细胞力学在压力性损伤中的作用及影响因素研究进展

随着压力性损伤的研究重心逐渐向细胞水平转移，发现力学因素下细胞结构和功能改变在压力性损伤发展过程中起重要作用。综述力学因素下压力性损伤发生机制、影响因素、评估以及预防管理。旨在提高护理人员对压力性损伤更为深入地认知，从而推动压力性损伤研究多元化发展。     

舌象仪临床应用研究的方法学及报告质量评价

目的 评价舌象仪临床应用研究的随机对照试验（RCT）、病例系列研究的方法学及报告质量。方法 检索PubMed、中国期刊全文数据库（CNKI）、维普数据库（VIP）和万方数据库（Wanfang database），从建库截至2018年12月开始检索，收集应用舌象仪观察临床疾病的RCT、病例系列研究和病例对照研究，分别参考Cochrane手册5.1.0版的偏倚风险评估工具和CONSORT 2010版的声明，对纳入的RCT研究进行方法学和报告质量进行评价；根据NICE和STROBE声明第四版进行方法学的报告质量评价研究。结果 初检出相关文献567篇，最终纳入59篇文献，包括2个RCT，57个病例系列研究。50%的RCT应用Cochrane偏倚风险工具评价后显示采用的随机分配方法比较合理，没有采用分配隐藏和盲法；均采用了意向性分析，遗憾的是并没有报告失访的情况；研究也缺乏选择性报告。NICE病例系列研究质量评价结果 病例系列研究中仅14.04%符合多中心研究；59.64%的研究纳入排除标准均不明确；数据未达到预期设定目标，未进行分层分析结局。CONSORT声明2010版评价结果显示：纳入的文献均不能从题目辨别出是否是随机临床试验，多项条目报告率为0；应用STROBE声明评价后结果显示：纳入的病例系列研究均未在题目中明确标明是病例系列研究，多项条目报告率为0。结论 舌象仪临床应用的RCT和病例系列研究报告质量不高，建议在设计和报告临床病例对照和随机对照试验时分别参考CONSORT声明、STROBE声明，纠正目前研究存在的方法学问题，进一步提高临床研究质量，增强舌象仪临床应用于疾病效用证据的强度，推进中医的客观化和现代化。     

miR-30c Impedes Glioblastoma Cell Proliferation and Migration by Targeting SOX9

miR-30c has been acknowledged as a tumor suppressor in various human cancers, such as ovarian cancer, gastric cancer, and prostate cancer. However, the role of miR-30c in glioblastoma (GBM) needs to be investigated. In our study, we found that the expression of miR-30c was significantly downregulated in GBM tissues and cell lines. We found that overexpression of miR-30c inhibited cellular proliferation of GBM cells in vitro and in vivo. More GBM cells were arrested in the G₀ phase after miR-30c overexpression. Moreover, we showed that miR-30c overexpression suppressed the migration and invasion of GBM cells. Mechanistically, we found that SOX9 was a direct target of miR-30c in GBM cells. Overexpression of miR-30c inhibited the mRNA and protein levels of SOX9 in GBM cells. Moreover, there was a negative correlation between the expression of miR-30c and SOX9 in GBM tissues. Finally, we showed that restoration of SOX9 in GBM cells reversed the proliferation, migration, and invasion of GBM cells transfected with miR-30c mimic. Collectively, our results demonstrated that miR-30c suppressed the proliferation, migration, and invasion of GBM cells via targeting SOX9.     

鲁迅与解剖学研究述略

鲁迅在《我怎么做起小说来》一文中写道,"但我的来做小说,也并非自以为有做小说的才能……大约所仰仗的全在先前看过的百来篇外国作品和一点医学上的知识,此外的准备,一点也没有"[1].可见,鲁迅青年时期接受的医学教育,与之精神与艺术有着深刻的渊源.而鲁迅所说的"医学上的知识"中,对其影响最大的莫过于 "解剖学的知识".在鲁迅的各类著作、书信与日记中,提及"解剖"者,凡34篇、67次,"解剖学"这一课程名称出现的频次也远高于其所学的生理学、组织学等其他课程[2].故"鲁迅与解剖学"这一研究场域,值得学者们深入的研究和探讨.     

