Accumulation of poly(adenosine diphosphate-ribose)by sustained supply of calcium inducing mitochondrial stress in pancreatic cancer cells

BACKGROUND The biochemical phenomenon defined as poly adenosine diphosphate(ADP)-ribosylation(PARylation)is essential for the progression of pancreatic cancer.However,the excessive accumulation of poly ADP-ribose(PAR)induces apoptosis-inducing factor(AIF)release from mitochondria and energy deprivation resulting in the caspase-independent death of cancer cells.AIM To investigate whether sustained calcium supply could induce an anticancer effect on pancreatic cancer by PAR accumulation.METHODS Two pancreatic cancer cell lines,AsPC-1 and CFPAC-1 were used for the study.Calcium influx and mitochondrial reactive oxygen species(ROS)were observed by fluorescence staining.Changes in enzyme levels,as well as PAR accumulation and energy metabolism,were measured using assay kits.AIF-dependent cell death was investigated followed by confirming in vivo anticancer effects by sustained calcium administration.RESULTS Mitochondrial ROS levels were elevated with increasing calcium influx into pancreatic cancer cells.Then,excess PAR accumulation,decreased PAR glycohydrolase and ADP-ribosyl hydrolase 3 levels,and energy deprivation were observed.In vitro and in vivo antitumor effects were confirmed to accompany elevated AIF levels.CONCLUSION This study visualized the potential anticancer effects of excessive PAR accumulation by sustained calcium supply on pancreatic cancer,however elucidating a clear mode of action remains a challenge,and it should be accompanied by further studies to assess its potential for clinical application.

Changes in P2Y purinoreceptor-mediated intracellular calcium signal pathways results in inositol-1, 4, 5-triphosphate-sensitive calcium stores in rat small trigeminal ganglion neurons

BACKGROUND： Most of the currently available information on purinergic receptors （P2Rs） involved in pain transmission is based on results obtained in dorsal root ganglion or the spinal cord. However, the mechanism of P2Rs in trigeminal neuralgia remains unclear. OBJECTIVE： To investigate changes in the P2R-mediated calcium signaling pathway in nociceptive trigemJnal ganglion neurons. DESIGN, TIME AND SETTING： In vitro experiments were conducted at the Patch-Clamp Laboratory of Comprehensive Experiment Center of Anhui Medical University, China from September 2008 to June 2009. MATERIALS： Thapsigargin, caffeine, suramin, and adenosine 5＇-triphosphate were purchased from Sigma, USA. METHODS： Using Fura-2-based microfluorimetry, intracellular calcium concentration （[Ca^2＋]i） was measured in freshly isolated adult rat small trigeminal ganglion neurons before and after drug application. MAIN OUTCOME MEASURES： Fluorescent intensities were expressed as the ratio F340/F380 to observe [Ca^2＋]i changes. RESULTS： In normal extracellular solution and Ca^2＋-free solution, application of thapsigargin （1 μmol/L）, a sarcoplasmic reticulum Ca^2＋ pump adenosine 5＇-triphosphate inhibitor, as well as caffeine （20 mmol/L）, a ryanodine receptor agonist, triggered [Ca^2＋]i increase in small trigeminal ganglion neurons. A similar response was induced by application of adenosine 5＇-triphosphate （100 μmol/L）. In Ca^2＋-free conditions, adenosine 5＇-triphosphate-induced [Ca^2＋]i transients in small trigeminal ganglion neurons were inhibited in cells pre-treated with thapsigargin （P 〈 0.01）, but not by caffeine （P 〉 0.05）. In normal, extracellular solution, adenosine 5＇-triphosphate-induced [Ca^2＋]i transients in small trigeminal ganglion neurons were partly inhibited in cells pre-treated with thapsigargin （P 〈 0.05）. CONCLUSION： Inositol-1,4, 5-triphosphate （IP3）- and ryanodine-sensitive Ca^2＋ stores exist in rat nociceptive trigeminal ganglion neurons. Two pathways are involved in the purinoreceptor-mediated [Ca^2＋]i rise observed in nociceptive trigeminal ganglion neurons. One pathway involves the metabotropic P2Y receptors, which are associated with the IP3 sensitive Ca^2＋store, and the second pathway is coupled to ionotropic P2X receptors that induce the Ca^2＋ influx.

