Assessment of homeostasis by body''s adaptative responses in patients with tuberculous pleurisy]

AIM: The study of the detection rate and potential pathogenetic significance of antibodies to low density oxidated lipoprotein (LDOL) in patients who had ischemic cerebral circulation disorder (ICCD) at young age. MATERIALS AND METHODS: The examination (enzyme immunoassay, general and neurological investigations, laboratory and instrumental tests) covered 148 patients who survived ICCD at young age (mean age 37.2 years). RESULTS: 48 of 108 (44%) patients had LDOL antibodies. Antibodies to cardiolipin, lupus anticoagulant were recorded in 33 (31%) patients. LDOL antibodies were higher and occurred more frequently in patients with Sneddon's syndrome (35% of patients, mean LDOL antibodies-44 units) and primary antiphospholipid syndrome (17% of patients, 45 units) than in atherosclerotic affection of the major head arteries (4%, 29 units) or occlusion of cerebral arteries of unclear genesis (8% of patients, 29 units). CONCLUSION: ICCD were not related to fast development of cerebral atherosclerosis or periaortitis due to production of LDOL antibodies as no relationships were found between their rise and atherosclerotic lesions of cerebral major arteries or periaortitis as shown by ultrasonic dopplerography or cerebral angiography. Feasibility of LDOL antibodies participation in the coagulation cascade and induction of hypercoagulatory condition causing ICCD needs special investigation.     

BCR-ABL induces neurite-like structures and BCR lacking the SH2-binding domain induces cell rounding in PC12 cells

The activated tyrosine kinase oncoprotein BCR-ABL is responsible for pathogenesis of Philadelphia chromosome-positive human leukemias. Because BCR carries a GAP (GTPase-activating protein) activity toward cytoskeleton-related small GTP-binding proteins, we utilized a neuronal PC12 cell system to test morphogenic potentials of BCR-ABL or BCR. We report here unique morphological phenotypes of PC12 cells expressing either BCR-ABL or a BCR mutant which lacks the SH2-binding domain (BCR Delta162-413). Although MAP kinase was not activated in PC12 cells expressing BCR-ABL, they showed incomplete neurite extensions even in the absence of the nerve growth factor (NGF). Overproduction of BCR Delta162-413 in PC12 cells, on the other hand, induced cell rounding in the absence of NGF. Interestingly, those cells could hardly make terminal differentiation in the presence of NGF and continued to grow without changing their round shape, although NGF receptor as well as MAP kinase appeared to be activated. Interestingly, the botulinum C3 toxin induced neurite-like structures in PC12 cells overexpressing BCR Delta162-413 without NGF.     

GLC determination of doxepin plasma levels

A procedure is described for extracting doxepin, a tricyclic antidepressant, from plasma and subsequently measuring its concentration by GLC. The developed technique permits the resolution and quantitative determination of the cis- and trans-isomers of doxepin as well as its desmethyl metabolite. The method allows precise, reliable measurement of the drug and one of its metabolities in concentrations as low as 10 ng/ml of plasma.     

正构烷烃的氧化以制取合成脂肪酸的研究

试验了国产的各种硬蜡及软蜡,确定了它们的氧化可能性。提出了可供工业上应用的加速氧化反应的二个方法:改善加入催化剂的方法及在泡沫状态下进行氧化。 对於简化分离氧化蜡亦提出了新方案。 文中还叙述了在氧化初期催化剂的作用,对工艺过程的控制有一定的帮助。     

Regional blood redistribution following blood loss in unanesthetized rats

The authors describe relative changes in the blood filling of 46 vascular areas of the body in rats after a moderate and severe blood loss. Moderate blood loss caused redistribution of the blood from the skin of the chest and from the skin of the posterior limbs, the majority of the abdominal and pelvis minor organs, muscular and bone tissues of the abdomen, pelvis minor and extremities into the brain, heart, lungs, kidneys, stomach and into the muscles of the head and neck. In severe blood loss the changes were analogous, but the blood content in the kidneys and the stomach decreased, and there was also a relative elevation of the blood in the muscles and bones of the chest. The intensity of the redistributive reaction in severe blood loss was less than in moderate blood loss.     

The functional activity of the portal vein as a reflection of the metabolic changes in experimental chronic kidney failure

Current therapeutic efforts to treat chronic and progressive neurodegenerative disease include, for the first time, attempts to regenerate affected nervous tissue using neurotrophic factors. The rationale for using trophic factors includes the understanding that they support neuronal survival and regrowth processes. The potential benefits of trophic factor therapy will be no more realized in the near future than in the treatment of amyotrophic lateral sclerosis (ALS). ALS is pathologically characterized by the selective degeneration of specific populations of cranial and spinal motoneurons. Evidence for the existence of factors that support motoneurons has come from studies demonstrating that motoneurons receive trophic influences from various tissues, both central and peripheral, within their local environment. Although the identity of these putative tissue-derived factors has remained enigmatic, recent studies have demonstrated that several previously characterized trophic factors exhibit trophic influences on motoneurons. Among these are several members of the neurotrophin family, most notably brain-derived neurotrophic factor. These neurotrophins meet most of the criteria to be considered motoneuron trophic factors: they are locally available to motoneurons in vivo; motoneurons express specific receptors for these factors; and exogenous application of these factors mimicks the effects of the uncharacterized endogenous agents. The clinical use of these factors for the treatment of ALS, therefore, appears to be scientifically justified.