Objective To explore the pattern and quantify the heat shock protein HSP)70 and HSP70 mRNA in Vero-E6 cells after infection with Hantann virus(HTNV).Methods The expres- sion of HSP70 and change of its mRNA level were detected by immunocytochemical staining,nucleic acid hybridization in situ and RT-PCR.Results In situ hybridization and RT-PCR were used to eval- uate the level of HSP70 mRNA during Hantaan 76-118 infection.HSP70 mRNA increased 0.5 h after infection,reached its peak by 12 h and gradually declined to steady state level by 72 h(vs.sham infec- ted group,P＜0.05).The expression of HSP70 protein induced by Hantaan 76-118 infection was e- valuated by quantitative immunocytochemical staining.HSP70 increased 0.5 h after infection,reached its peak by 12 h and decreased at 72 h after infection(vs.sham infected group,P＜0.05).Conclu- sions HSP70 can be induced directly by HTNV infection at both mRNA and protein levels,It pro- vides a basis for the further study of the pathogenesis,prevention and treatment of hemorrhagic fever with renal syndrome(HFRS).

Objective To investigate symptom characteristics and their their prevalence in terminally ill patients with ovarian carcinoma.Methods A retrospective study was carried out based on clinical data of 98 terminally ill patients with ovarian carcinoma who died in our hospital during January 1995 to December 2004.Fifteen most common symptoms were analyzed with a focus on the followings:symptom incidence,survival time after symptom occurrence,regularity of symptom cluster,and common causes of death.Fifteen symptoms were:pain,cachexia,pleural effusion and ascites,dyspnea,fever,intestinal obstruction,renal failure,bone marrow depression,lung infection,hemorrhage,deep venous thrombosis (DVT),intestinal or pancreatic fistula,mycotic infection,jaundice and emergency conditions.Results (1)The most prevalent symptom was pleural effusion and ascites(63%),followed by pain(60%), cachexia(59%),dyspnea(52%)and intestinal obstruction(49 %).(2)The symptom which lasted longest survival time was mycotic infection(77 days),followed by intestinal or pancreatic fistula(75 days), intestinal obstruction(67 days),pain(60 days)and eachexia(60 days).Symptoms such as bone marrow depression,renal failure,dyspnea and emergency conditions were comparatively critical associated with shorter survival times(14,13,12,7 days,respectively).(3)Terminal symptoms occurred typically in clusters,with 4.9?1.5 symptoms per case.Of 98 cases,84 cases(86%)had 4 or more symptoms,with the median survival time of 63 days from the last day of anti-cancer therapy,and a slow death process.The remaining 14 cases(14%)with 3 or fewer symptoms survived only 25 days,of which 10 cases(71%)died of emergency diseases.The survival time for two groups was significantly different(P

OBJECTIVETo evaluate the effects of paroxetine on protein kinase PKA, PKC and CaMKII activities in different brain regions in a rat model of depression.

METHODSThirty-six adult male SD rats were randomized into 6 groups, including one control group (I) and 5 groups of depression model established by forcing the rats to swim for 4 weeks. The 5 depression groups received no treatment (II) or were treated with paroxetine at a single dose (III), for a week (IV), 2 weeks (V) or 4 weeks (VI). The radioactivity of PKA, PKC and CaMKII in the hippocampus and prefrontal cortex was quantitatively measured using a liquid scintillation counter.

RESULTSIn the rat hippocampus, PKA and CaMKII activities were significantly lower in groups II, III, IV, and V than in groups I and VI (P<0.01 or P<0.05), but comparable between groups VI and I (P>0.05). PKC activity was significantly lower in group II than in group I (P<0.01), but showed no significant difference between the paroxetine-treated groups and group I (P>0.05). In the prefrontal cortex, the activity of PKA in groups I, II, III, and IV was similar (P>0.05), but all significantly lower than that in groups V and VI (P<0.01). PKC activity was significantly higher in groups II and III than that in group I and other paroxetine-treated groups (P<0.01), and similar between groups IV and I (P>0.05); groups V and VI had significantly lower PKC activity than group I (P<0.01). Group I had the highest CaMKII activity among the groups (P<0.01).

