Focal attenuation differences in pericystic liver tissue as seen on CT hepatic arteriography and CT arterial portography: observation using a unified helical CT and angiography system

BACKGROUND: To investigate nontumorous focal enhancement (FE) with computed tomographic hepatic arteriography (CTHA) and perfusion defect (PD) with computed tomographic arterial portography (CTAP) in pericystic liver tissue. METHODS: Incidence, shape, and size of nontumorous FE on CTHA and PD on CTAP were examined in 100 consecutive noncirrhotic and 100 consecutive cirrhotic patients. RESULTS: FE was observed on CTHA in 77 noncirrhotic and 61 cirrhotic patients, whereas PD was observed on CTAP in 50 noncirrhotic and 51 cirrhotic patients. When both findings were visualized in both CT studies, the shape of the FE on CTHA was similar to the overlapping PD on CTAP in 81% of patients but was larger in 92% of patients. CONCLUSIONS: FE on CTHA and PD on CTAP are frequently noted in pericystic liver tissue. The size of FE on CTHA is often larger than PD on CTAP, although the shapes are generally the same. Size discrepancy suggests the presence of both portal supply and splanchnic venous drainage.     

自制PV液与大鼠肝脏低温保存:与UW液的对比

背景:目前许多学者对UW液成分进行改进,其目的主要在于进一步探索器官保存的原理,提高保存的技术和延长保存的时限;简化UW液的成分,以进一步满足临床运输、储存和使用的方便;寻找合适的替代品,降低UW液的成本以满足市场需要.目的:观察自制PV液对大鼠肝脏低温保存的效果,并与UW液进行对比.方法:将90只Wistar大鼠按随机数字表法分成3组,即UW液组、PV液组和生理盐水组,制作大鼠肝脏非循环离体灌注模型,分别使用相应灌洗保存液.每组再根据不同的保存时间分为保存0,6,12,18,24 h 5个亚组,每个亚组6只大鼠.测定保存不同时间后肝脏谷丙转氨酶、谷草转氨酶、乳酸脱氢酶活性变化,以及灌注流出液中氧自由基代谢产物丙二醛浓度与超氧化物歧化酶活性;观察胆汁分泌量及镜下肝脏形态学变化.结果与结论:PV液组与UW液组比较,灌注流出液中谷丙转氨酶、谷草转氨酶、乳酸脱氢酶、超氧化物歧化酶活性相近,差异无显著性意义(P>0.05).保存6 h后,PV液组肿瘤坏死因子α质量浓度显著高于UW液组(P<0.05):保存12 h后,UW液组丙二醛浓度显著高于PV液组(P<0.05);保存18 h后,PV液组胆汁分泌量低于UW液组(P<0.05);两组光镜、电镜下组织形态改变相似.提示PV液与UW液对Wistar大鼠肝脏功能均具有保护作用,两者短时间保存效果相似,在抗氧化及清除氧自由基方面,PV液略优于UW液.     

Hemoglobin interference from in vivo hemolysis

Laboratory values for specimens from a case of intravascular hemolysis showed that hemoglobin was significantly increased and thus could interfere with the determination of other analytes. We studied this problem by adding increasing amounts of purified hemoglobin (to a maximum concentration of 19.3 mg/L) to aliquots of pooled serum samples. The hemoglobin significantly interfered with the determination of only five analytes: albumin, aspartate aminotransferase, direct bilirubin, and total protein on the SMAC, and creatinine on the Astra. We propose that for cases of proven intravascular hemolysis, values for only the analytes not affected by hemoglobin should be reported. We find lactate dehydrogenase activity useful in assessing the components of in vivo hemolysis; the differences between serum and plasma values for potassium, lactate dehydrogenase, and hemoglobin are related to in vitro hemolysis. Criteria for specimen collection and assessment of type of hemolysis are proposed.     

