介入治疗在急性动脉大出血中的应用价值

目的 探讨介入治疗在急性动脉大出血中的应用价值。方法 51例经内科保守治疗无法控制出血的急性动脉大出血患者,急诊作动脉血管造影术,根据术中出血原因和部位,分别采用动脉内栓塞或缩血管药物灌注治疗。结果 共51例,其中行动脉内栓塞48例,止血率100%;单纯动脉内灌注缩血管药物2例,1例未再出血,1例灌注止血72h后再出血者剖腹探察,手术证实为回盲部美克尔憩室;1例空肠部血管畸形,采用动脉灌注及栓塞治疗后止血。所有病例均未发生严重并发症。结论 介入治疗对急性动脉大出血多数可以通过栓塞或灌注止血,栓塞止血效果佳,灌注不能彻底止血者,可为患者进一步治疗创造条件。     

先天性珊瑚状白内障一家系

先证者,女,65岁,自幼双眼视力不佳,配戴远视镜后视力达0.5,近二年来视力明显下降,于2002年11月在我院眼科门诊检查:双眼裸眼视力均为0.1,(+5.00DS→0.25),无眼颤,眼位正常,瞳孔等大同圆,晶体皮质中央珊瑚状结晶样白色混浊(见图⑨、⑩),周边楔形混浊,散瞳查眼底未见异常.     

光子治疗应用于盐酸吡硫醇静脉注射血管外渗的疗效及护理体会

目的探讨光子治疗因盐酸吡硫醇静脉注射引起血管外渗的临床价值及护理对策。方法将36例因盐酸吡硫醇静脉注射发生血管外渗的患者随机分为观察组(光子治疗)和对照组(硫酸镁湿敷),比较两组患者的治疗有效率和愈合时间。结果观察组治疗有效率(94.4%)高于对照组(61.1%);治愈时间[(4.3±2.6)d]短于对照组[(6.1±3.5)d],差异均有统计学意义(P0.05)。结论将光子治疗应用于因盐酸吡硫醇静脉注射引起的血管外渗,具有效果好、治愈时间短的优点,值得临床推广。     

低血钾周期性麻痹伴二度型房室传导阻滞2例

1　病例报告　　例1　患者男,44岁,因清晨醒来四肢无力、酸痛,活动后症状加重伴行走障碍4h,于1993年4月23日入院。体温36.6°C,脉搏56/min,呼吸18/min,血压17/11kPa。眼球无突出,甲状腺无肿大。心界不大,心律不整,各瓣膜区未闻及杂音。颅神经检查无异常。四肢肌容积正常,肌力0级,肌张力低,双侧肱二、三头肌反射及膝腱反射消失,病理反射阴性。X线胸片无异常;心电图示窦性心动过缓,一度及二度型房室传导阻滞;血钾1.77mmol/L,血钠134mmol/L,血氯104mmol/L,血钙2.1mmol/L。入院诊断:低血钾性周期性麻痹伴二度型房室传导阻滞。立即心电监护下…     

小儿室间隔缺损血清内源性洋地黄因子测定的临床意义

用放射免疫法测定41例小儿室缺及31例正常对照组血清内源性洋地黄因子(SEDF)含量,发现正常儿SEDF含量为0.58±0.17nmol/L,室缺患儿SEDF为0.43±0.1nmol/L,两者差异显著(P<0.01)。年龄,性别对SEDF影响不大。41例室缺中心功能正常8例;Ⅱ级6例;Ⅲ级12例;Ⅳ级15例;其SEDF分别为0.62±0.11,0.59±0.17,0.36±0.12、0.33±0.16nmol/L。正常心功能组与Ⅱ、Ⅲ、Ⅳ级心功能比较P分别为>0.05,<0.01,<0.001。提示心功能受损可引起SEDF含量减少,其减少程度与心功能受损严重程度一致。笔者认为测定SEDF有助于了解婴幼儿心功能并可指导洋地黄的临床应用。     

睫状体无色素上皮瘤1例

患者，女，44岁，因“左眼红痛视力下降6a”于2006年8月18日来我院眼科就诊，当日入院。患者诉6a前出现左眼红痛、视力下降，5a前在当地医院诊断为“左眼虹膜睫状体肿块，左眼继发性青光眼，左眼并发性白内障”。肿块直径约3mm，在当地医院行“左眼Phaco＋IOL植入术”。入院检查：视力右1．0，左0．05；眼压：右16mmHg（1kPa=7．5mmHg），     

美容护理在骨科手术患者中的应用效果

目的 观察对骨科手术患者实施美容护理的临床效果。方法 选取2021年7月-2023年7月我院收 治的骨科手术患者100例作为对象,采用奇偶数字法分为对照组和研究组,各50例。对照组应用常规骨 科护理,研究组应用美容护理,比较两组瘢痕情况[温哥华瘢痕量表（VSS）]、心理状态[焦虑自评量表 （SAS）、抑郁自评量表（SDS）]、创口愈合美容效果以及护理满意度。结果 研究组护理后血管分 布、柔软度、色泽、厚度评分均低于对照组（P ＜0.05）;研究组护理后SAS、SDS评分均低于对照组 （P＜0.05）;研究组创口愈合美容效果优于对照组（P ＜0.05）;研究组护理满意度为98.00%,高于对照 组的84.00%（P＜0.05）。结论 对于骨科手术患者,美容护理措施可促进其创口愈合,减轻瘢痕程度,缓 解患者的负面心理,且患者对护理满意度更高。     

Role of TGF-β/Smad signaling pathway in pulmonary fibrosis after rheumatoid arthritis in mice北大核心CSCD

Aim To investigate the role of TGF-β/Smad signaling pathway in rheumatoid arthritis (RA) - associated postinterstitial pulmonary fibrosis in mice. Methods The mouse model of RA was constructed by subcutaneous administration of complete Freund's adjuvant (CFA) and chicken II collagen (Col-II) to the tail root of mice. The blank group was given the same amount of distilled water, and the control group was given the same amount of glacial acetic acid (solvent). The degree of toe swelling (joint swelling degree and arthritis index) was monitored to evaluate the mouse modeling. The pathological changes of mouse lung tissues were observed by HE and Masson staining. The expression of TGF-β in lung tissues were observed by immunohistochemical staining. The level of hydroxyproline in lung tissues was measured by chemiluminescence method. The expressions of Smad2, Smad3 and phosphorylated p-Smad2 and phosphorylated p-Smad3 in lung tissues were detected by Western blot. Results Compared with blank group and solvent group, the joint swelling and arthritis index of model group significantly increased. Twenty-one days after administration, HE staining showed inflammatory changes in lung interstitium of the model group, Masson staining showed collagen fiber deposition and obvious fibrosis in lung interstitium of the model group, and immunohistochemical staining showed that the expression of TGF-β in cytoplasm of lung interstitial cells of the model group increased, which was brown and yellow. Meanwhile, hydroxyproline was significantly raised in lung tissue homogenate of the model group. Further WB analysis showed that compared with blank group and solvent group, the expression of p-Smad2 and pSmad3 in lung tissues of the model group was significantly up-regulated (P < 0. 05, P < 0. 01). Conclusions RA can give rise to pulmonary fibrosis, and the expressions of p-Smad2 and p-Smad3 are up-regulated, which is be pivotal in pulmonary fibrosis and RA-related post-interstitial pulmonary fibrosis. © 2023 Publication Centre of Anhui Medical University. All rights reserved.