分析手足口病患儿心肌酶及C反应蛋白的临床意义

目的探讨对手足口病(Hand,foot and mouth disease,HFMD)患儿心肌酶活性和C反应蛋白检测的意义,预防并发心肌炎的发生。方法以30例健康儿童作对照,对51例HFMD患儿进行心肌酶及C反应蛋白检测。结果手足口病患儿AST、LDH、CK、CK-MB、LDH-1、α-HBDH活性和CRP水平均高于正常对照组(P<0.05或P<0.01)。其中18例有心电图异常的病例,其心肌酶谱及CRP水平更是明显高于正常。结论部分手足口病患儿存在不同程度的心肌损害,心肌酶谱及C反应蛋白可作为手足口病患儿合并心肌损伤诊断依据和观察病情及判断预后的有效指标。     

心肌酶联合超敏C-反应蛋白检测对早期手足口病的诊断价值

目的探讨心肌酶联合超敏C-反应蛋白检测对早期手足口病的诊断价值。方法选取2017年7月～2018年8月我院收治的手足口病患儿81例为观察组,选取同期接受健康体检的儿童83例为对照组。清晨空腹外周静脉血进行心肌酶联合超敏C-反应蛋白检测,分析心肌酶联合超敏C-反应蛋白检测对早期手足口病的诊断价值。结果观察组患儿心肌酶指标(肌酸激酶、肌酸激酶同工酶)、超敏C-反应蛋白等测定结果明显高于对照组,差异有统计学意义(P0.05);且手足口病高危患儿肌酸激酶同工酶、超敏C-反应蛋白检测结果明显高于一般患儿,差异有统计学意义(P0.05)。结论超敏C-反应蛋白以及心肌酶学指标在早期手足口病的诊断中应用价值显著,对提升诊断准确性有重要意义。值得临床推广和广泛应用。     

手足口病患儿心肌酶及C反应蛋白的临床意义

目的探讨快速联合检测(血糖、心肌酶谱、白细胞计数及C反应蛋白)对手足口病伴发热患儿病情判断的价值。方法以40例健康儿童作为对照,对55例初诊的手足口病伴发热患儿,及时抽取空腹静脉血并分别检测血糖、心肌酶谱、全血白细胞计数和CRP水平。结果患儿白细胞计数与心肌酶谱中AST、LDH、CK、CK-MB及CRP水平均明显高于健康对照组,提示存在心肌损伤。其中高热患儿空腹血糖水平与对照组无明显统计学差异,结论联合检测方便简单、快速实效,对于初诊HFMD伴发热患者的病情判断有很大作用,及时提供诊断依据及判断预后一定的有指导意义。     

联合检测对手足口病患儿心肌损伤早期诊断的意义

目的探讨cTnI、CK-MB及hs-CRP对手足口病患儿心肌损伤早期诊断的意义。方法观察组为手足口病患儿124例,其中合并心肌损伤的重症患儿37例,对照组为健康儿童50例,分别检测cTnI、CK-MB及hs-CRP水平。结果观察组患儿cTnI、CK-MB及hs-CRP均显著高于对照组（P〈0.05）,发生心肌损伤的高危患儿CK-MB、cTnI显著高于一般患儿（P〈0.05）。比较三个指标的灵敏度,cTnI、hs-CRP显著高于CK-MB（P〈0.05）。结论 cTnI、CK-MB及hs-CRP联合检测有助于提高对手足口病患儿心肌损伤的早期发现与诊断。     

酒精摄入量与心血管相关危险因子间关系的研究

目的研究酒精摄入量和吸烟、谷氨酰转肽酶(GGT)、缺糖基转铁蛋白百分比(?T)、超敏C反应蛋白(hs-CRP)、血脂等心血管相关危险因子的相关性。方法将73例研究对象分成轻度、中度、重度饮酒和不饮酒四组,分别检测GGT、?T、hs-CRP等检测指标。结果重度饮酒者GGT、?T与不饮酒者有明显差异(P<0.05),且随着酒精摄入量加重而升高;轻中度饮酒者hs-CRP与不饮酒者有明显差异(P<0.05),也随着酒精摄入量加重而降低;各组间TC、HDL、LDL、MCV均无明显差异(P>0.05)。重度饮酒者往往伴随着大量吸烟(P<0.05)。结论重度饮酒可引起GGT、?T升高,可能通过各种途径增加心血管疾病的危险性;少到中量饮酒与低水平的hs-CRP有关,可能通过抗炎作用对心血管系统部分起到保护作用。     

