OBJECTIVE:While M2 macrophage-mediated immunoregulation is critical for bone regeneration, the role of migrasomes-a newly identified organelle-remains unexplored. This study aims to investigate the effect of M2 macrophage-derived migrasomes on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). METHODS:Macrophages were polarized to the M2 phenotype using IL-4. Migrasomes were subsequently isolated and characterized by electron microscopy and Western blotting (WB).In vivo, murine femoral fracture models treated with 100 μg/mL M2 macrophage-derived migrasomes were analyzed for fracture healing via X-ray, microcomputed tomography (microCT), and immunofluorescence.In vitro, bone marrow mesenchymal stem cells (BMSCs) were co-cultured with 60 ng/mL migrasomes. Cell migration was assessed by wound healing assay at 24 h; expression of RUNX2, ALP, OCN, and Bmp-2 was detected via quantitative real-time polymerase chain reaction (qRT-PCR) and WB at 72 h; osteogenic activity was evaluated by ALP and alizarin red S (ARS) staining at 14 and 21 days, respectively. RESULTS:Increased Arg-1 and CD206 expression confirmed successful induction of M2 macrophages (P < 0.01, P < 0.0001). Transmission electron microscopy and Western blotting (WB) verified successful isolation and purification of M2 macrophage-derived migrasomes. X-ray and microcomputed tomography analyses demonstrated that migrasomes treatment significantly enhanced fracture healing. qRT-PCR showed migrasomes effectively upregulated mRNA levels of BMP-2, RUNX2, ALP, and OCN in BMSCs (P < 0.05, P < 0.01); WB revealed elevated protein levels of osteogenic markers (BMP-2, RUNX2, ALP) in the M2 migrasomes-treated group (P < 0.05). CONCLUSION:M2 macrophage-derived migrasomes promote fracture healing by inducing osteogenic differentiation of BMSCs.

ATP-dependent chromatin remodeling complexes regulate gene expression by altering chromatin structure through ATP hydrolysis. They are classified into four families-SWI/SNF, ISWI, CHD, and INO80-which remodel chromatin via nucleosome sliding, eviction, assembly, and editing to control transcription. These complexes play critical roles in DNA repair, tumorigenesis, and organogenesis. Recent advances in low-input proteomics have highlighted their importance in vertebrate embryonic development. In mammals, they regulate embryonic genome activation, lineage specification, and stem cell fate determination. In non-mammalian models (e.g., Xenopus laevis), they function from blastocyst formation to pre-organogenesis stages (gastrulation and neurulation)-key windows for chromatin reprogramming and cell fate decisions. This review provides a systematic overview of chromatin remodeling complexes, detailing their classification and conserved mechanisms, and discusses their functions in early embryogenesis and embryonic stem cell maintenance. The collective evidence underscores the implications of these chromatin remodelers for understanding developmental defects and advancing regenerative medicine.

Crosstalk between inflammatory macrophages and bone marrow mesenchymal stem cells (BMSCs) is crucial for fracture healing. Exosomes derived from inflammatory macrophages via the paracrine pathway have shown promise in cell-free therapies for bone healing. While inflammatory and mechanical microenvironments are known to regulate BMSC osteogenesis, the precise mechanism remains unclear, particularly the immunological influence of inflammatory macrophages on BMSC osteogenesis under mechanical stress. This study aims to explore the regulatory mechanism of miR-423-5p in M2 macrophage exosomes on the osteogenic differentiation of bone marrow mesenchymal stem cells under a mechanical microenvironment, providing a theoretical basis for cell-free fracture repair therapy. We extracted exosomes from M2-type macrophages cultured under shear stress using polymer precipitation and identified them using immunoblotting and transmission electron microscopy. Co-culturing these exosomes with BMSCs conjointly upregulates the expression of osteogenic proteins runt-related transcription factor 2(RUNX2), bone morphogenetic protein 2(BMP-2), and alkaline phosphatase (ALP), suggesting BMSCs' osteoblastic differentiation. miRNA sequencing revealed the downregulation of miR-423-5p in the secretions of M2 macrophages under shear stress, providing insights into the immunological regulation of bone formation. Cell transfection showed that miR-423-5p regulates osteogenesis in bone marrow mesenchymal stem cells. In conclusion, the present study demonstrated the mechanism of action of macrophages in fracture healing under a mechanical microenvironment. The present findings provide new insights into the study of fracture immunotherapy, with exosomes as targets.

