Abstract The causal link between the aging microenvironment and T cell aging remains elusive. Here, we demonstrate that adenosine within aging tissues actively reprograms CD8+ T cells into a pro-aging Granzyme K + (Gzmk+) population. Mechanistically, senescent cells create an adenosine-rich niche via p16-dependent CD39 upregulation, triggering A2aR signaling to induce Gzmk + T cell differentiation. Once released, Gzmk promotes systemic inflammaging through PAR1 and complement activation. Crucially, targeting this axis—either via genetic Gzmk ablation or pharmacological A2aR blockade—reverses multi-organ aging phenotypes and significantly extends healthy lifespan in mice. Human analysis reveals age-dependent Gzmk + T cell accumulation in multi organs, while coffee intake (an A2aR antagonist) inversely correlates with plasma Gzmk levels. Our findings uncover how metabolic niche changes drive T cell aging and establish the adenosine-Gzmk axis as a pivotal therapeutic target for combating age-related diseases.

The brain has long been considered an immune-privileged organ due to the presence of the blood-brain barrier (BBB). However, recent discoveries have revealed the underestimated role of T cells in the brain through the meningeal lymphatic system. Age is the primary risk factor for Alzheimer’s disease (AD), resulting in marked age-dependent changes in T cells. Manipulating peripheral T cell immune response has been shown to impact AD, but the relationship between T cell aging and AD remains poorly understood. Given the limited success of targeting amyloid beta (Aβ) and the growing evidence of T cells’ involvement in non-lymphoid organ aging, a deeper understanding of the relationship between T cells and AD in the context of aging is crucial for advancing therapeutic progress. In this review, we comprehensively examine existing studies on T cells and AD and offer an integrated perspective on their interconnections in the context of aging. This understanding can inform the development of new interventions to prevent or treat AD.

Silica is a very common and important chemical raw material with a wide range of uses. Long-term inhalation of silica particles could cause lung toxicity, of which the most important representative is silicosis. Silicosis is a serious and fatal occupational pulmonary disease, characterized by persistent pulmonary inflammation and fibrosis. Despite intensive research, the toxic mechanism of silicosis caused by silica particles is not completely clear, which deserves further research and exploration. Many studies have indicated that the epithelial cells partially participate in the formation, accumulation, and activation of fibroblasts through epithelial-mesenchymal transition (EMT), which is conducive to the occurrence of fibrosis. Galectin-3 (Gal-3), widely expressed in epithelial cells, was observed to induce EMT in fibrotic diseases and tumors by regulating the GSK-3β and β-catenin. Previous studies have demonstrated that silica particles is indeed involved in the silicosis process by inducing EMT. However, it remains to be further studied whether there is a certain relationship between silica particles and Gal-3 expression, and whether Gal-3 also mediates the development of the silica particles-induced silicosis by regulating GSK-3β/β-catenin signal pathway-mediated EMT. Our research results showed that silica particles could significantly induce Gal-3 expression to promote the development of EMT through activating the GSK-3β/β-catenin signal pathway in mice and in A549 cells, which then significantly exacerbated the pulmonary fibrosis caused by silica particles. And the inhibition of Gal-3 could effectively inhibit the occurrence of EMT, and then effectively alleviate silicosis caused by silica particles. These findings would help us to further clarify the toxicological mechanisms of silicosis caused by silica particles and provide a novel target for prevention and intervention of silicosis.

本科生导师制是高校管理制度的创新,是课堂教学外教书育人的重要载体.本文结合作者十年来做为本科生导师的实践工作,认为在指导方式上要注重人文关怀,强化民主精神.指导内容多样化,包括思想、生活、学习、创新思维和创新能力等方面.本科生导师还要通过参加培训和经验交流提升自己的带教能力.

社会和经济的高速发展赋予了营养与食品卫生学新的内涵,同时也对新时期医学人才的培养提出了更高的要求.微课教学模式具有短小精悍、情景性强、易于被学生接受等特点.将微课与营养与食品卫生学教学有机结合有助于提高教学效率和教学质量,提高学生的学习积极性.

当前是凸显创新型人才的时代,培养医学本科生的创新能力已成为高等医学教育的重要工作.科研训练是快速提高医学本科生创新能力的有效途径之一.本文就医学院校本科生科研训练浅谈下自己的体会.

