Brain ischemic conditioning (BIP) can improve the tolerance to ischemic injury in the brain. Nuclear factor-κB (NF-κB) is an important transcriptional regulatory factor.It presents in all types of cells in the nerous system. Studies have suggested that BIP may exert neuroprotective effects by mediating NF-κB through a series of cascade reactions. This may provide a new therapeutic strategy for BIP in the prevention and treatment of ischemic cerebrovascular disease in clinical practice.

Objective To investigate the relationship between the severity of coronary artery disease and malignant arrhythmia in the acute ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI), and guide clinical prevention and treatment .Methods By retrospective analysis method , 418 cases of hospitalized patients with a diagno-sis of STEMI undergoing direct PCI were continuously collected in the Department of Cardiology , the First Affiliated Hospital of China Medical University, from 2008 January to 2010 December.Electrocardiography (ECG) was given after admission.Those patients were divided into two groups according to whether the occurrence of malignant ventricular arrhythmias that was defined as sustained ventricu -lar tachycardia (sVT) or ventricular fibrillation (VF)].In sVT/VF patients, the preoperative and postoperative groups were divided according to sVT/VF time.The degree of coronary artery lesions was calculated in patients with STEMI .The incidence of sVT/VF was counted in each group with Gensini scores <60,≥60 and<120, and ≥120.The relationship between the severity of coronary le-sions and malignant arrhythmia was observed in STEMI undergoing direct PCI patients .Results ⑴In this study , a total of 47 cases ( 11.2%) occurred with sVT/VF in patients;Killip grade >I, fast heart rate , low blood pressure , and low ejection fraction were risk factors of sVT/VF( P <0.05).The occurrence of sVT/VF among the Gensini groups were significant difference (7.1%vs 10.8%vs 20.5%, P =0.012 ) .⑵The occurrence of sVT/VF was 44.8% ( 22 patients ) with direct PCI before operation; the preoperative sVT/VF rate among the Gensini groups had significant difference (2.1%vs 5.9%vs 9.6%, P =0.045).⑶The occurrence of sVT/VF is 53.3%(25 patients) with direct PCI after operation; the postoperative sVT/VF rate among Gensini groups had no significant difference(5.0%vs 4.9%vs 11.0%, P =0.142);⑷Paired with age ( x±2), gender, hypertension, and diabetes 1, Logistic re-gression analysis showed that the heart rate greater than 80 beats /min ( P =0.04 , OR:2.667 , 95%CI:1.043~6.815 ) was an independent risk factor of preoperative sVT/VF, that Gensini score was not an independent risk factor of preoperative malignant ar -rhythmia.Conclusions For STEMI PCI patients, the more serious the degree of coronary artery is , the higher may be preoperative malignant arrhythmia , while the postoperative malignant arrhythmia rate has no significant difference .

Nerve growth factor may play its particular role in promoting the development of neuroplasticity after central nervous system and peripheral nerve injury. Its possible mechanisms are associated with regulation of TrkA receptor, activation of L-type calcium channel, promoting the release of acetylcholine, regulation of long-term potentiation and long-term depression. The study of the mechanisms of nerve growth factors for promoting neuroplasicity may provide novel therapeutic approaches for the treatment and rehabilitation of stroke, Alzheimer's disease, and peripheral nerve injury, and it may facilitate the development of the therapeutic drugs.

Aim To explore the effect and mechanism of atorvastatin on lipopolysacchairde (LPS) inducing the expression of inhibitor of nuclear factor ?B? (I?B?) in human vascular endotheliar cells. Methods The human vascular endotheliar cell line ECV304 was cultured and divided into five groups as control group, LPS group, and low, moderate or high does atorvastatin groups. After incubated with different densities atorvastatin, the three atorvastatin groups and LPS group were stimulated with LPS 30min. Then the activation of I?B? was observed with immnofluorescence. The proteins expressions of I?B? and phosphorylated I?B? were detected with western blot. The ex-pression of I?B? mRNA was examined with reversetranscription-polymerase chain reaction. Results Atorvastatin could inhibit the translocation of p65 to the nucleus and reduce the phosphorylation and degradation of I?B? in a dose-dependent manner. The high density atorvastatin could increase the expression of I?B? mRNA. Conclusion The atorvastatin can inhibit the activation of nuclear factor ?B by regulating the expression and degradation of I?B?.

The post-stroke depression (PSD) is one of the common complications of stroke.It can not only delay the recovery of the neurological function in patients, seriously affect the quality of life of patients, but also increase the mortality and morbidity.More and more attention has been paid to the pathogenesis of PSD.Recent studies have confirmed that brain small vessel disease is closely related to the occurrence of PSD.This article reviews relationship between brain small vessel diseases and PSD.