Bladder cancer (BC) is one of the most prevalent genitourinary cancers. Despite the growing research interest in BC, the molecular mechanisms underlying its carcinogenesis remain poorly understood. The microarray datasets GSE38264 and GSE61615 obtained from the Gene Expression Omnibus (GEO) database were analyzed and differentially expressed genes (DEGs) were identified, which were then verified using a dataset from The Cancer Genome Atlas (TCGA). By taking the intersection of the two microarray datasets, the common DEGs were identified and these were selected as candidate genes associated with BC. The DEGs were further subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis, and the protein-protein interaction network was constructed. Further module analysis was performed using STRING and Cytoscape. A total of 362 DEGs were identified, including 13 hub genes, and the GO analysis revealed that these genes were mainly enriched in extracellular matrix organization, positive regulation of cell proliferation, angiogenesis and peptidyl-tyrosine phosphorylation. The expression changes of PTPRC, PDGFRA, CASQ2, TGFBI, KLRD1 and MT1X in the different datasets indicated that these genes were involved in the development of BC. Next, the differential expression of these genes was verified in the TCGA dataset, and ultimately, these 13 genes were determined to be related to the occurrence and development of BC. Finally, the cancer tissues and adjacent tissues of patients with BC were collected and subjected to reverse transcription-quantitative PCR, the results of which were consistent with the bioinformatics prediction. The present findings provide several vital genes for the clinical diagnosis and treatment of BC.

The objective of this study was to investigate the mechanism of prenatal stress on the cognitive function of offspring, and clarify the change of histone deacetylase 2 (HDAC2) expression in hippocampal neurons of offspring. 16 pregnant SD rats were randomly divided into control group and stress group, with eight rats in each group. The stress group received restrained stress from 15 to 21 days of pregnancy, while the control group did not receive any treatment. Anxiety-like behavior and spatial memory,learning and memory ability were detected in open field, elevated plus maze, novel object recognition test, and Barnes maze. Nissl staining was used to detect the function of hippocampal neurons. Western blot was used to detect the expression of HDAC2 protein in hippocampal neurons of adult offspring. Immunofluorescence staining was used to detect the expression of HDAC2 protein and hippocampal neurogenesis. The learning and memory ability of adult offspring was decreased.The prenatal stress damaged the function of hippocampal neurons , the expression of HDAC2 was down-regulated, and the number of neurons was reduced. Maternal prenatal stress can down -regulate the expression of HDAC2 in the hippocampus of offspring, inhibits hippocampal neurogenesis and impairs the cognitive function.

背景 氟可诱导破骨细胞分泌多种酶,使其吸收骨质的功能增强或减弱,从而溶骨或成骨,破骨细胞活化后骨吸收过程又与自噬密切相关.目的 探究氟通过AKT/mTOR/ULK1信号通路对破骨细胞自噬的影响.方法 采用RAW264.7细胞诱导形成的破骨细胞进行实验,分为对照组、NaF组、CQ组、CQ+NaF组、RAP组、RAP+NaF组,分别对相应组进行10 mg/L NaF、5 mmol/L CQ和5 mmol/L RAP给药,24 h后进行激光共聚焦显微镜检测,对破骨细胞自噬小体进行定量;荧光定量PCR检测Cathepsin K和TRAP的基因转录表达;Western blotting检测AKT/mTOR/ULKl磷酸化蛋白p-AKT、p-mTOR、p-ULK1水平,探究自噬在染氟破骨细胞的作用.结果 激光共聚焦显微镜结果显示10mg/L氟化钠溶液能够促进自噬小体的产生,自噬小体的数量明显增多,氟化钠协同RAP激动自噬.荧光定量PCR结果显示氟化钠使Cathepsin K基因和TRAP基因的表达降低,并且氟化钠与CQ对两种基因的表达降低有协同作用,氟化钠拮抗RAP,激发自噬,抑制Cathepsin K和TRAP基因上调.Western blotting显示氟化钠能够使p-AKT和p-mTOR蛋白表达量上调,并且能协同RAP使p-AKT、p-mTOR和p-ULK1表达量增高.结论 10 mg/L氟化钠溶液促进破骨细胞自噬,抑制其骨吸收能力从而成骨,可能与AKT/mTOR/ULK1信号通路有关.

