Adrenal crisis is a life-threatening emergency caused by the destruction or altered function of the adrenal gland with a primary deficit in cortisol secretion(primary adrenal insufficiency)or by hypotha-lamic-pituitary pathologies determining a deficit of adrenocorticotropic hormone(secondary adrenal insuffi-ciency).Infection and abrupt end glucocorticoid treatment are the major precipitating causes of adrenal crisis. Patients with adrenal crisis typically present with hypovolemic shock or hypotension,nausea,vomiting,and fe-ver responding well to parenteral hydrocortisone administration.The main laboratory findings include lower serum cortisol concentrations,hyponatremia,hypoglycaemia and/or hyperkalemia.Delay diagnosis of adrenal insufficiency leads to adrenal crisis which is potentially lethal complication.Empirical glucocorticoid replace-ment should be initiated as soon as the suspicious of adrenal crisis,or sooner if the patient presents in adrenal crisis in critically ill children.

The invasive fungal infection( IFI)in PICU has increased steadily during the recent years. Candida spp. and Aspergillus spp. are the most frequently fungi in children. Candida spp. is the leading cause and invasive Candida spp. Infection( ICI)is approximately five times frequency than invasive Aspergillus spp. Infection( IAI). The attributable mortality of ICI or IAI remains different mainly because of different basic diseases. Stay in the PICU presents risk factors for ICI especialy using central venous catheter,parenteral nutrition,dialysis,mechanical ventilation,and prolonged antibiotics application. The patients with hematologic malignancies and leukemia are higher prevalence of IAI who were treated with cytotoxic or immunosuppres-sive drugs,broad-spectrum antibiotics and stem cell transplantation. The most important challenge remains to propose targeted prophylaxis and to identify IFI earily in high risk critically ill children in PICU.

Sepsis is the leading cause of acute kidney injury (AKI) in pediatric intensive care unit.Development of AKI during sepsis increased patient morbidity,predicts higher mortality and days of stay in the intensive care unit.The mechanisms behind AKI in sepsis remain controversial but were believed to be complex and multi-factorial.The pathophysiology of AKI in sepsis involved intrarenal hemodynamic changes,endothelial dysfunction,infiltration of inflammatory cytokines.The new markers of neutrophil gelatinase-associated lipocalin as the representative is helpful for early diagnosis of AKI.Renal replacement therapy (RRT)is the main treatment of sepsis related AKI.At present,the model,dose and exact timing of RRT is not well defined.A widely accepted viewpoint is that the injury stage of RIFLE diagnostic criteria and fluid overload up to 10％ ～ 20％ is the beginning of the most appropriate chance of RRT.

Objective To evaluate the clinical efficacy of direct percutaneous coronary intervention (PCI) in ST segment elevation acute myocardial infarction (AMI) Methods From April 2000 to April 2004, 458 patients with ST segment elevation AMI were randomized to receive invasive therapy ( n =205) or non invasive therapy ( n =253) Comparison was made in the 30 day mortality rate, major cardiac events rate, reinfarction rate during hospitalization, left ventricular ejection fraction (LVEF) and end diastolic diameter (EDD) of echocardiograph in 2 weeks after AMI between the 2 groups The PCI group was divided into 3 sub groups according to number of stenosis artries found during angiography We try to find not the relation between left ventricular function and the number of coronary artery with stenosis Results The result of selective coronary artery angiography in 205 PCI patients was: 66 patients with single branch lesion (32 2%), 68 patients with double branches lesion (33 2%) and 71 patients with triple branches lesion (34 6%) 203 patients were operated successfully (99%), 228 stents were placed on lesions, 194 patients (94 6%) obtained TIMI grade Ⅲ perfusion of the IRA Compared the invasive with the non invasive group, the in hospital 30 day mortality rate was 2 9% vs 9 1% ( P

Objective To investigate the changes of cardiotrophin-1(CT-1) expression in rats with pressure overload-induced cardiac hypertrophy,and the effects of benazepril on this expression and the concerned cardiac hypertrophy.Methods The model of pressure overload was established by constriction of abdominal aorta and divided randomly into hypertrophied group(LVH,n=7) and benazepril intervention group(Ben,n=7,benazepril 1mg?kg~(-1)?d~(-1) orally)2 weeks later.A sham-operation group(Sham,n=7) served as control.Blood pressure and left ventricular mass index(LVMI) were investigated after 3 weeks' treatment.AngⅡ level in myocardium was measured by radioimmunoassay.The mRNA level of CT-1 was examined by RT-PCR.Results Compared with the sham group, blood pressure and LVMI in LVH group were increased significantly(P

Objective To clone shRNA (short hairpin RNA) recombinant plasmid targeting on COX-2 gene and analyze the nucleic acid sequence of the recombinant plasmid. Methods One pair of 21 bp reverse repeated sequence targeting on COX-2 mRNA spaced by 9 bp nucleotides were synthesized. The complement double strands was formed by annealing and inserted into plasmid pGenesil-1 to generate eukaryotic expression plasmid. The recombinant plasmid was transformed into Jm109 strain, and the recombinant plasmid extracted was identified by restriction enzyme and sequence analysis. Inhibition effects of COX-2 mRNA and protein were detected by RT-PCR and Western blotting respectively. Results The target DNA was directly cloned to vector and the result was correct by sequence analysis. Compared to untransfected group, recombinant expression plasmid pshRNA-COX-2 resulted in reduction of COX-2 mRNA and protein expression to 69.9% and 50.3% respectively. Conclusion The recombinant plasmid targeting on COX-2 gene was successfully constructed, and it inhibited the expression of COX-2 gene significantly.