Effect of Acupuncture on Monoamines and Adenosine Triphosphatase Activityin Lateral Hypothalamic Area of ObeseRats

Objective: To study the mechanism of acupuncture in treating simple obesity. Methods: Central nerve push-pull perfusion and biochemical technique were used to observe the effect of acupuncture on the obese parameters, changes of monoamine transmitters and activity of ATPase in the lateral hypothalamic area (LHA) of obese rats. Results: Noradrenaline (NA) level in LHA of obese rats was higher but serotonin (5-HT) level and ATPase activity were lower than those in normal rats. After acupuncture treatment, in the same time of reducing body weight, NA level in LHA of rats was reduced, and 5-HT level and ATPase activity in it were increased.(P<0.05 and P<0.01). Conclusion:The effective regulation on LHA of obese rats is possibly one of the key factors in anti-obesity effect of acupuncture.

Blocking Cyclic Adenosine Diphosphate Ribose-mediated Calcium Overload Attenuates Sepsis-induced Acute Lung Injury in Rats

Background： Acute lung injury （ALI） is a common complication of sepsis that is associated with high mortality, lntracellular Ca^2＋ overload plays an important role in the pathophysiology of sepsis-induced ALl, and cyclic adenosine diphosphate ribose （cADPR） is an important regulator of intracellular Ca^2＋ mobilization. The cluster of differentiation 38 （CD38）/cADPR pathway has been found to play roles in multiple inflammatory processes but its role in sepsis-induced ALl is still unknown. This study aimed to investigate whether the CD38/cADPR signaling pathway is activated in sepsis-induced ALl and whether blocking cADPR-mediated calcium overload attenuates ALl. Methods： Septic rat models were established by cecal ligation and puncture （CLP）. Rats were divided into the sham group, the CLP group, and the CLP＋ 8-bromo-cyclic adenosine diphosphate ribose （8-Br-cADPR） group. Nicotinamide adenine dinucleotide （NAD＋）, cADPR, CD38, and intracellular Ca^2＋ levels in the lung tissues were measured at 6, 12, 24, and 48 h after CLP surgery. Lung histologic injury, tumor necrosis factor （TNF）-a, malondialdehyde （MDA） levels, and superoxide dismutase （SOD） activities were measured. Results： NAD＋, cADPR, CD38, and intracellular Ca-＋ levels in the lungs of septic rats increased significantly at 24 h after CLP surgery. Treatment with 8-Br-cADPR, a specific inhibitor of cADPR, significantly reduced intracellular Ca^2＋ levels （P = 0.007）, attenuated lung histological injury （P = 0.023）, reduced TNF-a and MDA levels （P 〈 0.001 and P = 0.002, respectively） and recovered SOD activity （P = 0.031） in the lungs of septic rats. Conclusions： The CD38/cADPR pathway is activated in the lungs of septic rats, and blocking cADPR-mediated calcium overload with 8-Br-cADPR protects against sepsis-induced ALl.

Platelet-released ADP stabilizes PAF-induced rabbit platelet aggregation by stabilizing intracellular calcium

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Brain-derived neurotrophic factor signaling in the neuromuscular junction during developmental axonal competition and synapse elimination

During the development of the nervous system,there is an overproduction of neurons and synapses.Hebbian competition between neighboring nerve endings and synapses performing different activity levels leads to their elimination or strengthening.We have extensively studied the involvement of the brain-derived neurotrophic factor-Tropomyosin-related kinase B receptor neurotrophic retrograde pathway,at the neuromuscular junction,in the axonal development and synapse elimination process versus the synapse consolidation.The purpose of this review is to describe the neurotrophic influence on developmental synapse elimination,in relation to other molecular pathways that we and others have found to regulate this process.In particular,we summarize our published results based on transmitter release analysis and axonal counts to show the different involvement of the presynaptic acetylcholine muscarinic autoreceptors,coupled to downstream serine-threonine protein kinases A and C(PKA and PKC)and voltage-gated calcium channels,at different nerve endings in developmental competition.The dynamic changes that occur simultaneously in several nerve terminals and synapses converge across a postsynaptic site,influence each other,and require careful studies to individualize the mechanisms of specific endings.We describe an activity-dependent balance(related to the extent of transmitter release)between the presynaptic muscarinic subtypes and the neurotrophin-mediated TrkB/p75NTR pathways that can influence the timing and fate of the competitive interactions between the different axon terminals.The downstream displacement of the PKA/PKC activity ratio to lower values,both in competing nerve terminals and at postsynaptic sites,plays a relevant role in controlling the elimination of supernumerary synapses.Finally,calcium entry through L-and P/Q-subtypes of voltage-gated calcium channels(both channels are present,together with the N-type channel in developing nerve terminals)contributes to reduce transmitter release and promote withdrawal of the most unfavorable nerve terminals during elimination(the weakest in acetylcholine release and those that have already become silent).The main findings contribute to a better understanding of punishment-rewarding interactions between nerve endings during development.Identifying the molecular targets and signaling pathways that allow synapse consolidation or withdrawal of synapses in different situations is important for potential therapies in neurodegenerative diseases.