Lactate blood levels in the perioperative period of orthotopic liver transplantation

To investigate whether early postoperative changes in blood lactate concentration indicate the functional recovery of the newly grafted liver, changes in oxygen supply, oxygen consumption, acid-base equilibrium, and blood lactate concentrations were prospectively studied in a group of 53 postnecrotic cirrhotic patients during the various phases of orthotopic liver transplantation (preanhepatic, anhepatic, neohepatic) and for the first 48 h following reperfusion. The patients were divided into two groups according to the quality of the early graft function, as indicated by alanine aminotransferase, bile flow, and prothrombin activity: group A (49 patients), good immediate graft function and group B (4 patients), immediate graft non-function. Lactate levels rose in the same manner during the preanhepatic and anhepatic stages and peaked after revascularization of the graft. Following reperfusion, however, distinctly different blood lactate profiles were recorded in the two groups of patients. A fall in lactate concentration was recorded in group A patients, whereas a continuous rise occurred in group B patients: the difference becoming significant by the end of surgery (P<-0.05). During the first 48 h following revascularization of the graft, opposite trends in lactate concentration, bile flow, alanine aminotransferase, and prothrombin activity were evident in the two groups of patients: 24 h after reperfusion, lactate levels were below 2 mmol/1 in 47 of 49 patients from group A, while they plateaued above 4 mmol/1 in all patients from group B. Group A patients had lower alanine aminotransferase levels (P<-0.001), higher prothrombin activity, (P<-0.01), and greater bile flow (P<-0.02). If validated in larger series, the blood lactate profile, probably more than the absolute level, appears to be a useful indicator of the early recovery of liver metabolic capacities in the immediate postoperative period of orthotopic liver transplantation.     

肝硬化背景对肝细胞癌超声造影灌注曲线的影响

目的 对肝细胞癌(hepatocellular carcinoma,HCC)进行超声造影灌注曲线,f(t)分析,探讨肝硬化背景对灌注参数的影响.方法 使用Sonoliver软件对115例HCC患者的超声造影动态图像进行脱机分析,其中有肝硬化背景86例,无肝硬化背景29例,获得分析区和参考区的,f(t),对,f(t)参数:峰值强度(maximum of intensity,IMAX)、上升时间(rise time,RT)、达峰时间(time to peak,TTP)、平均渡越时间(mean trasit time,mTT)和始消时间(washout time,WT)进行统计学分析.结果 肝硬化组HCC分析区的IMAX为(124.25±5.56)%,RT为(12.98±0.48)s,TTP为(13.70±0.52)s,mTT为(138.61±9.20)s,RS为10.11±0.60,WT为(34.17±2.91)s.非肝硬化组HCC分析区的上述参数分别为(113.65±5.58)%,(13.68 ±0.92)s,(14.39 ±0.94)s,(149.49±21.70)s,8.89±0.77,(28.36±3.25)s.两组HCC的分析区和参考区灌注参数的差异均无统计学意义(P>0.05).结论 HCC的灌注参数可评估肿瘤内的血流灌注,肝硬化背景不影响HCC的,f(t)灌注参数.     

新型钙增敏剂哒嗪酮对低血容量性休克大鼠肝脏结构与功能的影响

目的：研究哒嗪酮（ＭＣＩ１５４）对低血容量性休克大鼠肝脏功能和结构改变的影响。方法：用大鼠低血容量性休克模型,设立ＭＣＩ１５４治疗组和生理盐水对照组,测定肝脏组织血流量以及肝脏组织提取液和线粒体悬液的生化指标,观察肝脏结构及超微结构的变化。结果：ＭＣＩ１５４治疗后肝脏组织血流量和Ｈ＋ＡＴＰ酶的活性显著高于相应的生理盐水对照组,组织提取液中丙氨酸转氨酶、乳酸脱氢酶、β葡萄糖醛酸酶和丙二醛以及线粒体内钙含量等指标显著低于相应的生理盐水对照组,肝脏细胞结构、超微结构损伤程度明显轻于生理盐水对照组。结论：ＭＣＩ１５４可显著增加大鼠肝脏组织血流量,减轻肝细胞损伤程度,延缓线粒体内钙超载进程,保护Ｈ＋ＡＴＰ酶的活性,对低血容量性休克大鼠肝脏结构和功能具有显著的保护作用。     

