蒙药绿松石的质量标准研究＊

目的 建立蒙药绿松石的质量标准。方法 收集不同产地绿松石，共10批。观察绿松石样品和粉末的性状并进行理化鉴别；按2020年版《中国药典》（四部）通则方法测定绿松石样品中水分、浸出物含量；采用原子吸收光谱法测定绿松石样品铜元素含量。结果 绿松石为不规则、周围带有黑石的块状物，表面蓝绿色，体重，质硬脆，难砸碎，断面呈贝壳状，蜡样光泽，粉末呈灰绿色，无臭，味淡；理化鉴别结果显示，呈铜盐反应；10批次样品中水分含量为0.41%-3.94%（SD=1.37%），浸出物含量为0.21%-0.81%（SD=0.21%），铜元素含量为3.03%-4.63%（SD=0.63%）。结论 初步拟定绿松石中水分含量不得超多5.0%、浸出物含量不得低于0.10%，铜元素含量应为2.60%-4.84%，制定的标准可用于蒙药材绿松石的质量控制。     

Additive Effects of Sevoflurane and Propofol on γ-Aminobutyric Acid Receptor Function

Background: Previous studies have shown that propofol and sevoflurane enhance the function of [gamma]-aminobutyric acid type A (GABAA) receptors. However, it is not known whether these two drugs modulate the same molecular pathways. In addition, little is known about receptor function in the presence of both propofol and sevoflurane. The aim of this study was to better understand the interactions of propofol and sevoflurane with the GABAA receptor.

Methods: Wild-type [alpha]1, [beta]2, [gamma]2s GABAA receptor subunit complementary DNAs were transfected into human embryonic kidney cells grown on glass coverslips using a calcium phosphate transfection method. After transfection (36-72 h), cells were whole cell patch clamped and exposed to combinations of the following: 0.3-1,000 [mu]m [gamma]-aminobutyric acid (GABA), 0-10 [mu]m propofol, and 0-1,650 [mu]m sevoflurane. Chemicals were delivered to the cells using two 10-channel infusion pumps and a rapid solution exchanger.

Results: Both propofol and sevoflurane alone enhanced the amplitude of GABAA receptor responses to submaximal concentrations of GABA in a dose-dependent manner. The enhancement was underpinned by an increase in the apparent affinity of the receptor for GABA. Coapplication of both anesthetics further enhanced the apparent affinity of the receptor for GABA.     

优克龙治疗输尿管结石(附60例报告)

目的　观察优克龙 (Urocalun )治疗输尿管结石的疗效和安全性。　方法　对 6 0例输尿管结石直径 <1cm的患者予口服优克龙治疗 ,4 5 0mg/次 ,3次 /d ,服药 5周。　结果　 6 0例患者中结石排出 4 5例 (75 % ) ;10例 (17% )结石位置下降 ;5例 (8% )位置无变化。 4例患者服药后有轻度胃部不适、恶心或口干。　结论　优克龙治疗输尿管结石效果良好。     

Mesogonadal shunts for extrahepatic portal vein thrombosis and variceal hemorrhage.

Extrahepatic portal vein thrombosis (EHPVT) may occur in children or adults and usually comes to clinical attention due to complications of portal hypertension such as variceal hemorrhage. A variety of standard surgical techniques exist to manage these patients, but when these fail surgical options are limited. We describe two novel portosystemic shunts that utilize the gonadal vein as an autologous conduit. Four patients were evaluated for EHPVT with variceal bleeding. None of the patients were candidates for a standard splenorenal shunt due to prior surgical procedures. The first patient underwent a left mesogonadal shunt and the remaining 3 patients underwent a right mesogonadal shunt. Postoperative ultrasound or computed tomography (CT) scan confirmed early patency of the shunt in each patient. There have been no further episodes of variceal hemorrhage with follow-up of 3.5 years in the child who underwent the left mesogonadal shunt, and 17, 19, and 20 months in the patients who underwent the right mesogonadal shunt. Three of the 4 shunts remain patent. One shunt thrombosis occurred in a patient homozygous for the Factor V Leiden mutation despite anticoagulation with coumadin. This is the first report of the successful use of the gonadal vein as an in situ conduit for constructing a portosystemic shunt. In conclusion, the right and left mesogonadal shunts may be useful as salvage operations for patients with EHPVT who have failed standard surgical shunt procedures.     

Development of metabolic alkalosis after massive transfusion during orthotopic liver transplantation

Five patients undergoing orthotopic liver transplantation were investigated for changes in acid-base homeostasis secondary to large volume transfusions. All patients developed a transient acidemia during the operative period, followed by alkalemia which persisted into the early postoperative period. The patients received an estimated mean of 750 mEq of citrate, which appeared to cause metabolic alkalosis. The biochemical basis underlying the regulation of citrate metabolism that may have led to the timing, extent, and duration of the subsequent metabolic alkalosis is presented. Finally, the time course for the development of metabolic alkalosis may be a potentially sensitive indicator of early allograft function.     

Decompression sickness incidence over 63 months of hypobaric chamber operation

U.S. Army hypobaric chamber operations over a 63-month period were retrospectively reviewed, and incidence rates for decompression sickness were calculated. The overall incidence rate was 1.38/1000 exposures. The rate for interior technicians monitoring chamber operations was 6.16/1000 exposures. The rate for students was 0.64/1000 exposures. The increased incidence of decompression sickness for technicians was especially pronounced for the 10,668-m and 13,106-m flight profiles. Rapid decompression after the 7,620-m flight profile did not appear to increase the incidence of decompression sickness.     

Comparative genomic hybridization (CGH) of augmentation cystoplasties

OBJECTIVE: Tumors arising within augmentation cystoplasties are aggressive, have poor prognosis and the majority are not detected at follow-up cystoscopy. Genetic changes in tumors precede morphological abnormalities. Therefore, the aim of this study was to investigate whether genetic abnormalities detected by comparative genomic hybridization (CGH) could be used to identify those patients with augmentation cystoplasties at increased risk of tumorigenesis. METHODS: Bladder biopsy samples were obtained from 16 augmentation cystoplasty patients both distant from and near to the enterovesical anastomosis. CGH was used to detect genetic abnormalities in DNA extracted from the biopsies, archival specimens of two augmentation cystoplasties and two de novo bladder adenocarcinomas. RESULTS: A greater number of amplifications on 2p, 3q, 8q, 9p, 17p, 18pq and 20pq, were observed in bladder biopsies obtained near to the enterovesical anastomosis compared to those taken distant to the suture line. CGH of archival augmentation cystoplasty tumor DNA indicated abnormalities at several loci with amplifications at 2q, 5q, 10p and 21pq, while deletions occurred at 5p and 16p. CONCLUSIONS: The results of this study suggest that the urothelium adjacent to the bladder and/or bowel anastomosis in augmentation cystoplasties is genetically unstable. Furthermore, longitudinal studies are required to establish whether or not patients exhibiting genetic instability following augmentation cystoplasty are at greater risk of developing tumors than those with genetically stable epithelia.