Background:Sarcopenia is prevalent in older adults and affects their quality of life and overall health, low handgrip strength is one of the main manifestations of sarcopenia. Resistance training is an effective intervention for improving muscle strength in older adults, but the optimal dose of resistance training remains unclear. Therefore, the aim of this meta-analysis was to investigate the dose-response relationship between different doses of resistance training and grip strength in older adults. Methods:This systematic review and network meta-analysis included a search in PubMed, Embase, and the Cochrane Library for randomized controlled trials from inception to 19 October 2024 of resistance training for patients with senile sarcopenia. Comprehensive data extraction covered dose, resistance training protocol, demographics, and study duration. Systematic review with Bayesian network meta-analysis (NMA) methodology was employed and results were presented as 95% credible intervals (Crl). Results:A total of 13 studies involving 711 participants (mean age: 68.29 ± 5.30 years; mean BMI: 24.03 ± 3.43; female: 79.5%) were included in this study. The results of our network meta-analysis showed that resistance training variables (e.g., frequency, intensity, period, and training volume) were effective in improving handgrip strength in older patients with sarcopenia. Among them, the effective dose range for frequency of resistance training was 2-5 times/week, resistance training intensity was 30%-75%, resistance training period was 4-24 weeks, resistance training exercise was 3-17 exercises per set, resistance training repetitions was 10-24 reps, resistance training sets was 2-8 sets, resistance training volume was 528-2,200 reps per week. The optimal dose of resistance training to improve handgrip strength in older adults with sarcopenia is 3 times per week (MD = 7.02, 95% CrI [4.62, 9.42]), 49% 1RM (MD = 7.11, 95% CrI [2.69, 11.52]), 19 weeks (MD = 7.87, 95% CrI [3.89, 11.85]), 15 exercises (MD = 8.16, 95% CrI [3.65, 12.66]), 16 reps (MD = 7.62; 95% CrI [4.77, 10.46]), 6 sets (MD = 8.63; 95% CrI [5.06, 12.21]), 1,400 reps/week (MD = 8.45; 95% CrI [5.50, 11.40]). Conclusion:Resistance training effectively improves handgrip strength in older adults with sarcopenia. A recommended 19-week program includes 3 sessions per week at 49% 1RM, featuring 15 exercises per set, 6 sets, and 16 repetitions per exercise, totaling up to 1,400 reps weekly. Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/recorddashboard.

OBJECTIVE:This study investigates the regulatory role of p53 on Lgals3 expression and its impact on preadipocyte differentiation, fatty acid synthesis, and oxidation in obesity. METHODS:Bioinformatics analysis of six obesity-related microarray datasets and single-cell RNA sequencing (scRNA-seq) data identified Lgals3 as a key obesity-associated gene. A high-fat diet (HF) mouse model was established to evaluate obesity-related phenotypes, including body weight, hepatic Lgals3 expression, adipose tissue pathology, blood lipid profiles, and glucose tolerance. In vitro experiments using 3T3-L1 cells were conducted to assess adipocyte differentiation, fatty acid synthase (FAS) activity, and glucose uptake. The interaction between p53 and the Lgals3 promoter was analyzed via dual-luciferase reporter and chromatin immunoprecipitation assays. Key metabolic genes and proteins were quantified by RT-qPCR and Western blot. RESULTS:HF mice exhibited significant weight gain, elevated Lgals3 expression, and altered lipid profiles. In vitro, p53 was shown to transcriptionally repress Lgals3, thereby reducing adipocyte differentiation, FAS activity, and glucose uptake. In vivo, p53 overexpression led to downregulation of Lgals3 and improvement in obesity-related metabolic outcomes, whereas Lgals3 overexpression counteracted these effects. CONCLUSIONS:p53 inhibits Lgals3 expression, suppressing adipocyte differentiation and improving obesity-related metabolic dysfunction, highlighting its potential as a therapeutic target in obesity management.

Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide, characterized by molecular and clinical heterogeneity. Interleukin (IL)-27, a heterodimeric cytokine composed of p28 and EBI3 subunits, has been reported to exert potent antitumor activity in several cancer models. However, the precise role of IL-27 in the pathogenesis of CRC remains unclear. Here, we show that during the azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced CRC development, IL-27p28 levels are dramatically increased in peripheral blood and tumor tissues, and the cytokine is mainly produced by tumor-infiltrating myeloid cells. IL-27p28 deficient mice display tumor resistances in both inflammation-associated CRC model and syngeneic MC38 colon cancer model. Administration with IL-27p28 neutralizing antibody also reduces the tumor formation in AOM/DSS-treated mice. Mechanically, CD8+ T cells in IL-27p28-/- mice exhibit enhanced tumor infiltration and cytotoxicity, which can be largely attributed to activation of the Akt/mTOR signaling pathway. Furthermore, selective depletion of CD8+ T cells in IL-27p28-/- mice markedly accelerate tumor growth and almost abrogate the protective effects of IL-27p28 deficiency. Most interestingly, the expression of IL-27p28 is also upregulated in tumor tissues of CRC patients and those with high expression of IL-27p28 tend to have a poorer overall survival. Our results suggest that loss of IL-27p28 suppresses colorectal tumorigenesis by augmenting CD8+ T cell-mediated anti-tumor immunity. Targeting IL-27p28 could be developed as a novel strategy for the treatment of colorectal cancers.

