Anticipatory perioperative management for patent ductus arteriosus surgery: Understanding postligation cardiac syndrome

Ligation of a hemodynamically significant ductus arteriosus results in significant changes in loading conditions which have predictable consequences. Postligation cardiac syndrome, defined as hypotension requiring inotropic support and failure of oxygenation and ventilation, may occur 6‐12 hours following ligation due to left ventricular systolic and diastolic failure, respectively. Afterload is the primary driver of this decompensation. In this review, we describe the pathophysiological changes in loading conditions associated with postligation cardiac syndrome and other contributors to cardiovascular dysfunction following ductal ligation. We present strategies for perioperative optimization and a physiology‐based algorithm for postoperative management guided by targeted neonatal echocardiography. The use of these strategies to reduce the frequency of postligation deterioration may be an avenue to improve outcomes for neonates in this vulnerable patient population.     

Curcumin ameliorates hepatic chronic inflammation induced by bile duct obstruction in mice through the activation of heme oxygenase-1

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Endoscopic band ligation for postpolypectomy gastric bleeding

We report a case of a patient in whom endoscopic band ligation was achieved for postpolypectomy gastric bleeding. A 76‐year‐old man visited our hospital because of anemia. Endoscopy revealed a gastric polyp, approximately 12 mm in diameter, on the lesser curvature in the distal gastric body. The polyp was considered to be the source of chronic anemia and was therefore removed by using standard careful snare‐cautery polypectomy technique. Four days later, follow‐up endoscopy was performed to evaluate the postpolypectomy site, and an active bleeding postpolypectomy ulcer was identified. Initial attempts to achieve hemostasis with ethanol injection were unsuccessful. Immediate hemostasis was obtained with a subsequent endoscopic band ligation device. There has been no recurrent bleeding. Endoscopic band ligation might be a good treatment modality for the treatment of a postpolypectomy gastric bleeding lesion.     

宫颈环形电切术对阴道镜活检诊断为宫颈上皮内瘤变的再评估

目的通过宫颈环形电切术(LEEP)对阴道镜活检诊断为宫颈上皮内瘤变(C IN)的准确性和全面性进行评估。方法对118例阴道镜活检诊断为C IN的患者行LEEP,对比术前术后的病理结果。结果32例阴道镜活检病理为C INⅠ级病例中有11例与LEEP术病理相符,6例LEEP术后病理级别上升,15例LEEP术后病理级别下降;26例阴道镜活检病理C INⅡ级病例中有17例LEEP术后病理示相符,5例LEEP术后病理级别上升,4例LEEP术后病理级别下降;60例阴道镜活检病理为C INⅢ级病例中有44例LEEP术后病理示相符,11例LEEP术后病理级别上升,5例术后病理级别下降。结论LEEP术是明确诊断和治疗C IN的有效而理想的方法,阴道镜活检有一定局限性。     

Partial Portal Vein Ligation Plus Thioacetamide: A Method to Obtain a New Model of Cirrhosis and Chronic Portal Hypertension in the Rat

To obtain a new model of chronic portal hypertension in the rat, two classical methods to produce portal hypertension, partial portal vein ligation and the oral administration of thioacetamide (TAA), have been combined. Male Wistar rats were divided into four groups: 1 (control; n?=?10), 2 [triple partial portal vein ligation (TPVL); n?=?9], 3 (TAA; n?=?11), and 4 (TPVL plus TAA; n?=?9). After 3 months, portal pressure, types of portosystemic collateral circulation, laboratory hepatic function tests (aspartate aminotransferase, alanine aminotransferase, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase) and liver histology were studied. The animals belonging to group 2 (TPVL) developed extrahepatic portosystemic collateral circulation, associated with mesenteric venous vasculopathy without hepatic destructurization or portal hypertension. Animals from group 3 (TAA) developed cirrhosis and portal hypertension but not extrahepatic portosystemic collateral circulation, or mesenteric venous vasculopathy. Finally, the animals from group 4 (TPVL?+?TAA) developed cirrhosis, portal hypertension, portosystemic collateral circulation, and mesenteric venous vasculopathy. The association of TPVL and TAA can be used to obtain a model of chronic portal hypertension in the rat that includes all the alterations that patients with hepatic cirrhosis usually have. This could, therefore, prove to be a useful tool to study the pathophysiological mechanisms involved in these alterations.     

Preparation of protected peptidyl thioester intermediates for native chemical ligation by Nα‐9‐fluorenylmethoxycarbonyl (Fmoc) chemistry: considerations of side‐chain and backbone anchoring strategies,and compatible protection for N‐terminal cysteine*,†

