Objective To detect the effects of glucocorticoids on the expression of toll-like receptor 4 (TLR4) on CD14+ monocytes in peripheral blood from patients with chronic obstructive pulmonary disease (COPD) and explore the relationship between inherent immunity deficiency and the pathogenesis of COPD.Methods A total of 30 hospitalized acute exacerbations of COPD (AECOPD) patients from 2012 January to March were divided them into 2 groups of mild-moderate (A,n =15) and severe-critical (B,n =15) according to pulmonary functions.The same basic treatment (anti-infection,oxygen inhalation,bronchial smooth muscle relaxing and cough relief) was administered.And glucocorticoids were added to Group B.Two weeks later,AECOPD achieved a clinical remission and it was designated as a stable COPD group.Another 30 healthy cases over the same period were selected as control group.Flow cytometry was used to measure the relative mean fluorescence intensity (rmfi) and relative positive cell percent (rpcp) of TLR4 onr CD14 positive peripheral blood monocytes.Conventional pulmonary function test (FEV1 percentage of predicted value,FEV1/FVC value) was performed.Results The value of rmfi for TLR4 of AECOPD group was 5.14 ±0.26 and rpcp (4.24 ±0.17)％ and they were similar to those of COPD group [4.46 ±0.24 and (3.49 ± 0.24) ％ respectively,all P ＞ 0.05].AECOPD and COPD groups were both significantly lower than normal control group [13.75 ±0.28 and (10.25 ±0.13)％ respectively,all P ＜0.01].The rmfi of TLR4 of Group B was 3.12 ±0.15 and rpcp (3.17 ±0.10)％.And both were significantly lower than those of Group A [5.48 ±0.23 and (5.12 ±0.20)％ respectively,all P ＜0.01].The value of rmfi for TLR4 of Group B before glucocorticoid treatment was 3.12 ±0.15 and rpcp (3.17 ±0.10)％.And both were significantly lower than those of later glucocorticoid treatment [5.24 ± 0.25 and (5.44 ± 0.19) ％ respectively,all P ＜ 0.01].Both values were significantly lower than those of normal control group [13.75 ± 0.28 and (10.25 ± 0.13) ％ respectively,all P ＜ 0.01].The expression of TLR4 on CD14 + monocytes in peripheral blood of AECOPD patients was positively correlated with FEV1 percentage of predicted value(r1 =0.824,P＜0.001) and FEV1/FVC (r2 =0.756,P＜0.001).Conclusions Innate immunodeficiency plays an important role in the pathogenesis of COPD.And the expression of TLR4 is an important indicator for disease severity.Glucocorticoids treat COPD through inhibiting airway inflammation response and enhancing defensive function of innate immune system.

BACKGROUND: Radiofrequency catheter ablation (RFCA) in dog triggers myocardial nerve sprouting and sympathetic hyperinnevation. It is possible that RFCA in humans has the same effect. Nerve growth factor (NGF) is a neurons nurture that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, it is hypothetic that RFCA can increases plasma NGF concentration in humans.OBJECTIVE: To test the hypothesis that RFCA increases plasma NGF concentration in humans.DESIGN: Self-control experiment.SETTING: Department of Cardiology, Tangdu Hospital, the Fourth Military Medical University of Chinese PLA.PARTICIPANTS: Forty-three patients were selected from the Cardiological Department of Tangdu Hospital, the Fourth Military Medical University of Chinese PLA from January to June 2005, including atrioventricular nodal reentrant tachycardia (AVNRT) (n=18), right-sided accessory pathways (RSAP) (n=13) and left-sided accessory pathways (LSAP) (n=12), 20 males and 23 females, ages 28-65 years, all agreed to participate in the study voluntarily.METHODS: Blood samples were obtained from the peripheral veins before ablation and at 6 hours, 1, 3, 5, 7 days after ablation. The plasma concentration of NGF was determined with enzyme-linked immunosorbent assay (ELISA).MAIN OUTCOME MEASURES: The plasma concentration of NGF was determined with ELISA before RFCA and at 6 hours, 1, 3, 5, 7 days after RFCA in each patient.RESULTS: Total 43 patients who were referred for ablation therapy for AVNRT, RSAP and LSAP were involved in the result analysis without loss. Plasma NGF increased at 6 hours after RFCA. Increased NGF continued to 7 days in the RFCA treated patients. The plasma NGF concentrations at 6 hours, 1, 3, 5, 7 days after RFCA in AVNRT, RSAP and LSAP ablations treated patients were (29.72±7.04), (30.94±5.68),(31.39 ±4.92), (31.06 ±4.56), (29.11 ±4.59), (31.77 ±6.25), (30.69 ±5.10),(31.46±4.96), (30.15±4.01), (30.43±3.14), (31.42±6.75), (31.00±5.20),(32.08±4.62), (30.67±3.71), (29.27±2.75) μg/L, respectively, and all more than that before RFCA [(14.89±2.84), (15.00±2.71), (15.51±2.75) μg/L, P ＜ 0.01]. However, there were no significant differences in the NGF levels at 6 hours, 1, 3, 5 and 7 days after RFCA (P ＞ 0.05). The plasma NGF concentration was not significant different among AVNRT, RSAP and LSAP ablation patients at any given time (P ＞ 0.05). The number of RFCA applications, the procedure time and the total energy have no correlation with NGF concentration at any given time instance.CONCLUSION: RFCA increases plasma NGF concentration in humans and lasts for at least 7 days. The number of RFCA applications, the procedure time and the total energy have no correlation with NGF concentration at any given time instance.

