外泌体在胰腺癌中的研究现状与进展

外泌体是一种双层脂质膜连接囊泡样小体，存在于各种体液中，参与细胞及肿瘤微环境之间的物质运输和信号传递。外泌体含有多种生物活性分子，包括脂质、蛋白质、DNA、mRNA以及非编码RNA，可以通过这些活性分子影响肿瘤的发生和发展，甚至可以影响肿瘤的治疗。胰腺癌是一种常见的恶性肿瘤，侵袭性强，预后较差，死亡率高。胰腺癌来源的外泌体是胰腺肿瘤微环境中的重要组成部分，促使胰腺癌细胞成功逃避细胞凋亡的重要因素，并且可以促进肝脏转移微环境的形成。近年来，与胰腺癌相关的外泌体逐渐成为新的研究热点，研究发现外泌体有望成为早期胰腺癌筛查的新型生物学标志，并将为胰腺癌靶向治疗提供可行的技术基础。     

辽宁省3129名成人的健康自评情况—基于中国家庭追踪调查数据

目的了解辽宁省成人的健康自评情况,为当地医疗与保健提供参考。方法使用北京大学中国社会科学调查中心中国家庭动态跟踪调查2010年横断面调查数据,描述辽宁省成人的健康自评情况,秩和检验比较不同特征人群健康自评的差异。结果 3 129名成人中有42.59%的人自评为健康,42.37%的人认为一般,3.94%的人认为比较不健康,9.08%的人认为不健康,2.02%的认为非常不健康。不同性别、年龄、收入水平的健康自评及健康自评变化情况不同。结论辽宁省女性、高龄人群在疾病防控中应予以关注。     

光镜组织切片结合数字切片在显微形态学实验教学中的应用

组织学教学需要将理论与实验紧密结合起来，促进学生学习机体的微观形态及相关功能。通过对比总结传统光镜组织切片与新兴数字切片的优势与局限，在显微形态学实验中采用光镜组织切片与数字切片相结合的教学；将每次实验课程（3~4学时）划分成教学录像观看、光镜组织切片与数字切片相结合观察、课程内容讨论、随机随堂测验四部分。该教学增加了学生的学习兴趣与能动性，提升了教师的教学效率，提高了整体教学质量。     

Comparison of diathermic high-frequency capsulorhexis and continuous curvilinear capsulorrhexis in white cataract surgery

AIM: To compare the corneal endothelial cell counts pre- and post-operation, ultrastructure of anterior lens capsule and surgical completion after diathermic high-frequency capsulorhexis (DHC) and continuous curvilinear capsulorrhexis (CCC) applied in phacoemulsification (PHACO) of white cataract surgery. METHODS: Sixty-six eyes of 66 patients (33 males and 33 females) with cataract aged between 60 and 80y (mean 72.5±5.5) were recruited and undergone the surgery from June 2014 to November 2016. Anterior lens capsule, derived from two kinds of capsulorhexis, were randomly divided into two groups according to random number table. The ultrastructure of the capsule edge and its closer tissue were observed by transmission electron microscopy (TEM) and optical microscopy respectively. The surgical completion conditions and corneal endothelial cell counts were analyzed pre- and post-operation after two capsulorhexis. RESULTS: The capsule derived from CCC had smooth edge, well-organized cellular structure and the cells filling into the cutting edge under TEM and optical microscopy. The capsule derived from DHC had an approximate 60 banded area of cell degeneration and necrosis, with dentiform prominences at the edge of the capsule, and no cell structure was observed at this area. The corneal endothelial cell counts of both groups were slightly declined 1wk post-operation compared with that of pre-operation. There was no statistical difference between the two groups (t=1.63, P>0.05). CONCLUSION: DHC shows good clinical value in white mature and hypermature cataract surgery.     

Melatonin impedes Tet1‐dependent mGluR5 promoter demethylation to relieve pain

Melatonin (N‐acetyl‐5‐methoxytryptamine)/MT2 receptor‐dependent epigenetic modification represents a novel pathway in the treatment of neuropathic pain. Because spinal ten‐eleven translocation methylcytosine dioxygenase 1 (Tet1)‐dependent epigenetic demethylation has recently been linked to pain hypersensitivity, we hypothesized that melatonin/MT2‐dependent analgesia involves spinal Tet1‐dependent demethylation. Here, we showed that spinal Tet1 gene transfer by intrathecal delivery of Tet1‐encoding vectors to naïve rats produced profound and long‐lasting nociceptive hypersensitivity. In addition, enhanced Tet1 expression, Tet1‐metabotropic glutamate receptor subtype 5 (mGluR5) promoter coupling, demethylation at the mGluR5 promoter, and mGluR5 expression in dorsal horn neurons were observed. Rats subjected to spinal nerve ligation and intraplantar complete Freund's adjuvant injection displayed tactile allodynia and behavioral hyperalgesia associated with similar changes in the dorsal horn. Notably, intrathecal melatonin injection reversed the protein expression, protein‐promoter coupling, promoter demethylation, and pain hypersensitivity induced by Tet1 gene transfer, spinal nerve ligation, and intraplantar complete Freund's adjuvant injection. All the effects caused by melatonin were blocked by pretreatment with a MT2 receptor‐selective antagonist. In conclusion, melatonin relieves pain by impeding Tet1‐dependent demethylation of mGluR5 in dorsal horn neurons through the MT2 receptor. Our findings link melatonin/MT2 signaling to Tet1‐dependent epigenetic demethylation of nociceptive genes for the first time and suggest melatonin as a promising therapy for the treatment of pain.     

Melatonin attenuates postmyocardial infarction injury via increasing Tom70 expression

Mitochondrial dysfunction leads to reactive oxygen species (ROS) overload, exacerbating injury in myocardial infarction (MI). As a receptor for translocases in the outer mitochondrial membrane (Tom) complex, Tom70 has an unknown function in MI, including melatonin‐induced protection against MI injury. We delivered specific small interfering RNAs against Tom70 or lentivirus vectors carrying Tom70a sequences into the left ventricles of mice or to cultured neonatal murine ventricular myocytes (NMVMs). At 48 h post‐transfection, the left anterior descending coronary arteries of mice were permanently ligated, while the NMVMs underwent continuous hypoxia. At 24 h after ischemia/hypoxia, oxidative stress was assessed by dihydroethidium and lucigenin‐enhanced luminescence, mitochondrial damage by transmission electron microscopy and ATP content, and cell apoptosis by terminal deoxynucleotidyl transferase dUTP nick‐end labeling and caspase‐3 assay. At 4 weeks after ischemia, cardiac function and fibrosis were evaluated in mice by echocardiography and Masson's trichrome staining, respectively. Ischemic/hypoxic insult reduced Tom70 expression in cardiomyocytes. Tom70 downregulation aggravated post‐MI injury, with increased mitochondrial fragmentation and ROS overload. In contrast, Tom70 upregulation alleviated post‐MI injury, with improved mitochondrial integrity and decreased ROS production. PGC‐1α/Tom70 expression in ischemic myocardium was increased with melatonin alone, but not when combined with luzindole. Melatonin attenuated post‐MI injury in control but not in Tom70‐deficient mice. N‐acetylcysteine (NAC) reversed the adverse effects of Tom70 deficiency in mitochondria and cardiomyocytes, but at a much higher concentration than melatonin. Our findings showed that Tom70 is essential for melatonin‐induced protection against post‐MI injury, by breaking the cycle of mitochondrial impairment and ROS generation.