Objective To investigate the effect of exogenous semaphorin 3A (Sema3A) on apoptosis in primary cultured rat cortical neurons and the roles of phosphoinositide 3-kinase (PI3K)/serine-threonine kinase (Akt) pathway in apoptosis induced by Sema3A.Methods Newborn Sprague-Dawley rat cortical neurons were cultured in vitro and they were identified by microtubule associated protein-2 (MAP-2) staining The cultured cortical neurons were treated with various concentrations of Sema3A (0,500,1 000,and 2 000 μg/ml) for 48hours.Neuronal survival rate was detected with CCK8 assay.Neuronal apoptosis was detected with Hoechst33342 staining and TUNEL staining.The expressions of P-Akt,Akt and Bcl-2 in cortical neurons were determined with Western blotting.Results The purity of cortical neurons culture was more than 95％.CCK8 assay showed that the survival rates of cortical neurons in the groups of 500,1 000and 2 000 μg/ml Sema3A were 80.9％ ± 5.3％,67.5％ ± 3.9％ and 50.2％ ± 4.4％ of the control group,respectively (F =165.042,P =0.000).Hoechst33342 staining showed that the apoptosis rate in the normal control group and the groups of 500,1 000and 2 000 μg/ml Sema3A were 22.4％ ± 1.2％,34.0％ ± 1.2％,39.3％ ± 1.4％ and 47.3％ ±2.3％,respectively (F =103.237,P =0.000).TUNEL staining showed that the apoptosis rate in the normal control group and the groups of 500,1 000and 2 000 μg/ml Sema3A were 23.9％ ± 1.1％,31.9％ ± 1.0％,40.1％ ± 1.5％ and 51.4％ ± 3.4％,respectively (F =103.118,P =0.000).Western blotting showed that the expressions of P-Akt (F =15.959,P =0.001) and Bcl-2 (F=18.776,P =0.001) decreased gradually,while the expression of Akt had no significant changes (F =0.590,P =0.639).Conclusions Sema3A can decrease the survival rate of the cultured cortical neurons,mainly by inducing apoptosis,and the mechanism of which might be related to the down-regulation of expressions of P-Akt and Bcl-2.

Objective To examine cerebrovascular reactivity to CO2 inhalation in mice. Methods In vivo Two-Pho?ton imaging technique was used to record the reaction of cerebral cortical vessels including penetrating artery, surface vein and capillary in 5 male C57 mice after CO2 inhalation under a thinned-skull cranial window. Nitric oxide syntheses inhibitor L-NAME and Prostaglandin syntheses inhibitor Indomethacin were used to block different vasodilator pathways, respectively. Results Different mouse cortical vessels displayed different degrees of dilation to 1-minute 5%CO2 inhala?tion. The penetrating artery exhibited the most obvious dilation (45.01%±4.45%). L-NAME intervention significantly di?minished cerebravascular CO2 reactivity(P<0.05). Indomethacin significantly attenuated the dilation of artery but not capillary comparing with L-NAME intervention(P<0.05). Conclusions Different vessels react differently to CO2 inhala?tion in which postaglandins and NO signal pathways are involved.

Wild Cordyceps sinensis strain was isolated from Mt. Batang in Yush District of Qinghai Province. Its optimal culture conditions were 1.5% Glucose, 1% malt extract, 1 peptone, 0.5% yeasts extract, pH6.0, temperature 23℃, 5—10% inoculum, vibration velocity 80—90r/min.

Objective To investigate the gene E670G SNP loci with coronary heart disease and its relationship Dongguan Han PCSK9 prognosis .Methods In our hospital 100 patients with coronary heart disease and 100 cases of non‐coronary heart disease patients for the study ,patients taking blood ,DNA was extracted and analyzed gene PCSK9 E670G SNP locus by PCR ,using gene sequencing validation .Lipid levels in patients using enzymatic detection and follow‐up of patients with coronary heart disease chan‐ges in serum lipid levels after statin therapy ,the incidence of cardiovascular events .Results CAD group TC ,LDL‐C levels were sig‐nificantly higher than the healthy control group ,HDL‐C was significantly lower than the healthy control group ,the difference was statistically significant (P<0 .05) .AA genotype that was mainly 298 bp and 152 bp of homozygotes ,followed by AG that was 450 bp and 298 bp ,152 bp heterozygotes ,had not been detected 450 bp GG homozygous genotype ,allele frequency distributions in Har‐dy‐Weinberg equilibrium .LDL‐C levels in patients with CAD patients was significantly lower than AA genotype AG genotype , HDL‐C levels were significantly higher in patients with AG genotype (P<0 .05) .Number of cardiovascular patients were followed up six months totaled 27 cases ,AA genotype accounted for 66 .7% ,AG genotype accounted for 33 .3% ,Gallele and the average number of cases of cardiovascular disease events count a statistically significant difference (P<0 .05) .Conclusion PCSK9 E670G polymorphism and LDL‐C ,HDL‐C levels and CAD severity gene‐related ,CAD patients carrying G allele may increase the risk of disease and the risk of again .