Objective To investigate the protective function and its mechanisms of eyclosporin A to immature brain tissue with convulsive brain damage. Methods 21-day-old SD rats were given lithium-pilocarpine to make the epilepsy model. Total 67 male rats had been investigated. Cyclosporin A (CsA) were injected three times at 6, 30, 54 hrs after model had been established. Three dosages had been chosen: 5, 10 and 25 mg/kg each time. The level of apoptotic cells, P-glycoprotein (P-gp), glial fibrillary acidic protein (GFAP) in CA1 area of hippocampus had been determined, and compared with the rats without giving CsA. Results Rats from epilepsy model group had higher level of apoptosis, P-gp, GFAP expression than those from pseudo-model group. CsA injection by dose 5 mg/kg each time for three times reduced the level of P-gp, GFAP. Model group and pseudo-model group were same. Both the interventions of CsA injection by 10 mg/kg and 25 mg/kg can reduce the level of P-gp, GFAP, however neither of their effectiveness was better than CsA 5 mg/kg each time. Conclusions Small dosage of CsA may protect the immature brain tissue from convulsive brain damage by reducing the level of P-gp, GFAP in CA1 area of hippocampus.

Objective To evaluate the long-term effective rate,retention rate and tolerability of the ketogenic diet (KD) in pediatric drug-resistant epilepsies.Methods Data of 36 children who were treated in Department of Pediatrics,the Second Affiliated Hospital of Xi'an Jiaotong University from Nov.2011 to Dec.2013 and had continuous follow-up of at least 12 months after initiation of the KD were analyzed prospectively.Response was defined as 50％ seizure reduction.The effective rate,retention rate, outcome-predictive value of various clinical factors were also assessed.The causes of the patients withdrew from KD and side effects were recorded and analyzed.Results Thirty-six children(29 boys,7 girls; mean age of 2.84 years)were included.The effective rate was 50.0％,52.8％,47.2％ and 41.7％ at the 1,3,6,12 months;the retention rate respectively was 94.4％,91.2％,69.4％ and 52.8％.Seventeen cases withdrew from KD.Seven cases (41.2％)ceased KD becau~ of a lack of compliance,5 patients because of poor outcome,and 2 cases because of repeated infection.None of the age,disease duration,etiology and seizure type could be used as the predictor for the favourable treatment for outcome.The antiepileptic drugs before KD might be predicted the efficacy of the KD.The less amount of the antiepileptic drugs,the more opportunity of the KD might have to succeed.The side effects on the start-up period were drowsiness,week and digestive discomfort,hyperlipoidemia,hypoglycemia and hepatic dysfunction.The side effects on the maintenance period were digestive discomfort,susceptibility to infection,hyperlipoidemia,the deficiency of trace elements.Conclusions The KD is a safe and potentially effective method in treatment of refractory epilepsy patients who do not respond to customary medication therapies.