Objective To investigate the significance and mechanism of intracerebroventricular injection viper venom nerve growth factor (Vngf) in rat neural plasticity after cerebral ischemia reperfusion injury.Methods Ninety Wistar male rats were randomly assigned into Vngf-25 U group (n = 18), Vngf-50 U group (n = 18), Vngf-100 U group (n = 18), ischemia reperfusion group (n = 18) and sham operated group.The expression of candidate plasticity-related gene 15(cpg-15) Mrna and nuclear factor of kappa B ( NF-Κb ) Mrna in rat brain tissues which were collection at 2,7,14 days after surgery were evaluated by the real time PCR.Results The expression of cpg-15 Mrna and NF-Κb Mrna began to increase after surgery( the F value of cpg-15:70.43, 34.11, 31.89, the F value of NF-Κb: 27.47, 34.56, 31.89,P＜0.01).At the same time, expression of cpg-15 Mrna and NF-Κb Mrna in the Vngf groups was significantly different from the I/R group and the sham operated group (the F value of cpg-15:48.18, 55.93, 78.43, the F value of NF-Κb: 45.92, 55.72, 50.49, P ＜0.01).The more Vngf were injected, the more cpg-15 Mrna and NF-Κb Mrna were expressed in Vngf groups.Conclusions The Vngf could accelerate neural plasticity and restore neurofunctional defect through up-regulated the expression of cpg-15 and NF-Κb.

Objective To observe the efficacy and adverse effects of MRC UKALL Ⅻ/ECOG E2993 regimen in inducing remission of Chinese adults with acute iymphoblastic leukemia(ALL). Methods 11 cases of previously untreated ALL patients were treated with MRC UKALL Ⅻ/ECOG E2993 regimen, then observe the efficacy and adverse effects. Results All of the 11 patients achieved complete rcmission(CR), the CR rate was 100 %. Among the 11 patients,8 patients achieved CR after the first course of chemotherapy. In the 8 patients which could be followed up, 5 patients achieved durative CR, among that the longest survival time was 30 months, and 3 patients had relapses. This regimen has a severe myelosuppression. There was an effect on liver function, mostly in the increase of glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase.After the symptomatic treatment, liver function could return to normal. No treatment-related deaths occurred. Conclusion MRC UKALL Ⅻ/ECOG E2993 regimen can be used as inducing remission therapy for Chinese adults with acute lymphoblastic leukemia.

Objective To investigate the cerebral ischemia/reperfusion protection mechanism of viper venom nerve growth factor(vNGF) by the change of expression of growth associated protein-43 (GAP-43) and neurological function.Methods 45 adult male Wistar rats (weight 220～280 g) were divided randomly into 3 groups: sham group(S, n=9), balanced salt solution group (BSS, n=9) and venom nerve growth factor group (vNGF, n=27). Each group was observed for 7 days. vNGF group was divided into 25 U, 50 U and 100 U subgroups respectively. The following indexes in 3 groups were observed respectively: neurologic deficits and the expression of GAP-43 (immunohistochemistry method).Results Neurological function: The scores of neurological function was 0 in S group. The neurological deficits score was lower at the same time in vNGF group than that in BSS group (P<0.05). Immunohistochemistry: GAP-43 expressed in both BSS group and vNGF group. The expression of GAP-43 in vNGF group increased in 25 U, and to maximum in 100 U. The expression of GAP-43 in BSS group was significantly lower than in vNGF group (P<0.05). Conclusion vNGF can effectively enhance and prolong the expression of GAP-43, increase the survival rats of nerve cells, and has the protection effect on nerve cells after cerebral ischemia injured.

ObjectiveTo explore the Apolipoprotein-E （ApoE） gene polymorphism in patients with Alzheimer's disease （AD）, vascular dementia (VD) or mild cognitive impairment (MCI). MethodsPeripheral blood was taken from patient with AD, VD or MCI to determine the ApoE genotypes. ResultsThe most of the patients were ε3/ε3 genotype, while the ε2/ε2 and ε4/ε4 could not be detected. ε3/ε4 genotype （P=0.001） and ApoE ε4 allele （P=0.013） was more frequent in AD than in MCI. ApoE ε4 was more frequent in VD than in MCI （P=0.044）. ConclusionApoE ε4 allele is a risk factor in AD, and may be associated with VD and MCI.

OBJECTIVETo detect potential mutation of the UGT1A1 gene in a child affected with Crigler-Najjar syndrome type II.

METHODSBlood samples were collected from the patient and his parents for the extraction of genomic DNA. Potential mutation of the UGT1A1 gene was detected with polymerase chain reaction (PCR) and direct sequencing. The child was followed up until the age of 3 years and 6 months.

RESULTSThe patient showed persistent unconjugated hyperbilirubinemia. Sequencing of the UGT1A1 gene has detected a rare heterozygous c.610 A>G (p.Met204Val) mutation in the exon 1, in addition with a heterozygous c.1091 C>T (p.Pro364Leu) mutation in exon 4. The two mutations were inherited from his father and mother, respectively. The patient was diagnosed with Crigler-Najjar syndrome type II and received oral phenobarbital treatment.

CONCLUSIONThe compound UGT1A1 gene mutation probably accounts for the disease in the patient manifesting persistent mild unconjugated hyperbilirubinemia. Genetic counseling and prenatal diagnosis should be provided for his family.