Objectives: To study the difference of Plasminogen Activation System in patients with coronary heart disease by different behavior types. Methods: 81 patients with coronary heart disease and 59 normal control were evaluated by Type A Behavior Scale. t-PA and PAI-1 activities of both groups were also measured. Results: The activity of PAI-1 was higher and t-PA was lower in patients with coronary heart disease, and this difference is also found between Type A and Non Type A patients. Conclusion: The activity of t-PA is decreased and PAI-1 increased in patients with CHD, this phenomenon are also related to Type A Behavior traits.

Objective To observe the intervention effect of Wuxing-Jiangu exercise for different syndrome types of elderly patients with chronic low back pain.Methods A total of 199 patients who met the criteria of chronic low back pain (CLBP) were divided into a Wuxing-Jiangu exercise group (86 cases), a control group (85 cases) and a health education group (28 cases). On the basis of health education, theWuxing-Jiangu exercise group was given Wuxing-Jiangu exercise; the control group was treated with the warm type frequency therapeutic instrument; health education group was only given health education guide. The changes of the score of CLBP patients before and after treatment with different syndrome types were observed.Results After 3 months of treatment, the score of the kidney deficiency syndrome and spleen deficiency syndrome in the Wuxing-Jiangu exercise group, the control group and the health education group had significant differences (H were12.554, 8.014, respectively;all P<0.01); After 3 months of treatment, the score of kidney deficiency syndrome and spleen deficiency syndrome in the Wuxing-Jiangu exercise group reduced than before the treatment (Z were -5.975,-5.025, respectively)and 1 month after the treatment(Z were -5.976,-5.026, respectively) (all P<0.01).Conclusion Wuxing-Jiangu exercise can reduce the score of the kidney deficiency syndrome and spleen deficiency syndrome and improve clinical syndrome.

Epilepsy, Generalized ; etiology ; Humans ; Infant, Newborn ; Male ; Malformations of Cortical Development ; complications

0.05).3.Thirty-three point three percent of animals from parental strain group were found fibrillations potentials and the po-sitive sharp waves in gastrocnemius electromyogram,no obvious abnormal waves were found in animals from both waaF mutant and control group.Conclusions The ganglioside-like epitope in LOS of CJ is critical antigen in inducing GM1-IgG antibody and in inducing conduction block of peripheral nerve,therefore,provide a support for the molecular mimicry theory as a pathogenesis in the axonal GBS following CJ infection.

Objective To measure the normal cerebrospinal fluid of the midbrain aqueduct peak velocity of different age groups by using magnetic resonance imaging (MRI) time‐spatial labeling inversion pulse (time‐SLIP) ,and to discuss the flow law of CSF . Methods Forty‐one cases of healthy volunteers ,including 23 cases of male ,18 cases of female ,aged 7 -73 .Patients were divided into 4 groups:7- <15 age group (n=11) ,15- <35 age group (n=10) ,35- <45 age group (n=9) ,≥45 age group (n=11) .We used the application of Toshiba 1 .5 T MRI head coil ,MRI sequence of time‐SLIP marked CSF to calculated the peak velocity of CSF in the midbrain aqueduct and measure the diameter and length of the midbrain aqueduct .Results The peak flow velocity be‐tween the 7- <15 age group and 15 - <35 age group ,35 - <45 age group ,≥45 age group were statistically significant (P<0 .05);inner diameter and length were no statistically significant difference (P>0 .05) between age .Conclusion In the midbrain aqueduct ,CSF is two‐way flow and supports the CSF of the pulsatile flow theory ;MRI sequence of time‐SLIP could measure CSF velocity and display the turbulence fluiding .