目的 了解新时代大健康背景下新疆地区乡村医师学生职业认同感现状及其与心理弹性的相关性,为其心理建设与职业认同的培养提供理论依据.方法 采用横断面调查法,于2020年11月选取新疆医科大学2018—2020级乡村医师专业学生为研究对象,共880人进行基本资料、心理弹性量表和职业认同量表的问卷调查.结果 ①乡村医师专业学生心理弹性存在性别差异,男生得分均高于女生(P<0.05);坚韧性、力量性和乐观性维度中,参加大学社团活动或担任学生会职务的学生得分高于未参加或未担任者、担任过学生干部经历的学生得分高于未担任者,差异均具有统计学意义(P<0.05).②乡村医师专业学生职业认同中,职业认知维度由2020级到2019级、2018级得分呈上升趋势(P<0.05);职业情感、职业期望和职业价值观维度由2020级到2019级、2018级得分呈下降趋势(P<0.05);职业行为和职业承诺维度中,2019级得分最高,2018级得分呈回落趋势(P<0.05).③多因素Logistic回归分析结果显示,坚韧性人格品质(OR=1.04,95％CI=1.02～1.31)、学生生涯班干部经历(OR=1.01,95％CI=0.98～6.04)是乡村医师学生职业认同感的独立正向影响因素(P<0.05).结论 学生生涯班干部经历及坚韧性人格品质的乡村医师学生在职业认同感与其心理弹性中表现出独立影响的正向因素特点,医学院校应采用针对个性化的教育和引导,更好地培养基层医疗卫生人才.

目的 观察不同剂量的氟（F - ）对成骨细胞MG-63的毒性效应，及在毒性作用过程中对DNA甲基化效应及相关基因的影响。方法 0.0、2.5、5、10和20 mg/L的F - 干预成骨细胞（MG-63）24、48、72和96 h后噻唑蓝比色法（MTT）检测细胞的增殖活力，Illumina甲基化850k芯片检测细胞的甲基化程度；实时荧光定量PCR（RT-PCR）、Western blotting检测染氟成骨细胞DNMT1、DNMT2、DNMT3a、Runx2和Osterix基因表达情况。结果 ≥72 h时，5 mg/L的F - 对成骨细胞MG-63增殖活力有明显的促进作用（P＜0.05）;≥72 h时，20 mg/L的F - 对成骨细胞MG-63增殖活力有明显的抑制作用（P＜0.05）;72 h时5 mg/L的F - 作用后DNA甲基化程度较0 mg/L组明显的降低（P＜0.05）;≥20 mg/L的F - 作用后DNA甲基化程度较0 mg/L组明显的升高(（P＜0.05）。5 mg/L的F - 干预成骨细胞MG-63后甲基化转移酶DNMT1、DNMT2、DNMT3a的mRNA和蛋白的表达量较0 mg/L组相比明显降低（P＜0.05）;成骨细胞特异性转录因子Runx2、Osterix的mRNA和蛋白的表达量较0 mg/L组相比明显增加（P＜0.05）;20 mg/L的F - 干预成骨细胞MG-63后甲基化转移酶DNMT1、DNMT2、DNMT3a的mRNA、蛋白表达量较0 mg/L组相比明显增加（P＜0.05）,成骨细胞特异性转录因子Runx2、Osterix的mRNA和蛋白的表达量较0 mg/L组相比明显降低（P＜0.05）。结论 低剂量的F - 对成骨MG-63的增殖具有促进作用，抑制了甲基化转移酶DNMT1、DNMT2、DNMT3a的mRNA和蛋白的表达量，降低了成骨细胞MG-63DNA甲基化程度，在一定程度上促进了成骨细胞特异性转录因子Runx2、Osterix的mRNA和蛋白的表达。高剂量的F - 对成骨MG-63的增殖起到抑制作用，但促进了甲基化转移酶DNMT1、DNMT2、DNMT3a的mRNA和蛋白的表达量，增加了成骨细胞MG-63DNA甲基化程度，在一定程度上抑制了成骨细胞特异性转录因子Runx2、Osterix的mRNA和蛋白的表达。