心肌酶联合超敏C-反应蛋白检测对早期诊断手足口病的临床意义

目的探讨心肌酶联合超敏C-反应蛋白（hs-CRP）检测对早期诊断手足口病的临床意义。方法检测65例早期手足口病患儿的血清心肌酶与hs-CRP水平,并与同期30例健康儿童检测结果进行对照分析。结果手足口病患儿病变早期肌酸激酶（CK）、肌酸激酶同工酶MBC（CK-MB）与hs-CRP分别为（236.3±89.2）U/L、（36.2±5.6）U/L、（10.4±8.5）mg/L,均高于健康对照组的（136.2±65.1）U/L、（15.0±3.4）U/L、（1.8±1.2）mg/L,差异有统计学意义（P〈0.01）,而α-HBDH水平与健康对照组比较差异无统计学意义（P〉0.05）。血清CK、CK-MB与hs-CRP之间,均呈正相关（rCK=1.26,rCK-MB=3.41,P〈0.05）。结论 CK-MB对判断心肌损害有高度特异性,hs-CRP为病变早期的敏感指标,在手足口病早期即迅速升高,且二者呈正相关,联合检测有助于为手足口病的早期诊断提供科学依据。     

不同类型冠心病超敏C反应蛋白的观察

目的:观察不同类型冠心病患者超敏C反应蛋白(hs-CRP)水平,以探讨hs-CRP与冠心病发生的关系.方法:检测并比较31例稳定劳力型心绞痛患者、30例不稳定型心绞痛患者、32例急性心肌梗死患者及90例健康人群hs-CRP水平和其他有关生化指标.结果:冠心病组患者hs-CRP水平、血压、血脂、血糖均明显高于健康人群,而不同类型冠心病相比hs-CRP水平也存在显著差异.结论:检测hs-CRP不仅有助于评估健康人群并发冠心病的风险,而且有助于对冠心病患者进行危险分层.     

重组瘦蛋白对实验性肥胖SD大鼠生长性能影响

用肥胖性大鼠检测重组瘦蛋白的生物学活性。方法：先利用75只SD大鼠（50～60g）分两组，一组对照，另一组建立肥胖模型，模型成功后分为五组：一组空白对照，另外Ⅱ、Ⅲ、Ⅳ、Ⅴ组，Ⅱ组注射生理盐水，其余按高、中、低剂量注射重组瘦蛋白1．0mg．0．5mg、0．1mg。检测大鼠的日增重、采食量、脏器系数及胴体脂肪率。结论：组间日增重差异显著p〈0．05、采食量差异显著（p〈0．05）、脂肪率（p〈0.05）。     

不同剂量阿托伐他汀对稳定性斑块的影响

目的探讨不同剂量阿托伐他汀对稳定性斑块的影响。方法入选经冠状动脉造影和血管内超声检查确定为稳定性斑块的174例患者,分为4组：阿托伐他汀10mg组47例,阿托伐他汀20mg组45例,阿托伐他汀40mg组43例,阿托伐他汀80mg组39例,随访3—6个月,观察给予他汀药物的4组低密度脂蛋白胆固醇（LDL—C）、高密度脂蛋白胆固醇（HDL—C）、超敏C反应蛋白（hs—CRP）、坏死核所占百分比及斑块体积的动态变化。结果各组患者LDL—C、HDL—C、hs—CRP、坏死核所占百分比及斑块体积的基线水平是相近的（P均〉0．05）。随访3～6个月后（1）阿托伐他汀治疗的4组LDL—C与基线相比均有明显下降（t值分别为3．12、4．23、3．26、5．21,P均〈0．01）,且阿托伐他汀20mg组和40mg组治疗后两组间LDL—C不同（P〈0．05）;（2）阿托伐他汀10、20、40mg组治疗后HDL—C与基线比较差异均无统计学意义,但阿托伐他汀80mg组HDL—C明显高于其余3组（P均〈0．05）,同时高于基线（t=2．35,P〈0．01）;（3）阿托伐他汀80mg治疗后hs—CRP较基线显著下降[分别为（3．59±1．07）mg／L与（6．10±2．12）mg／L,t=2．37,P〈0．01];（4）通过血管内超声虚拟组织成像技术（IVUS—VH）检测,斑块坏死核所占百分比在阿托伐他汀10mg组明显高于基线[16．54±1．76）％与（7．83±1．03）％,t=2．38,P〈0．01],提示斑块向不稳定进展（坏死核所占百分比〉10％定义为不稳定性斑块）,在阿托伐他汀20、40、80mg组与基线相比无进展（t值分别为1．24、0．21、0．69,P值分别为0．069、0．846、0．643）;（5）斑块体积在阿托伐他汀10、20mg组与基线相比无增大,但是在阿托伐他汀40、80mg组斑块体积明显缩小[（30．69±8．12）mm。与（37．09±12．01）mm^3,t=1．29,P=0．019;（24．99±1．01）mm。与（36．474-14．68）mm^3,t=2．62,P〈0．01]。结论不同剂量阿托伐他汀对稳定性斑块疗效不同。（1）对于LDL—C,20mg／d阿托伐他汀就能使LDL—c降低达标,但40mg／d阿托伐他汀降低幅度明显优于20mg／d,与80mg／d相似。（2）对于HDL—C,只有80mg／d阿托伐他汀能使之升高。（3）给予80mg／d阿托伐他汀能使hs—CRP下降。（4）≥20mg／d阿托伐他汀有稳定斑块的作用,80mg／d优于40mg／d及20mg／d,而且40～80mg／d阿托伐他汀有逆转斑块的作用。     

