Egr-1 is an important transcription factor, which regulates at least 30 kinds of gene expression. Egr-1 couples extracellular signals to long-term responses by altering expression of Egr-1 target genes. So egr-1 can directly or indirectly affect cell differentiation,apoptosis,immune response,injury and repair. This article reviewed the progress in Egr-1 and the lung disease.

Objective To explore the influence of IFN-? on anti-proliferation and apoptosis of the Caspase-8 silenced neuroblastoma cell line induced by doxorubicin and the influence mechanism.Methods MTT and flow cytometric analysis were used to detect the survival and apoptosis rates before and after the combined treatment of IFN-? and doxorubicin.Immunohistochemical staining was used to detect the expression of caspase-8 protein before and after the treatment of IFN-?.Results The survival rates of doxorubicin(0.03,0.10,0.30?g/ml)used alone for 24h were(95.62?13.03)%,(82.62?7.94)%,(64.84?9.19)%,IFN-?(10,100,1000U/ml)used alone for 48h were(98.37%?11.25)%,(97.15?5.36)%,(98.84?7.41)%.The survival rates of IFN-?(1000U/ml)combined with different concentration of doxorubicin(0.03,0.10,0.30?g/ml)were significantly lower than that of doxorubicin(0.03,0.10,0.30?g/ml)alone.The apoptosis rate of doxorubicin(0.30?g/ml)alone was(22.00?6.55)%,IFN-?(1000U/ml)alone was (8.22?4.00)%,whereas the apoptosis rate of the combined treatment of IFN-? and doxorubicin wassignificantly higher than that of doxorubicin alone;Immunohistochemical staining showed that caspase-8 protein was negative in SH-SY5Y cell line,whereas it become positiveafter the treatment of IFN-?(1000U/ml)for 48h.Conclusion Treating human neuroblastoma cell line SH-SY5Y cell with doxorubicin may induce anti-proliferation and apoptosis.Combined treatment with IFN-? may significantly increase this effect.The mechanism may be realized by upregulating the expression of caspase-8 protein.

Objective To explore perinatal risk factors associated with the neurobehavioral development of small for gestational age (SGA) full-term neonates.Methods This prospective cross-sectional study included 111 full-term newborn infants from Apr 2008 to Apr 2010 born in Yan-tai Yuhuangding Hospital.Detailed clinical data in perinatal period of all subjects were recorded.Infants aged 3 ～ 7 days were assessed with neonatal behavioral neurological assessment (NBNA) for neurobehavioral development.Logistic regression analysis was used to explore risk factors associated with the score of NBNA.Results Significant differences (P ＜ 0.05) were found between full-term SGA (10.72 ± 1.41,7.13 ± 0.96,7.32 ± 0.74,37.16 ±1.32) and normal neonates (11.27 ± 1.04,7.89 ± 0.72,7.62 ± 0.64,39.12 ± 0.76) in terms of capacity,active and passive muscle tension and NBNA score.Full-term SGA neonates had lower score than control.Univariate logistic regression showed that delivery,placenta abnormalities,umbilical cord abnormalities,infection in perinatal period,gestational hypertension,twin pregnancy,hyperbilirubinemia affected neurobehavioral development of full-term SGA infants.Multivariate logistic regression showed that mothers' infection in perinatal period (OR =2.175,95 ％ CI 1.981 ～ 2.408,P ＜ 0.05),twin pregnancy (OR =1.936,95％ CI 1.517 ～2.368,P ＜ 0.05) and hyperbilirubinemia (OR =1.518,95％ CI 1.072-2.149,P ＜ 0.05) were risk factors for neurobehavioral delay of full-term SGA infants.Conclusion Full-term SGA neonates showed poorer quality in neurobehavior.Risk factors associated with neurobehavior of full-term SGA infants included mothers' infection in perinatal period,twin pregnancy and hyperbilirubinemia.

