Ischemic stroke is a very complex disorder with many intracellular and extracellular factors such as excitatory amino acids, free radicals, calcium overload, apoptotic genes and inflammation involved in its pathophysiological mechanisms. It has been reported that neuronal death mainly derives from necrosis and/or apoptosis after cerebral ischemia. Those neurons in the ischemic core usually suffer from necrosis, however, apoptosis (also referred to as delayed neuronal death) occurs in the ischemic penumbra, which has been the major therapeutic target in the ischemic stroke.

Objective To explore the effects of human umbilical cord blood cells(HUCBCs) transplantation to treat experimental autoimmune encephalomyelitis(EAE) rats and the status of transplanted HUCBCs in the brain and spinal cord tissue of EAE rats.Methods The mononuclear cells abstracted from cord blood of infants were cultured in vitro and marked with 5-bromodeoxyuridine(Brdu) for 48 h.EAE rat models were made and the HUCBCs(3?106) were transplanted into the tail vein(transplanted group) 14 d later.The score of neurological function dificit and the number of the demyelinated foci in brain and spinal cord were undertaken at different time point after transplantation.The statue of survival,differentiation and migration of HUCBCs in vivo were determined by immunohistochemical technique,and compared with control group.Results The scores of neurological function dificit at 21 d,28 d post transplantation in transplanted group were much lower than those in the control group(all P

Protein Kinase C (PKC) is an important messenger in intracellular signal transduction. So far, at least 11 members of PKC isoforms have been isolated and purified. The mutation of the non-synonymous SNP (1425G/A) of the η isoform of protein kinase C (PKC η), a protein kinase Cη gene (PRKCH) may result in the increased PKCη activity, which is considered as a new risk factor for lacunar infarction. In recent years, the studies about the role of PRKCH in cell differentiation and apoptosis and its relation with some signal transduction pathways have made some new advances, especially, PKCη participates in the regulation of some key enzyme activity that mitogen-activated protein kinase, inducible nitric oxide-synthase and matrix metalloproteinase are closely correlated with the process of atherosclerosis. It will provide a new way of thinking for the clinical intervention of cerebral infarction in the future.

Granulocyte macrophage-colony stimulating factor (GM-CSF) is a muhifunctional growth factor. It stimulates the proliferation, differemiation and maturity of hematopoietic progenitor cell (HPC), and transfers from bone marrow to periphery, inducing multiple cell proliferation or differentiation. In recent years, some studies have indicated that GM-CSF plays an important role in anti-apoptosis, inducing neuronal differentiation and angiogenesis, which will he a new supplement to the treatment of ischemic cerebrovascular disease. This article reviews the effects of GM-CSF in the treatment of ischemic cerebrovascular disease.

A new method of mismatching PCR-RFL P was performed in our lab in ge- netic diagnosis of spinal muscular atrophy(SMA) and controls.Our data shows:9cases in 1 0 presumed SMA children are positive,i.e. deletion of telomeric SMN gene.One case is negative.2 0 cases of normal familial members and2 0 cases of normal controls are all nega- tive.Our results matches the criteria and reports of foreign countries.The method we used is highly specific,sensitive and useful and is suittable for genetic diagnosis of SMA and its prenatal diagnosis.

Objective To study the levels of ? amyloid protein(A?/?A 4) in cerebrospinal fluid(CSF) of patients with Alzheimer's disease(AD) and vascular dementia(VD) and its significance of diagnosis.Methods The levels of A? 1 40 and A? 1 42 in CSF of 24 patients with AD, 14 patients with VD and 30 normal controls(NC) were detected by enzyme linked immunosorbent assays(ELISA).Results (1)The levels of A? 1 42 in CSF of AD and VD patients were significantly lower than NC group ( P

Objective To study the best dose of batroxobin that protects forebrain ischemia reperfusion injury in gerbils.Methods 80 gerbils were randomly assigned to receive different dose of batroxobin (1 BU/kg, 2 BU/kg, 4 BU/kg, 8 BU/ kg, 16 U/kg or 32 BU/kg) in treatment group, NS in control group or nothing in sham-operation group. There were 10 gerbils in each group. NS (control group) or batroxobin (treatment group) was given intraperitoneally three hours before establishment of forebrain ischemia reperfusion model. Apoptotic cells were detected by TUNEL technique and the number of apoptotic cells in the hippocampal CA 1 territory was counted using Olympus microscope.Results The apoptotic cells in the treatment groups (8 BU/kg, 16 BU/kg, 32 BU/kg) markedly decreased than those in the control group and the other treatment groups (1 BU/kg, 2 BU/kg, 4 BU/kg) (all P0.05). Conclusions Batroxobin has a role of reducing neuron apoptosis after cerebral ischemia. The best dose of batroxobin that protects forebrain ischemia reperfusion injury in gerbils is 8 BU/kg.

Objective To explore the effect of human neural stem cells(hNSCs) transplantation to treat cerebral ischemic rats and the status of transplanted hNSCs in the ischemic brain tissue of these rats.Methods Human neural stem cells were separated from 10~13 weeks brains of human embryo and were cultured and induced to differentiate. The middle cerebral artery occlusion rat models were made and the human neural stem cells were transplanted through tail vein 1 day later. Neurological Severity Scores (NSS) tests were undertaken in two groups after transplantation. Immunohistochemistry was used to check the differentiation and migration of human neural stem cells in vitro and vivo.Results Neural stem cells from human embryonic brains had been successfully cultured. These cells formed typical neurospheres in suspension, and the majorities expressed nestin. Three weeks later, the neurological function of rats that received transplantation recovered much better than the rats without transplantation, as evidenced by NSS ( P

Objective To observe the apoptosis of neuron and protein kinase B (Akt) expression after intracerebral hemorrhage (ICH)in rats, and investigate the interference effect and mechanism of ?-aeacine sodium on ICH injury.Methods All Sprague - Dawley male rats were randomly divided into normal group, pseudo -operation group,model group and therapeutic group treated with ?-sodium aeacine.The latter three groups were divided into five subgroups respectively :6 h,12h,1d,3d and 7d.ICH models were performed by injection Ⅶ type collagenase into the the right globus pallidus.By the methods of in situ terminaldeoxynucleotidyl transferase- mediated dUTP nick end labeling (TUNEL) and immunohistochemistry, The dynamic changes of apoptosis and the expression of AKt protein were observed in the damaged cortex.Results TUNEL-positive cells appeared at 6h after collagenase injection in the model group and the expression of AKt increased at 12 h.They reached their peak at 3rd day, and were still present during 1 week. The numbers of TUNEL-positive cells in 1 d, 3 d, 1 week after ICH decreased markerly in treatment group than those of in model group ( P

Objective To explore the effect of human umbilical cord blood cells (HUCBCs) transplantation to treat cerebral ischemia of rats and the status of transplanted HUCBCs in the ischemic brain tissue of these rats. Methods The mononuclearcells abstracted from 60～100 ml of cord blood of full-term babies were cultured in vitro and marked with 5-bromodeoxyuridine (Brdu)(5 ?mol/L) for 2 days. The middle cerebral artery occlusion rat models were made and the HUCBCs (3?106) were transplanted into the lateral ventricular 1 day later. Neurological severity scores (NSS) tests were undertaken at different time point after transplantation, and iimmunohistochemistry method was used to check the migration and differentiation of HUCBCs. Results The HUCBCs had the capacity of proliferation in vitro and were induced to differentiate into astrocytes, oligodendrocytes and neurons in vivo. 3 weeks later, the neurological function of rats that received transplantation recovered much better than the rats without transplantation, as evidenced by NSS (all P