背景 研究表明睾丸间质细胞的凋亡是造成男性不育的重要因素之一,而菟丝子总黄酮(total flavonoids from semen cuscutae,TFSC)具有抗凋亡、抗炎等药理活性,并在治疗男性不育方面有一定疗效.目的 观察菟丝子总黄酮对小鼠睾丸间质细胞(TM3细胞)凋亡的影响并探究其可能作用机制.方法 体外培养TM3细胞,将其分为对照组(不含药物的完全培养基)、模型组[35 μmol/L丙烯醛(acrolein,ACR)]、TFSC低剂量组(100 μg/mL)、TFSC中剂量组(200 μg/mL)、TFSC高剂量组(400 μg/mL).采用CCK-8法筛选ACR的半数致死量和TFSC的作用剂量.采用流式细胞仪检测细胞凋亡情况、Western blotting检测凋亡相关蛋白Bcl-2、Bax、Caspase-3的表达情况.结果 TFSC浓度为100、200、400、600 μg/mL时明显促进TM3细胞增殖(P＜0.05);ACR浓度为33.97 μmol/L时,达到细胞半数致死量.与模型组比较,TFSC中、高剂量组可提高细胞存活率(P＜0.05).流式结果显示,与模型组相比,TFSC中、高剂量组细胞凋亡明显减少.Western blotting结果显示,与模型组比较,TFSC低、中、高剂量组Bcl-2蛋白表达明显升高(P＜0.05),TFSC中、高剂量组Bax、Caspase-3蛋白表达明显降低(P＜0.05).结论 TFSC能够促进TM3细胞的增殖,抑制TM3细胞的凋亡,其机制可能是通过降低凋亡蛋白Bax、Caspase-3的表达以及升高抗凋亡的蛋白Bcl-2的表达来改善抗凋亡与促凋亡蛋白之间的失衡.

Studies demonstrate that long non-coding RNAs (lncRNAs) play vital roles in cancer progression. However, the expression pattern and molecular mechanisms of lncRNA FAM83A-AS1 in lung cancer remain largely unclear. Here, we analyzed FAM83A-AS1 expression in lung cancer tissues from three RNA-sequencing (RNA-Seq) datasets and validated these results using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) in an independent set of lung adenocarcinoma. Cell proliferation, migration, invasion, and autophagy were analyzed after knockdown FAM83A-AS1 with siRNAs. The underlying molecular mechanisms of FAM83A-AS1 were performed by Western blot, qRT-PCR, and RNA-seq analysis. We found that FAM83A-AS1 was up-regulated in lung cancer and elevated expression was associated with poor patient survival. These results were confirmed using RT-PCR in an independent set of lung cancer. Functional study indicated that FAM83A-AS1 knockdown reduced cell proliferation, migration, invasion, and colony formation in cancer cells. FAM83A-AS1 silencing induced autophagy and cell cycle arrest at G2. Mechanistically, serval oncogenic proteins such as EGFR, MET, PI3K, and K-RAS were decreased upon FAM83A-AS1 silencing, while phosphor AMPKα and ULK1 were increased. Based on the above results, we believe that FAM83A-AS1 may have potential as a diagnosis/prognosis marker and its oncogenic role and autophagy regulation may be through MET-AMPKα signaling, which could lead to potential targeting for lung cancer therapy.

2020年《国务院办公厅关于加快医学教育创新发展的指导意见》(国办发[2020]34号)指出以"新医科"为抓手,分类培养研究型、复合型和应用型人才,以新的内涵强化医学培养,加强知识扎实的学术、本领过硬的技术、方法科学的艺术教育[1].医学生的培养注重知识更新、交叉融合,也要注重适应变化能力和创新能力的塑造.

为适应新科技革命和产业变革,教育部提出了以医学人文教育为主题之一的生命健康全周期理念——"新医科".《国务院办公厅关于加快医学教育创新发展的指导意见》提出以新内涵强化医学生培养.如何将人文教育与专业教育相结合,贯穿医学生教育教学全过程,已成为亟待解决的问题.组织学与胚胎学为医学生初次接触到的医学专业基础课程,该课程研究人体微细结构相关功能及发育,更蕴含着生命教育、职业素养、沟通协作、创新探索等丰富的人文精神.当前缺少针对各个章节精准融合人文素养的研究,多为对策性研究[1-5],部分研究仅将人文内容流于表面,缺乏横向联系且内容生硬.本研究旨在扩充组织学与胚胎学教学融入人文的精度、深度和广度,成为加强医学生人文素质培养最有效的手段,致力于培养切合新时代要求的医学人才.

