7810例乙肝表面抗原和谷丙转氨酶结果分析

乙型病毒性肝炎 Virus B hepatitis(VBH) ,是目前严重危害人类健康水平的重要疾病之一。乙型肝炎病毒在人群中流行面广 ,传播途径多等特点。而我国地广人多 ,是乙肝发病率较高的国家。故对乙型肝炎的易感人群的保护尤其重要。因此 ,我们对山东省德州市 7810人进行了谷丙转氨酶     

模拟医学生物化学实验血清标本的探讨

用蛋白胨、三油酸甘油酯、鼠肝、葡萄糖等材料模拟血清标本,通过测定该血清中蛋白、血脂、谷丙转氨酶、血糖以及部分物理参数,探讨了模拟血清从外观和实验项目上满足实验教学的可行性。结果表明,模拟血清实用、简便易得,既能解决医学生物化学实验教学标本来源困难问题,又能防止实验室污染和节省大量实验经费。     

Studies on the mechanism of paracetamol-induced protection against paracetamol hepatotoxicity.

In rats, 3 days treatment with paracetamol (1 oral dose of 1 g/kg daily) produced a complete protection against the hepatotoxic actions of a further dose of paracetamol as documented by determination of serum enzyme activities (glutamic-oxaloacetic transaminase, (GOT), glutamic-pyruvic transaminase (GPT), sorbitol dehydrogenase (SDH), bromsulphthalein retention and histological investigations. Subacute paracetamol treatment decreased liver glutathione levels by 46%, liver microsomal cytochrome P-450 content by 23%, hepatic hydroxylation of aniline by 29% and hepatic demethylation of aminopyrine by 46%. It afforded also some protection against the hepatotoxic actions of carbon tetrachloride, bromobenzene and thioacetamide, but did not influence the antiphlogistic activity of paracetamol (carrageenan paw edema test). Plasma and liver concentrations of free paracetamol after oral administration of 1 g/kg paracetamol were somewhat higher in the subacutely paracetamol-pretreated rats than in the non-pretreated control animals whereas no differences in the concentrations of conjugated paracetamol were found between the 2 groups. Pretreatment with paracetamol did not influence the urinary excretion of free paracetamol but caused some shift in the urinary excretion of paracetamol conjugates: pretreated rats excreted 23% less of the paracetamol glucuronide and sulfate and 33% more of the paracetamol mercapturate than the control animals. A depression of the microsomal mixed-function oxidase activity is presumed to be the main cause of the paracetamol-induced protection against paracetamol hepatotoxicity.     

N-acetylcysteine-induced inhibition of gastric emptying: A mechanism affording protection to mice from the hepatotoxicity of concomitantly administered acetaminophen

Swiss Webster male mice, 22 ± 3 g, killed 17–18 h following the concomitant oral administration of acetaminophen (350 mg/kg) and N-acetylcysteine (NAC, 100–500 mg/kg, treated) had statistically significant lower plasma transaminases (GOT and GPT) than control mice (acetaminophen + water). Possible mechanisms underlying this protective effect of NAC were examined. NAC (500 mg/kg) reduced [¹⁴C]acetaminophen-derived radioactivity in the blood and tissues but increased the percentage of the dose in the gastrointestinal tract. Depletion of hepatic sulphydryl compounds below 75% of the control value was prevented by NAC treatment, whereas urinary excretion of mercapturate and sulfate, metabolites derived from sulphydryls, were proportionally increased and excretion of unchanged drug was decreased by NAC. Absorption of acetaminophen from the small intestine was prevented by NAC and this was attributed to an inhibition in gastric emptying. Since all changes observed following NAC treatment could be attributed to inhibition of gastric emptying, it was considered the major mechanism responsible for affording in mice protection from acetaminophen-induced hepatocellular damage following concomitant oral administration.     

Impact of certain flavonoids on lipid profiles--potential action of Garcinia cambogia flavonoids

Flavonoids from Cocos nucifera, Myristica fragrance, Saraka asoka and Garcinia cambogia exerted hypolipidaemic activity in rats. Lipid lowering activity was maximum in rats administered flavonoids (10 mg/kg BW/day) from Garcinia cambogia. A dose response study revealed biphasic activity. Higher doses were less effective in reducing lipid levels in serum and tissues, although devoid of toxic effects.     