BACKGROUND: Schwann cell-derived neurotrophic factor is a bioactive protein isolated and purified from the kytoplasm of Schwann cell. It can obviously maintain the survival of spinal cord anterior horn motor neuron and promote the regeneration of peripheral nerve.OBJECTIVE: To observe the protective effect of Schwann cell-derived neurotrophic factor on the high injury of peripheral nerve-induced apoptosis of sensory neurons in spinal dorsal root ganglia.DESIGN: Randomized and controlled animal experiment.SETTING: Shenzhen Second People's Hospital.MATERIALS: Totally 30 3-week-old SD infant rats, of clean grade and either gender, were used in this experiment. They were randomly divided into neurotrophic factor group and control group with 15 rats in each one.Left sides of the animals in both two groups were set as normal sides and right sides as injured sides.METHODS: This experiment was carried out at the Experimental Animal Center, Medical College of Sun Yat-sen University from May 2003 to July 2003. ① L4.5 nerve root high-mutilation animal models were developed on the rats in two groups. Proximal nerve stump was connected with silicone tube. According to grouping, 60 mg/L Schwann cell-derived neurotrophic factors and 20 μL normal saline were injected into the silicone tubes respectively. Two ends of silicone tube were enveloped with vaseline.② Sample collecting was conducted at postoperative 4 weeks, survival rate and morphological change of sensory neurons in dorsal root ganglia of injured nerve was observed.MAIN OUTCOME MEASURES: ① Gross observation of sciatic nerve regeneration at injured side of the rats in two groups ② Survival of sensory neurons in dorsal root ganglia ③ Morphological change of sensory neurons in dorsal root ganglia.RESULTS: All the 30 rats entered the stage of result analysis. ① Gross observation of sciatic nerve regeneration: In the neurotrophic factor group,nerve new born axon grew along silicone tube, with 1cm in length; there were few and thin newborn axons in control group with 0.8 cm in length.② Survival of neuron in dorsal root ganglia of the rats in two groups: There was little fibrous tissue proliferation in the dorsal root ganglion in neurotrophic factor group. The loss of neurons was not obvious and the survival rate was 91.8%. Obvious fibrous tissue proliferation appeared in the dorsal root ganglia in control group, and a great many neurons were lost with the survival rate of 58.6%. Survival rate of neurons was 33.2% higher in neurotrophic factor group than in control group (P ＜ 0.01 ). ③ Morphological change of neurons in dorsal root ganglia: The diameter and area of neurons in dorsal root ganglia were significantly lower in control group than in neu rotrophic factor group and normal side [(21.8±1.4) μm,(373.1±50.9) μm2 vs (24.8±1.1) μm, (482.8±42.2) μm2 and (24.5±1.3) μm, (471.5±51.4) μm2,P ＜ 0.01], while there were no significant difference in diameter and area of neurons between neurotrophic factor group and normal side(P ＞ 0.05).CONCLUSION: Schwann cell-derived neurotrophic factors have obvious neurotrophic bioactivity for sensory neurons in the injured dorsal root ganglia.

BACKGROUND: Schwann cell derived neurotrophic factor, which is isolated and purified from the kytoplasm of Schwann cell with the relative molecular mass of 58000, is a kind of neurotrophic substance possessing obvious neurotrophic activity. It can be against neurovirulent substance of nitrogen monoxidum.OBJECTIVE:To create root avulsion animal models and observe the protective effects of Schwann cell derived neurotrophic factor (SDNF) on motoneurons of spinal anterior horn from spinal root avulsion induced cell death.DESIGN: Repeated observation and measure.SETTING: Third Department of Orthopaedics, Second People's Hospital of Shenzhen; Department of Micro-surgery , First Hospital Affiliated to Sun Yat-sen University.MATERIALS: This experiment was conducted at the Experimental Animal Center of Medical College of Sun Yat-sen University from March to May 2003. Twenty Sprague-Dawley rats with the age of 3-4 months, of clean degree, were selected and divided randomly into experimental group of Schwann cell derived neurotrophic factor and control group of normal saline with 10 rats in each group. The right side was injured, and the left side was intact served as normal control side.METHODS : ①A rat model of C6,7 spinal root avulsion induced motoneuron degeneration was established. ② A small piece of gelfoam presoaked in 40 μL SDNF solutions (1 g/L) was placed in contact with the injured spinal cord in the animals of the experimental group. Normal saline was added as the same way as above in the animals of the control group. ③ A silica pipe was put on the surface of gleform, one end of the silica was sutured to the glefoam , and the other end wasfixed subcutaneously with vaselinum. Local intramuscular injection of penicillinum was performed on the wound following closing the incision. All rats received an injection (20 μL) of either SDNF or normal saline solution at the lesion site through the silica pipe sutured to the glefoam once a week after the surgery. All the animals were killed by the end of the third weeks. ④The spinal region of C6,7 level was dissected out for observing survival rate and morphological change of motoneurons of spinal anterior horn as well as the expression of nitricoxide synthase(NOS).MAIN OUTCOME MEASURES: ① Survival and morphological change of spinal motor neurons. ②Change of nitricoxide synthase expression of spinal motor neurons.RESULTS: Totally 20 rats were enrolled in the experiment, and all of them entered the stage of result analysis. ① Survival and morphological changeof spinal motor neurons: 68.6% motoneurons of injured side of the control group died at 3 weeks after surgery. The survival rate was 31.4%,which was significantly lower than that of the intact side (P ＜ 0.01), and the survived neurons was shrinked significantly; the death rate of spinal motor neurons of injured side of experimental group was decreased by 35%as compared with control group (P＞ 0.05). The survival rate was 66.4%,and the survived neuron body was increased, similar to the intact side (P ＞ 0.05). ② Change of nitricoxide synthase expression of spinal motor neurons: In normal spinal cord, NOS positive neurons were shown in dorsal horn, surrounding the central canal and in the intermediolateral column.NOS was not seen in the anterior horn motonurons. At the end of the third week after C6,7 spinal root avulsion, increased NOS expression was not found at the injured side in the Schwann cell derived neurotrophic factor group and the intact side in the control side, while the significantly increased NOS expression of spinal motoneurons was found at the injured side of the control group.CONCLUSION: Degeneration of spinal motoneuron and increased expression of NOS can be induced by spinal root avulsion. SDNF has a significant effect in protecting spinal motoneurons from spinal root avulsion induced cell death and inhibiting the expression of NOS. These results suggest that the effects .of SDNF on motoneuron survival may be achieved by modifying the expression of certain cellular molecule such as NOS.