中国人肝细胞系1运用于生物人工肝的生物代谢功能

背景：前期研究发现,中国人肝细胞系1细胞分化程度高且生物代谢功能良好,并且中国人肝细胞系1细胞组织学上来源于正常肝组织,较其他来源于肿瘤源性的肝细胞系更为安全。目的：探讨中国人肝细胞系中国人肝细胞系1细胞在混合型生物人工肝中的生物代谢功能。方法：15只食蟹猴随机分成对照组（n=5）和治疗组（n=10）,均建立急性肝功能衰竭模型,治疗组接受以全接触灌流型生物反应器接种微载体微重力中国人肝细胞系1细胞建立的人源细胞混合型生物人工肝进行治疗。结果与结论：急性肝功能衰竭食蟹猴血清谷氨酸转氨酶、总胆红素、总胆汁酸、尿素氮、肌酐、血氨均明显上升,而白蛋白、Fischer指数则显著下降;人源细胞混合型生物人工肝治疗后,急性肝功能衰竭食蟹猴血清谷氨酸转氨酶、总胆红素、总胆汁酸、尿素氮、肌酐、血氨和白蛋白均恢复。提示中国人肝细胞系1细胞在混合型生物人工肝中生物代谢功能良好,表现出良好的肝特异性生物合成及生物代谢功能。     

Ginkgo biloba extract improves oxidative organ damage in a rat model of thermal trauma

This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) against oxidative organ damage distant from the original burn wound. Under brief ether anesthesia, the shaved dorsum of the rats was exposed to 90 degrees C (burn group) or 25 degrees C (control group) water bath for 10 seconds. EGb (50 mg/kg/day) or saline was administered intraperitoneally immediately and at 12 hours after the burn injury. Rats were decapitated 24 hours after burn injury and tissue samples from the liver and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by the chemiluminescence technique. Tissues also were examined microscopically. Blood urea nitrogen, creatinine, alanine aminotransferase, and aspartate aminotransferase levels and tumor necrosis factor- and lactate dehydrogenase activity were assayed in serum samples. Severe skin scald injury (30% TBSA) caused a significant decrease in GSH levels and significant increases in MDA levels, MPO activity, and collagen content of hepatic and renal tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum alanine aminotransferase, aspartate aminotransferase, and blood urea nitrogen levels, as well as lactate dehydrogenase and tumor necrosis factor-, were increased in the burn group as compared with the control group. However, treatment with EGb reversed all these biochemical indices, as well as histopathological alterations that were induced by thermal trauma. Our results show that thermal trauma-induced oxidative damage in hepatic and renal tissues is protected by the administration of EGb, with its antioxidant effects. Therefore, its therapeutic role as a "tissue injury-limiting agent" must be further elucidated in oxidant-induced tissue damage.     

In vitro analysis of human drug glucuronidation and prediction of in vivo metabolic clearance

The glucuronidation of a number of commonly used hepatic uridine diphosphate glucuronosyltransferase drug substrates has been studied in human tissue microsomes. Prediction of in vivo hepatic drug glucuronidation from liver microsomal data yielded a consistent 10-fold under-prediction. Consideration of protein binding was observed to be pivotal when predicting in vivo glucuronidation for acid substrates. Studies using human intestinal microsomes demonstrated the majority of drugs to be extensively glucuronidated such that the intrinsic clearance (CL(int)) of ethinylestradiol (CL(int) = 1.3 microl/min/mg) was twice that obtained using human liver microsomes (CL(int) = 0.7 microl/min/mg). The potential extrahepatic in vivo glucuronidation was calculated for a range of drug substrates from human microsomal data. These results indicate the contribution of intestinal drug glucuronidation to systemic drug clearance to be much less than either hepatic or renal glucuronidation. Therefore, data obtained with intestinal microsomes may be misleading in the assessment of the contribution of this organ to systemic glucuronidation. The use of hepatocytes to assess metabolic stability for drugs predominantly metabolized by glucuronidation was also investigated. Metabolic clearances for a range of drugs obtained using fresh preparations of human hepatocytes predicted accurately hepatic clearance reported in vivo. The use of cryopreserved hepatocytes as an in vitro tool to predict in vivo metabolism was also assessed with an excellent correlation obtained for a number of extensively glucuronidated drugs (R(2) = 0.80, p < 0.001).     

