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Elucidating the mechanisms by which short chain fatty acids (SCFA) reduce body weight may assist in the development of an effective weight control strategy. Dietary supplementation of acetate, propionate, butyrate or their admixture was shown to significantly inhibit the body weight gain induced by high-fat diet feeding. Supplementation of SCFAs caused significant changes in the expressions of G-protein coupled receptor 43 (GPR43) and GPR41 characterized by increases in the adipose tissue and reductions in the colon. Additionally, they influenced the bacterial community structure in feces, with a reduction in the proportion of Firmicutes and an increase in the proportion of Bacteroidetes. The effects of dietary SCFAs on the GPR expression and gut microbiota composition may further result in body weight reduction by enhancing triglyceride hydrolysis and FFA oxidation in the adipose tissue, promoting beige adipogenesis and mitochondrial biogenesis, and inhibiting chronic inflammation.

Specific adipokines, such as adiponectin and resistin, are secreted from adipose tissue and are associated with the development of obesity. Supplementation of dietary SCFA can prevent and reverse high-fat-diet (HFD)-induced obesity. However, it is not clear whether SCFA ameliorate abnormal expression of adiponectin and resistin in the obese state. The aim of this study was to investigate the effects of SCFA on adiponectin and resistin’s expressions in diet-induced obese mice, as well as the potential mechanisms associated with DNA methylation. C57BL/6J male mice were fed for 16 weeks with five types of HFD (34·9 % fat by wt., 60 % kJ) – a control HFD and four HFD with acetate (HFD-A), propionate (HFD-P), butyrate (HFD-B) and their admixture (HFD-SCFA). Meanwhile, a low-fat diet (4·3 % fat by wt., 10 % kJ) was used as the control group. The reduced mRNA levels of adiponectin and resistin in the adipose tissue of the HFD-fed mice were significantly reversed by dietary supplementation of acetate, propionate, butyrate or their admixture to the HFD. Moreover, the expressional changes of adiponectin and resistin induced by SCFA were associated with alterations in DNA methylation at their promoters, which was mediated by reducing the expressions of enzyme-catalysed DNA methyltransferase ( DNMT1 , 3a , 3b ) and the methyl-CpG-binding domain protein 2 ( MBD2 ) and suppressing the binding of these enzymes to the promoters of adiponectin and resistin. Our results indicate that SCFA may correct aberrant expressions of adiponectin and resistin in obesity by epigenetic regulation.

To examine the diffusion characteristics of airflow and dust particles, a multi-factor and multi-level physical self-developed testing system is established. In this study, bunker height, chute angle, feeding speed, coal granularity, and belt speed are selected as independent variables, and airflow velocity and dust concentration are the response variables. The two-factor interactive model is established to analyze the primary and secondary relationship between the independent variables and the response variables. The results demonstrate a denser contour distribution of three-dimensional curved surfaces, suggesting an obvious interaction between the factors. The bunker height increases from 0.75 m to 1.15 m, the maximum increment of the induced airflow velocity at the outlet of the guide chute is observed to be 0.35 m/s, meanwhile, and with the increase in the feed speed from 2t/h to 8t/h, the increment of the induced airflow velocity at the outlet of the guide chute is recorded to be 51%. The coal granularity and bunker height depicted the highest influence on induced air velocity and dust concentration, and the feeding speed proved to be the secondary parameter. This two-factor interactive model can accurately forecast the actual values with a deviation of the calculated values limited to 9%. These research results support the existing research and provide a theoretical foundation to guide the dust control at belt conveyor transfer stations.

Infant botulism in a 4-month-old boy in China who continued to excrete toxins for over a month despite antitoxin therapy was further treated with fecal microbiota transplantation. After treatment, we noted increased gut microbial diversity and altered fecal metabolites, which may help reduce intestinal pH and enhance anti-inflammatory capabilities.

