谷氨酰胺诱导大鼠热休克蛋白70mRNA的表达

热休克蛋白(heat shock protein,HSP)是感染或非感染(如创伤、休克)等致病因素作用于机体后,诱发机体细胞合成的一组高度保守的蛋白质,谷氨酰胺(Glu-tam ine,Gln)作为体液中最丰富的氨基酸之一,对机体多个脏器有保护作用。一些研究表明,Gln在体外可促进果蝇Kc细胞HSP的表达[1];Gln诱导的HSP表达对肠道上皮细胞有保护[2]。但Gln是否能在动物的各个脏器引起HSP的表达及时间和量效关系如何,尚未见明确报道。本研究对此进行了实验观察,拟为临床应用提供理论依据。1材料和方法1.1主要试剂力太(批号J20020081,Fresennius Kabi公司,德国),…     

HSP表达在炎症反应综合征中的作用与意义

热休克蛋白(HSPs)是生物体面临不利生存环境中快速表达的一类保护性蛋白家族，具有修复和维护细胞功能的作用。在炎症反应综合征(SIRs)病理过程中，机体细胞均有HSP表达，并通过分子伴侣、抗凋亡及抗炎机制发挥保护作用。本文对不同组织细胞HSP表达对SIRS发展及转归的意义作一综述。     

HSP表达在炎症反应综合征中的作用与意义

热休克蛋白(HSPs)是生物体面临不利生存环境中快速表达的一类保护性蛋白家族,具有修复和维护细胞功能的作用。在炎症反应综合征(SIRS)病理过程中,机体细胞均有HSP表达,并通过分子伴侣、抗凋亡及抗炎机制发挥保护作用。本文对不同组织细胞HSP表达对SIRS发展及转归的意义作一综述。     

热休克蛋白70家族的功能和在神经保护中的作用

脑缺血耐受的实验研究发现，诱导热休克蛋白70家族(HSP70)的表达增加可能是内源性脑保护机制之一。HSP70包括两种蛋白：Hsp70(诱导型)和Hsc70(结构型)。本文就这两种蛋白的功能、表达的调节及在不同应激反应中表达的相关性作一综述。     

热休克蛋白在子宫颈癌中的表达及其意义

目的探讨热休克蛋白(heat shock proteins,HSPs)在子宫颈癌组织中的表达情况及意义。方法采用PT—PCRH和免疫印迹法检测HSPs在子宫颈癌组织及正常子宫组织中的蛋白和mRNA的表达水平。结果癌组织中HSP70、HSP86及αB晶状体蛋白表达较正常组织明显增多(P<0.05),且HSP70表达最高(P<0.01)。结论 HSP70在子宫颈癌组织中表达显著增高。     

大鼠烫伤早期肠黏膜组织热休克蛋白HSP70和HSP90的表达

目的 研究烧伤早期肠黏膜组织热休克蛋白HSP70和HSP90的表达、组织含量和分布的变化规律,探讨烧伤早期肠黏膜组织细胞的热休克反应在机体的病理生理反应中的意义。方法 以烫伤大鼠为模型,利用ELISA、免疫印迹分析和免疫组织化学方法,分析和研究肠黏膜组织HSP70和HSP90的表达、组织含量和分布及其功能状态。结果 (1)大鼠烫伤早期肠黏膜游离HSP70的含量有非常显的短暂降低;(2)肠黏膜组织HSP70和HSP90的总体含量在烧伤后有显升高;(3)烧伤早期肠黏膜组织HSP70的分子结构存在显的不均一性。结论 肠黏膜组织细胞中两种热休克蛋白表达、含量和分布的规律性变化,在肠黏膜组织细胞的应激反应、进而在肠道的黏膜屏障机制中,可能有重要的意义。     

热休克反应与脓毒症

热休克反应主要表现为细胞在高于生理温度的环境中,快速表达一类特异性蛋白质,即热休克蛋白(HSPs),从而使细胞对继发的致死性高温产生耐受性。新近的研究发现,热休克反应对其他形式的多种细胞和组织损伤,包括脓毒症性损伤同样有保护使用,其机制与HSPs对炎症级联反应的广泛调节作用有关。将热休克反应用于脓毒症和急性肺损伤的防治是令人感兴趣的课题。     

热休克反应与脓毒症

热休克反应主要表现为细胞在高于生理温度的环境中，快速表达一类特异性蛋白质，即热休克蛋白（HSPs)，从而使细胞对继发的致死性高温产生耐受性。新近的研究发现，热休克反应对其他形式的多种细胞和组织损伤，包括脓毒症性损伤同样有保护使用，其机制与HSPs对炎症级联反应的广泛调节作用有关。将热休克反应用于脓毒症和急性肺损伤的防治是令 人感兴趣的课题。     

