Adolescent ; Female ; Humans ; Immunoglobulins, Intravenous ; administration & dosage ; Immunosuppressive Agents ; administration & dosage ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ; diagnosis ; therapy

Acupuncture Therapy ; methods ; Botulinum Toxins, Type A ; therapeutic use ; Cerebral Palsy ; therapy ; Child ; Child, Preschool ; Combined Modality Therapy ; Female ; Humans ; Male ; Massage

OBJECTIVETo explore the possible mechanism of electroacupuncture preconditioning (EAPC) and combined with ATP-sensitive potassium channel (KATP) blocker preconditioning for hypoxia/ischemic brain injury protection by observing the changes of the immediate genes (c-fos and c-jun protein content) in brain at the early stage after cerebral hypoxia/ischemic injury, and the effect of EAPC on these changes.

METHODSIntegrated density (ID) of c-fos and c-jun expression was measured by Western blot and computerized image processing.

RESULTSHypoxia/ischemia could induce c-fos and c-jun protein in both cerebral cortex and hippocampus simultaneously, with the peak appearing 2-4 hrs later, and the expression in hyppocampus was higher than that in cortex. EAPC could lower KATP blocker induced permanent high expression in hyppocampus.

CONCLUSIONThe effect of EAPC preconditioning in antagonizing cerebral hypoxia/ischemic injury may be related with its action in activating KATP, inhibiting the neuron apoptosis induced by the immediate genes at early stage of injury.

Animals ; Animals, Newborn ; Apoptosis ; Brain ; metabolism ; pathology ; Electroacupuncture ; Female ; Hypoxia-Ischemia, Brain ; metabolism ; prevention & control ; Ischemic Preconditioning ; methods ; Male ; Proto-Oncogene Proteins c-fos ; metabolism ; Proto-Oncogene Proteins c-jun ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThe cascade of physiological events underlying hypoxic-ischemic brain damage (HIBD) remains to be fully established. The perinatal brain shows both an increased tolerance to hypoxic-ischemic (HI) injury and a faster and more complete recovery than the adult. It is, therefore, important to understand the sequence of events following hypoxia and ischemia in young animals. The present study aimed to clarify the time-course of the activation of the mu-calpain, and the expression of c-Fos, c-Jun, HSP70 and HSP27 proteins following severe HI (2 h hypoxia) and their relationship with each other.

METHODSA modified newborn rat model of HIBD that included a combination of hypoxia and ischemia as described by Rice was used. Forty-two postnatal 7-day-old Sprague-Dawley rats were randomly divided into seven groups (6 rats in each): 6 time-window groups and a normal control group. Samples were collected at 0, 1, 2, 4, 12 and 24 h after HI insults. The protein concentration was determined using a modified Bradford assay. mu-calpain activation, c-Fos, c-Jun, HSP70 and HSP27 expressions were observed respectively by Western blot from cortical and hippocampal samples.

RESULTSThe cleavage of cytosolic mu-calpain was observed from both cortical and hippocampal samples in neonatal rats after HI. The ratio 76:80 of mu-calpain was increased significantly post-HI and reached a maximum at 24 h in cortex and at 12 h in hippocampus after HI. The expressions of c-Fos and c-Jun from both cortical and hippocampal samples in neonatal rats were up-regulated and peaked at 2 or 4 h after HI, demonstrating significant differences at 1, 2, 4, and 12 h compared with that observed in the control (P < 0.05). When compared with that observed in cortex, the nuclear c-Fos expression from hippocampal samples was highly elevated at 2, 4 and 12 h but significantly decreased at 24 h after HI (P < 0.05), while the nuclear c-Jun expression from hippocampal samples was highly elevated at 0 and 1 h but significantly decreased at 4 and 24 h after HI (P < 0.05). Similarly, the expressions of HSP70 and HSP27 from both cortical and hippocampal samples were up-regulated and reached a maximum at 12 or 24 h after HI, demonstrating significant differences at 12 or 24 h both in cortex and hippocampus for HSP70, and at 24 h in cerebral cortex as well as at 12 and 24 h in hippocampus for HSP27 compared with the control (P < 0.05). Furthermore, in comparison with that observed in cortex, the HSP70 expression from hippocampal samples was highly elevated at 1 h, but significantly decreased at 4, 12 and 24 h after HI (P < 0.05), while the HSP27 expression was permanently elevated in hippocampus after HI.

CONCLUSIONThe neuronal injury induced by HI insults appears to involve many ongoing and simultaneous mechanisms. HI activates the calpains immediately, which may contribute to neuron apoptosis, and induces a significant brain neuroprotection, since there is an increased HSP70 expression and a relatively late remarkable HSP27 expression in hypoxic-ischemic neonatal rat brain. Nuclear c-Fos and c-Jun may participate in the pathogenesis of HIBD.

