恙虫病并发中毒性肝炎40例临床分析

目的探讨恙虫病并发中毒性肝炎的临床特点。方法按诊断标准选择病例进行临床分析。结果本组除了具有恙虫病特征性的临床表现外，同时出现黄疸占25％(总胆红素平均164μmol/L)，出血点和瘀斑占15％，肝大占76％，脾大占63％。ALT和AST升高，平均分别为295U/L和240U/L。使用特效抗茵药物和护肝退黄治疗有良效。结论恙虫病并发中毒性肝炎较常见，少数可出现严重的肝功能损害。     

小骨窗开颅加尿激酶治疗高血压脑出血

目的　探讨微创小骨窗血肿清除加用尿激酶溶解血肿治疗高血压脑出血的效果。方法　将 32例入院的高血压脑出血病例在头颅CT片指导下行颞部直切口 ,小骨窗 2 0～ 3 0cm ,直视下吸除大部血肿 ,活动性出血予以电凝止血。血肿腔放置硅胶管 ,手术后 3d引流管注入 1万U尿激酶 ,再引流陈旧溶解的血肿液 ,并与大骨瓣开颅血肿清除术的效果相比较。结果　 32例中 ,18例完全恢复 ,半自理 8例 ,优良率 81 3% ,偏瘫 4例 ,无植物生存 ,死亡 2例 ,病死率 6 %。与前期大骨瓣开颅血肿清除术相比较有良好的效果。结论　小骨窗微创血肿清除加尿激酶血肿腔溶解血肿的结合 ,最佳化地发挥了各自的优势 ,同时避免了其缺点。     

吴立文教授治疗慢性前列腺炎经验

吴立文教授根据多年临床经验,认为慢性前列腺炎是由湿、热、虚、瘀等因素引起,临证时从病机、病性、论治三方面入手,强调以祛除湿邪为重点,活血化瘀贯彻始终,酌情配合扶正治疗。     

西雅图阻塞性肺疾病评分用于老年COPD患者优质护理效果相关因素分析

目的 探讨对老年慢性阻塞性肺疾病(COPD)患者实施优质护理效果的相关因素。方法 将130例COPD患者入院时均实施优质护理,出院时采用西雅图阻塞性肺疾病问卷(SOLDQ)评分,并根据其分值分观察组(≥240分)81例和对照组(<240分)49例。比较分析两组患者性别、年龄、病程、肺功能、住院天数、合并症等临床资料。结果 观察组患者的病程、肺功能、加重次数、住院天数均低于对照组,文化程度高于对照组(P<0.05);两组患者的性别、年龄、合并症、陪护、吸烟史、居住地及饮食标准差异无统计学意义(P>0.05)。logistic回归分析显示COPD病程、肺功能、加重次数、住院天数与COPD患者实施优质护理的效果呈负相关(β=-0.67、-3.49、-1.01、-1.75,P<0.05)。结论 老年COPD患者实施优质护理的效果与多种因素有关,肺功能可能是最重要的因素。     

培育颗粒对人绒毛滋养细胞侵袭与增殖的作用

目的观察培育颗粒对人绒毛滋养细胞的侵袭和增殖功能的影响。方法取人妊娠5~10周正常胎盘绒毛,进行滋养细胞培养。正常23~25 d雌性SD大鼠药物灌胃,取药理血清。培养液加20%血清,分组培养48 h后检测指标。用Transwell侵袭实验检测培育颗粒对滋养细胞侵袭功能的影响,MTT法检测培育颗粒对滋养细胞增殖能力的影响,流式细胞术检测培育颗粒对滋养细胞增殖核抗原(PCNA)表达的影响。结果Transwell侵袭实验检测结果表明,培育颗粒血清各剂量组与正常组侵袭细胞数均有差异,中剂量组侵袭细胞数最多。MTT法检测结果表明,培育颗粒血清各剂量组与正常组吸光度均有差异,中剂量组吸光度最高。流式细胞术检测结果表明,培育颗粒血清各剂量组与正常组PCNA阳性率均有差异,中剂量组PCNA阳性率最高。结论培育颗粒可促进人绒毛滋养细胞侵袭与增殖功能,可能与负反馈调节有关。     