Objective To study the effect of cyclooxygenase-2 (COX-2)selective inhibitor Celecoxib on the expression of P-glycoprotein(P-gp)in the brain of rats with status epilepficus,in order to assess the therapeutic value of intractable epilepsy.Methods Sixty adult male SD rats were randomly divided into blank control group,the epilepsy model group and Celecoxib intervention group.The status epilepticus was induced in rats by injecting Lithium pilocarpine.Forty-eight rats were included in the experiment.There were 16 rats in each of the blank control group,epilepsy model group and Celecoxib intervention group,respectively.Immunohistochemical method and Western blot method were used to detect the expression of P-gp in experimental group in the frontal cortex and hippocampus.Results Immunohistochemistry result showed that the expression of P-gp was significantly higher in epilepsy model group than the blank control group,and the difference was statistically significant (P ＜ 0.01);The P-gp expression in the Celecoxib intervention group was lower than that in the epilepsy model group,and the difference was statistically significant (P ＜0.01).Western blot results suggested that the expression of P-gp could be found both in the frontal cortex and hippocampus in each group.Compared with the blank control group,the P-gp expression was significantly higher than that in the epilepsy model group,and the expression of the P-gp was lower after the Celecoxib intervention than that in the epilepsy model group,and the difference was statistically significant (P ＜ 0.05).Conclusions COX-2 inhibitor Celecoxib could decrease the expression of P-gp in brain tissue with status epilepticus,which may provide a new method for the treatment of intractable epilepsy.

Objective To non-invasive assess coronary blood flow velocity changes of patients with slow coronary flow phenomenon (SCFP) by coronary blood flow imaging (CFI).MethodsTwenty-one patients who had no significant coronary artery stenosis but had thrombolysis in myocardial infarction (TIMI) slow-flow phenomenon were the experimental group,nine patients who has no significant coronary stenosis and TIMI flow normal were the control group.Using corrected TIMI frame count(CTFC) assess velocity of coronary artery.The left ventricular end diastolic diameter,end systolic diameter,ejection fraction,E peak velocity,A peak velocity,E/A ratio were measured by conventional echocardiography.The distal anterior descending coronary artery diastolic peak flow velocity(Vmax),mean velocity(Vmean) and blood flow velocity time integral(VTI) were measured by CFI.Results The corrected TIMI frame count (CTFC) of left anterior descending artery blood flow in slow blood group was (45.37 ± 8.62)frame,that in control group was (15.94± 4.66)frame,the difference was statistically significant (t = -9.596,P =0.000).The conventional echocardiographic measurements of two groups were not significantly different.The left anterior descending artery Vmax was (22.86 ± 3.04)cm/s,Vmean was (17.62 ± 2.89)cm/s,VTIwas (8.49± 2.01)cm in the slow blood flow group,the left anterior descending artery Vmax was (31.78 ± 9.28) cm/s,Vmean was (23.67 ± 7.60) cm/s,VTI was (10.91 ± 4.47) cm in the control group.The difference was statistically significant.The left anterior descending artery CTFC with Vmax and Vmean was negative correlation in the control group and the slow blood flow group.The left anterior descending artery CTFC was negatively correlated with VTI in the control group,there was no correlation between left anterior descending artery CTFC and VTI in the slow blood flow group.Conclusions Coronary artery flow velocity in the left anterior descending artery was declined.CFI can reflect changes in coronary TIMI flow,but in the diagnosis of coronary slow flow phenomenon CFI has limitations.

Objective To study influence on angiogenesis of placenta by gene silencing of netrin-1.Methods Netrin-1 gene in human umbilical vein endothelial cells(HUVEC)and placenta of pregnant rats were silenced by RNA interference.The following methods were used in this study,including the phenytetrazoliumromide(MTT)for viability,clone formation for proliferation,transwell for migration,and tube formation for angiogenesis in vitro.The change of fetal growth was recorded.Placental microvessel density in pregnant rats was measured by immunohistochemical CD34 staining in vivo.Results (1)HUVEC:viability and proliferation of HUVEC were remarkably inhibited by gene silencing of netrin-1.which number of clone formation,migration cell,tube formation were from(69±6)%,86±17,37±9 decreased to(46±5)%,46±13 and 17±5(P＜0.05)respectively.(2)Placenta of pregnant rats:after netrin-1gene silenced,fetal weight were decreased from(2.39 ±0.17)g to(2.12±0.10)g(P＜0.05).Placental microvessel density was decreased from(258±38)/mm2 to(197±32)/mm2 in vivo(P＜0.05).Conclusions Gene silencing of netrin-1 could inhibit viability,proliferation,migration,tubal formation of HUVEC and angiogcnesis of placenta.Netrin-1 plays an important role in regulating angiogenesis in placenta.

