Objective To explore the mechanism underlying the poor prognosis in cerebral infarction (CI) patients with low T3 syndrome by comparing the NIHSS scores in these patients with or without low T3 syndrome.Methods One hundred and sixty-two patients with CI,admitted to our hospital from January 2010 to December 2012,were chosen in our study; the levels of thyroid hormones,including triiodothyronine (T3),four iodine thyronine (T4),thyroid stimulating hormone (TSH),free Triiodothyronine (iT3) and free four iodine thyronine (fT4),were measured by radioimmunoassay.CI lesions and TOAST distribution were determined by cranial MRI,magnetic resonance angiography (MRA) or CT angiography (CTA),and carotid ultrasonography.NIHSS scores at the worst in cerebral infarction inpatients were detected.Results In the 162 patients with CI,29 patients (17.90％) were combined with low T3 symptom and 20 had fT3 level lower than the lowest normal level (2.63 pmol/L); and T4,fT4 and TSH levels were within normal limits.T3,fr3 and TSH levels in patients with low T3 symptom were significantly lower than those of patients without low T3 symptom (P＜0.05).The distribution of TOAST showed no significant difference between patients with low T3 symptom and patients without low T3 symptom (P＞0.05).In patients with large artery atherosclerosis-internal carotid artery,the NIHSS scores at the worst in patients with low T3 level were significantly higher as compared with those in patients with normal T3 levels (P＜0.05).Conclusion The neurologic impairment is more severe in large artery atherosclerosis-intemal carotid artery patients with low T3 level than those without low T3 level,which might be responsible for the poor prognosis of the illness with low T3 syndrome.

Objective To investigate the protective effect and its mechanism of DL-3-n-Butylphthalide on the brain damage in rats following whole brain irradiation.Methods A total of 120 male Sprague Dawley rats were randomly divided into sham-irradiation group,irradiatien group and DL-3-n-Butylphthalide group.The model of whole-brain irradiatien was established by exposuring rat brain to 4 MeV X-rays with a single-dose of 10 Gy.The rats were intraperitoneally injected with DL-3-n-Butylphthalide at the dosages of 0.3,1.0,and 3.0 mg/kg once a day.The contents of malondialdchyde and super oxide dismutase activity were measured,while the expressions of apoptosis-associated genes and the ultrastructural changes in hippocampus were examined by immunohistnchemisty staining and electron microscope,respectively.Results After irradiation,the content of malondialdehyde and the expression of apoptosis gene bax in rat brain tissue increased while the activity of super oxide dismutase(SOD) and the expression of anti-apoptosis gene bcl-2 decreased.Apoptosis was also observed in the neurons of hippocampus CA1.Compared with irradiation group,the content of malondialdehyde and the expression of bax gene in the DL-3-n-Butylphthalide group wen significantly reduced ( t =-3.89--1.96,2.72-3.48,P ＜ 0.05 ),while the activity of SOD and bcl-2 gene were significantly elevated ( t =2.94-3.76,-3.18--2.08,P ＜ 0.05),and the injury degree of neuron structure in the DL-3-n-Butylphthalide group was slighter than that in the irradiation group.Conclusions DL-3-n-Butylphthalide executes protective effects in a dose-dependent manner againest the radiation injury in rats brain by reducing the induction of malondialdehyde,raising the activity of SOD and inhibiting the generation of apoptosis.

Alzhelmer's disease (AD) is an important neurodegenerative disease. Recent evidence has indicated that the production and loss of the myelin,sheath are associated with AD because the particular vulnerability of oligodendrocytes produced in the late stage makes the loss of the myelin sheath take a core position in the changes of the earliest stage of AD. The loss of the myelin sheath disrupts synchronization of impulses on which normal brain functions highly depend, and ultimately results in the function disruption of cortical association regions and subsequent neuronal loss. Meanwfiile, there are diverse mechanisms that make oligodendrocytes degeneration exist in the brains of AD. Therefore, elucidating its specific mechanism may help better understanding of AD, and thus provide some help for its treatment.