CONCLUSIONChronic administration of paroxetine can reverse chronic stress-induced inhibition of PKA, PKC and CaMKII activity in rat hippocampus, while the effects of paroxetine on the protein kinases can be more complex in prefrontal cortex.

Animals ; Brain ; drug effects ; enzymology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; metabolism ; Cyclic AMP-Dependent Protein Kinases ; metabolism ; Depression ; enzymology ; Disease Models, Animal ; Hippocampus ; drug effects ; enzymology ; Male ; Paroxetine ; pharmacology ; Protein Kinase C ; metabolism ; Random Allocation ; Rats

Idiopathic pulmonary fibrosis (IPF) is characterized by myofibroblast foci in lung parenchyma.Myofibroblasts are thought to originate from epithelial-to-mesenchymal transition (EMT).Wnt1 and lithium chloride (LiCl) induce EMT in alveolar epithelial cells (AECs),but the mechanisms are unclear.AECs were treated with Wnt1 and LiCl,respectively;morphological change and molecular changes of EMT,including E-cadherin,fibronectin,and vimentin,were observed.SB203580 was administrated to test the role of p38 MAPK signaling in EMT.Then AECs were treated with siRNAs targeting p38 MAPK to further test the effects of p38 MAPK,and the role was further confirmed by re-expression of p38 MAPK.At last β-catenin siRNA was used to test the role of β-catenin in the EMT process and relationship of β-catenin and p38 MAPK was concluded.Exposure of AECs to Wnt1 and LiCl resulted in upregulation of vimentin and fibronectin with subsequent downregulation of E-cadherin.Wnt1 and LiCl stimulated the p38 MAPK signaling pathways.Perturbing the p38 MAPK pathway either by SB203580 or through p38 MAPK siRNA blocked EMT and inhibited fibronetin synthesis,which were reversed by transfection of p38 MAPK expression plasmid.β-catenin siRNA attenuated the EMT process and decreased p38 MAPK phosphorylation,indicating that β-catenin is involved in the EMT-related changes through regulation of p38 MAPK phosphorylation.These findings suggest that p38 MAPK participates in the pathogenesis of EMT through Wnt pathway and that p38 MAPK may be a novel target for IPF therapy.

OBJECTIVETo analyze the cloning result of CD40 mutant from RPMI8226 cells, a multiple myeloma (MM) cell line, and study the change of the expressions of costimulatory molecules and the apoptosis of RPMI8226 cells after activated with CD40.

METHODSCD40 gene mutant in RPMI8226 cell was detected by RT-PCR and DNA sequencing. The cell lines were cultured with sCD40L, L929/CD40L, soluble 5C11 (an anti-CD40 mAb) plate-bound 5C11 and their respective controls. Their growth curves, change of phenotypes and cell cycles were detected. The signalosome of CD40 on RPMI8226 cells were analyzed with laser scanning confocal microscope.

RESULTSThere was a single base substitution (TCA-->TTA) in the open reading frame of CD40 from RPMI8226 cells, resulting in the conversion of a amino acid (Ser124Leu). Only plate-bound antibody could inhibit RPMI8226 cell proliferation [(2.5 +/- 0.6) x 10(5) vs (7.8 +/- 1.2) x 10(5), P <0.05] and cause G1 arrested [(58.0 +/- 3.6)% vs (42.0 +/- 2.3)%, P <0.05]. muCD40 was translocated to CD40 signalosome while CD40 activated.

CONCLUSIONThe mutated CD40 in RPMI8226 cell might decrease its affinity to CD40L, leading to the disorder of CD40 signal.

Antibodies, Monoclonal ; pharmacology ; CD40 Antigens ; genetics ; immunology ; CD40 Ligand ; genetics ; pharmacology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; DNA Mutational Analysis ; Humans ; Multiple Myeloma ; genetics ; pathology ; Mutation ; Phenotype ; Transgenes

OBJECTIVETo investigate the effects of propofol combined with indomethacin on the contractile function of isolated human pulmonary arteries.