热休克对肝癌细胞HSP70、gp96表达的影响及与细胞周期关系

与肿瘤免疫密切相关的热休克蛋白（HSPs）主要有HSP70和gp96。因可诱导特异性抗肿瘤反应成为近期热点，不断有临床治疗试验报道。目前HSPs作用精确分子机制还不明确；特别是gp96，除发现其“管家”作用。还发现它在先天和获得性免疫中发挥重要调节作用。我们在不同条件下对BeL-7402肝癌细胞株的HSP70、gp96进行单项及共同表达的研究，结合细胞周期进行分析，对于HSP70、gp96表达，两者表达关联性，及其表达与细胞周期的关系进行了探讨。     

热休克蛋白27、70与恶性肿瘤

热休克蛋白(heat shock protein,HSP)广泛存在于生物体内,是一类在进化上高度保守的细胞应激蛋白.其中HSP27和HSP70在抗凋亡过程中发挥重要的作用,在多种肿瘤细胞中异常高表达,尤其是腺癌起源的肿瘤.HSP27和HSP70在恶性肿瘤的发生、发展中的作用及其机制是近年来研究的热点,有望对肿瘤的治疗提供新的平台.     

Shock: causes,initial assessment and investigations

Shock may result from a number of distinct disease processes and it is commonly associated with trauma, infection and cardiovascular dysfunction. Shock results in significant morbidity and mortality and is a leading causes of death in hospital patients. In order to improve patient outcomes it is important to recognize shock early, then assess and treat the shocked patient in a systematic way.The clinical classification of shock into cardiogenic, obstructive, hypovolaemic or distributive shock can help the clinician to understand the underlying cause of the shock. However, it is important to note that considerable overlap between these different types of shock can exist in practice.After identification of patients in shock, immediate resuscitation with goal-directed therapy to prevent further deterioration and improve outcome is vital. ABCDE approach can be useful systematic way for initial assessment and resuscitation. Basic monitoring should be instituted as soon as possible and in severe or unresponsive shock this should be escalated to invasive monitoring. Immediate generic laboratory, microbiological and radiological tests should be carried out as soon as possible and should include a blood lactate level. Further targeted tests should then be tailored to the history and clinical findings. These targeted investigations should help to pin point the specific cause of the shock and drive definitive management.     

Shock: causes,initial assessment and investigations

Shock may result from a number of distinct disease processes and it is commonly associated with trauma, infection and cardiovascular dysfunction. Shock results in significant morbidity and mortality and is a leading cause of death in hospital patients. In order to improve patient outcomes it is important to recognize shock early, then assess and treat the shocked patient in a systematic way. While the cause of the shocked state is sometimes obvious, in more difficult situations the use of the clinical classification of shock into cardiogenic, obstructive, hypovolaemic or distributive shock can help the clinician to discover the underlying cause of the shock. However, it is important to note that while this is a framework in practice there if often considerable overlap between these different types of shock in clinical practice. After identification of patients in shock, immediate life-saving resuscitation with directed therapy to prevent further deterioration, worsening organ failure and to improve outcome is vital. An ABCDE approach can be a useful systematic way for initial assessment and resuscitation. Basic monitoring should be instituted as soon as possible and in severe or unresponsive shock this should be escalated to invasive monitoring. Immediate generic laboratory, microbiological and radiological tests should be carried out as soon as possible and should include a blood lactate level. Further targeted tests should then be tailored to the history, clinical findings and presumed aetiology of the shocked state. These targeted investigations should help to pin point the specific cause of the shock and guide definitive management.     