Objective To study the effects of traumatic brain injury with or without hypotension on the development and severity of brain edema using the impact- acceleration model.Methods Brain tissue water content (BWC) was measured by the gravimetric technique in the cortex and striatum following traumatic brain injury (TBI) . The hypotension was induced by the combination of α - chloralose and pavulon after TBI.Results The mortality of this improved model of TBI was 48.6 %, but the rate of skull fracture was 6.4 %. Within the first 24 hours after TBI, the BWC of cortex and striatum in the survival rats showed a slight decrease at first, and then an increase. There appeared no difference in BWC between the two groups of TBI and the control. Nevertheless, the BWC in the area of parietal cortex at 24 hours after impact injury slightly increased by 0.5 % in comparison with that at 8 hours after impact [ (79.1 ± 0.5) % vs. (78.6 ± 0.5) %, P ＜ 0.05]. Meanwhile,the BWC of striatum didn't show the difference. However, while TBI was associated with hypotension, the BWC of both parietal cortex [ (81.5±0.9)% vs. (78.6±0.5)%, P＜0.001] and striatum [ (78.5±0.9)% vs. (75.5±0.9)%, P＜0.001) were significantly increased, by comparison with survival rats at 8 hours after impact. Moreover, the amplitude of increase in BWC achieved about 2.9 %.Conclusion The rats, suffering TBI without hypotension, presented the slight brain edema at the relatively late stage; by contrast, the rats,suffering from TBI with hypotension, had severe brain edema at the early stage.

Objective To investigate the pattern of fluctuations and clinical significance of fasting serum insulin(FINS) and C-peptide(CP) levels in patients with different subtypes of acute cerebral infarct(ACI) and its relationship with serum lipid. Methods FINS and CP were measured in 152 ACI patients by chemiluminescent immunoassay. All ACI patients were classified into 5 major ischemic stroke subtypes according to the trial of org10172 in acute stroke treatment(TOAST) criteria. And then the relationship between FINS and CP level and serum lipid in different TOAST subtypes were analysed. Results The percentage of each ischemic stroke TOAST subtype was as follow: stroke of undetermined etiology 40.13%, small-vessel occlusion 34.21%, cardioembolism 5.26%, large-artery atherosclerosis 15.79%, and stroke of other determined etiology 4.61%. Among 5 major stroke subtypes, large-artery atherosclerosis patients had the highest levels of FINS and CP. The levels of FINS and CP in small-vessel occlusion were (8.237?5.144) ?U/ml and (1.761?0.975)ng/ml,respectively. Stroke of other determined etiology subtypes were associated with the lowest levels of FINS and CP. Apparently, other factors, such as TC, TG, LDL, SBP, DBP, age and HDL, could also affect the levels of FINS and CP in serum. Conlusions Levels of FINS and CP varied in different subtypes of ACI. There was a significant correlation among insulin resistance, hyperinsulinemia(HIS) and lipid metabolic abnormality in ACI.

BACKGROUND: There are so many experimental and clinical researches on levels of nitrogen monoxide (NO) in serum and endothelins in plasma of patients with stroke; however, ratio and significance between them are still unclear.OBJECTIVE: To observe dynamic changes of levels of NO in serum and endothelins in plasma of patients with stroke.DESIGN: Case-controlled observation.SETTING: Neurological Department and Clinical Neurological Laboratory of the Second Hospital affiliated to Suzhou University.PARTICIPANTS: A total of 216 patients with acute cerebral infarction including 133 males and 83 females and 112 cases with cerebral hemorrhage including 68 males and 44 females were selected from Neurological Department of the Second Hospital affiliated to Suzhou University from September 1999 to December 2001. Another 106 subjects including 63males and 43 females were regarded as healthy control group.METHODS: Contents of NO in serum and endothelins in plasma were measured on 328 patients with stroke and 106 healthy subjects in the courses of 1-3 days, 1, 2, 4, 8 and 12 weeks with nitrate reductase and radio-immunity methods, respectively.MAIN OUTCOME MEASURES: Contents of NO in serum and endothelins in plasma; ratio between NO in serum and endothelins in plasma (NO/endothelins).RESULTS: ① As compared with those in the control group, content of NO in serum of patients with cerebral infarction and cerebral hemorrhage was decreased and reached the lowest value during acute period (within 1-3 days), and then increased gradually and closed to the normal level at about 4 weeks. In addition, content of endothelins in plasma was increased obviously during acute period, reached the peak at 2 weeks, and then decreased gradually. The level was still high at stage of recovery and closed to normal value within 4-8 weeks. ② As compared with that in the control group, NO/endothelins was decreased in cerebral infarction group at the courses of 1-3 days (P ＜ 0.05), reached the lowest value at 1 week (P ＜ 0.001), and increased to the normal level at 2 weeks. Moreover,NO/endothelins was remarkably decreased in cerebral hemorrhage group at the courses of 1-3 days (P ＜ 0.001), reached the lowest value at 1week (P ＜ 0.001), and increased gradually. The changes of course were great and the level reached above normal value at 8 weeks. There was significant difference of dynamic changes of NO/endothelins between cerebral hemorrhage group and cerebral infarction group (P ＜ 0.05).CONCLUSION: NO and endothelins play an important role in onset and development of ischemic cerebrovascular disease and hemorrhagic cerebrovascular disease, and their contents are related to prognosis.