ATP6V1A缺失导致脓毒症心脏驻留巨噬细胞清除能力损伤

目的 探讨脓毒症后心脏驻留巨噬细胞的清除能力及其机制。方法 利用盲肠穿孔结扎术建立脓毒症小鼠模型,将30只雄性C57BL/6小鼠(8周龄,体质量20~25 g)按随机数字抽样法分为假手术组(Sham组,n=15)和脓毒症模型组(Sepsis组,n=15)。使用免疫荧光技术标记心肌细胞与巨噬细胞观察小鼠心肌细胞凋亡及心脏驻留巨噬细胞对心肌细胞的吞噬情况。提取心脏驻留巨噬细胞进行转录组学测序,观察脓毒症后心脏驻留巨噬细胞的功能变化。在细胞水平建立心脏驻留巨噬细胞系,即正常组(RAC组);用LPS处理RAC组细胞后,即脓毒症组(RAC+LPS组)。观察2组间对凋亡心肌细胞清除能力的差异;使用DQ-BSA-RED溶酶体活性检测探针、Lyso-Sensor yellow/bule染料、ELISA以及蛋白质印迹实验法检测心脏驻留巨噬细胞溶酶体功能、溶酶体重要水解酶活性及蛋白表达、囊泡型腺苷三磷酸酶(vacuolar-type adenosine triphosphatases,V-ATPase)含量及其相关亚基的改变。结果 与Sham组相比,Sepsis组小鼠心肌细胞凋亡数量增加(P<0.05),心脏巨噬细胞对心肌细胞的吞噬增加(P<0.05),转录组学结果分析发现脓毒症后心脏驻留巨噬细胞的溶酶体相关功能显著失调。体外实验结果显示,与RAC组相比,RAC+LPS组对凋亡心肌细胞的碎片化能力降低,溶酶体的黄色荧光强度明显减弱(P<0.05),溶酶体水解酶活性降低(P<0.05)。此外,LPS处理显著降低了心脏驻留巨噬细胞V-ATPase及其主要亚基ATP6V1A的活性和表达(P<0.05)。结论 脓毒症后心脏驻留巨噬细胞对凋亡心肌细胞的清除能力降低,其机制可能与其溶酶体V-ATPase重要亚基ATP6V1A和溶酶体水解酶活性降低有关。

严重烫伤大鼠心、肝、肾组织Na^+,K^+-ATP酶、Ca^(2+)-ATP酶活性的变化

目的：观察严重烫伤大鼠心、肝、肾组织Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ和Ｃａ２＋－ＡＴＰａｓｅ活性及组织含水量的变化。方法：雄性ＳＤ大鼠制作３０％Ⅲ度烫伤模型，在伤后４，８，１２，２４ｈ取心、肝、肾组织，测定含水量，匀浆后用比色法测定Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ和Ｃａ２＋－ＡＴＰａｓｅ活性。结果：对照组大鼠肾组织Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ活性最高，心肌组织Ｃａ２＋－ＡＴＰａｓｅ活性最高；严重烫伤后各器官ＡＴＰａｓｅ活性均进行性下降，伤后１２ｈ达最低点，但不同组织间酶活性下降的模式不尽相同；组织含水量均在伤后４ｈ明显升高，伤后８ｈ最高。结论：Ｎａ＋，Ｋ＋－ＡＴＰａｓｅ和Ｃａ２＋－ＡＴＰａｓｅ分布存在组织特异性。

