Amiloride is an epithelial Na+ channel(EnaC)blocker.As a potassium-sparing diuretic,it has been used in clinical practice for decades of years.Studies have shown that many ion channels were semitive to amiloride in the central nervous system,such as acid-sensitive ion channel(ASIC)and Na+/H+ exchanger.These channels have important physiological functions,and paticipate in pathological processes such as cerebral ischemia and tissue acidosis.It has demonstrated that amailoride reduces the effects of ischemia-and acid-mediated neuronal injury by blocking these channels,which may become a novel neuroprotective agent for the treatment of cerebral ischemia.

Bone marrow mesenchymal stem cell (BMSC) provides the merits such as easy to obtain and small injury. Its low immunogenicity and its potential to easily induce immune tolerance make allogeneic transplant feasible without human leucocyte antigen matching to reduce the adverse effects of immunosupprassants. Density gradient centrifugation has been mostly used to isolate and culture BMSCs in vitro, which can be identified according to biological characteristics, cell surface markers, multi-differentiation potential, low immunogenicity and immune regulation. BMSCs are form the mesoderm, but they can be induced towards the calls from endoderm or ectoderm. Generally, BMSCs of the fifth passage are selected. In addition to use of conventional inducing agents, such as nerve growth factors, ratinoic acid, brain-derived growth factors, basic fibroblast growth factors, and epidermal growth factors, docesahexenoic acid and arachidonic acid are added to accelerate the neuron-like cell differentiation of BMSCs and concomitantly to promote the growth of neuronal axon. However, the security of BMSCs transplantation, in particular the tumorigenicity of tissue, requires further investigation.

Objective To observe the effect of acute cerebral infarction treated with FPD.Methods 50 cases of acute cerebral infarction patient were treated with FPD as observation group according to the diagnostic standard that made in 1986,Other 50 cases of comparable patirnt were as control so that to compare the curative effect.Results The nerve function deficiency in observation group was maredry hower than.Concusions FDP could reach an obvions effect that treat acute cercbral infarction via some aspecta.

Objective:To observe the clinic effect of wild apricot in Xinjiang Uighur nationality on fatty liver.Methods:With a western medicine group as the control group,the treatment courses of both two groups were 12 weeks.The trial group was given wild apricot decoction orally,the control group was given vitamin B,C and Glucurolactone tables.Results:Wild apricot exerted a significant effect in lowering the fat and treating the fatty liver without any toxic and side-effects.Conclusion:Wild apricot in Xinjiang Uighur nationality served as a vital treatment to fatty livers,which was worth being further promoted in the clinical therapy.

One hundred patients with acute ischemic stroke were enrolled in the study as the trial group, and 20 healthy individuals as control group. Intima-media thickness and plaque of the carotis were detected by carotid ultrasonography, cerebral infarction was detected by CT/MRI, and serum concentrations of sCD40L were measured by enzyme-linked immunosorbent assay. Neurologie impairment score was evaluated in all patients. The results showed that in patients with acute ischemic stroke the serum concentrations of sCD40L in plaques group were significantly higher than those in no plaque group. The levels of serum sCD40L of infarction group (diameter>1.5 cm) were higher than those of lacunar infarction group ( diameter<1.5 cm ) and temporary ischemic attack ( TIA ) group. The levels of serum sD40L in trial group were all higher than those in control group. In the trial group, serum concentrations of sCD40L were correlated with neurologic impairment score. The results indicate that CD40/CD40L signaling pathway may be involved in the carotid atherosclerosis formation and the rupture of plaques, and the increase of serum CD40L levels might be a risk factor for acute ischemic cerebrovascular diseases.