肝损伤酶活性联合检测在肝胆疾病诊断中的相关分析

目的探讨肝损伤酶活性联合检测在肝胆疾病诊断中的临床意义。方法对健康对照组36例和各类肝胆疾病组204例患者的丙氨酸氨基转移酶、天门冬氨酸氨基转移酶、乳酸脱氢酶、腺苷脱氨酶、线粒体天门冬氨酸转氨酶、碱性磷酸酶、γ-谷氨酰转移酶、5′-核苷酸酶活性进行测定与分析。结果肝胆疾病组丙氨酸氨基转移酶、天门冬氨酸氨基转移酶、乳酸脱氢酶、腺苷脱氨酶、线粒体天门冬氨酸转氨酶、碱性磷酸酶、γ-谷氨酰转移酶、5′-核苷酸酶活性均高于健康对照组（P〈0．01）。结论肝损伤酶活性联合检测有利于肝胆疾病的鉴别诊断及疗效观察。     

前列腺素E1对大鼠供肝灌注冷保存的保护作用

目的应用高渗构橼酸盐腺嘌呤液（HCA液）加前列腺素E1（PGE1）对大鼠供肝进行灌注,探讨PGE。在供肝灌注冷保存中对肝脏的保护作用。方法采用雄性SD大鼠肝脏单纯冷保存离体灌注模型,随机分为实验组和对照组。每组30只。实验组是HCA灌注液中加入PGE．加器官保存液（UW液）注取肝,对照组则单纯使用HCA液加UW液灌注取肝。经不同冷保存时间后,检测丙氨酸转氨酶（ALT）、乳酸脱氢酶（LDH）、髓过氧化物酶（MPO）以及丙二醛（MDA）、超氧化物歧化酶（SOD）及病理学变化。结果在10h和20h保存时间点,实验组ALT和LDH以及MDA和MPO均明显低于对照组,且酶值水平均随冷保存时间延长增高（P〈0．01）;实验组SOD高于对照组,且随时间延长降低（P〈0．01）。病理变化可见实验组肝窦、肝细胞索结构清晰,肝轻度肿胀,无细胞坏死。结论HCA液中加入PGE1后对肝脏冷保存损伤具有一定的保护作用,其机制可能与PGE1在灌注过程中通过改善微循环提高组织的抗氧化能力,减少中性粒细胞与肝窦库普弗细胞及内皮细胞的黏附,减轻多种组织和细胞损伤等因素有关。     

In vivo and in vitro evidence for a hepatic modulation of the leptin signal in rats

BACKGROUND: Leptin is primarily secreted by the adipose tissue. It binds not only to hypothalamic structures involved in energy regulation but also to many peripheral tissues including the liver. Leptin circulates in free and receptor-bound forms. Both components are differentially regulated under various pathophysiological conditions and serve different physiological functions. They are released from adipose tissue but previous data suggest an additional formation outside the fat compartment. Here we tested the contribution of the liver in binding and modulating leptin in the circulation. MATERIALS AND METHODS: In vivo experiments were performed with radioactive labelled leptin with and without pretreatment with unlabelled leptin in freely moving, chronic intravenously cannulated male rats. Livers were investigated by immunohistochemistry and in situ hybridization and immunoblotting was performed, followed by ex vivo liver perfusion studies with human recombinant leptin. RESULTS: In in vivo experiments radioactively labelled leptin (at low concentrations) is avidly bound to rat liver (greater than 80% of basal serum values 90 min following i.v. infusion). Pre-treatment with excess of unlabelled leptin in vivo revealed a rapid hepatic down-regulation of leptin receptor isoforms when tested by in situ hybridization, immunoblotting or immunohistochemistry. Ex vivo perfusion of rat liver with human recombinant leptin induced a dose- and time-dependent formation of receptor-bound leptin in the perfusate. CONCLUSIONS: The present data support an active role of the liver in the modulation of the leptin signal through different regulation of the soluble leptin receptor, the bound and free forms of the hormone, which may have important implications for leptin's central efficacy and the development of 'leptin resistance'.     

Protection against liver injuries induced by low-temperature preservation with ulinastatin]