氟烷和七氟醚对缺血心肌功能和代谢及Ca^(2+)-ATP酶活性的影响

目的 :研究氟烷、七氟醚 (1 5MAC)对缺血心肌的影响。方法 :应用离体大鼠心脏Langendorff逆行灌注模型研究氟烷、七氟醚对心肌缺血前心率 (HR)、左室舒张末期压力 (LVEDP)、左室发展压 (LVDP)、左室压力升高速率 (+dp/dt)、左室压力下降速率 (-dp/dt)和冠脉流量 (CF)的影响 ,测定缺血前、缺血 1 0min、缺血 2 5min 3个不同时间的心肌ATP含量、Ca2 + -ATP酶活性 ,同时记录缺血间期左室内压的变化情况。结果 :七氟醚显著增加正常离体心脏的CF ,氟烷、七氟醚均不同程度地抑制心肌收缩功能和Ca2 + -ATP酶活性 ,能够增加正常心肌的能量贮备。缺血 1 0min时 ,二药能够减缓心肌ATP含量及Ca2 + -ATP酶活性的下降 ,氟烷的作用比较明显。缺血间期 ,氟烷明显推迟缺血性挛缩的起始时间 ,降低挛缩幅度。结论 :氟烷的抗缺血损伤作用优于七氟醚 ,延缓缺血期心肌ATP含量及Ca2 +

丙泊酚对大鼠脑突触体Na^+,K^+-ATP酶和Ca^(2+)-ATP酶活性的影响

丙泊酚（ｐｒｏｐｏｆｏｌ）是一种新型短效静脉麻醉药，具有起效迅速，苏醒快，醒后无宿醉感等优点［１］，因而被广泛地应用于麻醉维持，但其全麻作用的确切机理仍不十分清楚．Ｎａ＋，Ｋ＋－ＡＴＰ酶对维持神经细胞的兴奋性，传导性和影响神经递质的释放等方面具有极为...

牛磺酸对缺血大鼠心肌线粒体Ca^(2+)-Mg^(2+)-ATP酶活性与MDA含量影响

目的和方法：用Ｗｉｓｔａｒ大鼠皮下注射异丙肾上腺素（ＩＳＰ，５ｍｇ／ｋｇ）诱导心肌缺血模型。观测心肌线粒体（Ｍｉｔ）中丙二醛（ＭＤＡ）含量、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性及牛磺酸（Ｔａｕ）的影响。结果：缺血组大鼠心肌Ｍｉｔ中ＭＤＡ升高８７８３％、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性分别降低３７５６％和５０２０％（Ｐ＜０．０１）。Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性与ＭＤＡ含量也呈显著负相关（ｒ＝－０．８７，Ｐ＜０．０１）。Ｃａ２＋－ＡＴＰ酶活性与ＭＤＡ含量也呈显著负相关（ｒ＝－０７９，Ｐ＜０．０１）。在注射异丙肾上腺素（ＩＳＰ）前３０ｍｉｎ腹腔注射Ｔａｕ（２００ｍｇ／ｋｇ）则Ｍｉｔ中ＭＤＡ含量、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性均未见显著异常改变。结论：Ｔａｕ可能通过抑制ＭＤＡ的生成实现其保护Ｃａ２＋－ＡＴＰ酶和Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性的作用。

硫喷妥钠对大鼠不同脑区ATP酶活性的影响

目的 探讨硫喷妥钠对大鼠不同脑区ATP酶活性的动态影响 ,是否与麻醉作用有关。方法 采用♂SD大鼠 4 0只 ,随机分为 5组 ,生理盐水 (10mL·kg- 1,ip)对照期组及给硫喷妥钠 (30mg·kg- 1,ip)后的诱导期组、麻醉期组、恢复期组、清醒期组。断头取脑 ,用分光光度法测定大脑皮层、脑干、海马和纹状体Na+,K+ ATP酶、Ca2 + ATP酶活性。结果给硫喷妥钠后大脑皮层的Na+,K+ ATP酶活性在诱导期和恢复期显著降低 ,而Ca2 + ATP酶活性在诱导期和麻醉期显著升高 ,到清醒期时 ,两种酶活性均恢复到对照期组水平 ;脑干的Na+,K+ ATP酶、Ca2 + ATP酶活性在给硫喷妥钠后诱导期、麻醉期和恢复期均显著低于对照期组 ,直至清醒期仍与对照组有显著性差异 ,而以诱导期最低。海马、纹状体的Na+、K+ ATP酶和Ca2 + ATP酶活性则在整个麻醉期间无明显变化。