Histology and embryology is a science that studies the micro structure and function of the body and embryogenesis, and has insight into the microcosmic world of human body. It is delicate and ingeniousness, which greatly satisfy our thirst for knowledge and visual appreciation. This paper expounds the beauty of Science in histology and Embryology from the perspectives of aesthetics on cell morphology, tissue mode, organogenesis and life birth. Aesthetic education in histology and embryology can possible cultivate medical students' humanistic quality and aesthetic thinking, So that they are able to have an access to the essence of life.

基础医学学科拔尖人才的培养不仅是现代医学进步的基石,也是实施"健康中国"战略的迫切需求.根据专业培养目标及学业职业规划需求,新疆医科大学通过本科全程导师制分阶段培养学生的创新能力,不断推进课程建设,构建立体式教学科研平台,并以项目为依托,将科研创新能力整合到本科教育全过程,对基础医学拔尖人才培养进行了探索与实践,取得了良好的效果,以期为基础医学高层次拔尖人才培养提供实践参考.

目的 探究不同浓度骨髓间充质干细胞外泌体对巨噬细胞向M1型极化的影响.方法 提取骨髓间充质干细胞外泌体,电子显微镜观察外泌体形态,并通过Western blot检测骨髓间充质干细胞外泌体特异性蛋白TSG101、CD63、Alix表达水平;将不同浓度骨髓间充质干细胞外泌体与巨噬细胞共培养,RT-qPCR检测巨噬细胞极化相关基因IL-6、iNOS、Arg-1、CD206等的表达.结果 电镜检测显示,外泌体为杯口状结构;Western blot检测显示骨髓间充质干细胞外泌体表达特异性蛋白TSG101、CD63、Alix;外泌体内吞实验表明,在60μg/ml外泌体时,巨噬细胞对外泌体的内吞效率最高.RT-qPCR分析显示,60μg/ml外泌体处理使M1型巨噬细胞相关基因IL-6和iNOS表达升高最明显.结论 骨髓间充质干细胞的外泌体可以诱导巨噬细胞向M1型巨噬细胞极化.

Muscina pascuorum (Diptera: Muscidae) represents an important hygiene pest. The complete mitochondrial genome (mitogenome) of M. pascuorum was first sequenced and annotated in this study. The full length of mitogenome was 14, 940 bp, consisting of 13 protein-coding genes (PCGs), two ribosomal RNA (rRNA), 22 transfer RNA (tRNA), and one AT-rich region. The nucleotide content of these flies was 40.0% A, 13.2% C, 9.1% G, and 37.6% T. This study illustrates that the arrangement of the genes was identical to classical metazoans. Besides, the phylogenetic analyses indicated that the branch of M. pascuorum was clustered separately from the common three Muscina spp in the tree. This genome provides an essential reference for understanding the phylogenetic relationships of Muscidae.

专业型社团以专业知识为背景,通过各类社团活动,强化实践教学环节、增强学生技能,是第一课堂的有效延伸.组织学与胚胎学是作为医学生最初接触到的医学基础专业课程,教学过程中可与专业社团进行优质整合和优势互补,给学生提供更多的实践探究机会的同时,培养学生临床思维,发展终生学习的能力.

Background Studies demonstrate that long non-coding RNAs (lncRNAs) play critical roles in the occurrence and development of cancer. However, many of the molecular mechanisms underlying lncRNAs role in this process remains unclear. Methods Here, we analyzed lncRNA expression in lung cancer tissues based on RNA-Seq analysis and found that lncRNA FAM83A-AS1 was one of the top up-regulated lncRNAs in lung adenocarcinoma and elevated expression of FAM83A-AS1 was significantly associated with poor patient survival. We validated these results using RT-PCR and an independent cohort of lung cancer. Results Functional studies indicated that knockdown of FAM83A-AS1 decreased cell proliferation, colony formation, migration and invasion in H1299 and H838 lung cancer cells. Knockdown of FAM83A-AS1 induced the autophagy and cell cycle arrest at G2. Mechanistically, we found that MET, p62 and phosphor S6K proteins were decreased upon FAM83A-AS1 knockdown. Conclusion In conclusion, FAM83A-AS1 may have potential as a diagnosis/prognosis marker and its oncogenic role could lead to potential targeting for lung cancer therapy.