ObjectiveTo investigate the effect of mescenchymal stem cell (MSC) transplantation on Tourette syndrome(TS)model rats.MethodsStereotypies can be successfully induced in rats by intrastriatal microinfusion of TS sera.MSC suspension was bilaterally injected into the striatum.Survival and differentiation of transplanted MSC were tested through immunohistochemical analyses.ResultsFlow cytometry results demonstrated that the cells strongly expressed CD29(95.2％ ),CD105(97.2％ ),CD44(96.3％ ) and CD106 (94.1％).TS rats with MSC grafts exhibited significantly decreased stereotypic behaviors at 10 and 14 days(95.5 ±6.6,73.1 ± 6.5 vs.114.1 ± 6.0,108.0 ± 6.4).Immunohistochemistry analyses revealed survival of transplanted MSC and differentiation into neurons and astrocytes in the rat brain.ConclusionIntrastriatal transplantation of human MSC can provide therapeutic potential for TS.

Objective:To establish animal model on the basis of the autoimmune etiology for a subset of cases of Tourette syndrome.Methods:Blood samples were drawn from patients with TS(by DSM-IV)and were sent for further enzyme-linked immunosorbent assays(ELISA)to a laboratory.Eight serum samples with the highest concentration of anti-neural antibody were selected for TS model group,and 8 serum sampled with the lowest concentration of anti-neural antibody were selected for the control group.Osmotic mini pump filled with undiluted TS or control serum were microinfused into the rat striatum at a rate of 0.5 μl /h for 72 h.Stereotypic movements were recorded at 1 d,7 d,14 d and 21 d after microinfusion.Several categories of stereotypy including bites(teeth touching the cage,wood chips,vacuous chewing or other objects except the body),taffy pulling(raises of the forepaw to the mouth and face),self-gnawing,licking not associated with grooming,grooming,head shaking,paw shaking,rearing and episodic utterances(EU)were recorded.Results:The anti-neural antibody serum concentration used for TS model was(0.29±0.06) U/L,and that used in control group was (0.10±0.04) U/L.After infusion of TS sera,stereotypic behaviors in rats was increased significantly[(37.2±7.1) vs.(106.3±11.7),P=0.000].Significant difference were observed in stereotypies scores of TS rats compared to control rats after microinfusion[(106.3±11.7) vs.(31.2±6.2),P=0.000].Conclusion:Stereotypic behaviors are increased in rats after intrastriatal microinfusion of Tourette Syndrome sera under noninflammatory conditions.

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Immunoglobulins, Intravenous ; therapeutic use ; Infant ; Infant, Newborn ; Male ; Prednisone ; therapeutic use ; Purpura, Thrombocytopenic, Idiopathic ; drug therapy

Objective To investigate the protective effect of sevoflurane on the brain against focal ischemia-reperfusion(I/R)injury and its mechanism.Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into 3 groups(n=8 each):group Ⅰ sham operation;grouop Ⅱ I/R and group Ⅲ I/R + sevoflurane.The rats were anesthetized with intraperitoneal chloral hydrate 300 mg?kg~(-1).Middle cerebral artery occlusion(MCAO)was produced by insertion of a 4-0 mono-filament nylon thread with rounded tip at bifurcation of right common carotid artery into internal carotid artery.The nylon thread was advanced cranially until resistance was felt.The depth of insertion was 18-20 mm.After 3 h MCAO the thread was withdrawn to allow reperfusion.In group Ⅲ the animals inhaled 1.0 MAC sevoflurane for 30 min at 30 min before reperfusion.The rectal temperature of the animals was kept at 36.5-37.5℃.At the end of 24 h reperfusion the animals were weighed again.The animals'neurological deficit was evaluated using Zea Longa score(0=no defcit,4=unable to walk and unconscious).The animals were then killed.The neuronal apoptosis in striatum was assessed(TUNEL)and the PKC protein expression in striatum was determined by immunocyto-chemistry.Results The body weight of the animals in I/R group was significantly reduced after 24h reperfusion as compared to the body weight before ischemia (P＜0.01),while in control group and sevoflurane group there was no significant difference in the body weight before and after sham operation or I/R.The neurological deficit scores were significantly higher in I/R group than in sevoflurane group.The number of apoptotic neurons in striatum was significantly higher in I/R group than in sevoflurane group.The PKC expression in striatum was significantly higher in sevoflurane group than in I/R group (P＜0.01).Conclusion 1.0 MAC sevoflurane inhalation has protective effect on the brain against I/R injury. Upregulation of PKC expression in striatum decreased by I/R is involved in the mechanism.