SD大鼠皮下移植瘤模型的建立

目的建立SD大鼠W256细胞皮下移植瘤模型。方法将W256细胞冻融后传代,调整细胞浓度后接种于大鼠腹腔,建立大鼠腹腔积液模型;以浓缩的腹腔积液接种于大鼠右侧后腿皮下,建立大鼠皮下移植瘤模型,定期测量肿瘤大小;接种2周后切取长势良好肿瘤2个,并于试验结束后切取所有肿瘤,行组织病理学检查。结果所有接种SD大鼠全部接种成功,生长良好,肿瘤周围无感染病灶;肿瘤接种后第4天可触及皮下小结节,接种后第3周肿瘤平均体积2.0cm×2.5cm×3.2cm,最大肿瘤长径达5.5cm;2周后切取肿瘤结节,大体观察可见多个灰白色结节,质软;光学显微镜下瘤细胞排列密集,细胞间无间质,瘤细胞呈团状或片状排列,核大,核仁明显,核分裂相多见,肿瘤内可见丰富的小血管;实验结束时肿瘤内均见不同程度片状坏死。结论采用浓缩腹腔积液注射法制作SD大鼠W256皮下移植瘤模型方法简单、成瘤率高,能为实验提供理想的动物模型。     

Biochemical studies on the cardioprotective effect of glutamine on tissue antioxidant defense system in isoprenaline-induced myocardial infarction in rats

Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial infarction of human beings. Levels of diagnostic marker enzymes in plasma, reduced glutathione (GSH) and lipid peroxides and the activities of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase in heart tissue were determined. Injection of isoprenaline caused significant increases in the levels of diagnostic marker enzymes in plasma and lipid peroxidation in heart tissue. A parallel decline in the levels of ATP (Adenosine triphosphate) and GSH and the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes in heart tissue was also observed. Prior oral administration of glutamine significantly prevented isoprenaline-induced adverse effects and maintained myocardial antioxidant status at near normal status. The cardioprotective effect of glutamine is probably related to a strengthening of the myocardial membrane by its membrane stabilizing action, or to a counteraction of free radicals by its antioxidant property, or to its ability to maintain near to normal status the activities of free radical scavenging enzymes and the level of GSH, which protect myocardial membrane against oxidative damage by decreasing lipid peroxidation.     

SD大鼠皮下移植瘤模型的建立

目的建立SD大鼠W256细胞皮下移植瘤模型。方法将W256细胞冻融后传代,调整细胞浓度后接种于大鼠腹腔,建立大鼠腹腔积液模型;以浓缩的腹腔积液接种于大鼠右侧后腿皮下,建立大鼠皮下移植瘤模型,定期测量肿瘤大小;接种2周后切取长势良好肿瘤2个,并于试验结束后切取所有肿瘤,行组织病理学检查。结果所有接种SD大鼠全部接种成功,生长良好,肿瘤周围无感染病灶;肿瘤接种后第4天可触及皮下小结节,接种后第3周肿瘤平均体积2.0cm×2.5cm×3.2cm,最大肿瘤长径达5.5cm;2周后切取肿瘤结节,大体观察可见多个灰白色结节,质软;光学显微镜下瘤细胞排列密集,细胞间无间质,瘤细胞呈团状或片状排列,核大,核仁明显,核分裂相多见,肿瘤内可见丰富的小血管;实验结束时肿瘤内均见不同程度片状坏死。结论采用浓缩腹腔积液注射法制作SD大鼠W256皮下移植瘤模型方法简单、成瘤率高,能为实验提供理想的动物模型。     

