions via adipose tissue, vascular, intestinal, skeletal muscle, and brain, this process is associated with adipose tissue inflammation, inflammatory factors in the blood, intestinal inflammation, skeletal muscle inflammation, and brain tissue inflammation.

Background Curcumin has been reported to have activity for prevention and therapy of CRC, yet its underlying mechanisms remain largely unknown. Recently, emerging evidence suggests that the gut microbiota and its metabolites contribute to the causation and progression of Colorectal cancer (CRC). In this study, we aimed to investigate if curcumin affects the tumorigenesis of CRC by modulating gut microbiota and its metabolites. Methods Forty male C57BL/6JGpt mice were randomly divided into four groups: negative control (NC), curcumin control, CRC model, and curcumin treatment (CRC-Cur) groups. CRC mouse model was induced by using azoxymethane (AOM) and dextran sodium sulfate (DSS), and the mice in CRC model and curcumin treatment groups received oral PBS or curcumin (150 mg/kg/day), respectively. Additionally, fecal samples were collected. 16 S rRNA sequencing and Liquid Chromatography Mass Spectrometry (LC-MS)-based untargeted metabolomics were used to observe the changes of intestinal flora and intestinal metabolites. Results Curcumin treatment restored colon length and structural morphology, and significantly inhibited tumor formation in AOM/DSS-induced CRC model mice. The 16S rRNA sequencing analysis indicated that the diversity and richness of core and total species of intestinal microflora in the CRC group were significantly lower than those in the NC group, which were substantially restored in the curcumin treatment group. Curcumin reduced harmful bacteria, including Ileibacterium , Monoglobus and Desulfovibrio , which were elevated in CRC model mice. Moreover, curcumin increased the abundance of Clostridia_UCG-014 , Bifidobacterium and Lactobacillus , which were decreased in CRC model mice. In addition, 13 different metabolites were identified. Compared to the NC group, ethosuximide, xanthosine, and 17-beta-estradiol 3-sulfate-17-(beta-D-glucuronide) were elevated in the CRC model group, whereas curcumin treatment significantly reduced their levels. Conversely, glutamylleucine, gamma-Glutamylleucine, liquiritin, ubenimex, 5’-deoxy-5’-fluorouridine, 7,8-Dihydropteroic acid, neobyakangelicol, libenzapril, xenognosin A, and 7,4’-dihydroxy-8-methylflavan were decreased in the CRC group but notably upregulated by curcumin. Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analysis revealed enrichment in seven pathways, including folate biosynthesis ( P  < 0.05). Conclusions The gut microecological balance was disrupted in AOM/DSS-induced CRC mice, accompanied by metabolite dysbiosis. Curcumin restored the equilibrium of the microbiota and regulated metabolites, highly indicating that curcumin may alleviate the development of AOM/DSS induced colorectal cancer in mice by regulating intestinal flora homeostasis and intestinal metabolites.

College students experience ever-increasing levels of stress, leading to a wide range of health problems. In this context, monitoring and predicting students’ stress levels is crucial and, fortunately, made possible by the growing support for data collection via mobile devices. However, predicting stress levels from mobile phone data remains a challenging task, and off-the-shelf deep learning models are inapplicable or inefficient due to data irregularity, inter-subject variability, and the “cold start problem”. To overcome these challenges, we developed a platform named Branched CALM-Net that aims to predict students’ stress levels through dynamic clustering in a personalized manner. This is the first platform that leverages the branching technique in a multitask setting to achieve personalization and continuous adaptation . Our method achieves state-of-the-art performance in predicting student stress from mobile sensor data collected as part of the Dartmouth StudentLife study, with a ROC AUC 37% higher and a PR AUC surpassing that of the nearest baseline models. In the cold-start online learning setting, Branched CALM-Net outperforms other models, attaining an average F1 score of 87% with just 1 week of training data for a new student, which shows it is reliable and effective at predicting stress levels from mobile data.

Adenine monophosphate‐activated protein kinase (AMPK) is a fuel sensing enzyme that is activated in shortage of energy and inhibited in its surplus. Cancer is a metabolic disease characteristic of aerobic glycolysis, namely Warburg effect, and possesses heterogeneity featured by spatiotemporal hypoxia and normoxia, where AMPK is deeply implicated. The present study delineates the regulation of mitochondrial functions by AMPK in cancer cells. On the one hand, AMPKα subunit binds to mitochondria independently of β subunit and targeting AMPK to mitochondria facilitates oxidative phosphorylation and fatty acid oxidation, and inhibits glycolysis. As such, mitochondrial AMPK inhibits the growth of cancer cells and tumorigenesis. On the other hand, ablation of the β subunits completely abolishes AMPK activity and simultaneously leads to decreases in mitochondria DNA and protein contents. The effect of the β deletion is rescued by overexpression of the active mutant of bulky AMPKα1 subunit. In conjunction, the transcriptional factors PGC1α and Nrf‐1 are up‐regulated by LKB1/AMPK, an event that is abolished in the absence of the β subunits. Intriguingly, the stimulation of mitochondria biogenesis is not achieved by mitochondria‐targeted AMPK. Therefore, our study suggests that AMPK inhibits cancer cell growth and tumorigenesis via regulation of mitochondria‐mediated metabolism.

