不同通气方式对机械通气引起急性肺损伤兔模型的影响

目的：通过表面活性物质缺乏的兔肺模型,评估传统通气模式（ｃｏｎｖｅｎｔｉｏｎａｌ ｍｅｃｈａｎｉｃａｌ ｖｅｎｔｉｌａｔｉｏｎ,ＣＭＶ）与允许性高碳酸血症加最佳ＰＥＥＰ（ｐｅｒｍｉｓｓｉｖｅ ｈｙｐｅｒｃａｐｎｉａａｓｓｏｃｉａｔｅｄ ｗｉｔｈｉｄｅａｌＰＥＥＰｖｅｎｔｉｌａｔｉｏｎ,ＰＨＹ＋ ＰＥＥＰｉ）的通气模式对肺损伤的影响,了解肿瘤坏死因子α（ｔｕｍｏｒ ｎｅｃｒｏｓｉｓｆａｃｔｏｒα,ＴＮＦα） 与机械通气引起肺损伤（ｖｅｎｔｉｌａｔｏｒｉｎｄｕｃｅｄｌｕｎｇｉｎｊｕｒｙ,ＶＩＬＩ） 的关系。方法：１２ 只成年兔,以反复肺灌洗法制备表面活性物质缺乏兔肺模型。以ＣＭＶ（Ｃ组） 或ＰＨＹ＋ ＰＥＥＰｉ （Ｐ 组） 通气４ ｈ 后,测定通气前、后的支气管肺泡灌洗液（ｂｒｏｎｃｈｏａｌｖｅｏｌａｒ ｌａｖａｇｅ ｆｌｕｉｄ,ＢＡＬＦ）中ＴＮＦα含量和白细胞分类计数,测定肺水量,进行动脉血气分析和病理检查。结果：ＣＭＶ 组表现为明显的低氧血症,ＢＡＬＦ中较多的中性粒细胞数,总肺水量及血管外肺水量明显增多,肺内病理改变为较明显透明膜形成及炎性细胞聚集;而ＰＨＹ＋ ＰＥＥＰｉ 组引起较少的上述病理、生理变化。且ＣＭＶ 组ＢＡＬ     

眶上神经的走行层次及其临床意义

目的探讨眉区和额部不同手术层面眶上神经的保护方法。方法在１５例成人头部标本上,对眶上神经在眉区和额部的行程、走行层次和入肌点的位置进行解剖观测。结果眶上神经出眶上孔后,以５２．８±７．４°角向外上经额肌筋膜附着处入帽状腱膜下隙,达发际附近穿帽状腱膜和额肌至皮下。眶上神经起始部直径１．４±０．３ｍｍ,本干入肌点至眶上孔的直线距离为４０．２±９．１ｍｍ,水平距离和垂直距离分别为３０．５±８．８ｍｍ和３３．８±８．４ｍｍ。结论根据手术层面的不同,额眉区的深层面手术应注意保护眶上神经     

肉毒碱治疗TPN大鼠肝脂肪变性的研究

目的 探讨在全胃肠外营养（ＴＰＮ）中补充肉毒碱减轻肝脂肪变性的作用。方法 １８只正常Ｗｉｓｔａｒ大鼠和１９只肝硬化Ｗｉｓｔａｒ大鼠分别随机分为６组,Ａ１组、Ａ２组,自由进食和进水（各６只）;Ｂ１组、Ｂ２组,ＴＰＮ（分别６只、７只）;Ｃ１组、 ,ＴＰＮ加肉毒碱（各６只）。各组实验结束后测肝功能,肝脂肪及行肝脏的组织学检查。结果 ＴＰＮ组肝内脂肪显著２,ＴＰＮ＋肉毒碱组肝内脂肪明显减少。结论 在ＴＰＮ     

《伤寒论》水气证治论析

就《伤寒论》水气的涵义、致病特点、形成与发病、证治等方面进行了分析和探讨。认为：水气是一个病理概念,具有病理产物和致病因素的双重性,其本质是体内停蓄之水,其致病过程具有动而不居的特点;痰饮、水肿、湿痹皆是水气为患。水气的形成机制是阳虚,阳不制阴。治疗以“温药和之”为常法,振奋阳气以祛除水气;非尽以温药和之为变法,攻逐、清热、滋阴皆在其中。     

大鼠实验性视网膜光损伤中的视细胞凋亡

目的 进一步探讨视网膜光损伤的发病机制。 方法 20只Wistar大鼠分为实验组、对照组,分别在光照后12,24,36小时摘除眼球,视网膜组织行HE染色和核苷酸末端转移酶介导的DUTP缺口翻译法(TdT-mediated dUTP nick end labelling method,TUNEL)标记凋亡细胞。 结果 光照后12小时,视杆细胞外节出现少量空泡变性;24小时后,外核层出现明显的细胞核破碎、浓染和DNA裂解;36小时后,视杆细胞内、外节溶解,外核层大量细胞核丢失。 结论 视细胞凋亡是大鼠实验性视网膜光损伤的重要机制之一。 (中华眼底病杂志, 1999, 15: 167-169)     

An international registry for toxic inhalation and pulmonary edema: notes from work in progress