急性过量饮酒对大鼠心脏功能的影响

目的　研究急性过量酒精摄入后大鼠心脏的病理、功能变化的特点及可能的机制。方法　 2 8只成年雄性SD大鼠随机分成饮酒组与对照组。饮酒组按 5 35 7ml/kg体重 (即 2 4g纯酒精 /kg体重 )胃管灌入 5 6 %酒精 ,对照组给予同等量生理盐水。两组均分别于灌胃后 4 5和 12 0min通过颈总动脉插管观察左心室内压力、血压、心率和心肌力学指标的变化 ,同时测定血中酒精含量。实验结束后光镜下观察大鼠心脏病理变化。结果　①饮酒组急性酒精摄入后 ,光镜下可见大鼠心肌细胞肿胀明显 ,出现嗜酸性变性。②与对照组比较 ,饮酒组急性酒精摄入后 4 5min时出现显著性的左心室压力指标下降 ,血压下降 ,心率减慢 ,心肌力学指标下降 (P <0 0 5 )。结论　①酒精可对心肌细胞造成直接的损害作用。②急性过量酒精摄入可明显损害心肌收缩和舒张功能。     

联合检测CRP、心肌酶谱及血气分析在新生儿肺炎中的临床意义探讨

目的探讨联合检测C反应蛋白(CRP)、心肌酶谱及血气分析在新生儿肺炎中的临床意义,为其诊治提供依据。方法选择该院2013年10月至2014年8月收治的新生儿肺炎患儿152例作为观察组,并根据病情检查结果分为重症肺炎组(101例)、轻症肺炎组(51例),根据病原学检查结果分为病毒性肺炎组(76例)、细菌性肺炎组(62例)和其他肺炎组(14例),同时联合检测CRP、心肌酶谱和血气分析,观察各组的差异性并与50例健康足月新生儿(对照组)进行比较。结果重症肺炎组、轻症肺炎组患儿心肌酶谱及血气分析均有不同程度异常,除轻症组患儿门冬氨酸氨基转移酶、乳酸脱氢酶、α-羟丁酸脱氢酶与对照组比较差异均无统计学意义(P0.05)外,其余检测项目与对照组比较差异均有统计学意义(P0.05);细菌性肺炎组患儿CRP增高最明显,与病毒性肺炎组、其他肺炎组及对照组比较差异均有统计学意义(P0.05);重症肺炎组患儿以混合性酸中毒为主,轻症肺炎组患儿以呼吸性酸中毒为主。结论新生儿肺炎可致心肌损害、肺通气和换气功能障碍,同时检测CRP、心肌酶谱及血气分析有助于及早发现患儿心肌损害和损害程度,对掌握和纠正酸碱失衡、低氧血症,改善肺泡通气功能,正确判断细菌性和非细菌性肺炎并给予正确治疗具有重要意义。     

川芎嗪对急性心肌梗死模型大鼠的保护作用及机制

目的探讨川芎嗪对急性心肌梗死模型大鼠的保护作用及机制。方法利用结扎清醒大鼠冠状动脉左前降支复制急性心肌梗死模型,将大鼠随机分为假手术组,模型组、银杏叶提取物(20 mg/kg)组及川芎嗪(10、204、0 mg/kg)组。测定清醒大鼠心肌酶学、心肌梗死面积、细胞凋亡和组织病理HE染色的变化。结果急性心肌梗死模型大鼠SOD显著降低,MDA、LDH和心肌梗死面积显著增大,心肌细胞凋亡数量亦明显增多(P<0.01~0.001)。川芎嗪能明显提高SOD、降低MDA、LDH的含量,减小心肌梗死面积和细胞凋亡数量(P<0.05~0.001)。结论川芎嗪对急性心肌梗死模型大鼠具有一定的保护作用,其机制可能是通过缩小心肌梗死面积、改善心肌酶学、保护受损心肌细胞凋亡等多种途径实现的。     