Animals ; Animals, Newborn ; Blotting, Western ; Brain ; metabolism ; pathology ; Calpain ; metabolism ; Enzyme Activation ; Female ; HSP27 Heat-Shock Proteins ; HSP70 Heat-Shock Proteins ; metabolism ; Heat-Shock Proteins ; metabolism ; Hypoxia, Brain ; metabolism ; Male ; Neoplasm Proteins ; metabolism ; Proteins ; metabolism ; Proto-Oncogene Proteins c-fos ; metabolism ; Proto-Oncogene Proteins c-jun ; metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors

Objective To investigate the relationship between the Apolipoprotein(Apo)A5-1131T>C polymorphism and strokes.Methods Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP)and polyacrylamide gel eletrophoresis(PAGE)wefe used to analyze the genotypic polymorphism in 327 patients with stroke(including 194 cerebral infarction patients and 133 cerebral hemorrhage patients)and 311 healthy controls.The levels of serum lipids profiles were also measuredby enzymatic methods. Results The frequency of the-1131C allele in cerebral infarction patients was significantly higher than that of the control group(44.1% vs 32.3%,P<0.05),but there was not statisticai difference between cerebral hemorrhage patients and controls on the-1131C allele frequeney(35.4%vs 32.3%,P>0.05).Compared with the noncamers,the C carriers also had a higher triglyceride(TG)levels in stroke group[(1.45±0.77)vs(1.69±1.06)mmol/L,P<0.05],but the total cholesterol(TC),high density lipoprotein cholesterol(HDL-C)and low density lipoprotein cholesterol (LDL-C)levels did not show statistical differences in various genotypes(P>0.05).Unadjusted Logistic regression analysis indicated that TC+CC genotype of A5-1131T>C was significantly associated with the presence of cerebral infarction,but not with hemorrhage stroke.Logistic regression analysis adjustedfor BMI,presence of hypertension or diabetes and HDL-C levels revealed that TC+CC genotype was an independent risk factor for cerebralinfarction(OR=1.932,95%CI:1.057-3.532,P=0.032). Conclusion The ApoA5-1131C allele frequency of the patients with cerebral infarction is significantly higher than controls.ApoA5-1131T>C polymorphism has a significant influence on serum TG levels.The ApoA5-1131T>C variant is associated with an increased susceptibility for ischemic stroke.

Objective To asses the value of proton magnetic resonance spectroscopy (1H-MRS) combined with neuropathological findings in early detection of metabolic abnormities and damages of the brain neurons following heat stress (HS) and febrile convulsion (FC). Methods Febrile convulsion models were established in weaning rats (21 days old) by means of hot water bath. -1H-MRS was performed to measure the changes in N-acetylaspartate (NAA), choline (cho), lactate (Lac) and creatine (Cr) contents in the brain tissue following HS or FC, and in sire hybridization was used to detect Zinc transporter 3 (ZnT3) mRNA expression in the hippocampus. Results In the control group, HS group and FC group, the NAA/Cr ratio (1.5±0.42, 1.57±0.59, and 1.61±0.37, respectively) and Cho/Cr ratios showed no significant differences, but a significant increase in Lac/Cr ratio was observed in FC group. ZnT3 3 mRNA expression was detected in the dentate gyms of the rats following the onset of FC. Conclusions As Lac increase is a putative marker of seizure-induced neuronal damage, and ZnT3 is associated with mossy fiber sprouting in the hippocampus, our results suggest that even a single temporary FC may result in marked changes in neuronal metabolism and cause subtle brain injury.

OBJECTIVETo investigate the expression of brain-derived neurotrophic factor (BDNF) mRNA and immunoreactivity in experimental acute inflammatory brain injury.

METHODSTen rats were inoculated with pneumococcus to establish the model of bacterial inflammatory brain injury and other 6 rats were used as normal controls. At 24 h after inoculating, the expression of BDNF mRNA and BDNF protein in brain tissue was detected by in situ hybridization and immunohistochemical methods, respectively.

RESULTThe necrosis of neuron in cerebral cortex and hippocampus was observed after infection. The increase of BDNF mRNA expression in the cerebral cortex and hippocampus of experimental animals was demonstrated at 24 h after inoculation: (0.1194 +/- 0.02941 compared with 0.0662 +/- 0.01176)A and (0.1608 +/-0.01854 compared with 0.0680 +/- 0.00946)A (P<0.01), respectively. Compared with controls the expression of BDNF protein in the cerebral cortex and hippocampus was enhanced at 24 h of inoculation:(177.04+/-43.66 compared with 79.79+/-7.23)mm(2) (P<0.01) and (81.78 +/-37.47 compared with 42.98 +/-20.44)mm(2) (P<0.01), respectively. Strong positive hybridization and immunoreactivity were observed in the infiltrated inflammatory cell in leptomeninges, subarachnoid cavity, ventricles and brain parenchyma in the brain from the experimental rats.

CONCLUSIONThe expression of BDNF mRNA and BDNF protein increases following brain inflammatory injury, which supports the hypothesis that BDNF may constitute intrinsic neuroprotective mechanism as a part of the inflammatory response.