Multiple-Temperature Gas-Kinetic Scheme for Type IV Shock/Shock Interaction

In this paper, a gas-kinetic scheme (GKS) method coupled with a three temperature kinetic model is presented and applied in numerical study of the Edney-type IV shock/shock interaction which could cause serious problems in hypersonic vehicles. The results showed very good agreement with the experimental data in predicting the heat flux on the surface. It could be obviously seen that the current method can accurately describe the position and features of supersonic jets structure and clearly capture the thermal non-equilibrium in this case. The three temperature kinetic model includes three different models of temperatures which are translational, rotational and vibrational temperatures. The thermal non-equilibrium model is used to better simulate the aerodynamic and thermodynamic phenomenon. Current results were compared with the experimental data, computational fluid dynamics (CFD) results, and the Direct Simulation Monte Carlo (DSMC) results. Other CFD methods include the original GKS method without considering thermal non-equilibrium, the GKS method with a two temperature kinetic model and the Navier-Stokes equations with a three temperature kinetic model, which is the same as the multiple temperature kinetic model in current GKS method. Comparisons were made for the surface heat flux, pressure loads, Mach number contours and flow field values, including rotational temperature and density. By Comparing with other CFD method, the current GKS method showed a lot of improvement in predicting the magnitude and position of heat flux peak on the surface. This demonstrated the good potential of the current GKS method in solving thermodynamic non-equilibrium problems in hypersonic flows. The good performance of predicting the heat flux could bring a lot of benefit for the designing of the thermal protection system (TPS) for the hypersonic vehicles. By comparing with the original GKS method and the two temperature kinetic model, the three temperature kinetic model showed its importance and accuracy in this case.     

Continuum Formulation for Non-Equilibrium Shock Structure Calculation

Are extensions to continuum formulations for solving fluid dynamic problems in the transition-to-rarefied regimes viable alternatives to particle methods? It is well known that for increasingly rarefied flow fields, the predictions from continuum formulation, such as the Navier-Stokes equations lose accuracy. These inaccuracies are attributed primarily to the linear approximations of the stress and heat flux terms in the Navier-Stokes equations. The inclusion of higher-order terms, such as Burnett or high-order moment equations, could improve the predictive capabilities of such continuum formulations, but there has been limited success in the shock structure calculations, especially for the high Mach number case. Here, after reformulating the viscosity and heat conduction coefficients appropriate for the rarefied flow regime, we will show that the Navier-Stokes-type continuum formulation may still be properly used. The equations with generalization of the dissipative coefficients based on the closed solution of the Bhatnagar-Gross-Krook (BGK) model of the Boltzmann equation, are solved using the gas-kinetic numerical scheme. This paper concentrates on the non-equilibrium shock structure calculations for both monatomic and diatomic gases. The Landau-Teller-Jeans relaxation model for the rotational energy is used to evaluate the quantitative difference between the translational and rotational temperatures inside the shock layer. Variations of shear stress, heat flux, temperatures, and densities in the internal structure of the shock waves are compared with, (a) existing theoretical solutions of the Boltzmann solution, (b) existing numerical predictions of the direct simulation Monte Carlo (DSMC) method, and (c) available experimental measurements. The present continuum formulation for calculating the shock structures for monatomic and diatomic gases in the Mach number range of 1.2 to 12.9 is found to be satisfactory.     

Shock and haemodynamic monitoring

Shock is the clinical syndrome that arises from inadequate cellular oxygen metabolism which can occur when there is either insufficient oxygen delivery or impaired oxygen utilization. As a clinical syndrome, shock is associated with significant morbidity and mortality particularly if there is a delay in recognition or initiation of treatment. There are multiple mechanisms that can result in a shocked state; often clinical examination is insufficient to differentiate between such mechanisms. Clinicians must instead rely on haemodynamic monitoring devices for both diagnosis and the targeting of therapies. In this article we review the basic principles of haemodynamics, the different aetiologies of shock and explore the various haemodynamic monitoring devices available to clinicians.     

Heat shock protein 70: correlation of expression with degree of graft-versus-host response and clinical graft-versus-host disease

BACKGROUND: The heat shock proteins are increasingly becoming associated with immunopathologic phenomena, being induced in response to inflammation. They are highly immunogenic and are postulated as playing a role in both innate and adaptive immunity. Their proposed role in peptide binding and antigen presentation could suggest a potential role in the alloreactive process that leads to graft-versus-host disease (GVHD) after bone marrow transplantation. METHODS: In this study we examined the expression of the widely studied heat shock protein 70 (hsp70) in an in vitro-generated graft-versus-host reaction in human skin, using streptavidin biotin immunohistochemistry and laser scanning confocal microscopy. RESULTS: Hsp70 expression was correlated with high graft-versus-host responses (P<0.001) and was confirmed using laser scanning confocal microscopy. Increased expression of hsp70 was further defined due to increases in the inducible form of hsp70. Expression of inducible hsp70 was predictive of both clinical acute GVHD (P=0.001) and incidence of chronic GVHD (P<0.001). CONCLUSIONS: This investigation has demonstrated for the first time the expression of hsp70 in a human model of GVHD, suggesting involvement in the pathogenesis of the disease and providing the basis for further investigation. Increased expression of inducible hsp70 in the model could provide a biologic marker for the prediction of clinical acute and chronic GVHD.     

