Hypoxic-ischaemic brain injury is a main cause to neonatal death and children neural handicap,and therapeutic efficacy is bad for the completely injured nerve cells.The development research of mesenchymal cells transplantation has a good prospect to treat this disease.

Just as "the market failures" in business or "the government failures" in government department, the non - profit organizations failures is displaying on kinds of forms. The reason that the non - profit organizations failed includ: seeking profit, the serious insufficiency of the organization funds, the morals out of control, the unscientific achievements evaluation system. The countermeasure settle of non - profit organizations failures include: to establish the information publishing system and the corresponding punishing system, perfecting the organization management system, forming the multiplicated financeing mechanism leading by government, perfecting the moral restraint mechanism which the autonomy and the heteronomy unifies.

Objective To investigate the change of gamma-aminobutyric acid A (GABAA) receptor α1 subunit mRNA expression in nitroglycerin induced migraine rat model,thus suggesting the relationship between GABAA receptor and migraine.Methods Thirty adult female Sprague-Dawley (SD) rats were randomly divided into control group,migraine model group,sodium valproate-treated group,each of the last 2 groups was divided into the attacking group and intermission group.The model of migraine was established using Cristina method,once a week for 5 weeks.After the second injection,rats in sodium valproate-treated group were given sodium valproate(0.5 g/L,10 ml/kg) everyday,and those in control group and model group were given normal saline solution(10 ml/kg).After the fifth injection,at the second hour(attacking groups) or the fourth day(intermission groups and control group),reverse transcription-polymerase chain reaction was used to detect the expression level of GABAA receptor α1 mRNA in brainstem and trigeminal ganglion.Results The expression level of GABAA receptor α1 mRNA in modeling attacking group(1.50 ±0.13) was higher than any other group(control group:1.01 ±0.24,modeling intermission group:1.04 ±0.10,sodium valproate-treated attacking group:0.99 ± 0.22,sodium valproate-treated intermission group:0.72 ± 0.03),and it was significantly higher than modeling intermission group(x2 =9.490,P =0.009).There was no statistical difference between modeling group and any other group,and compared with control group,there was no statistical difference in sodium valproate-treated attacking group or intermission group.Conclusion The pathogenesis of migraine may be related to the expression level of GABAA receptor α1 mRNA.

Objective To investigate the protective effect of allopurinol in kainic acid-induced epileptic rats and to explore new ideas and methods for the clinical treatment of epilepsy. Methods 120 Wistar rats were randomly divided into sham group, KA epilepsy group and allopurinol groups. Six rats of each group were randomly selected and were given electrodes into their left frontal and hippocampal regions. After injection, behavior changes were observed in all rates without electrodes. 24 h later, MDA level and SOD enzymatic activity of the left hippocampi were measured. One week later, the EEGs were recorded in rates with electrode, as well as total time of seizures /30 min and numbers of seizures / 30 min. Results Compared with the KA model group, latency period of the epilepsy in the allopurinol group was longer (P < 0.05) and the extent was lighter (P < 0.05); the MDA level was significantly lower (P < 0.01), the SOD enzymatic activity was significantly higher (P < 0.01). The total time of seizures / 30min and numbers of seizures / 30 min in allopurinol group reduced significantly (P < 0.01). Conclusion Allopurinol has potential antiepileptic and antioxidative activities in kainic acid-induced epileptic rats.

