Comparison of the efficacy of cell preparations from embryonic ventral mesencephalon of various prenatal age transplanted intrastriatally to rats with 6-OHDA-induced Parkinsonism

Cell preparations of ventral mesencephalon obtained from 8-, 14-, and 16-17-day rat embryos were stereotactically transplanted to homologous rats with 6-hydroxydopamine-induced hemiparkinsonism. Automated analysis of apomorphine-induced motor asymmetry for 3 months after neurotransplantation revealed higher efficacy of cell preparations from 8- and lower from 16-17-day-old embryos. These data correlated with histomorphological findigs, in particular, with the size of grafts, glial reaction, and the number of dopaminergic neurons in the grafts.     

Tryptophan 650 of human granulocyte colony-stimulating factor (G-CSF) receptor, implicated in the activation of JAK2, is also required for G- CSF-mediated activation of signaling complexes of the p21ras route

Granulocyte colony-stimulating factor (G-CSF) induces rapid phosphorylation of JAK kinases as well as activation of the p21ras route through interaction with its specific receptor (G-CSF-R). The cytoplasmic membrane-proximal region of G-CSF-R (amino acids 631 to 684) is necessary for proliferation induction and activation of JAK2. In contrast, activation of Shc and Syp, signaling molecules implicated in the p21ras signaling route, depends on the phosphorylation of tyrosine residues located in the membrane-distal region (amino acids 685 to 813) of G-CSF-R. We investigated whether G-CSF-induced activation of signaling complexes of the p21ras route depends on the function of the membrane-proximal cytoplasmic region of G-CSF-R. A G- CSF-R mutant was constructed in which tryptophan 650 was replaced by arginine and expressed in BAF3 cells (BAF/W650R). In contrast to BAF3 cell transfectants expressing wild-type G-CSF-R, BAF/W650-R cells did not proliferate and did not show activation of JAK2, STAT1, or STAT3 in response to G-CSF. Immunoprecipitations with anti-Shc and anti-Grb2 antisera showed that mutant W650R also failed to activate Syp and Shc. These data indicate that the membrane-proximal cytoplasmic domain of G- CSF-R is not only crucial for proliferative signaling and activation of JAK2 and STATs, but is also required for activation of the p21ras route, which occurs via the membrane-distal region of G-CSF-R.     

p38 MAPK对嗜酸性粒细胞和支气管上皮细胞共培养时细胞因子释放的调控作用

目的 了解嗜酸性粒细胞和支气管上皮细胞相互作用诱导细胞因子释放的p38 MAPK信号转导通路.方法 用CD16磁珠抗体分离外周血中嗜酸性粒细胞,以嗜酸性粒细胞和支气管上皮细胞(BEAS-2B)接触共培养为实验模型,观察SB 203580对细胞培养上清液中细胞因子浓度的影响.细胞因子浓度采用ELISA和流式细胞微珠方法测定.结果 SB 203580能够有效抑制BEAS-2B细胞释放IL-6、IL-8(P＜0.05)和嗜酸性粒细胞释放IL-8(P＜0.01).SB 203580对嗜酸性粒细胞与BEAS-2B细胞接触共培养诱导的IL-6、IL-8和IP-10释放具有显著抑制作用(P＜0.001).结论 嗜酸性粒细胞、BEAS-2B细胞单独或相互作用时均通过p38 MAPK信号转导通路释放细胞因子.     

Drug prevention of cardiac rhythm disorders during the acute period of myocardial infarct]

Among 152 patients with myocardial infarction admitted to a specialized department within a few hours (1st day) of the onset of the disease without cardiac rhythm disorders, or with "minor" arrhythmias, 31 patients were receiving Panangine intravenously, 10--20 ml daily, for 7 days since the moment of admission. Another group of patients was comprised of 75 persons who, in addition to the above regimen of Panangine therapy, received at the moment of their admission a single intramuscular injection of Retabolil (50 mg). The control group was formed by 46 patients receiving no antiarrhythmic drugs. Monitoring of the cardiac rhythm during the acute period of myocardial infarction demonstrated that with preventive employment of Panangine prognostically dangerous rhythm disorders (especially paroxysmal tachycardia) developed less often than in the controls. A combined employment of Panangine and Retabolil resulted in a still better preventive effect, largely preventing, among other developments, the appearance of multiple polytopic extrasystoles. No ventricular fibrillation was observed in the examined patients.     

Actual aspects of phlebothromboses and thromboembolism of the pulmonary artery in trauma

Risk factors of the development of phlebothrombosis and thromboembolism of the pulmonary artery (TEPA) were estimated in 257 patients as associated both with the patient and the trauma. The factors influencing the development of risk factors were: bed immobilization, age older than 40, heart failure and respiratory insufficiency, fractures of the lower extremities, skeleton traction, obesity, thrombosis of lower extremities, previous thrombosis or pulmonary embolism, floating clot. Risk factors of the development of vein thrombosis associated with trauma included the presence of lower extremity fractures, skeletal traction or immobilization in bandage, mechanism of injury and type of trauma.