Abstract: Native chemical ligation has proven to be a powerful method for the synthesis of small proteins and the semisynthesis of larger ones. The essential synthetic intermediates, which are C‐terminal peptide thioesters, cannot survive the repetitive piperidine deprotection steps of N^α‐9‐fluorenylmethoxycarbonyl (Fmoc) chemistry. Therefore, peptide scientists who prefer to not use N^α‐t‐butyloxycarbonyl (Boc) chemistry need to adopt more esoteric strategies and tactics in order to integrate ligation approaches with Fmoc chemistry. In the present work, side‐chain and backbone anchoring strategies have been used to prepare the required suitably (partially) protected and/or activated peptide intermediates spanning the length of bovine pancreatic trypsin inhibitor (BPTI). Three separate strategies for managing the critical N‐terminal cysteine residue have been developed: (i) incorporation of N^α‐9‐fluorenylmethoxycarbonyl‐S‐(N‐methyl‐N‐phenylcarbamoyl)sulfenylcysteine [Fmoc‐Cys(Snm)‐OH], allowing creation of an otherwise fully protected resin‐bound intermediate with N‐terminal free Cys; (ii) incorporation of N^α‐9‐fluorenylmethoxycarbonyl‐S‐triphenylmethylcysteine [Fmoc‐Cys(Trt)‐OH], generating a stable Fmoc‐Cys(H)‐peptide upon acidolytic cleavage; and (iii) incorporation of N^α‐t‐butyloxycarbonyl‐S‐fluorenylmethylcysteine [Boc‐Cys(Fm)‐OH], generating a stable H‐Cys(Fm)‐peptide upon cleavage. In separate stages of these strategies, thioesters are established at the C‐termini by selective deprotection and coupling steps carried out while peptides remain bound to the supports. Pilot native chemical ligations were pursued directly on‐resin, as well as in solution after cleavage/purification.     

门静脉主干缩窄法制备SD大鼠门静脉高压症模型时最佳口径的探讨

目的 探讨缩窄门静脉主干法制备SD大鼠门静脉高压症模型时的最佳缩窄口径.方法 SD大鼠70只,随机分为正常组和6个实验组,每组各10只.正常组行假手术.各实验组分别按照5、6、7、8、9、12号针头的缩窄口径行门静脉主干缩窄术.观察各组大鼠术后累积死亡率,术后状态,术前、术后即刻及术后2周时的门静脉压力,术后2周时的食管组织学变化和脾指数.结果 5、6、7、8、9、12号针头缩窄组术后3 d时大鼠的累积死亡率分别为100%、80%、70%、20%、10%、0%,与缩窄程度正相关.8、9、12号组的大鼠存活状态明显好于5、6、7号组.5、6、7、8、9、12号组术后即刻门静脉压力分别为:(5.836±0.275)、(4.557±0.419)、(3.856±0.576)、(3.343±0.433)、(2.708±0.309)、(1.957±0.358)kPa,7、8、9、12号组术后2周时门静脉压力分别为:(2.163±0.424)、(1.956±0.172)、(1.841±0.202)、(1.232±0.154)kPa,均较正常(0.881±0.165)kPa显著升高(P＜0.05).术后2周,7、8、9、12号组大鼠食管下段黏膜下层平均血管数目分别为:(3.94±0.83)、(3.58±0.63)、(3.14±0.64)、(2.02±0.62)个,与正常组(1.65±0.62)个比较,除12号组外均有增多(P＜0.01);固有层平均血管数目分别为:(2.24±0.64)、(2.05±0.29)、(1.52±0.28)、(0.93±0.19)个,与正常组(0.82±0.18)比较,除第12组外均增多(P＜0.01);黏膜下层血管口径分别为:(4.52±1.51)、(4.05±1.23)、(3.75±1.11)、(2.03±0.86)μm,除第12组外均增大(P＜0.01);脾指数分别为:(4.21±0.93)、(4.06±0.68)、(3.84 4±0.71)、(3.31±0.69)除12号组外也较正常增加(P＜0.01).结论 缩窄门静脉主干可成功制成大鼠门静脉高压症模型;其最佳缩窄口径应该是:大鼠体重200 g左右时用8号针头(直径0.8mm),大鼠体重300 g左右时用9号针头(直径0.9 mm).     

腹腔镜治疗精索静脉曲张235例

目的探讨腹腔镜治疗精索静脉曲张的疗效. 方法回顾分析1993年9月～2003年7月235例经腹腔镜精索静脉高位结扎术的临床资料. 结果 235例手术均获成功,手术时间5～20 min,平均12 min.术后住院2～5 d,平均3 d.210例随访6～18个月,9例复发,复发率4.3%(9/210),不育11例术后6～12个月后其妻受孕. 结论腹腔镜精索静脉高位结扎术微创、美观、疗效好,对双侧精索静脉曲张、开放性手术后复发和有腹股沟区手术史者尤为适用.     

Research review: DNA polymerases as molecular markers of the regenerating capacity of hepatocytes

Hepatocyte regeneration has been widely investigated, with the mitotic index and the incorporation of [³H]thymidine being used as regeneration markers. We focused on the induction of DNA replication enzymes, particularly DNA polymerases (pol) α, δ, and ε. Using rat models, we have shown that the activity of pol α in crude liver extract well represents the regenerating capacity of hepatocytes. Using pol α as an indicator, we analyzed liver regeneration in rat models under various conditions: obstructive jaundice, external or internal biliary drainage, and the obstruction of portal vein branches. It has been revealed that the ligation of the common bile duct alone induces a certain amount of hepatocyte proliferation. It was striking that external biliary drainage suppressed regeneration capacity in cholestatic rat liver after partial hepatectomy. The strong regeneration in nonligated lobes induced by portal branch ligation was similar to the liver regeneration seen after partial hepatectomy with respect to the induction of DNA polymerases. Taken together, the aspects of DNA replication, particularly the induction of DNA polymerases, may contribute to shedding new light on the regeneration of human liver. This work was supported in part by a Grant-in-Aid for General Scientific Research and for Cancer Research from the Ministry of Education, Science and Culture, Japan, and by grants from the Uehara Memorial Foundation