Acomplexcascadeofmoleculareventsisconsiderdtobeinitiatedfollowingcerebralis chemia ,whichincludereleaseofexcitatoryaminoacid ,calciumdyshomeostasis ,freeradicalinjury ,increased cytokines,caspaseactivationandalteredgeneexpression .Thisreviewprovidesanoverviewofmolecular mechanismsinvolvedinpostischemicneuronaldeathandanalysesthepotentialfortherapeuticintervention .

Oxidative stress has been implicated in brain injury after ischemia, which is a complex cascade. These oxidants produced by oxidative stress are directly involved in oxidative damage with cellular macromolecules such as lipids, proteins and nucleic acids, which lead to cell death. Oxidants are also mediators in signaling involving mitochondria pathway, DNA repair enzymes, and transcription factor that may lead to apoptosis after cerebral ischemia. Antioxidangt enzymes (such as superoxide dismutase,etc) provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury. This review focuses on the mechanisms of oxidative stress during brain ischemia.

In this study we found that while pituitrin induced a significant decline of nutritional blood flow of myocardium in mice, oxygen free radical concentration andmalondialdehyde content significantly increased, and superoxide dismutase activity signifi-cantly declined in the ischemic myocardium. These results suggest that this pituitrin-inducedmyocardial ischemia in mice may serve as an easy-to-operate, cheap and in vivo model forscreening oxy-radical scavengers in the study of anti-ischemic myocardial injury.

Cell protection from stresses by heat shock protein (HSP) was previously attributed to its ability to prevent aggregation and to accelerate refolding of damaged proteins. It plays an important role in cell survival after extremely harsh protein damaging treatment leading to necrotic cell death. On the other hand, protein repair function of HSP cannot explain how it protects cell from stresses which do not cause direct protein damage. These stresses kill cell through activation of apoptotic program. Recently it has been found that HSP can meditate suppression of a stress-activated protein kinase, JNK, an early component of stress-induced apoptotic signaling pathway.These observations can provide a basis for HSP's function of anti-apoptosis.

C. Conclusion The optimal SINI TANG composition comprises three active components combined at clinical maximal dosage showed the best therapeutic efficacy, of which A is a key factor and B, C are necessary factors for the composition in SINI TANG.

Cell protection from stresses by heat shock protein (HSP) was previously attributed to its ability to prevent aggregation and to accelerate refolding of damaged proteins. It plays an important role in cell survival after extremely harsh protein damaging treatment leading to necrotic cell death. On the other hand, protein repair function of HSP cannot explain how it protects cell from stresses which do not cause direct protein damage. These stresses kill cell through activation of apoptotic program. Recently it has been found that HSP can meditate suppression of a stress-activated protein kinase, JNK, an early component of stress-induced apoptotic signaling pathway.These observations can provide a basis for HSP's function of anti-apoptosis.

To explore the presence of informative protein biomarkers in the salivary proteome of breast cancer patients with thick white or thick yellow tongue fur.

AIM: To study dose-effect and time-effect changes of endothelin (ET) in myocardium and plasma during myocardial ischemia and its mechanism. METHODS:After inducing myocardial ischemia of rats in vivo with different dose of pituitrin(Pit) and the optimal dosage in the Pit at different time point, ET concentration in the myocardium and plasma was measured.Moreover, immunohistochemical study and RT-PCR were also applied in this study. RESULTS:ET concentration in myocardium increased gradually with the increase of Pit dose. ET concentration elevated significantly ( P

AIM: The study was undertaken to explore the dynamic changes of the concentration of nitric oxide(NO) in ischemic myocardium and its mechanism.METHODS: In vivo myocardial ischemia of mice and in vitro perfused isolated heart of rat were used in the experiment. The effects of severity and time of ischemia on NO production, NOS activity and mRNA were examined, respectively. RESULTS: There was a considerable difference (P