We report evidence of a detailed epigenetic modification of the leptin promoter and the effects of n-3 polyunsaturated fatty acids (n-3 PUFAs), which is closely associated with the leptin gene transcription in obesity. In the adipose tissue of diet induced obese (DIO) mice, methylation of the CpG island and the binding of methyl-CpG-binding domain protein 2 (MBD2) and DNA methyltransferases (DNMTs) at the leptin promoter are increased and RNA Pol II is decreased. Additionally, histones H3 and H4 are hypoacetylated, lysine 4 of histone H3 (H3K4) is hypomethylated and the binding of histone deacetylases (HDACs) 1, 2 and 6 is increased at the leptin promoter in the DIO mice. These modifications may serve a feedback role to maintain leptin concentrations within a normal range. The regulation of leptin transcriptional expression by n-3 PUFAs is mediated, at least in part, by epigenetic targets, such as MBD2 and histone modifications.

Our study aimed at assessing the impact of β-blocker treatment on the mortality of patients with sepsis-associated acute kidney injury (SA-AKI). Clinical data for patients with SA-AKI were collected from the Medical Information Mart for Intensive Care (MIMIC)-IV database. Baseline characteristics between β-blocker users and non-users were adjusted through propensity score matching (PSM). Kaplan-Meier curves and the Cox proportional hazards model were employed to analyze the relationship between β-blocker use and mortality, with the primary outcome being 30-day mortality. This study included data from 8,620 patients, with 3,159 receiving treatment and 5,461 not. After PSM, 2,896 matched pairs were created. The analysis revealed that 30-day (hazard ratio [HR]: 0.58, 95% CI: 0.52-0.65;  < 0.001), 90-day (HR: 0.55, 95% CI: 0.50-0.61;  < 0.001), and 365-day mortality (HR: 0.59, 95% CI: 0.54-0.64;  < 0.001) were significantly reduced in β-blocker users. Treatment with long-acting β-blockers was linked to notable improvement in 30-day (17.0 29.2%;  < 0.001), 90-day (24.1 36.0%;  < 0.001), and 365-day survival (31.9 45.0%;  < 0.001). In contrast, short-acting β-blockers showed no significant effect on 30-day (33.8 28.3%;  = 0.08), 90-day (37.5 34.2%;  = 0.07), or 365-day mortality (46.3 38.8%;  = 0.14). β-blocker therapy was associated with reduced mortality rates at 30, 90, and 365 days in SA-AKI patients. Long-acting β-blockers have demonstrated significant protective effects, while short-acting β-blockers, like esmolol, failed to improve patient survival in SA-AKI.

Calcium plays important roles in lipid metabolism and adipogenesis, but whether its status in early life affects later lipid profiles needs to be clarified. Three to four-week old C57BL/6J female mice were fed with three different reproductive diets containing normal, low (insufficient) and high (excessive) calcium concentrations respectively throughout pregnancy and lactation. At postnatal 21 days, the weaning male and female pups from each group were sacrificed for experiments and the remaining were fed with the normal chow diet for 16 weeks. Meanwhile, some of the weaning female pups from maternal low calcium diet group were fed with the normal calcium, low calcium and high calcium mature diets respectively for 8 weeks. Maternal insufficient or excessive calcium status during pregnancy and lactation programmed an abnormal expression of hepatic and adipose genes (PPAR-γ, C/EBP-α, FABP4, Fasn, UCP2, PPAR-α, HMG-Red1, Acc1, and SREBP-1c) in the offspring and this may lead to dyslipidemia and accumulation of hepatic triglyceride (TG) and total cholesterol (TC) in later life. The effects of maternal calcium status on lipid metabolism were found only in the female adult offspring, but were similar between offspring males and females at postnatal 21 days. Additionally, the dyslipidemia and hepatic lipid accumulation caused by insufficient calcium status in early life may be reversed to some extent by dietary calcium supplementation in later life.