子宫动脉栓塞术治疗子宫肌瘤42例临床分析

目的 探讨子宫动脉栓塞术（UAE）治疗子宫肌瘤的疗效。方法 选择42例子宫肌瘤患者,以Seldinger技术完成单侧股动脉插管,根据数字减影血管造影（DSA）检查结果,选用管径为4－5F（1F=0.33mm)的脾管、肝管或cobra导管,或选用3F微导管,插管至双侧子宫动脉并经DSA检查证实后,以携带有抗生素的明胶海绵颗粒栓塞该处血管。结果 DSA检查发现,子宫肌瘤血液供应丰富。UAE治疗6－12个月后,子宫肌瘤患者的临床症状明显缓解,月经量减少26．3％－75．2％;UAE治疗后第12个月、第18个月肌瘤体积分别缩小77．7％、83．0％,子宫体积分别缩小54．9％、62．7％。术后有不同程度的下腹痛、低热,持续1－3周,经对症处理后症状逐渐消失。结论 UAE可有效地缩小肌瘤及子宫的体积,并明显改善子宫肌瘤患者的临床症状。     

叙事暴露疗法在儿童和青少年创伤后应激障碍患者中应用效果的Meta分析

背景 叙事暴露疗法（NET）结合叙事疗法和暴露疗法的优点,对缓解创伤后应激障碍（PTSD）症状有效,有助于患者对创伤进行深入的认识,也具有较好的安全性。儿童和青少年是PTSD的高发人群,但NET对该人群干预效果的研究结果存在差异。目的 系统评价NET对儿童和青少年PTSD患者的干预效果,为NET的临床应用提供参考。方法 于2022年8月1日,计算机检索Cochrane Library、PubMed、Web of Science、CINAHL、中国知网（CNKI）、中国生物医学文献数据库（SinoMed）、维普数据库和万方数据库,检索时限为建库至2022年6月。采用主题词与自由词相结合的方式进行检索,收集NET治疗儿童和青少年PTSD的文献。根据Cochrane协作网更新的偏倚风险评估手册中对随机对照试验的真实性评价标准（2011）,评价文献质量。采用RevMan 5.4对纳入的随机对照试验进行Meta分析。结果 纳入9篇文献,共包括394例儿童和青少年PTSD患者。Meta分析结果显示,在PTSD症状缓解程度方面,干预后1~3个月（SMD=0.22,95% CI：-0.84~1.28）以及干预后6个月（SMD=0.21,95% CI：-0.75~1.17）,NET与放松疗法的效果比较,差异无统计学意义;干预后1~3个月（SMD=-0.66,95% CI：-1.04~-0.27）以及干预后6个月（SMD=-0.77,95% CI：-1.36~-0.19）,NET的效果均优于常规治疗,差异均有统计学意义。在抑郁症状缓解程度方面,治疗后1~3个月,NET与常规治疗的效果比较,差异无统计学意义（SMD=-0.39,95% CI：-0.98~0.21）;干预后6个月,NET与常规治疗的效果比较,差异无统计学意义（SMD=-0.74,95% CI：-2.23~0.75）。在心理困扰缓解程度方面,干预后1~3个月,NET与常规治疗的效果比较,差异无统计学意义（SMD=-0.54,95% CI：-2.14~1.07）。在食欲亢进缓解程度方面,NET与常规治疗的效果比较,差异无统计学意义（SMD=-0.17,95% CI：-0.54~0.19）。结论 与常规治疗相比,NET对缓解儿童和青少年PTSD症状的效果更佳,且具有中长期效果,但在改善抑郁症状、心理困扰以及食欲亢进方面无明显优势。     

Corosolic acid analogue,a natural triterpenoid saponin,induces apoptosis on human hepatocarcinoma cells through mitochondrial pathway in vitro

Context 2a,-3a,-24-Trihydroxyurs-12-en-28-oic acid (TEO, a corosolic acid analogue) is a triterpenoid saponin isolated from Actinidia valvata Dunn (Actinidiaceae), a well-known traditional Chinese medicine.

Objective This study investigated the anti-proliferation and inducing apoptosis effects of TEO in three human hepatocellular carcinoma (HCC) cell lines.