OBJECTIVE: To study whether ulinastatin has a protective role in cold preservation of liver and its mechanism. METHODS: To study the role of ulinastatin in protection of liver after cold preservation, the isolated rat liver with perfused either with cold perfusion fluid or perfused with cold perfusion fluid with ulinastatin. Liver tissue was harvested at 0, 12 and 24 hours after cold perfusion, and morphological changes were examined, alanine aminotransferase (ALT), lactate dehydrogenase (LDH), thoperoxidase (MPO), malondialehyde (MDA) and superoxide dismutase (SOD) contents were also determined. RESULTS: ALT, LDH, MPO and MDA contents were significantly lower in ulinastatin group than those in the control group at 12 and 24 hours, and levels of ALT, LDH, MDA and MPO were increased along with prolongation of preservation time (all P<0.01), but SOD was higher in ulinastatin group than the control group and it was increased along with the prolongation of time (all P<0.01). Compared with ulinastatin group, the control group showed obvious pathological changes. CONCLUSION: Protective effect of UW solution used in clinic weakens gradually as cold preservation time is prolonged. Ulinastatin has protective effect on liver against cold preservation injury, and its effect is better than the simple UW solution. Its mechanism is related to inhibition of anti-oxidation and aggregation neutrophil's accumulation effect of ulinastatin.     

啤酒对血清酶活性影响的体内外实验

目的:观察体内外实验中受试者饮用啤酒后各种血清酶活性的变化情况。设计:观察对比实验。单位:泰山医学院基础医学研究所。对象:实验于2005-03/04在泰山医学院基础医学研究所完成。选择泰山医学院学生17名,年龄19～35岁,包括本科生和研究生,实验前均签署同意书。方法:①体内实验:受试者统一正常饮食后3h采静脉血3mL,作为对照。然后立即口服啤酒4mL/kg,分别于15,30,45,60,90,120,180min后各采血3mL,测定血液中丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶、碱性磷酸酶、肌酸激酶、乳酸脱氢酶、淀粉酶、脂肪酶活性的变化。②体外实验:选取17份新鲜受试者血清,分别加入两个试管中,每管0.5mL。对照管加入20μL生理盐水;测定管中加入20μL啤酒溶液,观察啤酒对以上各种酶活性的直接影响。主要观察指标:体内外实验中血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶、碱性磷酸酶、肌酸激酶、乳酸脱氢酶、淀粉酶及脂肪酶的活性。结果:纳入17名学生,全部进入结果分析,无脱落。①体内实验:啤酒可显著降低血清天冬氨酸氨基转移酶活性(418.08±58.68,383.41±63.01)nkat/L,显著升高血清碱性磷酸酶活性(3678.57±436.25,3962.96±400.91)nkat/L(χ2=19.00～20.00,P<0.01),其余酶活性均有不同程度的升高。②体外实验:啤酒在体外对各种酶活性均有一定程度的抑制作用。结论:啤酒在体内外对酶活性均有一定影响,从而影响机体代谢,过量饮用会影响健康。在常规血清酶学检测中,应避免患者饮用啤酒所造成的干扰,以确保实验结果的准确可靠。     

Evaluation of arylimidamides DB1955 and DB1960 as candidates against visceral leishmaniasis and Chagas' disease: in vivo efficacy, acute toxicity, pharmacokinetics, and toxicology studies

Arylimidamides (AIAs) have shown outstanding in vitro potency against intracellular kinetoplastid parasites, and the AIA 2,5-bis[2-(2-propoxy)-4-(2-pyridylimino)aminophenyl]furan dihydrochloride (DB766) displayed good in vivo efficacy in rodent models of visceral leishmaniasis (VL) and Chagas' disease. In an attempt to further increase the solubility and in vivo antikinetoplastid potential of DB766, the mesylate salt of this compound and that of the closely related AIA 2,5-bis[2-(2-cyclopentyloxy)-4-(2-pyridylimino)aminophenyl]furan hydrochloride (DB1852) were prepared. These two mesylate salts, designated DB1960 and DB1955, respectively, exhibited dose-dependent activity in the murine model of VL, with DB1960 inhibiting liver parasitemia by 51% at an oral dose of 100 mg/kg/day × 5 and DB1955 reducing liver parasitemia by 57% when given by the same dosing regimen. In a murine Trypanosoma cruzi infection model, DB1960 decreased the peak parasitemia levels that occurred at 8 days postinfection by 46% when given orally at 100 mg/kg/day × 5, while DB1955 had no effect on peak parasitemia levels when administered by the same dosing regimen. Distribution studies revealed that these compounds accumulated to micromolar levels in the liver, spleen, and kidneys but to a lesser extent in the heart, brain, and plasma. A 5-day repeat-dose toxicology study with DB1960 and DB1955 was also conducted with female BALB/c mice, with the compounds administered orally at 100, 200, and 500 mg/kg/day. In the high-dose groups, DB1960 caused changes in serum chemistry, with statistically significant increases in serum blood urea nitrogen, lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase levels, and a 21% decrease in body weight was observed in this group. These changes were consistent with microscopic findings in the livers and kidneys of the treated animals. The incidences of observed clinical signs (hunched posture, tachypnea, tremors, and ruffled fur) were more frequent in DB1960-treated groups than in those treated with DB1955. However, histopathological examination of tissue samples indicated that both compounds had adverse effects at all dose levels.     