Heat shock protein and high-dose aspirin: effects on random skin flap survival in a rat model.

The heat shock response is known to have a protective effect against flap ischemia. It has been shown that heat shock protein (hsp) expression can be augmented in vivo with the administration of high-dose aspirin before heat treatment. The authors hypothesized that administration of aspirin before hsp induction through heat stress would enhance further the protective effects of the heat shock response against skin flap ischemia. They used a random dorsal skin flap model in 32 rats divided into four groups (N = 8 each): control, heat shock, aspirin plus heat shock, and aspirin. Before surgery, rats in the two heat shock groups were placed in a 45 degrees C water bath until core body temperature measured 42 degrees C, and they were maintained at 42 degrees C for 15 minutes. Rats in the two aspirin groups received a single oral dose of aspirin (100 mg per kilogram) 1 hour before heat bath or surgery. Immunohistochemistry confirmed hsp expression in the two heat groups. Skin flap survival was improved significantly (p < 0.05) in the heat shock (55%), aspirin plus heat shock (58%), and aspirin (60%) groups when compared with controls (45%). Contrary to their hypothesis, aspirin combined with hsp induction did not offer greater protection from ischemia than hsp induction alone (p > 0.05). However, high-dose aspirin administration alone did improve skin flap survival when compared with controls. Future studies are needed to investigate further the role of pharmacological therapy combined with hsp induction in improving skin flap survival and to delineate the dose-response relationship between aspirin and hsp.     

Effects of quercetin on the heat-induced cytotoxicity of prostate cancer cells

BACKGROUND: It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress. We have reported that heat treatment at 43 degrees C increases the expression of heat shock protein 70 (hsp70) in prostate cancer cells, leading to apoptosis. Hsp70 is a protein that protects cells against heat damage. Cells with lower levels of hsp70 have been shown to have a higher sensitivity to heat stress. Therefore, downregulation of hsp70 is expected to enhance heat-induced inhibitory effects on cell growth. Quercetin has been reported to be an agent that inhibits hsp70 expression. The present study was undertaken to investigate the effects of quercetin and/or heat on the growth of prostate cancer cells in vitro. METHODS: Three human prostate cancer cell lines were used: Lncap; PC-3; and JCA-1. The cells were treated with quercetin and/or heat. Alterations in the cell cycle and hsp70 expression were examined by means of flow cytometry (FCM). The apoptotic cells were detected by FCM using fluorescein isothiocyanate (FITC) labeled annexin V. RESULTS: Treatment with quercetin alone resulted in an apparent decrease of hsp70-positive cells and an increase of subG1 cells in JCA-1 and LNcap cells. Quercetin inhibited an increase of hsp70 expression after heat treatment and increased the number of subG1 cells with lower levels of hsp70 in JCA-1 and LNcap cells. Quercetin was found to enhance heat-induced inhibitory effects on cell growth and heat-induced apoptosis in both JCA-1 and LNcap cells. CONCLUSION: These results suggest that quercetin may enhance heat-induced cytotoxicity in prostate cancer cell lines through the inhibition of hsp70 production.     

多沙普仑纳络酮对失血性休克犬等容输血后血流动力学的影响

目的：在实验犬中观察多沙普化、纳络酮对失血性休克等容输血后血流动力学的影响。方法：实验犬分为对照组、多沙普化组和纳络酮组，每组５条，三组动物均以动脉快速放血３０ｍｌ／ｋｇ、造成严重失血性休克模型，３０ｍｉｎ后等容输血，多沙普仑组和纳络酮组分别于输血后立即静脉注射多潲普仑２ｍｇ／ｋｇ或纳络酮０．０１５ｍｇ／ｋｇ，采用Ｓｗａｎ－Ｇａｎｚ漂浮导管及心脏电脑监护仪等手段分别于动物休克、等容输血前后测定血流     

Shock: causes,assessment and investigation

Shock is a life-threatening clinical state in which cellular hypoxia develops due to an imbalance between oxygen supply and demand resulting in end organ dysfunction. It is the end result of a number of pathophysiological processes, and multiple processes may coexist. Shock may be reversible in early stages; however, if appropriate treatment is delayed the effects become irreversible, resulting in multiorgan failure and death. Given the morbidity and mortality associated with shock, its significance has been emphasized in medical education and public health campaigns globally in recent years. Early recognition and timely interventions to treat shock and address the underlying cause(s) are essential to improve outcomes.This article provides an overview of shock syndromes, presents an approach to assessment and investigations, and reviews the management of shock in a general context. It is beyond the scope of one article to discuss the vast subject of shock in as much depth as it deserves.