The effect of melatonin on endotoxemia-induced intestinal apoptosis and oxidative stress in infant rats

Objective To evaluate the effect of melatonin on the intestinal apoptosis along with oxidative damage in endotoxemic infant rats. Design and setting Prospective animal study in a university-based experimental research laboratory. Subjects and interventions Wistar albino 7-day-old rat pups (n = 21). The animals were randomized into three experimental groups: (1) controls; (2) endotoxemia; (3) endotoxemia treated with melatonin (10 mg/kg). Endotoxemia was induced in rats by intraperitoneal injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 3 mg/kg). Measurements and results Four hours after LPS injection, the antioxidant enzyme activities, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and thiobarbituric acid reactive substance (TBARS) levels as an indicator of lipid peroxidation, were determined. Intestinal apoptosis was assessed by hematoxylin-eosin staining and terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling. The administration of melatonin into endotoxemic rats prevented the increase in the TBARS levels, and increased the activities of antioxidant enzymes and attenuated apoptotic cell death in both intestinal epithelium and lamina propria. Conclusions Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infant rats.     

The effect of age on the enzyme activities of tryptophan metabolism along the kynurenine pathway in rats

BACKGROUND: Quinolinic acid and other kynurenine metabolites of the oxidative metabolism of tryptophan play an important role in several pathophysiological conditions. We aimed to study the effect of age on the enzyme activities of tryptophan metabolism along the kynurenine pathway. METHODS: Enzyme activity was investigated in liver, kidneys and small intestine obtained from Sprague-Dawley rats of various ages (1 week, 2-3, 12 and 18 months). RESULTS: We found age-related differences in the liver tryptophan 2,3-dioxygenase, small intestine indole 2,3-dioxygenase, liver and kidney kynurenine 3-monooxygenase activities, which decreased significantly with age. Also liver kynureninase activity declined with age, while the activity in kidneys did not show an evident age-related pattern from 2-3 months to 18 months of age. Liver kynurenine oxoglutarate transaminase was quite similar through all considered age groups, while the activity in kidneys was significantly lower in newborn rats and progressively increased up to 12 months, then significantly decreased at 18 months of age. Liver and kidney 3-hydroxyanthranilate 3,4-dioxygenase progressively and significantly increased from newborns to 12 months of age; in the group of rats aged 18 months, the enzyme activity tended to diminish, although not significantly. The liver aminocarboxymuconate-semialdehyde decarboxylase activity increased up to 12 months of age, then tended to decrease at 18 months, while in the kidneys, in which the activity was higher than in the liver at all the considered ages, the activity remained constantly elevated from 2-3 months to 18 months of age. CONCLUSIONS: A progressive decline in the enzyme activities involved in tryptophan metabolism along the kynurenine pathway in rat tissues was found with age, except for aminocarboxymuconate-semialdehyde decarboxylase, which, on the contrary, was increased after 2-3 months to the other older groups of age. The altered metabolism of tryptophan with ageing can lead to a decreased biosynthesis of nicotinic acid, tryptophan being the major source of body stores of NAD coenzymes, which are involved in almost all biogenetic and biosynthetic pathways of the organism.     

不同剂量阿托伐他汀对急性心肌梗死患者早期炎症反应的临床研究

目的探讨不同剂量阿托伐他汀早期干预治疗对急性心肌梗死患者血脂及血清高敏C反应蛋白的影响。方法60例AMI患者随机分为大剂量阿托伐他汀（40mg／d）治疗组（30例）和常规剂量阿托伐他汀（20mg／d）治疗组（30例）,分别在入院24h内及服药后3、7d测定患者血脂、高敏C反应蛋白,比较两组患者血脂、高敏C反应蛋白的变化。结果治疗7d后20mg／d及40mg／d阿托伐他汀治疗组总胆固醇、低密度脂蛋白水平较治疗前有降低（P〈0．05）,而且40mg／d阿托伐他汀治疗组高敏C反应蛋白水平显著降低,与20mg／d阿托伐他汀治疗组比较有显著差异（P〈0．01）,而治疗前后两组间总胆固醇、低密度脂蛋白比较无统计学意义（P〉0．05）。结论早期大剂量阿托伐他汀应用更能降低急性心肌梗死患者的高敏C反应蛋白水平,且阿托伐他汀的抗炎治疗独立于降脂之外。