Changes in serum enzymes in moderate drinkers after an alcohol challenge

When 14 "moderate" drinkers abstained from alcohol for four weeks, the activity of gamma-glutamyltransferase (GGT; EC 2.3.2.2) in their serum showed a large decrease. Immediately after the period of abstention, an orally given ethanol challenge of 1 g/kg produced a marked increase in serum GGT at 24 h, followed by a slow decline thereafter. Aspartate amino-transferase activity in serum was significantly increased at 24 h; however, alkaline phosphate, alanine aminotransferase, and lactate dehydrogenase showed much smaller or no changes. An abnormal increase in lactate dehydrogenase isoenzyme 5 was observed in seven subjects. In some of the moderate drinkers, liver biopsies showed mild chronic hepatitis or nonspecific changes. Eight nondrinking controls showed only slight increases in serum GGT following the same alcohol challenge; results for the other enzyme tests were unchanged. We consider it probable that pre-existing liver disease affects the response to ethanol, so that greater amounts of GGT are released from hepatic tissue; alternatively, drinkers may have a higher GGT activity in this tissue as a result of enzyme induction by ethanol. The alcohol challenge test was an effective discriminator between moderate drinkers and abstainers.     

Dipeptidyl aminopeptidase IV in hospitalized patients and in galactosamine hepatitis of the rat: Activity and lectin affinity chromatography in serum and hepatic plasma membranes

The activity of dipeptidyl aminopeptidase IV was studied in the sera of 378 hospitalized patients. The mean activity of dipeptidyl aminopeptidase IV was elevated significantly in patients with neoplasmata and hepatitis, but not in patients with liver cirrhosis. Significant correlations (p less than 0.001) existed with gamma-glutamyl transferase, glutamate dehydrogenase, alkaline phosphatase and leucine aminopeptidase. A significant correlation with lactate dehydrogenase existed only in patients with neoplasmata. Principal component analysis, performed with aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, leucine aminopeptidase, lactate dehydrogenase and dipeptidyl aminopeptidase IV, revealed correlations between the activities of aspartate aminotransferase and alanine aminotransferase, and between alkaline phosphatase and leucine aminopeptidase, but neither dipeptidyl aminopeptidase IV nor lactate dehydrogenase showed any correlation with either of these two groups. In lectin affinity chromatography with concanavalin A and wheat germ lectin sepharose, serum dipeptidyl aminopeptidase IV from liver cirrhosis patients showed the same binding pattern as that from healthy subjects. The activity and glycosylation of dipeptidyl aminopeptidase IV in serum and hepatic plasma membranes was investigated in rats, following the induction of hepatitis with galactosamine. In the serum, dipeptidyl aminopeptidase IV activity was elevated as early as 6 h after galactosamine injection, and the elevated activity persisted until the 7th day. At the same time dipeptidyl aminopeptidase IV activity was also elevated in the hepatic plasma membrane. Ninety eight percent of hepatic dipeptidyl aminopeptidase IV bound to concanavalin A as well as to wheat germ lectin and this value was unchanged during hepatitis. In the serum of control rats, 90% of dipeptidyl aminopeptidase IV bound to concanavalin A but only 39% to wheat germ lectin.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enzyme-activities in serum and plasma of man, dog and rat, and the variation of these enzyme activities during storage of the blood]

The following enzymes were determined in the serum and plasma of man, dog and rat: alanine aminotransferase, asparate aminotransferase, alkaline phosphatase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. The enzyme assays were performed on an Eppendorf-Enzymautomat 5010 using optimised conditions at 25 degrees C. The enzyme-activities changed by variable amounts during standing of the blood. This concerned mainly lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase and aspartate aminotransferase in the serum of the rat. In human serum and in dog serum, and in the plasma of man, dog and rat this effect was only less pronounced.