目前肉及肉制品与癌症的相关性已成为人们关注的热点.已有的研究显示,肉类食品在加工生产过程中会产生包括N-亚硝基化合物、多环芳烃类和杂环胺类在内的大量有害物质,过量食用会提高人体的氧化应激水平,产生炎症反应,引起基因的异常表达,最终导致多种癌症的发生.

小儿营养性缺铁性贫血(iron deficiency anemia,IDA)又称营养不良缺铁性贫血,好发于6个月～3岁的婴幼儿,是常见的儿童疾病之一[1].根据世界卫生组织(WHO)的调查,亚洲地区儿童IDA的发病率高于50％,IDA不仅使机体多器官、系统的功能下降,还会影响认知和行为发育[2-3].为了解马鞍山市市区0～3岁婴幼儿IDA患病状况及其相关影响因素,2017年2～3月对市区220名婴幼儿进行了调查,现将结果报道如下.

CBL是一种以案例为先导,在教师的引导下,学生探索问题、发现问题和解决问题的教学方法.目前在国内外院校中广为推崇,许多学科开展了CBL教学,包括营养与食品卫生学.案例是CBL教学效果的关键所在,学生正是在教师的引导下,对案例所提供的信息进行讨论,从而发现问题、解决问题,既掌握了知识,也提高了自主学习的意识和能力.笔者就营养与食品卫生学CBL案例编写过程中的心得体会进行了总结.

PBL教学法是一种以学生为主体的新型教学方法,近年来受到教育工作者的广泛关注.PBL教学法利用复杂而有意义的问题情境,学习者通过小组合作的形式共同解决各种问题,学习问题中隐含的科学知识,促进问题的解决,加强自主学习和终身学习能力.笔者经过3年的教学实践,体会到PBL具有提高学生的自主学习能动性、增强学生的交流和组织能力、提高学生的查找文献资料的能力、激发学生向小组中其他同学学习、引发对社会人文问题的关注和思考等优点.

目的：探讨在我校开设营养学课程的必要性。方法：对我校本科生进行问卷调查，内容包括营养学知识、对开设营养相关课程的态度、对营养知识的兴趣和知识来源。结果：83.3%的学生认为有必要开设营养学相关课程；约50%的同学通过网络、报刊书籍和电视了解营养学知识；60%~70%的学生认为营养学相关课程对其日后在医疗工作中指导病人，并对自身、家人或朋友的饮食行为有帮助。结论：为提高医学生营养知识及满足日后临床工作需要，有必要开设营养相关课程。

为探讨营养学相关选修课程对我校医学生营养知识、态度及饮食行为的影响，本文对选修过营养学相关课程和未选修过的两组医学生进行知—信—行（KAP）调查。结果显示，已选修营养学相关课程组的医学生对含胆固醇高的食物、含钙丰富的食物、维生素A与晚上长时间看不见物体有关的知晓率显著高于未修课程组，部分营养态度、饮食行为的正向率均高于未修课程组，差别有统计学意义。由此得出结论，开设营养学选修课对医学生营养知识、态度、行为产生有利影响，有必要在学校开设营养学相关选修课程。

目的 :探讨双酚A（bisphenol A,BPA）对人前列腺癌PC-3细胞增殖和mi R-19表达的影响。方法 :不同浓度BPA处理人前列腺癌PC-3细胞,以雌二醇（E2）作为阳性对照,6 d后采用四甲基偶氮唑盐（MTT）法和Hoechst 33258荧光染色法测定BPA对PC-3细胞增殖的影响,real-time PCR检测mi R-19a和mi R-9b表达水平的变化,Western blot检测细胞中mi R-19的靶基因PTEN及细胞增殖相关基因p-AKT、AKT、PCNA和Cyclin D1的蛋白表达变化。结果:5×10-6~5×10-5 mol/L BPA显著促进PC-3细胞增殖,增加PC-3细胞中mi R 19a和mi R 19b的表达水平,降低PTEN表达并上调p-AKT、PCNA和Cyclin D1表达水平。结论:BPA可促进前列腺癌PC-3细胞增殖,其机制可能与BPA引起mi R-19表达上调有关。

