槲皮素磷酸酯钾对实验性心肌梗塞的影响

iv10～20mg/kg(木解)皮素磷酸酯钾使兔急性心肌梗塞范围明显缩小,ST段明显降低,并能对抗冠脉结扎后引起的血清CPK含量增加及心律失常,这些作用与普萘洛尔相似。但iv40mg/kg后作用不明显。     

Pheophytin a, a low molecular weight compound found in the marine brown alga Sargassum fulvellum, promotes the differentiation of PC12 cells

We identified and characterized a neurodifferentiation compound from the marine brown alga Sargassum fulvellum collected from the Japanese coastline. Several instrumental analyses revealed the compound to be pheophytin a. Pheophytin a did not itself promote neurite outgrowth of PC12 cells. However, when PC12 cells were treated with a low concentration of pheophytin a (3.9 microg/ml) in the presence of a low level of nerve growth factor (10 ng/ml), the compound produced neurite outgrowth similar to that produced by a high level of nerve growth factor (50 ng/ml). Pheophytin a also enhanced signal transduction in the mitogen-activated protein kinase signaling pathway, which is also induced by nerve growth factor. The effect of pheophytin a on neurite outgrowth of PC12 cells was completely blocked by U0126, a representative mitogen-activated protein kinase kinase inhibitor. These results suggest that pheophytin a enhances the neurodifferentiation of PC12 cells in the presence of a low level of nerve growth factor and that this effect is mediated by activation of a mitogen-activated protein kinase signaling pathway.     

乌司他丁对严重烧伤患者伤后早期心肌损害的防治作用

目的观察乌司他丁（UTI）对烧伤“休克心”的防治作用，探讨其可能的机制。方法选择笔者单位收治的伤后24h内入院、烧伤面积〉50％TBsA的34例特重度烧伤患者，分为烧伤组和UTI治疗组，每组17例。两组患者均进行常规治疗，且UTI治疗组患者入院后立即给予UTI10万U静脉滴注，3次／d，连续7d。于两组患者伤后2、4、7d采血，检测其血浆中性粒细胞弹性蛋白酶（PMN elastase）、心肌肌钙蛋白I（cTnI）含量和心肌型肌酸激酶同工酶（CK—MB）活性，以公认的各指标正常值作参考，并对3项指标进行相关性分析。结果（1）伤后2、4、7d，两组患者血浆PMN elastase及cTnI含量均显著高于正常值（P〈0．01）；UTI治疗组与烧伤组比较，两指标偏低。（2）与正常值比较，伤后2、4、7d烧伤组患者CK—MB活性明显升高（P〈0．01），第4天达高峰；UTI治疗组伤后2、4d CK—MB活性明显高于正常值（P〈0．05或0．01），但与烧伤组比较升幅较小，第7天降至正常值水平（P〉0．05）。（3）34例烧伤患者PMN elastase、cTnI含量及CK—MB活性三者间均呈现显著正相关，前两者的相关系数为0．904，后两者的相关系数为0．922，PMN elastase含量与CK-MB活性的相关系数为0．829（均为P〈0．01）。结论UTI能够显著减轻严重烧伤患者心肌损害的程度，有效抑制PMN elastase的过度释放。     

禁食对蛋鸡肝脏腺苷-磷酸激活的蛋白激酶活性的影响

腺苷 -磷酸 (AMP)激活的蛋白激酶 (AMP- acti-vated protein kinase,AMPK)是丝氨酸激酶家族的一员 ,由 AMP和其上游激酶 AMPK激酶所活化 ,对细胞内 AMP/ATP的变化非常敏感 [1] ,被称为真核细胞的“代谢感受器”[2 ]。研究发现在跑步 [3 ,4 ]、电刺激肌肉 [5,6]或禁食应激后 [7] ,大鼠肝脏和肌肉中的AMPK活性升高数倍 ,乙酰辅酶 A羧化酶 (ACC)活性显著下降甚至丧失 ,丙二酸单酰辅酶 A产量降低甚至为零 ,脂肪酸合成受抑。同时 ,AMPK活化后 ,脂肪酸的氧化率显著提高 ,CO2 和酮体生成量明显增加[4 ,8] 。这些均表明 ,AMPK活化…     

A rare polymorphism affects a mitogen-activated protein kinase site in synapsin III: possible relationship to schizophrenia.

BACKGROUND: Synapsin III plays a role in neuronal plasticity and maps to chromosome 22q12-13, a region suggested to be linked to schizophrenia. To determine if synapsin III plays a role in this disease, we searched for polymorphisms in this gene in patients with schizophrenia and controls. METHODS: The synapsin III gene was initially sequenced from 10 individuals with schizophrenia to identify polymorphisms. Association analysis was then performed using 118 individuals with schizophrenia and 330 population controls. Synapsin III expression was studied by immunoblot analyses, and phosphorylation sites were mapped by sequencing trypsin-digested synapsin III fragments phosphorylated with phosphorus-32. RESULTS: A rare, missense polymorphism, S470N, was identified in the synapsin III gene and appeared more frequently in individuals with schizophrenia than in controls (p =.0048). The site affected by the polymorphism, Ser470, was determined to be a substrate for mitogen-activated protein kinase, a downstream effector of neurotrophin action. Phosphorylation at Ser470 was increased during neonatal development and in response to neurotrophin-3 in cultured hippocampal neurons. CONCLUSIONS: Our observations suggest an association of a rare polymorphism in synapsin III with schizophrenia, but further studies will be required to clarify its role in this disease.     