Importance Acute necrotizing encephalopathy (ANE) is a rare but life‐threatening pediatric neurological disorder characterized by rapid progression and high mortality. Tocilizumab, an interleukin‐6 receptor antagonist, combined with high‐dose methylprednisolone [MP, ≥20 mg/(kg·day)], may improve outcomes, yet the optimal MP dosing strategy remains uncertain. Objective To evaluate the comparative effectiveness and safety of two high‐dose MP regimens [20 mg/(kg·day) vs. 30 mg/(kg·day)], each in combination with tocilizumab for ANE. Methods This retrospective cohort study included 23 ANE patients treated with tocilizumab and high‐dose MP at Beijing Children's Hospital from January 2023 to January 2025. Patients were divided into two groups based on the initial MP dosage: 20 mg/(kg·day) (n = 11) and 30 mg/(kg·day) (n = 12). Primary outcomes included mortality and anti‐inflammatory response. Secondary outcomes were the incidence of severe neurological sequelae, assessed using the pediatric overall performance category (POPC) score, and the frequency of treatment‐related adverse events. Results Overall mortality rate was 26.1% with a lower rate observed in the 30 mg/(kg·day) group (16.7%) compared to the 20 mg/(kg·day) group (36.4%). Most patients (78.3%) had severe ANE (ANE Severity Score ≥5), and 91.3% presented with multi‐organ dysfunction and brainstem involvement. Both groups demonstrated significant reductions in procalcitonin, cerebrospinal fluid protein, and cerebrospinal cytokines after 3 days of MP therapy (P < 0.05). Compared with the 20 mg/(kg·day) group, the 30 mg/(kg·day) MP group had significantly lower rates of severe neurological sequelae (POPC score 4–6) at discharge (41.7% vs. 90.9%; P = 0.027) and at 6–12 months follow‐up (30.0% vs. 85.7%; P = 0.050). No statistically significant differences in adverse event rates were observed between the two groups (P > 0.05), and no tocilizumab‐related adverse events were reported. Interpretation In pediatric ANE, tocilizumab combined with 30 mg/(kg·day) MP was associated with improved neurological outcomes compared with 20 mg/(kg·day), with comparable mortality and safety profiles. These findings suggest that a higher initial MP dose may offer neuroprotective advantages, warranting further validation in prospective, multicenter studies. Tocilizumab combined with high‐dose methylprednisolone improved outcomes in children with acute necrotizing encephalopathy. A dose of 30 mg/(kg·day) may be more effective than 20 mg/(kg·day).

Background TORCH infections are the most common prenatal infections causing congenital malformation and infant mortality, especially in developing countries. Migrant women might be vulnerable to TORCH infections, but little is known about the association between migration-related characteristics and TORCH infection risk. This study aimed to investigate the impact of migrant status, migration distance, and the spouse’s migrant status on the TORCH epidemic among women of childbearing age. Methods Based on the National Free Preconception Health Examination Project, we analyzed a representative dataset of TORCH infections among women of childbearing age (15–49 years old) in Guangdong Province of China (2014–2019, n  = 2,451,297). The past and/or recent infection status of TORCH infections (Toxoplasma gondii [TOX], Cytomegalovirus [CMV], and Rubella virus [RV]) were identified. Demographic and migration-related characteristics were collected. We thoroughly assessed the prevalence of TORCH infections in both migrant and native women and estimated adjusted odd ratios (aOR) for migration-related characteristics using multivariable logistic regression after adjusting the other sociodemographic factors. Results Among all 2,451,297 participants, 443,725 (18.1%) were migrant women. Migrant women presented a lower risk of past TOX infection (aOR: 0.89, 0.88–0.91) suggesting a healthy migrant effect (HME), but a higher risk of recent TOX infection (aOR: 1.88, 1.77–1.99), past CMV infection (aOR: 1.26, 1.25–1.28) and RV infection in natural ways (aOR: 1.05, 1.04–1.06). Compared with intra-provincial migrants, inter-provincial migrants had a lower past TOX infection (aOR: 0.88, 0.85–0.91), but a higher risk of recent TOX infection (aOR: 1.16, 1.05–1.27) and RV infection (aOR: 1.33, 1.31–1.36). In addition, having a migrant spouse was associated with a higher risk for all types of infection. Conclusion This study reported the association of migrant status and migration distance with TORCH infections, although the significance and directionality of these associations varied between pathogens. The spouse’s migrant status further amplified the infection risk for all types of pathogens. Our findings suggested interventions for preventing the spread of CMV and RV infection and new acquisition of TOX infection for migrants in southern China, to narrow the native-migrant health inequity and decrease the incidence of prenatal infections and related adverse outcomes.