Background: Inflammatory bowel disease (IBD) is an increasingly common and globally emergent immune-mediated disorder. The etiology of IBD is complex, involving multiple factors such as immune dysregulation, environmental factors, genetic mutations, and microbiota dysbiosis, exacerbated by a lack of effective clinical therapies. Recently, studies hypothesized that dysbiosis of intestinal flora might participate in the onset of IBD. Metformin is widely used to treat type 2 diabetes and has shown beneficial effects in mouse models of IBD, although its underlying mechanisms remain poorly understood. Accumulating studies found that metformin shows beneficial effects for diabetes by affecting microbiota composition. This study explores possible regulatory effects of metformin on intestinal microecology during treatment for IBD. Methods: Inflammation was induced using 3% Dextran Sulfate Sodium (DSS) solution to generate mice models of IBD. Metformin treatments were assayed by measuring body weights and colon lengths of mice and H&E staining to observe histological effects on colon tissue structures. Changes in bacterial community composition and diversity-related to IBD and metformin treatment were assessed by high-throughput metagenomic sequencing analysis. Results: Metformin administration significantly ameliorated body weight loss, inhibited colon shrinking, and contributed to preserving the integrity of colon histological structures. The gut microbiota profiles revealed that the biodiversity of intestinal flora lost during inflammation was restored under metformin treatment. Metformin administration was also associated with decreased pathogenic Escherichia shigella and increased abundance of Lactobacillus and Akkermansia . Conclusion: Metformin appears to induce anti-inflammatory effects, thus ameliorating colitis symptoms, concurrent with enrichment for beneficial taxa and restored microbial diversity, suggesting a viable strategy against IBD.

Background Obesity has emerged as a global health crisis, with its prevalence having increased alarmingly over recent decades. There is significant damage to pancreatic islets due to obesity, as well as metabolic syndrome. Improving the function of β-cells in obese patients is meaningful for treatment. Thus, GLP-1 receptor agonists like semaglutide may be beneficial for islet structural remodeling and their endocrine function in diet-induced obese mice and associated with food intake. However, whether the specific impact of semaglutide on obesity is the same as calorie restriction(CR) has not been investigated. Methods In this study, Five-week-old male C57BL/6 mice were divided into two dietary groups and fed for 12 weeks a control diet or a high-fat diet (HFD). Then, for an additional four weeks, the main groups were resampled to include treatment (Semaglutide, SME, 40 µg/kg), or CR, totaling four groups: Control, Model, Model + SME, Model + CR. Immunofluorescence, Western blot, and RT-qPCR were used in the study. Results Semaglutide or CR was capable of ameliorating hyperglycemia and insulin sensitivity, and reduces the lesion on the islet, increases islet cell proliferation, and recovers islet size and alpha- and beta-cell masses. Moreover, the changes include improvement of METTL3/14, pancreatic duodenal homeobox 1 (PDX-1), and insulin signaling. Meanwhile, Semaglutide or CR significantly decreases the abundance of Firmicutes, Proteobacteria, and Verrucomicrobia, but increases the Bacteroides content. Conclusions Semaglutide plays a positive role in alleviating β-cell dysfunction by regulating gut microbiota, and METTL3/14, PDX-1, insulin signal pathway-related genes may be associated with CR.

Generating insulin-producing cells (IPCs) poses a significant hurdle in diabetes cell therapy. The liver is an advantageous cell source for pancreatic cell production due to its similar origin, potent proliferation, and regeneration capabilities, and shared glucose-sensing system. Hence, it is crucial to further comprehend the molecular regulatory mechanism of liver cell reprogramming into IPCs to refine the induction protocol and boost the induction efficiency. The expression of LncRNA MALAT1 and PI3K was elevated, in contrast to a significant diminution in miR-124-3p expression, during the progression of in vitro induced differentiation of primary mouse hepatocytes. In the overexpression group of lncRNA MALAT1 transfected, the level of PI3K diminished considerably during the IPCs induction phase, Consequently, effects on differentiation into IPCs were diminished in mice primary hepatic cells. Furthermore, the in vitro responsiveness of primary mouse hepatocytes-derived β islet-like cells to high glucose stimuli and insulin release by these cells were significantly diminished in the overexpression of lncRNA MALAT1 transfection group, while the outcomes were converse in the si-lncRNA MALAT1 group. And the transplanted IPCs(Si-MALAT1) have better cell function in T1DM mice. The experimental findings suggest that transfection of lncRNA MALAT1 alters the expression levels of miR-124-3p and PI3K genes in the final IPCs phase, accomplishing regulation of primary mouse hepatocytes directed β islet-like cell differentiation efficiency.

