T管出口预定位在肝胆管结石病人术后护理中的应用

目的:探讨T管出口预定位在肝胆管结石病人术后护理中的应用效果。方法:采用便利抽样法纳入2018年1月—2019年12月行腹腔镜胆囊切除术(LC)联合腹腔镜胆总管探查术(LCBDE)术后留置T管引流并携管出院的96例病人为研究对象。选择2018年1月—2018年12月的48例病人为对照组,其T管出口位置的确定方法为管道的头端到皮肤最短最直的距离为引流管出口位置,选择2019年1月—2019年12月的48例病人为观察组,术前由医生、护士和病人三方共同进行T管出口的预定位。比较两组病人术后舒适度、满意度及置管3月后刺激性皮炎的发生情况。结果:观察组病人管道出口位置相对理想,方便病人自我维护,术后舒适度、满意度均高于对照组(P<0.05),刺激性皮炎的发生率和严重程度均低于对照组(P<0.05)。结论:T管术前预定位利于病人术后护理,可提高病人术后舒适度和满意度,减少T管留置并发症的发生。     

可吸收缝线缝扎兔胆总管致良性狭窄模型的建立

目的 利用可吸收缝线缝扎部分胆总管建立兔损伤性胆管狭窄动物模型.方法 24只新西兰兔按完全随机方法分为3组:正常对照组、假手术对照组和手术组.手术组用6-0可吸收缝线缝扎1/2胆总管,手术当天和术后15、30 d检验血清肝功能指标,取狭窄段胆总管行HE染色、Masson三色染色检测胶原纤维和肌纤维的表达,免疫组化DAB法检测狭窄段胆管组织Ⅰ、Ⅲ型胶原的表达.结果 手术组动物直接胆红素、间接胆红素、丙氨酸氨基转移酶和天门冬氨酸氨基转移酶在30 d均高于术前(P＜0.01).术中观察胆总管损伤处明显狭窄,手术组病理切片中,胶原纤维大量增生形成瘢痕组织,Ⅰ、Ⅲ型胶原随着时间推移表达强度逐渐增强.结论 可吸收缝线缝扎法可有效建立兔胆总管良性狭窄模型.     

Primary malignant peripheral nerve-sheath tumor of the common bile duct

Primary malignant peripheral nerve-sheath tumors of the common bile duct are extremely rare. To our knowledge, the published literature contains no previous case report of this disease. Here we report on a 58-year-old Japanese woman with a primary malignant peripheral nerve-sheath tumor of the common bile duct, which was completely resected. A hypoechoic mass was identified in the hepatic hilus, using ultrasonography and computed tomography. Endoscopic retrograde cholangiography revealed a smooth stricture and deviation of the common bile duct. Laparotomy exposed a firm mass around the common bile duct that had not invaded the surrounding tissues. Partial resection of the common bile duct and cholecystectomy were performed as the treatment of choice. The final histopathological diagnosis was malignant peripheral nerve-sheath tumor arising from the wall of the common bile duct.     

A case of septum formation of the common hepatic duct combined with an anomalous hepatic duct of the caudate lobe

A 66-year-old Japanese woman was admitted to our hospital with upper right quadrant pain and jaundice. Laboratory data indicated the presence of obstructive jaundice. A diagnosis of cholecystocholedocholithiasis was made by ultrasonography. Endoscopic retrograde cholangiography revealed choledochal stones with septum formation in a portion of the common hepatic duct up to where an anomalous bile duct drained from the caudate lobe of the liver. We performed a cholecystectomy, T-tube drainage, and partial resection of the septum when these findings were confirmed at surgery. Histological examination of the removed septum showed fibrous stroma under atrophic mucosa. To our knowledge, this is the eighteenth reported case in Japan of septum formation of the bile duct. However, no other such case to date has been seen combined with an anomalous hepatic duct of the caudate lobe of the liver. Selective cholangiography by choledochoscope and computed tomography with a thin guide-wire inserted to the bile duct were useful in confirming the origin of the anomalous bile duct. This case may serve as further evidence of the assumption that septum formation of the common (hepatic) bile duct is a malformation of congenital origin. An erratum to this article is available at .     

"肌少-骨质疏松症"的共同发病机制

"肌少-骨质疏松症"(sarco-osteopenia)的提出是基于两者共同的病理生理学基础,其中涉及八类主要影响因素.简要概括为机械因素作用于骨细胞构成的机械支架和肌管;肌肉-骨骼系统相互影响彼此化学因子的释放;甲基转移酶样蛋白21C(METTL21C)和肌肉生长抑制素(myostatin,MSTN,简称肌抑素)以及硬骨抑素(sclerostin,SOST)作为共同的遗传因素调控肌肉-骨骼系统;肌肉和骨骼在旁分泌和内分泌水平上的串扰、脂肪浸润因素导致肌力的下降和骨折发生率增加;炎性反应、糖尿病和糖皮质激素过量影响肌肉的丢失以及骨丢失;营养缺乏加速骨丢失和肌肉蛋白质合成减少;个体运动量的减少和神经-肌肉功能减弱间接影响肌肉和骨骼的合成代谢.深入研究"肌少-骨质疏松症"共同的致病机制,以推动生物检测特异性指标的确定、临床疾病的评估和诊断以及有效治疗药物和设备开发工作,最终目标是有效地治疗和预防"肌少-骨质疏松症".本文对"肌少-骨质疏松症"共同病理生理学机制研究现状与进展进行系统综述.     

Common variable immunodeficiency revisited: normal generation of naturally occurring dendritic cells that respond to Toll‐like receptors 7 and 9

Patients with common variable immunodeficiency (CVID) have reduced numbers and frequencies of dendritic cells (DCs) in blood, and there is also evidence for defective activation through Toll‐like receptors (TLRs). Collectively, these observations may point to a primary defect in the generation of functional DCs. Here, we measured frequencies of plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) in peripheral blood of 26 CVID patients and 16 healthy controls. The results show that the patients have reduced absolute counts of both subsets. However, the decreased numbers in peripheral blood were not reflected in reduced frequencies of CD34⁺ pDC progenitors in the bone marrow. Moreover, studies at the single cell level showed that DCs from CVID patients and healthy controls produced similar amounts of interferon‐α or interleukin‐12 and expressed similar levels of activation markers in response to human cytomegalovirus and ligands for TLR‐7 and TLR‐9. The study represents the most thorough functional characterization to date, and the first to assess bone marrow progenitor output, of naturally occurring DCs in CVID. In conclusion, it seems unlikely that CVID is secondary to insufficient production of naturally occurring DCs or a defect in their signalling through TLR‐7 or TLR‐9.