甘草酸对缺血再灌注犬脑线粒体ATP酶活性的影响

研究甘草酸对完全性缺血再灌注犬脑线粒体ＡＴＰ酶、脑组织乳酸脱氢酶（ＬＤＨ）、脑水含量和神经功能的影响。采用犬心脏停跳再复苏模型，１６只家犬随机分成３组：非缺血对照组（ｎ＝４）；缺血再灌注组（ｎ＝６）；甘草酸治疗组（ｎ＝６）。结果显示：甘草酸明显提高再灌注犬脑ＡＴＰ酶和ＬＤＨ活性，减轻脑水肿，改善神经功能。表明甘草酸通过提高线粒体ＡＴＰ酶和组织ＬＤＨ活性，改善能量代谢，减轻犬脑再灌注损伤，促进脑功能恢复。

高血压病患者红细胞内Ca浓度及ATP酶活性与红细胞变形性的关系

目的 探讨高血压病患者红细胞变形性 (RCD)与红细胞内Ca2 + 浓度及细胞膜ATP酶活性的关系。方法 用粘度法、化学比色法测定了 2 0例正常人及 30例高血压病患者的红细胞变形指数 (DI)、红细胞内Ca2 + 浓度、红细胞膜Na+ K+ ATP酶和Ca2 + Mg+ ATP酶活性。结果 高血压病组与正常对照组比较 ,DI值显著升高 ,ATP酶活性显著降低 ,红细胞内Ca2 + 浓度升高 ;高血压病患者DI与ATP酶活性呈负相关 ,与红细胞内Ca2 + 浓度及DBP呈正相关。结论 高血压病患者RCD降低 ,并与细胞膜ATP酶活性降低及红细胞内Ca2 + 浓度、血压升高相关。

长期摄取高钠盐饮食引发的高血压发病机制实验研究

目的 :探讨高钠盐引发的高血压发病机制。方法 :雄性SD大鼠 4 0只 ,分为对照 (NC)组、高盐 (HS)组、高盐 +L -精氨酸 (HS +Arg)组、高盐 +依那普利 (HS +En)组和高盐 +特拉唑嗪 (HS +Ter)组 ,每组 8只。各组饲料相同。NC组饮去离子水 ;HS组饮 1 5 %氯化钠溶液 ;HS +Arg组、HS +En组和HS +Ter组分别饮用 1 5 %氯化钠溶液配制的L -精氨酸 ( 4g·kg-1·d-1)、依那普利 ( 3 0mg·kg-1·d-1)和盐酸特拉唑嗪 ( 4mg·kg-1·d-1)。第 8周末 ,大鼠在戊巴比妥钠麻醉下 ,直接测量颈总动脉血压 ,开腹抽取下腔静脉血及剖取肾脏、肾上腺。测定前海葱苷原A样物质 (PLC)水平 ,Na+ K+ ATP酶活性 ,NO(x)、内皮素 (ET)及血管紧张素II(AngII)水平。结果 :HS组大鼠血压显著高于NC组 ,血浆PLC、ET及肾上腺AngII水平皆显著高于NC组 ;血浆和肾组织NO(x)和AngII水平、肾脏Na+ K+ ATP酶活性皆明显低于NC组 ;HS +Arg组、HS +En组和HS +Ter组大鼠血压和血浆PLC水平皆显著低于HS组 ,血浆和肾组织NO(x)水平及Na+ K+ ATP酶活性皆明显高于HS组 ;HS +Arg组、HS +En组和HS +Ter组肾上腺AngII水平及HS +Arg组血浆ET水平明显低于HS组 ,并与NC组相近。结论 :在高钠盐引发的高血压发病机制中 ,除钠泵抑制因子释放增加致细胞膜Na+ K+ ATP酶活性?