Objective To evaluate the neuroprotective effect and possible mechanisms of edaravone(3-methyl-1-phenyl-2-pyrazolin-5-one) in neonatal Harlequin(Hq) mutant mice brain after hypoxia-ischemia brain injury(HIBD) insult.Methods The nine-day-old male Hq mutant mouse pups were assigned randomly either edaravone(n=16) and vehicle(n=17) treatment group.The Hq mice were subjected to left common carotid artery occlusion combined with inhalation 100 mL/L oxygen for 45 minutes.The mice were injected intraperitoneally either with edaravone(10 mg/kg) or equivalent volume of saline immediately after artery occlusion and after hypoxia.Nitrotyrosine and lipid peroxidation formation were evaluated at 3 h and 24 h after hypoxia-ischemia(HI) by using immunohistochemistry staining.Nitrotyrosine formation and caspases activation were evaluated either by immunoblotting or fluorogenic activity measurement at 24 h after HI.Brain injury was evaluated at 72 h by neuropathological score and calculating the infarct volume.Results Brain injury encompassed cortex,hippocampus,striatum and thalamus.Edaravone treatment reduced brain injury significantly in all the brain regions.The total infarct volume was reduced 52.8% in edaravone treatment group compared with vehicle group(P

Objective To evaluate the effect of N- acetylcysteine(NAC) on lipopolysaccharide (LPS) - sensitized neonatal rats with hypoxic- ischemic brain damage(HIBD) and possible mechanism except the antioxidant. Methods With the total number of 98 Wistar pups at postnatal day 8 of either sex was used in this study. There were 86 pups which were divided into three groups to evaluate the brain injury:vehicle group ( n = 29) ,low dose (25 mg/kg) ( n = 31 ) and high dose NAC (200 mg/kg) ( n - 26) treatment group. The pups were injected with LPS(0.1 mg/kg)intraperitoneally 3 days before hypoxic- ischemic(HI) insult. Multiple dose of NAC (25 mg/kg or 200 mg/kg) or vehicle was injected intraperitoneally before and after HI. Brain injury was evaluated 7 days after HI. For the Caspase - 3 activity and immunoblotting analysis, the samples were collected at 24 h after HI treated either with vehicle or high dose NAC ( n = 6 per group). Results The brain injury volume was significantly reduced by high dose NAC (200 mg/kg) treatment compared with that of vehicle (77% reduction, P ＜ 0.001 ). The tissue loss was reduced 67 % ( P ＜ 0.001 ) in high dose NAC treated group compared with that of vehicle. However,there was no significant reduction of brain injury in the low dose NAC treatment group compared with vehicle group. Caspase - 3 like activity measurement showed that the activity decreased 53 % after high dose NAC treatment ( P ＜ 0. 001 ) compared with that of vehicle treatment. The immunoblots showed that the active form of Caspase - 3, 17 kDa band, was abolished by the high dose NAC treatment. Conclusions NAC treatment attenuate LPS - sensitized neonatal HI brain injury is dose dependent. The neuroprotective effect involves Caspase - 3 inhibition.