Acute Disease ; Animals ; Brain-Derived Neurotrophic Factor ; analysis ; genetics ; Calcium ; metabolism ; Female ; Immunohistochemistry ; Male ; Meningitis, Pneumococcal ; metabolism ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effects of ST1571 on the development of dendritic cells (DC) derived from bone marrow mononuclear cells of patients with chronic myeloid leukemia (CML).

METHODSBone marrow mononuclear cells (BMMNC) from CML patients and healthy volunteers were cultured initially using multiple cytokine combinations as follows: recombinant human granulocyte/ macrophage colony-stimulating-factor (rhGM-CSF) plus recombinant human interleukin-4 (rhIL-4) as CML and normal control groups, rhGM-CSF plus rhIL-4 and ST1571 as CML experimental groups, and from day 8 recombinant human tumor necrosis factor-alpha ( rhTNF-alpha) was added to stimulate DC maturation. The morphologic features of cells were observed by Wright's staining and phenotypes were assessed by flow cytometry. Cytogenetic analysis was performed by fluorescence in-situ hybridization (FISH), and the antigen-presenting function was assayed by mixed lymphocyte reaction (MLR). The concentration of VEGF was detected by ELISA.

RESULTSCML experimental groups treated with STI571 displayed morphological features similar to those of control groups with delicate membrane projections. However, in comparison with the CML control groups, the CML experimental groups showed an increased expression of CD80, CD86, CD83 and HLA-DR and showed more intense abilities of allogeneic antigen presentation, which were similar to those of normal control groups. FISH confirmed that DCs of both CML, groups were of leukemic origin. The concentration of VEGF was dramatically reduced in CML experimental groups.

CONCLUSIONIn vitro, STI571 promotes the activation/maturation of DCs derived from BMMNCs of patients with CMI, and decreases VEGF production by the leukemic cells. The promotion of DC maturation may be partially due to decreased inhibitory effect of VEGF.

Adult ; Antigens, CD ; metabolism ; Benzamides ; Bone Marrow Cells ; drug effects ; metabolism ; pathology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Dendritic Cells ; drug effects ; metabolism ; pathology ; Female ; Flow Cytometry ; Fusion Proteins, bcr-abl ; genetics ; metabolism ; HLA-DR Antigens ; metabolism ; Humans ; Imatinib Mesylate ; In Situ Hybridization, Fluorescence ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; blood ; pathology ; Male ; Middle Aged ; Piperazines ; Pyrimidines ; pharmacology ; T-Lymphocytes ; drug effects ; metabolism ; pathology ; Vascular Endothelial Growth Factor A ; metabolism

OBJECTIVE: To identify possible risk factors for cerebral palsy (CP) in children. METHODS: A Population-based survey was conducted (including 92 CP cases) in 66 townships of 15 cities of Zhejiang Province from October to November, 1998. 184 of matched controls were selected for comparison. RESULTS: Factors identified which were statistically significant for risk of subsequent childhood Cerebral Palsy included some neonatal diseases, some maternal diseases, low birth weight (<2500 g), maternal irregular menstruation, toxic, substances during pregnancy, malnutrition during pregnancy,and paternal age. CONCLUSION: Several risk factors for Cerebral Palsy were identified. Their prevention may result in redduction of the incidence of Cerebral Palsy.

OBJECTIVETo investigate the clinical value of different magnetic resonance (MR) pulse sequences in diagnosis of spinal metastatic tumor.

METHODSFifteen patients with clinically suspected spinal metastatic tumor were included in this study. These patients were with documented primary tumors. Four MR pulse sequences, T1-weighted spin echo (T1WI SE), T2-weighted fast spin echo (T2WI FSE), short time inversion recovery (STIR), and gradient echo 2-D multi echo data imaging combination (GE Me-2D) were used to detect spinal metastasis.

RESULTSFifteen vertebral bodies were entire involvement, 38 vertebral bodies were section involvement, and totally 53 vertebral bodies were involved. There were 19 focal infections in pedicle of vertebral arch, 15 metastases in spinous process and transverse process. Fifty-three vertebral bodies were abnormal in T1 WI SE and GE Me-2D, 35 vertebral bodies were found abnormal in T2WI FSE, and 50 vertebral bodies were found abnormal in STIR. The verges of focal signal of involved vertebral bodies were comparatively clear in T1WI SE, comparatively clear or vague in T2WI FSE, vague in STIR, and clear in GE Me-2D.

CONCLUSIONSGE Me-2D may be the most sensitive technique to detect metastases. So three sequences (T1WI SE, T2WI FSE, GE Me-2D) can demonstrate the early changes of spinal metastasis roundly.

Cervical Vertebrae ; diagnostic imaging ; Coccyx ; diagnostic imaging ; Humans ; Lumbar Vertebrae ; diagnostic imaging ; Magnetic Resonance Imaging ; methods ; Neoplasm Metastasis ; pathology ; Radiography ; Sacrum ; diagnostic imaging ; Sensitivity and Specificity ; Spinal Neoplasms ; pathology ; secondary ; Spine ; diagnostic imaging ; Thoracic Vertebrae ; diagnostic imaging