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ObjectivesThe study aims to systematically identify the alterations in gut microbiota that observed in gastric cancer through comprehensive assessment of case–control studies.MethodsThe systematic literature search of PubMed, Embase, Cochrane Library, and Web of Science was conducted to identify case–control studies that compared the microbiomes of individuals with and without gastric cancer. Quality of included studies was evaluated with the Newcastle-Ottawa Quality Assessment Scale (NOS). Meta-analyses utilized a random-effects model, and subgroup and sensitivity analyses were performed to assess study heterogeneity. All data analyses were performed using the “metan” package in Stata 17.0, and the results were described using log odds ratios (log ORs) with 95% confidence intervals (CIs).ResultsA total of 33 studies involving 4,829 participants were eligible for analysis with 29 studies provided changes in α diversity and 18 studies reported β diversity. Meta-analysis showed that only the Shannon index demonstrated statistical significance for α-diversity [−5.078 (−9.470, −0.686)]. No significant differences were observed at the phylum level, while 11 bacteria at genus-level were identified significant changed, e.g., increasing in Lactobacillus [5.474, (0.949, 9.999)] and Streptococcus [5.095, (0.293, 9.897)] and decreasing in Porphyromonas and Rothia with the same [−8.602, (−11.396, −5.808)]. Sensitivity analysis indicated that the changes of 9 bacterial genus were robust. Subgroup analyses on countries revealed an increasing abundance of Helicobacter and Streptococcus in Koreans with gastric cancer, whereas those with gastric cancer from Portugal had a reduced Neisseria. Regarding the sample sources, the study observed an increase in Lactobacillus and Bacteroides in the gastric mucosa of people with gastric cancer, alongside Helicobacter and Streptococcus. However, the relative abundance of Bacteroides decreased compared to the non-gastric cancer group, which was indicated in fecal samples.ConclusionThis study identified robust changes of 9 bacterial genus in people with gastric cancer, which were country-/sample source-specific. Large-scale studies are needed to explore the mechanisms underlying these changes.Systematic ReviewUnique Identifier: CRD42023437426 https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023437426.

As the incidence of type 2 diabetes mellitus (T2DM) is increasing rapidly and its consequences are severe, effective intervention and prevention, including sleep-related interventions, are urgently needed. As a component of sleep architecture, naps, alone or in combination with nocturnal sleep, may influence the onset and progression of T2DM. Overall, napping is associated with an increased risk of T2DM in women, especially in postmenopausal White women. Our study showed that napping >30 minutes (min) increased the risk of T2DM by 8-21%. In addition, non-optimal nighttime sleep increases T2DM risk, and this effect combines with the effect of napping. For nondiabetic patients, napping >30 min could increase the risks of high HbA1c levels and impaired fasting glucose (IFG), which would increase the risk of developing T2DM later on. For diabetic patients, prolonged napping may further impair glycemic control and increase the risk of developing diabetic complications (e.g., diabetic nephropathy) in the distant future. The following three mechanisms are suggested as interpretations for the association between napping and T2DM. First, napping >30 min increases the levels of important inflammatory factors, including interleukin 6 and C-reactive protein, elevating the risks of inflammation, associated adiposity and T2DM. Second, the interaction between postmenopausal hormonal changes and napping further increases insulin resistance. Third, prolonged napping may also affect melatonin secretion by interfering with nighttime sleep, leading to circadian rhythm disruption and further increasing the risk of T2DM. This review summarizes the existing evidence on the effect of napping on T2DM and provides detailed information for future T2DM intervention and prevention strategies that address napping.

