Objective To investigate the influence of influenza virus A（H1N1,A/PR/8/34 strain）on alveolar fluid clearance（AFC）in vivo and the effects of β1-adrenergic agonist on AFC in rat lungs infected by H1N1.Methods Fortyfive rats were divided into control group（n =12）,H1N1 infection group（the rats were infected with influenza virus strain A/PR/8/34,n =18）,β1-adrenergic agonist groups（the rats were administrated with β1-adrenergic agonist after HIN1 infection,n =15）.AFC was estimated by the progressive increase in the albumin concentration over 30 minutes.The activity of cAMP and cGMP in the lung tissues of control,H1N1 infection and β1-adrenergic agonist groups was measured.Results The infection with H1N1 resulted in a decline in AFC 9.15±1.01% vs control group 17.25±1.01% and increased lung water content（W/D was 6.77±0.13 vs control group 4.99±0.02）.H1N1-mediated inhibition of AFC could be reversed to 14.41±1.41% by the administration of β1-adrenergic agonist denopamine.H1N1 infection increased cGMP levels 7.34±0.40 pmol·mg-1· mg-1 vs control group 5.10±1.88 pmol·mg-1·mg-1 and decreased cAMP levels 1.43±0.06 nmol·mg-1·mg-1 in lung tissues compared with control group.β1-agonist denopamine reversed the level of cAMP to 2.06±0.16 nmol·mg-1·mg-1 and cGMP to 6.16±1.36 pmol·mg-1·mg-1.Conclusion H1N1 infection decreased AFC and increased lung edema.β1-agonist denopamine could reverse AFC and the ratio of cAMP/cGMP in H1N1 infected lung tissues.β1-agonist might regulate AFC through the pathway of cAMP-PKA.

The use of optimal regulatory sequences for simultaneous expression of the transgenes might play a significant role in engineering plants with increased disease and insect resistance.The plant expression vector pOMS-GUS,which contained the GUS gene under the control of a chimeric promoter based upon the mannopine synthase(mas)promoter and the octopine synthase(ocs)enhancer,was constructed.Used as control,another vector pMAS-GUS,carried the GUS gene driven by only the mas promoter.The two vectors were introduced into tobacco plants by Agrobacterium-mediated transformation.Fluorometric assays for GUS activity and reverse transcription-polymerase chain reaction(RT-PCR)analysis revealed that GUS gene expressed weakly with untreated transgenic tobacco while the level of GUS activity increased steadily after 1 h subjected to wounding.The expression of the mas and ocs/mas promoters was induced a further 1.8-fold and 5.7-fold,respectively.SA(1 mmol/L)or MJ(250 ?mol/L)treatment also caused a large induction of the ocs/mas chimeric promoter;And the application of SA in combination with MJ(1 mmol/LSA & 250 ?mol/L MJ)produced an additive effect that exceeded the wounding response.The results showed that the ocs/mas chimeric promoter is a strong inducible promoter that can be activated by various stresses.The chimeric promoter should have utility in development of disease and insect resistant transgenic crops.

Child ; Colitis ; diagnosis ; Colon, Sigmoid ; pathology ; Diagnosis, Differential ; Diarrhea ; etiology ; Eosinophilia ; complications ; diagnosis ; Female ; Gastroenteritis ; complications ; diagnosis ; pathology ; Humans ; Sigmoid Diseases ; complications ; diagnosis ; pathology ; Sigmoidoscopy

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Apolipoproteins E ; blood ; genetics ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Venous Thromboembolism ; blood ; genetics ; Young Adult ; alpha-2-Antiplasmin ; analysis ; genetics

Objective To investigate the therapeutic effects and adverse drug reactions of different doses of rosuvastatin in patients with acute ST segment elevation myocardial infarction (STEMI). Methods A total of 115 patients with STEMI were collected from Department of Cardiology, the Second Hospital of Tianjin Medical University. According to different oral doses of rosuvastatin, patients were divided into two groups including 5 mg/d rosuvastatin treatment group (low-dose group, n=44) and 10 mg/d Rosuvastatin treatment group (moderate-dose group, n=71). Patients of two groups were treated with Rosuvastatin at least 1 month after discharge. Data of total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed and compared before and after treatment between two groups. The major cardiovascular adverse events (MACE) and adverse reactions were recorded in two groups of patients. Results There were no significant differences in blood lipid and liver function levels before and after one month treatment between the two groups. After one month treatment, levels of TC, LDL-C, ALT and AST were significantly decreased in both groups of patients compared with those before treatment (P<0.05). There were no significant differences in levels of TG, and HDL-C before and after treatment between two groups. The incidence of MACE (heart failure and angina pectoris) was significantly lower in moderate-dose group than that in low-dose group (P<0.05). There was no significant difference in the proportion of malignant arrhythmia between the moderate-dose group and the low-dose group (P<0.05). No target vessel repair and death were found in the two groups. No obvious adverse drug reactions were found during the follow-up period. Conclusion The hypolipidemic effects are epuivalent between 5 mg/d rosuvastatin and 10 mg/d on the basis of conventional treatment for STEMI patients, but the moderate dose can reduce the incidence of MACE and improve prognosis.

