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.

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.

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.

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 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.

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: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:Reperfusion injury salvage kinase (RISK) pathway plays an important role in protective mechanism against ischemia reperfusion injury (IRI) induced by both ischemic pre-and post-conditioning. Many researches have been carried out on RISK pathway mechanism underlying ischemic post-conditioning conferring cardioprotection against IRI;however, there is less research about its effect on IRI in the skeletal muscle.
OBJECTIVE:To investigate the protective effect of an optimized protocol of ischemic post-conditioning on IRI in rat skeletal muscle and its underlying mechanism.
METHODS:Eighteen male Sprague-Dawley rats were equivalently randomized into IRI, ischemic post-conditioning and control groups. Rats were given occlusion or disocclusion of the right femoral artery of the right lower limb. Subsequently, the IRI group rats were subjected to 24 hours of reperfusion;the ischemic post-conditioning group immediately given 4 cycles of 30 seconds reperfusion/30 seconds ischemia, followed by 24 hours of reperfusion;the control group given no intervention.
RESULTS AND CONCLUSION:Hematoxylin-eosin staining showed that in the ischemic post-conditioning group, the morphology of muscle fibers changed little, with fewer inflammatory lesions and milder edema compared with the IRI group. The infarct size with TTC staining in the ischemic post-conditioning group was smaller than that in the IRI group. Western blot analysis revealed that the expressions of phospho-Akt and phosphorylated endothelial nitric oxide synthase-S1177 were significantly increased, but the expression of phosphorylated type endothelial nitric oxide synthase-Thr495 was much decreased in the ischemic post-conditioning group compared with the IRI group. The measurement of mitochondrial permeability transition pore opening with Ca2+induction showed that the absorbance values in the ischemic post-conditioning group were significantly lower than those in the IRI group (P<0.05). These results indicate that ischemia-reperfusion injury can be improved by applying an optimal protocol of ischemic post-conditioning in rat skeletal muscle. The underlying mechanism may be associated with the activation of RISK signaling pathway to inhibit opening of mitochondrial permeability transition pore, thereby contributing to the enhanced tolerance to IRI in rat skeletal muscle.