空心莲子草对钉螺酶组织化学的影响

目的观察空心莲子草抑制钉螺运动及灭螺的机制。方法将实验钉螺随机分为4组,分别于空心莲子草浸液(1g/L)及去氯水中各浸泡12h和20h后,用酶组织化学方法染色,显微镜下观察钉螺的头足部、中枢神经节、鳃叶及肝脏的三磷酸腺苷酶(Mg2+-ATPase)、胆碱脂酶(ChE)、乳酸脱氢酶(LDH)和琥珀酸脱氢酶(SDH)的活性;并用计算机图像分析系统(HPIAS-1000)检测各组不同部位染色片的灰度值,进行定量分析。结果空心莲子草浸液12h和20h组,在钉螺头足部、中枢神经节及鳃部的ChE酶染色均明显变淡,显示该酶的活性减弱。图像分析系统检测各组不同部位染色片的灰度值,结果显示,空心莲子草浸液12h和20h组ChE活性在头足部(130.95±8.08,129.91±7.05)、中枢神经节(127.43±7.27,126.78±7.38)和鳃叶(121.38±7.31,126.41±8.28)与对照组的相应部位(分别为64.65±8.54、65.18±7.96,57.86±6.57、50.71±6.15,88.96±6.78、89.86±7.01)比较,差异均有统计学意义(P<0.01)。空心莲子草浸液20h组钉螺的Mg2+-ATPase活性在头足部(89.91±5.08)、中枢神经节(71.15±5.43)及肝脏(112.40±7.81)与对照组(分别为78.81±8.10、60.09±6.05和95.50±8.35)比较,差异有统计学意义(P<0.05),但浸泡12h组的Mg2+-ATPase活性与对照组比较,差异无统计学意义(P>0.05)。空心莲子草浸液12h和20h组的LDH和SDH活性与对照组的比较,差异均无统计学意义(P>0.05)。结论空心莲子草浸液主要通过迅速抑制钉螺体内ChE活性,随后抑制Mg2+-ATPase活性,而导致ATP的释放与利用障碍致钉螺死亡。

猫心肌缺血再灌注对Ca2+┐ATPase活力及肌浆网钙摄取能力的影响

目的：观察猫心肌缺血再灌注过程中心肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力、肌浆网钙摄取能力、线粒体丙二醛及心肌ＡＴＰ含量变化。方法：利用猫体外循环模型，心脏低温停搏６０ｍｉｎ后，恢复正常血液灌注６０ｍｉｎ。测定心肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力、肌浆网钙摄取能力、心肌ＡＴＰ及线粒体丙二醛含量。结果：心脏缺血６０ｍｉｎ时，随着心肌ＡＴＰ含量的下降，Ｃａ２＋－ＡＴ－Ｐａｓｅ活力及肌浆网钙摄取能力下降，而丙二醛含量仅有轻微增加；恢复灌注６０ｍｉｎ后，Ｃａ２＋－ＡＴＰａｓｅ活力及肌浆网钙摄取能力进一步下降，同时丙二醛含量明显增加。结论：缺血期间心肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力及肌浆网钙摄取能力的下降主要与心肌能量储备降低有关，而复灌后Ｃａ２＋－ＡＴＰａｓｅ活力及肌浆网钙摄取能力进一步下降，可能与复灌过程中氧自由基大量产生。

亚低温对大鼠脑缺血损伤的保护作用

目的：验证亚低温对脑缺血损伤的保护作用。方法：２４只ＳＤ大鼠随机分为对照组（ｎ＝７），缺血组（ｎ＝９），亚低温组（ｎ＝８），参照Ｐｕｌｓｉｎｅｌｉ和Ｂｒｉｅｒｌｅｙ的方法建立脑缺血动物模型，观察Ｎａ＋－Ｋ＋－ＡＴＰ酶活性、脑组织含水量和丙二醛（ＭＤＡ）含量的改变。结果：与对照组和缺血组相比，亚低温组能阻止Ｎａ＋－Ｋ＋－ＡＴＰ酶活性的降低（Ｐ＜０．０１）、降低脑组织含水量（Ｐ＜０．０５）和ＭＤＡ含量（Ｐ＜０．０１）。结论：亚低温具有保护血脑屏障，减轻脑水肿，减少Ｃａ２＋内流，抑制氧自由基的产生等作用。

银屑病辨证分型与红细胞变形能力及膜ATP酶活性的关系

本文报告３２例不同证型银屑病患者及３０例健康对照者红细胞变形能力及膜ＡＴＰ酶活性的检测结果。银屑病患者红细胞变形能力下降，Ｎａ＋－Ｋ＋－ＡＴＰ酶活性增高而Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性降低。异常的程度依次是血瘀型＞血燥型＞血热型。提示银屑病的确具有血瘀证指征，为本病的辨证分型提供了客观资料。

循环血中有微血栓时大鼠心肌细胞膜Na~＋－K~＋－ATP酶活性与心肌损害的关系

在循环血中出现微血栓的大鼠模型中分析心电图改变、微血栓数目及心肌细胞膜上Ｎａ￣＋－Ｋ￣＋－ＡＴＰ酶活性间关系，结果发现心电图上Ｓ－Ｔ段变化与酶活性间呈负相关（ｒ＝－０．７７，Ｐ＜０．０５），微血栓数目与酶活性间呈负相关（ｒ＝－０．９５，Ｐ＜０．０５），同时观察心肌纤维的形态学改变。讨论了上述变化的临床意义。