GPT法和超声稀释法在动静脉内瘘流量监测中的应用和比较

目的观察和比较GPT法（glucose pump test）、超声稀释法在监测动静脉内瘘流量中的应用。方法选择第二军医大学附属长征医院肾内科,全军肾脏病研究所透析中心长期维持性透析的39例患者,上机前用GPT法测定内瘘流量,正常上机后0.5h后用HD02型血液透析监测仪测定内瘘流量,对GPT法、超声稀释法测得流量〈500ml/min的患者2周内行内瘘彩超检查。结果2例患者GPT法、超声稀释法均未能测出流量,4例患者GPT法前后血糖变化轻微无法计算流量。33例患者数据纳入分析,GPT法测定的内瘘流量均值高于超声稀释法,且具有统计学差异,两种方法测得内瘘流量存在直线相关。对GPT法、超声稀释法流量〈500ml6例患者行内瘘彩超检查,动静脉内瘘均有吻合口狭窄或近吻合口静脉段狭窄。结论两种方法测定动静脉内瘘流量在临床均是可行的,能预先发现存在的血管通路狭窄。     

Novel compound heterozygous mutations in GPT2 linked to microcephaly,and intellectual developmental disability with or without spastic paraplegia

We here describe novel compound heterozygous missense variants, NM_133443:c.[400C>T] and NM_133443:[1435G>A], in the glutamic‐pyruvic transaminase 2 (GPT2) gene in a large consanguineous family with two affected siblings diagnosed with microcephaly intellectual disability and developmental delay (IDD). In addition to these clinical phenotypes, the male sibling has spastic paraplegia, and the female sibling has epilepsy. Their four extended family members have IDD and microcephaly. Both of these variants, c.400C>T (p.R134C) and c.1435G>A (p.V479M), reside in the pyridoxal phosphate‐dependent aminotransferase domain. The missense variants affect highly conserved amino acids and are classified to be disease‐causing by meta‐SVM. The candidate variants were not found in the Exome Aggregation Consortium (ExAC) dataset or in dbSNP. Both GPT2 variants have an allele frequency of 0% (0/ ∼ 600) in the whole‐exome sequenced Turkish cohort. Upon Sanger sequencing, we confirmed these mutations in all affected family members and showed that the index patient and his affected sister inherited one mutant allele from each unaffected parent. To the best of our knowledge, this is the first family in which a novel compound heterozygous variant in the GPT2 gene was identified.

     

GPT2 mutations cause developmental encephalopathy with microcephaly and features of complicated hereditary spastic paraplegia

Various genetic defects can cause intellectual and developmental disabilities (IDDs). Often IDD is a symptom of a more complex neurodevelopmental or neurodegenerative syndrome. Identifying syndromic patterns is substantive for diagnostics and for understanding the pathomechanism of a disease. Recessive glutamate pyruvate transaminase (GPT2) mutations have recently been associated with IDD in 4 families. Here, we report a novel recessive GPT2 stop mutation p.Gln24* causing a complex IDD phenotype in a homozygous state in 5 patients from 2 consanguineous Arab families. By compiling clinical information of these individuals and previously described GPT2 patients a recognizable neurodevelopmental and potentially neurodegenerative phenotype can be assigned consisting of intellectual disability, pyramidal tract affection with spastic paraplegia, microcephaly and frequently epilepsy. Because of the consistent presence of pyramidal tract affection in GPT2 patients, we further suggest that GPT2 mutations should be considered in cases with complex hereditary spastic paraplegia.     

钉螺转氨酶的初步研究

纸层析法证明丙氨酸、天门冬氨酸及精氨酸经过钉螺匀浆作用后可使α-酮戊二酸转变成谷氨酸,说明钉螺存在谷-丙、谷-草及谷-精转氨酶。比色法也测得谷-草转氨酶和谷-丙转氨酶的活力。溴乙酰胺对上述两酶活力无明显影响,而烟酰苯胺有抑制钉螺谷-丙转氨酶作用。小剂量溴乙酰胺与烟酰苯胺盐酸盐伍用,无增强杀螺作用。