OBJECTIVE To investigate the management situation of cross infection in outpatient service of stomatology in hospital and clinic in Zhanjiang city and conduct effective measure to control hospital infection.METHODS In our investigation,we selected 105 hospitals and private clinics to inspect their management situation of cross (infection) via dental(instrument).RESULTS The management in the hospitals of the city was quite qualified but the some private dental clinics were terrible.The main problems were as follows: no effective disinfection for dental instrument and the bad environment in procedure room,especially the worse sterilization situation of the dental handpieces.Most of the doctors in private clinics were short of knowledge in the sterilization for dental(instruments.) CONCLUSIONS There is no time to delay for the health administration department to normalize the management of the private dental clinics.It is essential to train the medical staffs,and implement measures for dental instrument disinfection management in private dental clinics.

Objective To investigate the clinical effect of large dosage of Methylprednisolone on epilespy combined with electrical status epilepticus during sleep(ESES) in children.Methods Forty-six epielpsy patients with ESES were treated with additive large dosage of Methylprednisolone.The seizures and video electroencephalogram discharges were observed before and after using Methylprednisolone.The Methylprednisolone effect in eliminating the methylprednisolone of ESES and controlling of clinical seizures and improving cognitive function were analyzed.Results Two cases were lost and 44 cases were included,male 30,female 14,the age at onset was (5.37 ±2.52) (2-9) years old.The duration of follow-up was (4.12 ± 2.00)(1-9) years old.The age at diagnosis of ESES was (8.17 ± 2.09) (4.0-12.5) years old.The efficacy of Methylprednisolone on seizures was 72.7％ (32/44 cases),while the efficacy of Methyl prednisolone on electroencephalograph (EEG) was 59.1％ (26/44 cases).For patients who were resistant to Levetiracetam or Clonazepam,Methylprednisolone was still effective.Intelligence quotient had no significant changes before and after treatment(P ＞ 0.05).The earlier onset age,the worse effect of Methylprednisolone.The efficacy of methylprednisolone for atypical benign epilepsy with cento-temporal spike(BECT) was higher than other syndromes.Conclusions Large dosage of Methyl prednisolone therapy for children with ESES,especially for those resistant to traditional or new antiepileptic drug for ESES,was effective and safe.The onset age and syndrome classification may have a certain value for prognosis and prediction of the effect of Methylprednisolone treatment.

OBJECTIVE:To discuss the expression of voltage-gated potassium channel(KV1.3)and calcium activated potassi-um channel(KCa3.1)in peripheral monocyte from patients with coronary artery disease(CAD)and the regulatory effect of simvas-tatin. METHODS:20 patients with CAD and 8 control patients without CAD diagnosed by percutaneous coronary intervention but correlated to risk factor of CAD were enrolled. The expression of KV1.3 mRNA and KCa3.1 mRNA were measured by RT-PCR in 2 groups,and those of CAD group were measured by RT-PCR after 1 month of simvastatin treatment. RESULTS:Compared with control group,mRNA expression of KV1.3 [(1.54±0.08)vs.(0.77±0.06),P<0.01] and KCa3.1 [(1.32±0.08)vs.(1.06±0.06), P<0.05] were significantly increased in CAD group. mRNA expression of KV1.3 was significantly correlated to the concentration of C reactive protein (CRP)(P=0.003)and was decreased by simvastatin for one month [(1.54 ± 0.08)vs.(1.14 ± 0.05),P<0.01]. However,mRNA expression of KCa3.1 was not correlated to the concentration of CRP and simvastatin didn’t affect it’s expression. CONCLUSIONS:KV1.3 and KCa3.1 in peripheral monocytes may be two new markers of CAD. Regulating KV1.3 may be one of mechanisms of statin’s pleiotrophic effect.