RESUMEN
Ischemic stroke, gravely affecting human health with its increasing incidence rate , is a common disease of old age . JAK/STAT way , a recently discovered signaling pathway , is not only widely involved in processes of cell growth ,differentiation, and apoptosis ,but also closely related to the pathophysiology of stroke.However,the pathway function and mechanism in ische-mic cerebral stroke has not yet been fully elucidated .We will review the role and mechanism of JAK/STAT signal transduction pathway in ischemic stroke ,and scientifically draw network chart between various related signal molecules in the process of ische-mic stroke neuropathy combining both domestic and foreign re-search reported in this paper , in order to better understand the pathological mechanism process of brain stroke , find new drugs for the treatment of cerebral ischemic diseases ,then provide more systematic scientific literature support .
RESUMEN
We sought to determine whether VEGF and other angiogenic growth factors and their receptors might be subject to negative feedback regulation during two weeks of treadmill-exercise conditioning in inbred strains of mice. C57BL/6 mice exhibited greater VEGF mRNA and protein responses in gastrocnemius muscle to a single bout of treadmill exercise compared to BALB/c mice. The patterns of VEGF, VEGFR1, VEGFR2, Ang2 and Tie2 mRNA expression in gastrocnemius muscles of C57BL/6 mice during long-term exercise support the hypothesis that they may be subject to negative feedback regulation. The combination of expression patterns for growth factors and their receptors suggests that multiple layers of control mechanisms may exist to prevent angiogenesis following a single bout of exercise and to promote angiogenesis following long-term exercise.
RESUMEN
The intracellular signal transduction pathway of histamine H 3 receptor was reviewed. The modulatory effect to some neurotransmitters on cardiovascular system and the therapeutic potential of histamine H 3 receptor agonist was summarized.
RESUMEN
The effect of hydrocortisone (135 nag i.v. as a bolus) on the levels of serum N-POMC was studied in the patients with Cushing's disease [including three groups: untreated (CD, n=8), post-adrenolectomy without Nelson's syndrome (CDA, n=5), and Nelson's syndrome (NS, n=4)]; Addison's disease (AD, n = 13) and congenital adrenal hyperplasia (CAH, n=4). The results showed that the levels of serum N-POMC were decreased after the administration of hydrocortisone in all three groups of Cushing's disease, however the suppression rate of N-POMC was much lower in these groups than that in AD and CAH (P