结直肠癌(colorectal cancer,CRC)发病率高且难以治愈.越来越多的证据表明肠道微生物群生态失调与CRC发生发展密切相关,具核梭杆菌(Fusobacterium nucleatum,Fn)已经被确定为肠道微生物群中的病原体,有助于结直肠发生癌变.本文综述了Fn诱导CRC发生发展的重要机制,包括毒力因子、慢性炎症、miRNA、免疫调节和肠道代谢物,并描述了Fn在诊断治疗中的临床价值,以期为新型肿瘤生物标志物的筛查与新兴免疫治疗靶点的开发提供参考.

为了解肺癌肿瘤组织白细胞介素-10(interleukin-10,IL-10)的表达和来源,并探究IL-10对肿瘤的作用,采用MSD超敏电化学发光技术检测Lewis肺癌小鼠模型血清中IL-10的水平,使用流式细胞术分析肿瘤组织IL-10的主要来源,再通过CCK-8实验、膜联蛋白V-碘化丙啶(annexin V-PI)凋亡实验、划痕实验,检测IL-10重组蛋白对肺癌细胞增殖、凋亡、迁移的影响.结果表明:Lewis肺癌小鼠血清中IL-10水平较正常小鼠显著升高,肿瘤组织中的IL-10主要由免疫细胞产生.其中,B细胞和髓源性抑制细胞(myeloid-derived suppressor cells,MDSCs)是IL-10的主要来源,IL-10重组蛋白可以显著抑制LLC(小鼠Lewis肺癌细胞:Lewis lung carcinoma line)的增殖和迁移并促进其凋亡.综上可见,IL-10水平与肺癌密切相关,B细胞和MDSCs是产生IL-10的主要来源,IL-10可能通过激活CD8 T细胞或者直接作用于肿瘤细胞而发挥抗肿瘤作用.

全球每年有超100万例结直肠癌(colorectal cancer,CRC)新诊断病例.CRC是世界第三大常见恶性肿瘤及第四大常见癌症死亡原因.炎症相关结直肠癌(colitis associated cancer,CAC)是CRC的主要临床类型之一,患有长期炎症性肠病(inflammatory bowel disease,IBD)患者发生CAC的风险显著增加,这可能与慢性炎症的累积密切相关.本文就遗传性基因突变,慢性炎症与免疫,肠道菌群丰度及产物变化三种致病因素分析,了解三种因素相互作用关系对CAC发病机制的影响,对理解炎症环境下肿瘤发生具有重要意义.

Objective: Curcumin is a natural active product extracted from turmeric, has been reported to have anticancer properties against various tumors. However, the effect of curcumin on colon cancer remains still unclear. Our aimed to investigate the anti-colon cancer properties of curcumin in vitro , and determine the molecular mechanisms underlying these effects. Methods: Viability assays including CCK8 and LDH were used to measure cell proliferation. Flow cytometry was performed to detect cell apoptosis and cell cycle distribution. qRT-PCR and Western blotting was used for measuring genes/protein expression/activation in apoptotic and pro-carcinogenic cellular signaling pathways. Finally, the results were confirmed using a xenograft tumor model that comprised of mice. Results: In vitro , Our data showed that curcumin preferentially and, in a dose, dependent way inhibited colon cancer cells proliferation, but was not toxic to normal colon mucosa epithelial cells. Curcumin induced apoptosis through a p53-mediated mechanism, pro-apoptotic proteins Bax was upregulated, and cell cycle arrest at S phase by inhibited the expression of cell cycle related proteins, phosphorylation of Rb signaling pathway proteins and E2F family transcription factors. Finally, the mouse xenograft model confirmed the suppressive effect of curcumin on tumor growth in vivo . Conclusion: Curcumin may be a potential strategy for the treatment of colon cancer.(c) 2022 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ )

Objective To explore the clinical diagnostic value of LTA in lung canaer Methods Patients were divided into two groups: non-small cell lung cancer(n=72);bengin lung disease(n=68).The LTA levels in BLAF、pleural effusion f;luid and serum were detected by latex agglutination method.Results The NSCLC group:positive rate for LTA in BLAF、pleural effusion and serum were 58%、67%、75%.While 22%、17%、20% in the control group.The difference between the two groups is significant(P0.05).Positive rate of LTA in serum of the NSCLC group was the highest,75%.The peculiarty for LTA in pleural effusion at the NSCLC group was the highest,82%.Conclusion These results suggested that detection of LTA in BLAF、pleural effusion and serum is a valuable method for the diagnosis of lung cancer.