Acute toxic inhalation by irritant, and particularly oxidant, gases has until recently been considered to be no more complicated conceptually than a chemical burn of the epithelial surface. More recently, however, toxic inhalation has been appreciated to be a complex process involving biochemical, morphological and functional changes which are quantitatively similar, although inducible by different agents. Recent advances in pulmonary pathophysiology, inhalation toxicology, and particularly endothelial biology have clarified the events occurring at the moment of, and immediately following, exposure to oxidant gases. Studies of the pathophysiologic mechanisms associated with toxic inhalation by oxidant gases have been relatively static, however. Implications of recent findings in related fields illuminate the pathophysiology of toxic inhalation. Several principal speakers in this workshop are collaborating in an effort to develop a research facility for the study of toxic inhalation injury. This would be an international registry to serve as a teaching and research facility for documentation of cases of occupational and environmental toxic inhalation, considered as lung injury resulting from the inhalation of a toxic substance in a workplace setting or an uncontrolled release affecting residents of a community. The registry, as proposed, would encourage submissions by clinicians and institutions of a data set on each patient and on each incident; the registry would further encourage long-term follow-up of subjects and documentation of residual effects.Work presented at the 23rd Congress on Occupational and Environmental Health in the Chemical Industry (Medichem 1995) The Chemical Industry as a Global Citizen - Balancing Risks and Benefits, 19–22 September 1995, Massachusetts Institute of Technology, Cambridge, Massachusetts     

恶性肿瘤体内外生长和发展过程与细胞外基质相关性的研究

目的探讨细胞外基质在肿瘤侵袭转移中的作用。方法利用小鼠肺腺癌细胞母系ＬＡ７９５移植于Ｔ７３９小鼠皮下和肾包膜下,以及人鼻咽癌细胞系ＣＮＥ－２Ｚ移植于裸小鼠皮下等体内移植模型,通过间接免疫酶标和间接免疫荧光技术,测定纤维粘连蛋白（ＦＮ）、层粘连蛋白（ＬＮ）与Ⅳ型胶原（ⅣＣ）在肿瘤移植后不同时间的表达,并利用多种体外实验方法（琼脂糖滴瘤细胞移动实验、软琼脂上瘤细胞集落生长速度测定、斑点杂交等）,分析瘤细胞运动能力、瘤细胞集落生长速度等与ＬＮ、ＦＮ和ⅣＣ之间的关系。结果随着肿瘤的生长,ＦＮ、ＬＮ与ⅣＣ的表达均增强,且呈不同的分布;外源性ＦＮ、ＬＮ及ⅣＣ能提高瘤细胞的体外运动能力和促进瘤细胞集落的体外生长。结论细胞外基质的分布及其合成和降解的变化,与恶性肿瘤的侵袭和转移有关,对预测肿瘤生物学行为有参考价值。观察细胞外基质与瘤细胞侵袭的关系,肾包膜下移植模型较为理想     

Neutropenia, fever, and infection

With the advances in the management of various neoplastic diseases and subsequent improvement in "disease-free" states, complications of therapy--particularly, infectious complications--have evolved as stumbling blocks to survival. Among neutropenic (absolute neutrophil count below 1,000/mm3) patients with cancer, infection is the major autopsy-determined cause of death. With expected "cure rates" of childhood leukemia approaching 60 to 70 percent, it seems unreasonable to lose such patients to an infectious cause of death, yet this, indeed, happens. The purpose of this review is to (1) define the magnitude of the problem; (2) describe the various agents responsible for infections in neutropenic patients; (3) attempt to more sharply define degrees of neutropenia and mechanical defenses; and (4) consider various approaches to studying and treating these infections.     

Application of Akaike's information criterion (AIC) in the evaluation of linear pharmacokinetic equations

According to linear pharmacokinetics, the time course of plasma concentration of a drug, C_p,is expressed by a sum of exponential functions, C_p= _i=1 ⁿ a_i .This article describes a statistical technique to estimate the number of exponential terms, n,for the time course of drug by the application of Akaike's information criterion (AIC). Plasma concentrations of ethoxybenzamide, sulfisoxazole, bishydroxycoumarin, and diazepam measured following bolus intravenous injection were used as clinical examples for this method. Selection of models is compared between the AIC method and an Ftest method at significance levels of 5% and 1%.     

Experimental approach to the pathogenesis of the anomalies of amniotic disease

By intra-adnexal injection of glucose in the rabbit embryo, we were able to stimulate all the anomalies associated with "Amniotic Disease". Since we were even able to obtain amniotic bands, this study provides an excellent experimental model of this disease. Resulting lesions occur early in development, corresponding to the first trimester of human gestation. All of the anomalies can ultimately be explained by the destruction of the most superficial cells: epiblastic cells of the embryo and the amnion, subjacent mesenchyme, and endothelial cells. The subsequent lack of interaction between these cells and the importance of the anatomical localizations of resulting hematomas can lead to the pathogenetic approach to this disease. In light of the present study, the disease appears to be caused by an external factor within the amniotic fluid. The exact nature of the destructive agent(s) remains a mystery in man.