Objective To investigate the effect of Buyanghuanwu decoction(BYHWD) on angiogenesis and Ang-1/Tie-2 expression after focal cerebral ischemia in mice. Methods Focal cerebral ischemia was induced by 30 min of middle cerebral artery occlusion followed by reperfusion. BYHWD (20 g/kg) was administered orally 24 h after ischemia and once a day. The neurological score and the corner test were used to evaluate sensorimotor function during 28 days after ischemia. The microvessels density and the expression of Ang-1/Tie-2 in the ischemic boundary zone were determined by immunohistochemistry on 28 days after ischemia. Results Compared with the model group, BYHWD significantly ameliorated neurological dysfunction and reduced the number of right turn during 3 to 28 days after ischemia(P＜0.05 ). In addition,the numbers of CD31 ,Ang-1 and Tie-2 immunopositive cells were (437 ±59) ,(389 ±61 ) and (251 ±42) at the boundary zone in model group 28 days after ischemia,respectively. However, BYHWD treatment significantly increased the numbers of CD31(609 ± 68 ), Ang-1 (551 ±66) and Tie-2 (342 ±46) immunopositive cells(P＜0. 01 ). Conclusion BYHWD promotes angiogenesis,which may contribute to recovery of neurological function after focal cerebral ischemia,and Ang-1/Tie-2 pathway appears to mediate BYHWD-induced angiogenesis.

Objective To identify predictive factors of survival to in-hospital children with post-cardiorespiratory arrest.Methods Eighty-seven patients who had cardiorespiratory arrest(CRA)and received cardiopulmonary resuscitation(CPR)were reviewed from January 2006 to December 2008.The clinical data was analyzed to identify predictive factors of survival by Pearson X~2 test and multivariate and unconditioned Logistic regression analysis.Results Forty-three of eighty-seven cases received return of spontaneous circulation,the initial sunvival rate was 48.3%,31(35.6%)cases survived for 24 hours,19(21.8%)cases survived to hospital discharge.Primary diseases and complications,the type of arrest,tracheal intubation or not,the duration of CPR,the dose of adrenaline,the body temperature post-resuscitation for 24 hours,the glucose post resuscitation for 6 hours and complications were obviously associated with both initial and long-term survival.Logistic regression analysis revealed that primary diseases and the duration of CPR were predictive factors of both survival for 24 hours and hospital discharge,additionally,the body temperature post-resuscitation for 24 hours were predictive factor of survival to hospital discharge.Conclusion Initial and long-term survival rate of in-hospital children with post-resuscitation was both low.Primary diseases and complications,good quality CPR and management of post-resuscitation affect survival,especially primary diseases and the duration of CPR may predict initial survival and primary diseases,the duration of CPR and the body temperature post-resuscitation for 24 hours may predict long-term survival.

The relationship between the expression of resistin in polycystic ovary syndrome (PCOS) and insulin resistance was investigated. The plasma resistin concentrations in 35 patients with PCOS and 40 controls were measured by ELISA. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and fasting insulin (FIN) were tested by radioimmunoassay. Insulin resistance index (HOMA-IR) was calculated. Fasting plasma glucose (FPG) was determined by oxidase test. Western blot and reverse transcriptase PCR (RT-PCR) methods were used to detect the expression of resistin in adipose tissues. The levels of plasma resistin, LH, LH/FSH and FIN and HOMA-IR in patients with PCOS were significantly higher than those in control group (all P<0.05). Plasma resistin was correlated positively with FPG, FIN, HOMA-IR, LH and LH/FSH (r=0.56, 0.60, 0.65, 0.48, and 0.42 respectively). Resistin protein and mRNA expression levels in patients with PCOS were significantly higher than those in normal tissues (all P<0.01). It was concluded that resistin might be involved in the pathogenesis of insulin resistance of PCOS.