Abstract Introduction The main emphasis of the research about adjuvant imatinib for high‐risk gastrointestinal stromal tumors (GISTs) is prolonging the treatment duration and ignores the heterogeneous that 10‐year recurrence rates ranged from about 20%–100%. Thus, this study evaluated the effect of different durations of adjuvant imatinib on outcomes in high‐risk GISTs to explore the feasibility of individual treatment. Methods We analyzed 855 high‐risk GIST patients from three centers who underwent macroscopically complete resection between December 2007 and September 2020. The patients were divided into training (n =564) and two validation cohorts (n = 238 and53) based on their source. Recurrence‐free survival (RFS) was the primary point. Cox multivariate analysis was used to develop the nomogram. C‐index, time‐dependent area under the curves, and calibration plots were used to assess the performance of the nomogram. Results Univariate analysis showed that longer adjuvant imatinib was significantly associated with better 5‐year RFS (p

Based on the Bethe-Richardson-Gaudin ansatz for the standard pairing model, extended Bethe- Richardson-Gaudin ansatzes for eigenvectors of a spherical mean-field plus separable pairing model with three non-degenerate j-orbits are proffered. It is shown that the number of variables appearing in the general extended ansatz eigenvectors for given number of pairs N is N(N+1)/2. More importantly, when one of the j orbits is 1/2, there are only 2N variables involved in the alternative extended ansatz eigenvectors, which, like the standard pairing model, can be solved efficiently. Numerical results for an application of the model in the ds-shell up to its half-filling are presented, which serves to validate the procedure and illustrates the completeness of the solutions it renders.

In China, animal feeds are frequently contaminated with a range of mycotoxins, with Aflatoxin B1 (AFB1) and T-2 toxin (T-2) being two highly toxic mycotoxins. This study investigates the combined nephrotoxicity of AFB1 and T-2 on PK15 cells and murine renal tissues and their related oxidative stress mechanisms. PK15 cells were treated with the respective toxin concentrations for 24 h, and oxidative stress-related indicators were assessed. The results showed that the combination of AFB1 and T-2 led to more severe cellular damage and oxidative stress compared to exposure to the individual toxins (p < 0.05). In the in vivo study, pathological examination revealed that the kidney tissue of mice exposed to the combined toxins showed signs of glomerular atrophy. The contents of oxidative stress-related indicators were significantly increased in the kidney tissue (p < 0.05). These findings suggest that the combined toxins cause significant oxidative damage to mouse kidneys. The study highlights the importance of considering the combined effects of mycotoxins in animal feed, particularly AFB1 and T-2, which can lead to severe nephrotoxicity and oxidative stress in PK15 cells and mouse kidneys. The findings have important implications for animal feed safety and regulatory policy.

Cadmium (Cd) contamination in soil-rice systems has become a global public concern. However, influencing factors and the contamination threshold of Cd in soils remain largely unknown owing to soil heterogeneity, which limits our ability to assess the risk to human health and to draft appropriate environmental policies. In this study, we selected the soil-rice system of Longtang and Shijiao town in southern China, which was characterized by multi-metal acidic soil contamination due to improper electronic waste recycling activities, as a case to analyze the influence of different soil properties on the Cd threshold in the soil and Cd accumulation in rice. The results showed that soil organic matter (SOM) was the main factor regulating Cd accumulation in the soil-rice system. Moreover, compared with the total Cd concentration, the DTPA-extractable Cd concentration in the soil was a better predictor of Cd transportation in the soil-rice system. According to the prediction model, when SOM was < 35 g kg−1, the CdDTPA threshold was 0.16 mg kg−1 with a 95% likelihood of Cdrice accumulation above the Chinese food standard limit (0.2 mg kg−1). Conversely, when SOM was ≥ 35 g kg−1, the CdDTPA threshold was only 0.03 mg kg−1. This study of the influence of SOM on Cd accumulation in a soil-rice system confirms that SOM is a crucial parameter for better and safer rice production, especially in multi-metal contaminated acidic soils.

Pseudorabies, caused by pseudorabies virus (PRV), is the main highly infectious disease that severely affects the pig industry globally. T-2 toxin (T2), a significant mycotoxin, is widely spread in food and feeds and shows high toxicity to mammals. The potential mechanism of the interaction between viruses and toxins is of great research value because revealing this mechanism may provide new ideas for their joint prevention and control. In this study, we investigated the effect of T2 on PRV replication and the mechanism of action. The results showed that at a low dose (10 nM), T2 had no significant effect on porcine kidney 15 (PK15) cell viability. However, this T2 concentration alleviated PRV-induced cell injury and increased cell survival time. Additionally, the number of PK15 cells infected with PRV significantly reduced by T2 treatment. Similarly, T2 significantly decreased the copy number of PRV. Investigation of the mechanism revealed that 10 nM T2 significantly inhibits PRV replication and leads to downregulation of oxidative stress- and apoptosis-related genes. These results suggest that oxidative stress and apoptosis are involved in the inhibition of PRV replication in PK15 cells by low-concentration T2. Taken together, we demonstrated the protective effects of T2 against PRV infection. A low T2 concentration inhibited the replication of PRV in PK15 cells, and this process was accompanied by downregulation of the oxidative stress and apoptosis signaling pathways. Our findings partly explain the interaction mechanism between T2 and PRV, relating to oxidative stress and apoptosis, though further research is required.