Objective To investigate the relationship between the matrix metalloproteinase-3(MMP-3)and the stability of carotid artery plaque,and explore MMP-3's prediction role on the attack and relapse of acute ischemic cerebrovascular events.Methods 100 patients with the first ever acute cerebral infarction,100 patients with chronic cerebral circulation insufficiency(CCCI)and 40 persons without cerebrovascular diseases were enrolled in this study.According to the carotid ultrasound examination,100 cerebral infarction patients were divided into three subgroup: unstable plaque group(45 patients,mixed plaque,soft plaque),stable plaque group(35 patients,plaque Group)and endometrial coarse group(25patients).Matrix metalloproteinase-3(MMP-3)levels of all the subjects were measured by enzyme-linked immunosorbent assay(as basal level).All the subjects were followed up for one year to observe cerebral infarction events.Serum MMP-3 levels of each group,and the basic serum MMP-3 levels were compared among patients who were attacked or relapsed cerebral ischemic with those who had not been attack cerebral ischemic during this period of time.Results 5 patients in the cerebral infarction group had relapse (5%),2 patients in the CCCI group were attacked by cerebral ischemic(2%),and no one in the normal control group was attacked by cerebral ischemic.Serum MMP-3 levels in the acute cerebral infarction group were significantly higher than CCCI group,and both groups were significantly higher than normal control group (P ＜0.05).The basic serum MMP-3 levels in all patients who were attacked by cerebral ischemic were significantly higher than those who had not been attack by cerebral ischemic during this period of time(P ＜0.05).The serum MMP-3 levels of the unstable plaque group were significantly higher than stable plaque group.And both groups were significantly higher than endometrial coarse group(P ＜0.05).Conclusions Elevated levels of matrix metalloproteinase-3(MMP-3)might have something with the stability of carotid atherosclerotic plaque,and participate the attack and the relapse of acute cerebral infarction.Determination of MMP-3 might be used to predict the attack and relapse of acute cerebral infarction.

Objective:To investigate the relationships between matrix metalloproteinase-3 (MMP-3),high-sensitivity C-reactive protein(hs-CRP)and carotid atherosclerosis and acute cerebral infarction.Methods: Sixty-four patients with the first ever cerebral infarction and 20 normal control subjects were selected.Their serum MMP-3 levels were determined by double antibody enzyme-linked immunosorbent assays,and serum hs-CRP levels were measured by immunonephelometric assay.Their carotid intima-media thicknesses were assessed by carotid ultrasonography,and neurological deficit scores were performed in patients with acute cerebral infarction.Results:The levels of serum MMP-3 and hs-CRP in patients with acute cerebral infarction were significantly higher than those in the normal control group(P＜0.01).The levels of serum MMP-3 and hs-CRP in unstable plaque group(mixed plaque group,soft plaque group)were significantly higher than those in stable plaque group(hard plaque group)and rough intima group(P＜0.01).The levels of serum MMP-3 and hs-CRP were positively correlated with the neurological deficit scores respectively in patients with acute cerebral infarction. Conclusions:The levels of serum MMP-3 and hs-CRP in patients with acute cerebral infarction may reflect the character and stability of carotid artery plaque,and they are the important indexes in understanding the severity of cerebral infarction in clinical practice.

Objective To investigate whether iron mass induces HO-1 overexpression and explore the role of HO-1 in rat intracerebral hemorrhage(ICH). Methods In this study,144 hydrated chloride aldehyde-anesthetized Sprague- Dawley rats were used,autologous blood were injected into the right caudate nucleus to establish the ICH model.Saline injection and health were served as controls.Deferoxamine(DFO)with an intraperitoneal injection served as intervention group.Enhanced Perl's reaction was used for iron staining and brain iron deposits were determined.Brain HO-1 level were examined by immunohistochemical analysis and reverse transcription polymerase chain reaction(RT-PCR). Results There was a 21-fold increase in iron deposits around the hematoma 7 days after the infusion of 100 μl of autologous blood.Markedly increased levels of perihematomal HO-1 immunoreactivity and HO-1 mRNA in all ICH rats were detected at 3-14 days.The addition of DFO significantly reduced iron deposits in the ipsilateral basal ganglia at 7-14 days after ICH.DFO also inhibited HO-1 overexpression at day 7,14.Correlations test showed that there were positive correlations of iron sediments with HO-1mRNA(r=0.647)and HO-1 immunopositive cells(r=0.209). Conclusions ICH causes iron accumulation in the brain.Iron overloading may induce HO-1 upregulation after ICH.Ratherly,the HO-1 moderate increasing possibly fits with the events,whereas HO-1 overexpression may result in its dysfunction.It may be prudent to intervene ICH with HO-1 inhibitor.