两例父源性17q12微缺失综合征胎儿的产前诊断和遗传学分析

目的探讨两例父源性17q12微缺失综合征胎儿的产前诊断和遗传咨询。方法一名孕妇的两例胎儿的孕中晚期超声检查均提示肾脏异常和羊水过多,应用单核苷酸多态性分析(single nucleotide polymorphism array,SNP-array)分别对第1胎的脐血样本和第2胎的羊水样本进行产前诊断。发现第1胎染色体17q12微缺失后,父母进行外周血SNP-array检测以确定遗传来源。结合双亲临床病史,其父亲进行泌尿系统相关的565个基因的高通量测序,以排除泌尿系统及生殖器官先天性结构畸形相关的已知致病变异或疑似致病变异可能。结果该家系两例胎儿SNP-array结果均为arr[hg19]17q12(34822465~36243365)×1,大小约1.4 Mb,为17q12微缺失综合征,遗传自父亲。胎儿父亲未发现泌尿系统相关的致病或疑似致病变异。结论父源性17q12微缺失可能为两例胎儿超声肾脏异常和羊水过多的遗传学病因。产前SNP-array检测可明确诊断,为该家系的遗传咨询及产前诊断提供依据。     

仿生矿化后的丝素电纺复合支架体内成骨性能的实验研究

目的探讨仿生矿化后的丝素电纺复合支架体内修复颅骨缺损的能力。方法利用静电纺丝技术制备丝素电纺支架(非矿化组),通过模拟体液(SBF)浸泡法对支架仿生矿化(矿化组),扫描电镜观察其微观形貌。18只8周龄的雄性SD大鼠购自南京医科大学动物实验中心,采用随机数字表示法分为3组,分别为矿化组、非矿化组和对照组,每组6只。构建SD大鼠颅骨缺损模型,在直径为5 mm的骨缺损区分别植入矿化组及非矿化组支架,对照组不作处理,分别于术后4、8周取材,通过微计算机断层扫描技术(micro-CT)、苏木精-伊红(HE)及马松染色(Masson染色)比较评估不同支架的体内骨再生情况。应用GraphPad Prism 8统计软件分析,采用单因素方差分析。结果扫描电镜结果显示仿生矿化后的丝素电纺支架表面形成明显的羟基磷灰石矿化层。动物实验结果显示,术后4周和8周,通过对CT三维重建、HE及Masson染色的观察以及对骨体积分数(BV/TV),骨小梁数(Tb.N),骨小梁厚度(TB.Th)和骨小梁间隙(TB.Sp)定量指标的分析结果显示,在矿化组和非矿化组均能观察到新骨的形成,且矿化组的修复效果均优于非矿化组,差异有统计学意义[矿化组、非矿化组及对照组BV/TV在4周时分别为(22.880±2.324)、(12.600±1.965)、(4.967±1.580)%,F=61.838,P<0.05,8周时分别为(45.770±4.433)、(29.400±4.086)、(19.310±2.272)%,F=38.686,P<0.05;Tb.N在4周时分别为(0.029±0.001)、(0.019±0.003)、(0.008±0.003)mm-1,F=52.890,P<0.05,8周时分别为(0.053±0.002)、(0.037±0.003)、(0.023±0.001)mm-1,F=171.433,P<0.05;TB.Sp在4周时分别为(10.810±0.179)、(11.350±0.098)、(11.730±0.163)μm,F=27.655,P<0.05,8周时分别为(8.792±0.175)、(10.060±0.339)、(11.150±0.275)μm,F=56.807,P<0.05]。结论仿生矿化后的丝素电纺复合支架能有效促进骨再生,有望用于骨组织工程。     

Prognostic and immunological roles of Fc fragment of IgG binding protein in colorectal cancer

Valuable diagnostic and prognostic biomarkers are urgently needed for colorectal cancer (CRC), which is one of the leading causes of mortality worldwide. Previous studies have reported altered expression of a mucin-like protein Fc fragment of IgG binding protein (FCGBP) in various types of cancer, but its potential diagnostic, prognostic and immunological roles in CRC remain to be determined. Therefore, the aim of current study was to investigate the potential roles of FCGBP in CRC. The present study investigated FCGBP mutations and changes in its expression levels using a combination of microarray and public dataset analyses, as well as immunohistochemistry. The results demonstrated a 10.5% mutation frequency in the FCGBP coding sequence in CRC tissues, and identified decreased FCGBP mRNA or protein expression levels in colorectal adenoma and CRC (compared with those in normal colorectal tissues from healthy control subjects), including pathologically advanced CRC (stage III+IV vs. I+II). Survival analysis using the GEPIA and Kaplan-Meier Plotter databases revealed that low FCGBP expression levels were associated with short overall, disease-free, relapse-free and event-free survival times in patients with CRC. Notably, analysis using the online Tumor IMmune Estimation Resource database revealed a positive correlation between FCGBP expression levels and the extent of infiltrating immune cells, such as B cells and dendritic cells. Consistently, the expression levels of most markers (51/57) for various types of immune cells were significantly correlated with FCGBP expression levels in CRC tissues. These findings suggested that FCGBP may serve as a diagnostic and prognostic biomarker, and that FCGBP may be associated with immune infiltration in CRC.