目的探讨全反式维甲酸（ATRA）对卵巢癌肿瘤标志物DNA拓扑异构酶Ⅱα（TopoⅡα）的下调作用及卵巢癌组织TopoⅡα含量与血清ATRA含量的关系。方法以0-10μmol/L的不同浓度ATRA处理人卵巢癌细胞A2780及SKOV3;24h后,用Western blot和免疫组化法检测卵巢癌组织中TopoⅡα的表达,高效液相色谱法测定23例卵巢癌患者血清ATRA含量。结果人卵巢癌细胞A2780及SKOV3中ATRA下调TopoⅡα的蛋白表达;卵巢癌组织TopoⅡα含量与血清ATRA含量具有负相关的关系（r=-0.63,P＜0.05）。结论 ATRA能下调人卵巢癌细胞A2780及SKOV3中TopoⅡα蛋白的表达,卵巢癌的发生可能与血清ATRA含量下降有关。

目的：探讨丙烯酰胺（AA）对人SH-SY5Y神经细胞凋亡和miR-21表达的影响。方法：不同浓度丙烯酰胺作用于人神经母细胞瘤SH-SY5Y细胞24 h后,采用四甲基偶氮唑盐（MTT）法测定丙烯酰胺对SH-SY5Y细胞活力的影响,Hoechst 33258荧光染色法检测细胞凋亡,real-time PCR检测miR-21表达水平,Western blot检测PTEN、p-AKT、AKT、Bcl-2、Bax、caspase 9和caspase 3蛋白表达。结果：丙烯酰胺剂量依赖性地降低SH-SY5Y细胞活性,Hoechst 33258染色显示明显细胞凋亡形态变化;丙烯酰胺显著降低SH-SY5Y细胞miR-21的表达,同时升高PTEN、Bax、caspase 9、caspase 3水平并降低p-AKT和Bcl-2表达。结论：丙烯酰胺可通过线粒体途径诱导SH-SY5Y神经细胞凋亡,其机制可能与丙烯酰胺引起miR-21表达下调有关。

Objective: To explore the effect and the related mechanisms of fucoidan on hepatoma cell proliferation.Methods: Proliferation inhibition rate of hepatoma HepG2 cells was measured by MTT.A variety of dosage of fucoidan(0 μg/ml,10 μg/ml,100 μg/ml and 500 μg/ml) was treated to HepG2 cells.The morphology changes of the cells were observed under microscopy.Apoptosis was detected by Hoechst 33258 staining and DNA Ladder analysis.CyclinD1 and topoisomerase IIα(TopoIIα) were as the proliferation biomarker.Their protein expression levels were examined by Western blot.Results: Fucoidan inhibited HepG2 cells proliferation in a dose-dependent manner.There was a remarkable morphological change when cells were treated with 500 μg/ml of fucoidan.Apoptosis was occurred when the cells were incubated with 100 μg/ml and 500 μg/ml of fucoidan.In addition,fucoidan also suppressed the expression of cyclinD1 and TopoIIα in HepG2 cells.Conclusion: Fucoidan can inhibit the proliferation of HepG2 cells and induce apoptosis.Meanwhile,fucoidan also has the ability to suppress the protein expression of cyclinD1 and topoIIα,which may be involved in the mechanisms of inhibiting hepatoma cells proliferation.

Interferon-stimulated gene 15(ISG15) encodes a protein named ISG15,which is the first identified ubiquitin-like protein.The expression of ISG15 is induced not only by type I IFN and viral infection,but also by some anticancer drugs.Recently,it was found that ISG15 and its modification system were also involved in tumor suppression or tumorigenesis.Enzyme such as ubiquitin-activating enzyme E1-like(UBE1L) appears tumor-suppressive,while other enzymes such as de-ISGylation enzyme,UBP43 promotes tumorigenesis.Overexpression of ISG15 has been observed in metastasis of some malignant tumors.Alteration of ISG15 expression can affect the chemosensitivity of some chemotherapy drugs.We reviewed the biological effect of ISG15 in tumor-related target,which will provide fundamental knowledge of ISG15 in cancer research and may provide new insight for tumor therapy.