The agricultural production process contributes to the global issue of pesticide pollution. Based on the static toxicity test of diuron (DCMU) on Daphnia magna (D. magna) for EC50-48 h, a concentration range of 0.2 to 1 mg/L was set as sublethal concentrations, while lethal concentrations were set at 2 mg/L and 4 mg/L. This study analyzes the toxic response patterns of the swimming behavior indicators of D. magna exposed to different concentrations of DCMU. The results showed that the average speed (V) of D. magna decreased step by step with exposure time, regardless of exposure to sublethal concentration or lethal concentration. However, during the same short-term exposure period, the V of D. magna at lethal concentration was higher than that at sublethal concentration, which indicates that the swimming behavior of D. magna exposed to DCMU may be stimulated and accelerated. Compared to the control group, there is a statistically significant difference in the V of D. magna after short-term exposure, especially showing an extremely significant difference after 5 min of exposure. Evidently, compared to the traditional 48 h static toxicity testing method, the swimming behavior indicators of D. magna show a more sensitive response to DCMU after 5 min of exposure, making it more suitable for rapid toxicity detection. By expanding the range of exposure concentrations, it was found that the V indicator of D. magna responded significantly to a DCMU concentration of 0.05 mg/L after only 5 min of exposure, and a high degree of correlation was observed between the indicator and the exposure concentration. Through nonlinear fitting, the relationship between V and the dose–effect of DCMU toxicity presents an S-shaped curve, with R2 > 0.9. Consequently, it becomes possible to study the dose–effect relationship between the changes in the swimming behavior indicators of D. magna and the stress concentration based on this theory. This further establishes a foundation for the development of comprehensive aquatic toxicity rapid detection technology based on the toxic response of swimming behavior indicators.

Although pancreas and islet cell transplantation are the only ways to prevent the late complications of insulin‐dependent diabetes, a shortage of donors is a major obstacle to tissue and organ transplantation. Stem cell therapy is an effective treatment for diabetes and other pancreatic‐related diseases, which can be achieved by inducing their differentiation into insulin‐secreting cells. The liver is considered an ideal source of pancreatic cells due to its similar developmental origin and strong regenerative ability as the pancreas. This article reviews the traditional and emerging strategies using hepatocytes for pancreatic regenerative medicine and evaluates their advantages and challenges. Gene reprogramming and chemical reprogramming technologies are traditional strategies with potential to improve the efficiency and specificity of cell reprogramming and promote the transformation of hepatocytes into islet cells. At the same time, organoid technology, as an emerging strategy, has received extensive attention. Biomaterials provide a three‐dimensional culture microenvironment for cells, which helps improve cell survival and differentiation efficiency. In addition, clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing technology has brought new opportunities and challenges to the development of organoid technology. Highlights At present, the traditional and emerging strategies using hepatocyte‐derived islet‐like cells for diabetic cell replacement therapy have made extensive and far‐reaching progress. Gene reprogramming and chemical reprogramming technology are traditional strategies with potential, and organoid technology as an emerging strategy has also been widely studied. Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing also provides new opportunities and challenges for the development of organoid technology.

Silver films are key building blocks for plasmonic and nanophotonic devices, whose optical performance and device reliability are highly sensitive to particulate contamination introduced during fabrication and operation. Herein, a non-destructive surface cleaning strategy specifically applicable to silver film systems is proposed, based on the synergistic regulation of the mechanical properties of a polymer layer and its interfacial adhesion to the silver film. Such regulation is achieved by tuning hydrogen-bond-mediated interactions within a modified poly(vinyl alcohol) (PVA) layer, enabling effective control over the locus of fracture during peeling, such that fracture preferentially occurs at the polymer/silver interface. Unlike conventional polymer-assisted cleaning methods that suffer from an inherent trade-off between bulk cohesion and interfacial adhesion, this approach decouples the two properties through molecular-level hydrogen-bond redistribution. As a result, particulate contaminants can be efficiently removed from the silver surface while preserving the structural integrity of the silver film. The proposed method achieves a particle removal efficiency of up to 98% for contaminants larger than 30 nm and can be stably applied to silver films with lateral dimensions ranging from 1 inch to 12 inches, demonstrating excellent scalability. By further adjusting the processing parameters and compositional ratios of the polymer layer, this strategy is expected to be adaptable to silver films with different thicknesses and structural configurations, providing a reliable surface cleaning solution for improving the performance and reliability of plasmonic and optoelectronic thin-film devices.