Materials and methods Cytotoxic activity of TEO was determined by the MTT assay at various concentrations from 2.5 to 40?μg/mL in BEL-7402, BEL-7404 and SMMC-7721 cell lines. Cell morphology was assessed by acridine orange/ethidium bromide and 4′-6-diamidino-2-phenylindole dihydrochloride staining and fluorescence microscopy. Cell-cycle distribution and DNA damage were determined by flow cytometry and comet assay. Mitochondrial dysfunction was assessed by JC-1 staining and transmission electron microscopy. Apoptosis changes were explored by Western blot, TNF-α and caspase-3, -8, -9 assays.

Results TEO exhibited inhibition effects on BEL-7402, BEL-7404 and SMMC-7721 cells treated for 24?h, the IC₅₀ values were 34.6, 30.8 and 30.5?μg/mL, respectively. TEO (40?μg/mL)-treated three cell lines increased by more than 21% in the G1 phase and presented the morphological change and DNA damage. TEO also declined the mitochondrial membrane potential and altered mitochondrial ultra-structure. Furthermore, caspase-3, caspase-8, caspase-9 and TNF-α were also activated. Mechanism investigation showed that TEO could decrease anti-apoptotic Bcl-2 protein expression, increase proapoptotic Bax and Bid proteins expressions and increase Bax/Bcl-2 ratio.

Conclusion Our results demonstrate for the first time that TEO inhibited growth of HCC cell lines and induced G1 phase arrest. Moreover, proapoptotic effects of TEO were mediated through the activation of TNF-α, caspases and mitochondrial pathway.     

Inhibitory effect of Ginkgo biloba extract on hyperhomocysteinemia-induced intimal thickening in rabbit abdominal aorta after balloon injury

Ginkgo biloba extract (GBE) has been widely used to treat cardiovascular and cerebrovascular disorders. Hyperhomocysteinemia (Hhcy) is associated with the risk of atherosclerosis and restenosis after angioplasty. The objective of this study was to investigate whether GBE could attenuate the Hhcy-induced intimal thickening after balloon injury in rabbit abdominal aorta. It was observed in this study that GBE could decrease the neointima area (NA) and the ratio of the neointima area to the media area (NA/MA), down-regulate the mRNA expression of matrix metalloproteinase-9 (MMP-9) and up-regulate the protein expression of p21 (WAF1/CIP1) (p21). It suggests that GBE can reverse the Hhcy-induced neointima formation in rabbits following balloon injury, and the suppressive effect of GBE on the migration and proliferation of vascular smooth muscle cells (VSMCs) may contribute to its actions.     

Inhibiting DNA methylation alleviates cisplatin-induced hearing loss by decreasing oxidative stress-induced mitochondria-dependent apoptosis via the LRP1–PI3K/AKT pathway

Cisplatin-related ototoxicity is a critical side effect of chemotherapy and can lead to irreversible hearing loss. This study aimed to assess the potential effect of the DNA methyltransferase (DNMT) inhibitor RG108 on cisplatin-induced ototoxicity. Immunohistochemistry, apoptosis assay, and auditory brainstem response (ABR) were employed to determine the impacts of RG108 on cisplatin-induced injury in murine hair cells (HCs) and spiral ganglion neurons (SGNs). Rhodamine 123 and TMRM were utilized for mitochondrial membrane potential (MMP) assessment. Reactive oxygen species (ROS) amounts were evaluated by Cellrox green and Mitosox-red probes. Mitochondrial respiratory function evaluation was performed by determining oxygen consumption rates (OCRs). The results showed that RG108 can markedly reduce cisplatin induced damage in HCs and SGNs, and alleviate apoptotic rate by protecting mitochondrial function through preventing ROS accumulation. Furthermore, RG108 upregulated BCL-2 and downregulated APAF1, BAX, and BAD in HEI-OC1 cells, and triggered the PI3K/AKT pathway. Decreased expression of low-density lipoprotein receptor-related protein 1 (LRP1) and high methylation of the LRP1 promoter were observed after cisplatin treatment. RG108 treatment can increase LRP1 expression and decrease LRP1 promoter methylation. In conclusion, RG108 might represent a new potential agent for preventing hearing loss induced by cisplatin via activating the LRP1-PI3K/AKT pathway.KEY WORDS: Cisplatin, DNMT, Apoptosis, Hair cell, Spiral ganglion neurons, RG108, Mitochondrial dysfunction, ROS