Objective To investigate the carotid arterial stiffness in patients with coronary slow flow ( CSF) .Methods forty-five patients with CSF and Forty -five persons having normal coronary arteries ( NCA) detected by coronary angiography with a similar distri-bution of risk factors were recruited .Stiffness parameter (β), pressure-strain elastic modulus (Ep), arterial compliance (AC) and lo-cal pulse-wave velocity (PWV) were obtained at the level of bilateral carotid artery by a real time echo -tracking system.Serum levels of high-sensitivity C-reactive protein ( hs-CRP) were measured in two groups of subjects .Linear regression analysis were performed to evaluate the correlation between hs -CRP and the parameters of the carotid artery stiffness .Results We found that stiffness parameter (β), Ep and PWV were significantly higher in CSF group those that of control group (β:11.80 ±3.19 vs 9.70 ±3.76,P<0.01;Ep:149.90 ±44.47 vs 130.10 ±41.56,P<0.05;PWV:7.40 ±0.84 vs 7.00 ±1.08,P<0.05), AC was lower than that of control group (0.640 ±0.180 vs 0.760 ±0.192 ,P<0.01).The levels of high-sensitivity C-reactive protein (hs-CRP) was significantly higher in CSF group than that of control group (13.90 ±10.66 vs 9.30 ±6.33,P<0.05).The levels of hs-CRP was positively correlated with theβ(r=0.272,P=0.005), Ep(r=0.411,P=0.003), and PWV(r=0.452,P=0.001), but negatively correlated with AC (r=-0.293,P=0.025).Conclusion Echo-tracking technology is a simple practical method to evaluate carotid artery stiffness in patients with CSF and correlation well with coronary slow flow and artery stiffness .

Objective Toinvestigatetheroleofcontrolledanticoagulationinocclusionofvertebral arteriesforthetreatmentofgiantfusiformaneurysmsofthebasilartrunkinchildren.Methods The clinical data of 3 children with giant fusiform aneurysms of the basilar trunk were analyzed retrospectively. Three children underwent bilateral vertebral artery occlusion with endovascular intervention,and conducted controlled anticoagulation by intravenous infusion of heparin sodium (10-30 U/[kg·h])after procedure. Results Intheprocessofanticoagulation,2patientshadsomeseverebleedingcomplications,including epistaxis,gastrointestinal bleeding,and after transient cessation of anticoagulation,they had severe brainstem ischemic symptoms,including vomiting,hemiplegia,loss of consciousness and respiratory dysfunctions (one recovered after using low-molecular weight heparin and one died),another patient did not have any serious complicationsandwascuredafteradjustingtheanticoagulationstrategy.Conclusion Inthetreatmentof basilar artery trunk giant fusiform aneurysms in children through the bilateral vertebral artery occlusion,the controlled anticoagulation after procedure may reduce the occurrence of brain stem infarction and severe bleeding complications. It may be an important measure for improving the safety and effectiveness of bilateral vertebral artery occlusion.

SUMMARY Pheochromocytomaisrareinpregn’ancy.Clinicalfeaturesofacaseofpheochromocytoma during pregnancy in the Peking University People’s Hospital was investigated and the literature reviewed to discuss the diagnosis and treatment of this disease.The patient manifested with hypertension and pro-teinuria,who was easily misdiagnosed with gestational hypertension disease.When she was transferred to our hospital,the symptoms such as,paroxysmal palpitation,dizziness,vomiting were noticed,and the possibility of pheochromocytoma was considered due to the accompanying abdominal mass.An emergent cesarean section was performed successfully due to preterm labor during the treatment of the disease.Af-ter the delivery the drug preparation continued.And the laparoscopic resection of pheochromocytoma pro-ceeded when the blood pressure was steady.The patient recovered fully after the surgery.The final diag-nosis of pheochromocytoma was confirmed with the pathology.Its diagnosis and treatment experiences could improve our understanding and treatment of secondary hypertension due to pheochromocytoma in pregnancy.