P-glycoprotein is one of the members in the superfamily of ATP-binding cassette transporters. It is expressed in many sites in vivo, and is correlated with multidrug resistance. Under physiological conditions, as an efflux pump, P-glycoprotein in the blood-brain barrier can eliminate endogenous substrates and xenobiotics to maintain the balance of internal environment. But at the same time, it also limits the concentration of therapeutic drugs in brain, and thus reduces therapeutic efficacy. P-glycoprotein inhibitors can get drugs across the blood-brain barrier. It is of great importance to improve the blood concentration in brain and bioavailability of central nervous system drugs.

Objective To investigate the effects of aquaporin4 (AQP4) on the brain injury after cerebral ischemic reperfusion and to search the new method that can prevent and cure the injury. Methods Locally injection of naked DNA ( pcNDA3.1/Zeo), which carries AQP4 gene and reporter gene green fluorescent protein(GFP), in the brain was performed 12 h before ischemic challenge to up-regulate the AQP4 expression. The expressed level of AQP4, the infarction size and neurological deficit scores were estimated in three groups. Results (1) Exogenous AQP4 expression in the brain did not affect the healthy rat neurological deficit score; (2) Rat neurological deficit scores were 7.9?0.7, and 7.1?0.9 respectively in 12 h and 24 h after reperfusion in AQP4 injected group, which were lower than that in plasmid control group when both groups were challenged with reperfusion after ischemia; (3) Expression of AQP4 in the brain was higher in AQP4 injected group than plasmid control group and control group in early stage after reperfusion; (4) Expression of exogenous AQP4 in the brain increased the cortex and striatum infarction size 24 h after reperfusion, which were (261.0?18.2) mm 3 and (21.9?1.9) mm 3, respectively, in AQP4 injected group more than plasmid control group. Conclusions (1) Increased local AQP4 expression in brain does not affect neurological function in the healthy rat; (2) Pre-expression of AQP4 increase infarction size and neuro-functional injury; (3) Modification of AQP4 activity and regulation of AQP4 expression level would be the new strategy for the prevention of cerebral edema and the reduction of cerebral injury after stroke.

Objective To investigate the relationship between the neurotoxicity of A? and monoamine neurotransmissions in brain.Methods 32 male SD rats were divided into four groups: The model group, Nimodipine treatment group, Shenmai treatment group and the control group,there are 8 rats in each group.Under the stereotaxis A? was injected into NBM of rats to establish AD model, The extracellular monoamine neurotransmissions were detected by microdialysis in vivo with high performance liquid chromatography.Results The contents of frontal lobe NE,DA,5 HT in the model group were lower than those in the control group, which recovered to normal level,DA in hippocampus was higher than the control group;after the treatment of Shenmai,the result was similar to Nimodipine group.There was no difference between the two treatment groups.The rising levels of three kinds of transmitters in different brain area were different.Conclusion Neurotoxicity of A? might relate to dysfunction in monoamine system. A? on monamine system of inhibition was shown through multiple pathways, including the loss of Ca 2+ homeostasis.

Objective To explore a better method to establish temporal lobe epilepsy model by administrating drug in brain region.Methods Kainic acid(KA)4 ?g/kg was injected into rat's hippocampus by stereotactic operation.The rat's behavior,EEG and pathological changes were observed.Results After the rat's hippocampus injected with KA,staring,wet-dog shakes,masticatory movement and clonus of limbs occurred successively.The seizures were paroxysmal with rotation,unsettled state of jump and tic of limbs.The rats' behavior gradually recovered to normal after 10 hours.Then the spontaneous seizure(mostly rating 2～4)occurred 1～3 times every week.Cluster electric discharge,spike waves and sharp waves were recorded in cerebral cortex.KA-treated rats could result in hippocampal CA1 and CA3 fields neuronal degeneration and necrosis,especially significant neuron loss was observed in the CA3 field of KA injected ipsilateral side.Conclusions Injection KA in brain region of rat can establish temporal epilepsy model.The symptom,electrophysiology and pathological changes of temporal lobe epilepsy in the rat model are almost the same as those in human being.The KA induced rat model is an ideal tool to research human temporal lobe epilepsy.