Objective To explore the method of primary isolation, cultivation and identification of rat brain microvessel pericytes. Methods The brain tissue of 10 3 week-old Wistar rats was separated sterilely. The brain microvessel fragments were separated using two-step enzyme digestion and one-step gradient centrifugation and were seeded in 35-mm dishes for primary culture. The cell morphology was observed by phase contrast microscopy; the immunofluorescence assay was used to identify the associated antigns, such as the α-smooth muscle actin (α-SMA), neuron-glial antigen 2 (NG2), von Willebrand factor (vWF), and glial fibrillary acidic protein (GFAP). Methyl thiazolyl tetrazolium was used to determine the cell growth curve. Results Pericytes climbed out from the adherent brain microvascular fragments around,showing polygonal, and the cell fusion was 95％ after 12-14 days. Immunofluorescence staining revealed that the molecular markers of the pericytes α-SMA and NG2 related antigens showed double positive, while the vWF and GFAP related antigens showed double negative and the cultured cells were confirmed as brain microvascular pericytes. The growth rate of primary cells was slower. The passage cells entered into logarithmic growth phase after 36 to 60 hours and entered into plateau phase after 72 to 108 hours. Conclusions This method may successfully isolate rat brain microvascular pericytes with higher purity.

Objective To investigate the relationship of placental vascular anastomosis and physical development and morbidity of the disease in twin neonates.Methods Fourteen pairs of twin neonates deliveried from Sep.2005 to Aug.2009 were enrolled in Newborn Intensive Care Unit,the Third Affiliated Hospital of Zhengzhou University.These twins were divided into 2 groups according the conditions of placental vascular anastomosis:significant placental vascular anastomosis group(group A) and no significant vascula anastomosis group(group B).Birth weight,head circumference,length,the morbidity of disease were all investigated in 2 groups.Clinic follow-up included neonatal behavioral neurological assessment(NBNA) and children′s development center of China(CDCC).The correlation of neonates placental vascular anastomosis between twin neonates were compared.Results There were statistically significant differences between group A and group B in birth weight,head circumference and body length(t=6.070,5.237,5.784,Pa

Microcirculation dysfunction is involved in the onset of diabetes and its complications.The pathophysiological mechanisms behind the relationship between microcirculation and diabetes are multifactorial.Islet microcirculation dysfunction affects function of islet β cells.Impairment of microvascular vasomotion might be associated with insulin resistance.Microcirculation dysfunction of target organs mediates diabetic complications.

Aim To detect the effects of cetuximab combined with adriamycin on the proliferation and ap-optosis of triple-negative breast cancer cells.Methods Cell viability was evaluated by MTT assay.The cell apoptosis was analyzed by flow cytometry with propidi-um iodide staining.JC-1 staining was used to deter-mine mitochondrial membrane potential.The expres-sions of glucose regulated protein78 (GRP-78),Bcl-2 and Caspase-3 were measured with Western blot.Re-sults MTT assay showed that cetuximab had inhibi-tion effect on the breast cancer cell MDA-MB-231 growth,and the effect was related to concentration of drug.The inhibition effect of adriamycin on MDA-MB-231 had remarkabe relationship with time and concen-tration.When combined with each other,they could re-markably increase inhibition effect.The viability of cells in combination group for 1 2 h,24 h,48 h,sig-nificantly lower than that in cetuximab or adriamycin group (P <0.05 or P <0.01 ).Apoptosis results showed that cell apoptosis was significantly increased when cetuximab combined with adriamycin,reached (43.93 ±3.59)% for 24 h,had remarkably statistical significance compared to cetuximab or adriamycin
group (P <0.01 ).JC-1 staining indicated that cetux-imab or adriamycin could reduce the mitochondrial membrane potential,but the reduction effect was more remarkable in the combination group.Western blot re-vealed that cetuximab could reduce the expression of GRP-78 and Bcl-2,and increased the expression of Caspase-3 and its activity.The expressions of Bcl-2, Caspase-3 had no significant change in adriamycin group,but GRP-78 was increased.In combination group,the expression of GRP-78 and Bcl-2 was signifi-cantly decreased,but Caspase-3 was increased nota-blely compared to adriamycin group.Conclusions The combination of cetuximab and adriamycin enhances the inhibition effect on the triple-negative breast cancer MDA-MB-231 cells,and increases cell apoptosis.The mechanism may be that cetuximab reduces the endo-plasmic reticulum stress level,then activates the mito-chondrial pathways by decreasing the expression of Bcl-2,reducing the mitochondrial membrane potential,and promoting cell apoptosis.