Objective:To analyze the expression of E-cadherin in the epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1) in neuroblastoma.Methods:TGF-β1(1 μg/L, 5 μg/L, 10 μg/L), was applied to SK-N-SH cells in vitro compared with the blank control group.EMT-related genes mRNA and protein expression were detected by carrying out real-time PCR assays and Western blot.A scratch test and migration assay were performed to verify the alteration of SK-N-SH cell migration capacity.Data collected from 18 cases of neuroblastoma patients were selected from the Department of Hematology Oncology, Shanghai Children′s Hospital from January 2008 to December 2012.The expression of E-cadherin in the tumor tissue of the neuroblastoma patients after operation was detected by immunohistochemistry.The clinical features and survival prognosis of these patients were analyzed. Results:Compared with the control group, after SK-N-SH cells were treated with TGF-β1(1 μg/L, 5 μg/L, 10 μg/L), real-time PCR assays and Western blot revealed that the mRNA(0.603±0.081, 0.606±0.008, 0.716±0.166 vs.1.000) and protein expression levels(0.855±0.026, 0.600±0.017, 0.495±0.011 vs.1.000) of E-cadherin were significantly decreased ( F=8.144, P=0.040; F=74.810, P<0.001), while the mRNA(2.132±0.167, 3.494±0.017, 4.184±0.021 vs.1.000) and protein expression levels (1.175±0.053, 1.189±0.058, 1.225±0.106 vs.1.000)of α - smooth muscle actin were significantly increased ( F=547.300, P<0.001; F=68.810, P=0.007), suggesting that EMT changes occur in cells.Scratch test and Transwell migration assay revealed that the number of migrating cells increased obvious with the treatment of TGF-β1 (5 μg/L) ( t=16.070, P=0.040). The 10-year overall survival(OS) rates of neuroblastoma patients with E-cadherin strong positive expression, positive expression, weak positive expression and negative expression in the pathology were (77.78±13.86)%, (75.00±21.66)%, (25.00±21.65)% and 0, respectively ( F=8.160, P=0.040). Conclusions:TGF-β1 can induce the EMT in SK-N-SH cells and increase cell migration.The decrease expression of E-cadherin in neuroblastoma patients is closely associated with clinical progress and recurrence or metastasis of the disease.

BACKGROUND: Ischemic postconditioning protects the myocardium from ischemia/recursion injury via maintaining 3-minute acidosis initially. But its effect on the skeletal muscle remains unclear. OBJECTIVE: To dynamically measure the pH values in rat skeletal muscle after ischemia, and then to simulate acidic perfusate infusion to investigate the effect of ischemic postconditioning on ischemia/reperfusion injury. METHODS: Based on the ischemia/reperfusion injury model and ischemic postconditioning protocol in previous study, dynamic measurement of pH values in rat skeletal muscle was conducted using pH instrument at the global ischemia, ischemic postconditioning (30/30 seconds) and reperfusion period, and then the acidic perfusate equivalent to pH in ischemic postconditioning period was prepared with lactic acid and normal saline. Twenty-five healthy adult male Sprague-Dawley rats were randomly divided into sham, ischemia/reperfusion, ischemic postconditioning, lactic acid, and normal saline groups (n=5 per group). Blood samples were collected to detect lactate dehydrogenase level. The samples from gastrocnemius were harvested to calculate the wet/dry ratio, level of myeloperoxidase, and infarct size through triphenyltetrazolium chloride staining. The samples from the right tibialis anterior muscle were taken to detect the expression level of Erk1/2 in the MAPK signaling pathway by western blot assay. RESULTS AND CONCLUSION: A prolonged acidic platform was detected in the early reperfusion during ischemic postconditioning, on which the pH value was 6.81±0.133, and the duration was 2 minutes and 40 seconds. The levels of lactate dehydrogenase and myeloperoxidase as well as the wet/dry ratio in the ischemic postconditioning and lactic acid groups were significantly lower than those in the ischemia/reperfusion group (P < 0.05). Western blot assay results showed that the expression level of p-Erk in the ischemic postconditioning, lactic acid and normal saline groups was significantly higher than that in the ischemia/reperfusion group (P < 0.05). Triphenyltetrazolium chloride staining results showed that compared with the ischemia/reperfusion group, the infarct area was significantly reduced in the postconditioning and lactic acid groups (P < 0.05). These findings suggest the existence of a short acidosis during ischemic postconditioning in the early reperfusion, and acidic perfusate can simulate the ischemic postconditioning and effectively attenuate ischemia/reperfusion injury in the rat skeletal muscle via activating Erk1/2 in RISK signaling pathway.