PRKCG mutation (SCA-14) causing a Ramsay Hunt phenotype.

Progressive myoclonic ataxia, also referred to as Ramsay Hunt syndrome, is characterized by a combination of myoclonus and cerebellar ataxia, infrequently accompanied by tonic-clonic seizures. Its differential diagnosis overlaps with progressive myoclonic epilepsy, a syndrome with myoclonus, tonic-clonic seizures, progressive ataxia and dementia. In patients with progressive myoclonic epilepsy, specific diseases can frequently be recognized, but the diagnostic yield in progressive myoclonic ataxia is much lower. We describe a patient who presented with multifocal myoclonus in his thirties and who later developed cerebellar ataxia and focal dystonia. His father was similarly affected. Genetic studies revealed a mutation in the protein kinase C gamma (PRKCG) gene, known to cause spinocerebellar ataxia type 14 (SCA-14). This case illustrates that both myoclonus and dystonia are part of the clinical spectrum in SCA-14 and that myoclonus can even be the presenting symptom. We suggest that SCA-14 should be considered in the differential diagnosis of progressive myoclonic ataxia.     

Management of status dystonicus: our experience and review of the literature.

Status dystonicus (SD) is a life threatening disorder that develops in patients with both primary and secondary dystonia, characterized by acute worsening of symptoms with generalized and severe muscle contractions. To date, no information is available on the best way to treat this disorder. We review the previously described cases of SD and two new cases are reported, one of which occurring in a child with static encephalopathy, and the other one in a patient with pantothenate kinase-associated neurodegeneration. Both patients were admitted to an intensive care unit and treated with midazolam and propofol. This approach proved to be useful in the former while the progressive nature of the dystonia of the second patient required the combination of intrathecal baclofen infusion and bilateral pallidal deep brain stimulation. We believe that a rapid and aggressive approach is justified to avoid the great morbidity and mortality which characterize SD. Our experience, combined with the data available in the literature, might permit to establish the best strategies in managing this rare and severe condition.     

脂质体介导的单纯疱疹胸苷激酶基因在人前列腺癌细胞中的表达

目的：提取并鉴定已构建的EB病毒表达载体pDR2-TK，利用脂质体介导的基因转染技术将pDR2-TK转染人前列腺癌细胞并对单纯疱疹胸苷激酶（HSV－TK）表达状况进行检测。方法：采用DNA大量制备及纯化系统提取pDR2-TK，酶切和DNA测序进行鉴定，采用阳离子脂质体法将pDR2-TK导入激素非依赖性人前列腺癌细胞系PC－3m，逆转录PCR（RT－PCR）法和SABC免疫组化法检测TK mRNA和蛋白的表达。结果：扩增提取的质粒经PstⅠ和EcoR Ⅴ酶切后各获得4个及2个片段，与原基因酶切图谱一致；所提取质粒PCR产物经DNA测序，与NCBI公布的HSV－TK基因序列对照，证实所提取质粒含目的基因序,旨质体法转染PC－3m细胞后，mRNA和蛋白均有HSV－TK的表达，其蛋白表达率约为22％。结论：pDR2-TK质粒含有目的的基因HSV－TK，阳离子脂质体法可将pDR2-TK导入人前列腺癌细胞并获得较高效率的表达。     

抗氧化剂对糖尿病大鼠肾小球蛋白激酶C的影响

目的　通过大鼠糖尿病模型 ,观察抗氧化剂对糖尿病大鼠肾小球蛋白激酶的影响。方法　将 75只雄性Wistar大鼠分为正常对照组、糖尿病未治疗组、抗氧化剂治疗组各 2 5只 ,共观察 8周 ,分别测定尿白蛋白排泄量(UAE) ,内生肌酣消除率 (Ccr)、血浆及肾脏组织一氧化氮 (NO)、一氧化氮合成酶 (NOS)、内皮素 (ET)和肾小球蛋白激酶C(proteinkinaseC ,PKC)。结果　给予维生素E治疗组 8周时 ,Ccr[(5 .2 8± 0 .5 4)ml/(min·kg) ]及尿白蛋白排泄量 [(14.2 7± 1.16 ) μg/2 4h]显著低于未治疗组 ,肾小球细胞膜PKC[(6 8.2 7± 12 .33) pmol/(min·mgprotein) ],2周时N0 [(34 .2 3± 3.91) μmol/L]及NOS[(32 .0 7± 3.76 )U/L]明显低于未治疗组 ,维生素E治疗组 2周时与 8周时的NO及NOS下降幅度明显小于未治疗组。结论　维生素E具有抑制PKC活性作用。     

蛋白激酶C激活调控FOS表达参与缺血诱导神经元凋亡的研究

目的：探讨蛋白激酶C（PKC）与神经元凋亡的可能机制，方法：采用大鼠全脑缺血模型，观察脑缺血／再灌流后PKC活性，FOS表达及神经元凋亡的变化。结果：脑缺血／再灌流可以导致PKC的移位激活伴FOS表达及神经元凋亡的增加；用蛋白激酶C抑制剂灯盏花可以阻止上述变化。结论：蛋白激酶C的激活可能通过促进FOS表达参与了脑缺血／再灌流诱导的神经元凋亡。