The generation of genetically modified mouse models derived from gene targeting (GT) in mouse embryonic stem (ES) cells (mESCs) has greatly advanced both basic and clinical research. Our previous finding that gene targeting at the Myh9 exon2 site in mESCs has a pronounced high homologous recombination (HR) efficiency (>90%) has facilitated the generation of a series of nonmuscle myosin II (NM II) related mouse models. Furthermore, the Myh9 gene locus has been well demonstrated to be a new safe harbor for site-specific insertion of other exogenous genes. In the current study, we intend to investigate the molecular biology underlying for this high HR efficiency from other aspects. Our results confirmed some previously characterized properties and revealed some unreported observations: 1) The comparison and analysis of the targeting events occurring at the Myh9 and several widely used loci for targeting transgenesis, including ColA1, HPRT, ROSA26, and the sequences utilized for generating these targeting constructs, indicated that a total length about 6 kb with approximate 50% GC-content of the 5' and 3' homologous arms, may facilitate a better performance in terms of GT efficiency. 2) Despite increasing the length of the homologous arms, shifting the targeting site from the Myh9 exon2, to intron2, or exon3 led to a gradually reduced GT frequency (91.7, 71.8 and 50.0%, respectively). This finding provides the first evidence that the HR frequency may also be associated with the targeting site even in the same locus. Meanwhile, the decreased trend of the GT efficiency at these targeting sites was consistent with the reduced percentage of simple sequence repeat (SSR) and short interspersed nuclear elements (SINEs) in the sequences for generating the targeting constructs, suggesting the potential effects of these DNA elements on GT efficiency; 3) Our series of targeting experiments and analyses with truncated 5' and 3' arms at the Myh9 exon2 site demonstrated that GT efficiency positively correlates with the total length of the homologous arms (R = 0.7256, p

Objective This study aimed to assess the associations between multidimensional sleep features and type 2 diabetes mellitus (T2DM).Methods We conducted a systematic search across the PubMed, Embase, Web of Science, and Scopus databases for observational studies examining the association between nighttime sleep duration, nighttime sleep quality, sleep chronotype, and daytime napping with type 2 diabetes mellitus (T2DM), up to October 1, 2024. If I2 < 50%, a combined analysis was performed based on a fixed-effects model, and vice versa, using a random-effects model.Results Our analysis revealed that a nighttime sleep duration of less than 7 h (odds ratio [OR] = 1.18; 95% CI = 1.13, 1.23) or more than 8 h (OR = 1.13; 95% CI = 1.09, 1.18) significantly increased the risk of T2DM. Additionally, poor sleep quality (OR = 1.50; 95% CI = 1.30, 1.72) and evening chronotype (OR = 1.59; 95% CI = 1.18, 2.13) were associated with a notably greater risk of developing T2DM. Daytime napping lasting more than 30 min augments the risk of T2DM by 7-20%. Interactively, the incidence of T2DM was most significantly elevated among individuals with poor sleep quality and nighttime sleep duration of more than 8 h (OR = 2.15; 95% CI = 1.19, 3.91).Conclusions A U-shaped relationship was observed between sleep duration and type 2 diabetes mellitus (T2DM), with the lowest risk occurring at a sleep duration of 7 to 8 h. Additionally, poor sleep quality, evening chronotypes, and daytime napping exceeding 30 min emerged as potential risk factors for T2DM. These high-risk sleep characteristics interacted with one another, amplifying the overall risk of developing the disease.