METHODSHuman pulmonary artery preparations were obtained from patients undergoing surgery for lung carcinoma. The intrapulmonary arteries were dissected and cut into rings under microscope for treatment with propofol or propofol combined with indomethacin. In each group, the rings were divided into endothelium-intact and endothelium-denuded groups and mounted in a Multi Myograph system. In propofol group, the rings were preconstricted by U46619 to induce a sustained contraction, and propofol (10-300 mmol/L) was then applied cumulatively. In the combined treatment group, the rings were pretreated with indomethacin (100 µmol/L) for 30 min before application of U46619 to induce sustained contraction, and propofol (10-300 µmol/L) was added cumulatively after the tension became stable.

RESULTSPropofol (10-100 µmol/L) induced constrictions at low concentrations and caused relaxations at higher concentrations (100-300 µmol/L) in the pulmonary artery rings with prior U46619-induced contraction. Propofol caused stronger constrictions in endothelium-intact rings [EC=4.525∓0.37, Emax=(30.44∓2.92)%] than in endothelium-denuded rings [EC=4.699∓0.12, Emax=(31.19∓5.10)%, P<0.05]. Pretreatment of the rings with indomethacin abolished constrictions, and the relaxation was more obvious in endothelium-intact group [pD=3.713∓0.11, Emax=(98.72∓0.34)%] than in endothelium- denuded group [pD=3.54∓0.03, Emax=(94.56∓0.53)%, P<0.05].

CONCLUSIONPropofol induces constriction at low concentrations and relaxation at high concentrations in human intrapulmonary arteries with U46619-induced contraction. Indomethacin abolishes the constriction induced by propofol in isolated intrapulmonary arteries, suggesting that propofol potentiates U46619-mediated pulmonary vasoconstriction by promoting the concomitant production of prostaglandin by cyclooxygenase in pulmonary artery smooth muscle cells, and the mechanism for its relaxation effect may partly depend on the endothelium.

Objective To explore whether autoreactive antibody presents in patients with sporadic idiopathic hypoparathyroidism(sIHP).Methods The subjects including 26 patients with sIHP and 112 genealogical members as well as 60 age-and sex-matched healthy controls.Anti-parathyroid antibodies in the sera were assayed by indirect immunofluorescence.The levels of calcium,phosphorus and magnesium as well as intact parathyroid hormone(iPTH)in the sera were tested.Results Positive autoantibodies against parathyroid tissue were demonstrated in 10 patients(38%)with sIHP,significantly higher than that of in genealogical members(10%,?~2=13.42,P

Objective To explore the risk factors of cardiovascular disease in adolescents with a family history of hypertension.Methods A cross-sectional study was conducted in 3874 adolescents ages 13-18 years,with normal BP in 3724 people.Based on family history of hypertension (FH),the cohort of adolescents were dichoto- mized as postive family history (FH~+,n=1145) and negative (FH~-,n=2579).Height,weight,waist circum- ference,hip circumference,blood pressure and fasting plasma glucose(FPG),total cholesterol(TC),triglyceride (TG) and high-density lipoprotein cholesterol(HDL-C) were determined.Results FH~+ adolescents had signifi- cantly higher levels of body mass index(BMI),waist circumference,WHR,FPG,TC and LDL-C(P

Objective To delineate the relationship between body mass index(BMI),waist-to-height ratio (WHtR)and hypertension in adolescents.Methods A cross-sectional study was conducted in 3874 adolescents ages 13-18 years.They were classified into four groups according to BMI and WHtR,group A:normal BMI and WHtR

Objective To investigate the expression and correlation of NKG2D and sMICA in lung cancer patients. Methods By collecting 30 lung cancer patients as the test group,and taking 30 healthy volunteers as the contrast group, the expression of NKG2D and sMICA in the two groups were examined separately by FACS and ELISA method. Results The expressions of NKG2D in the two groups were (81.56±8.78) %, (85.63±6.62) %. The lung cancer patients were high remarkable. There was a significant difference between the two groups (P <0.05). The expression of sMICA in the two groups were (354.13 ±80.575) pg/ml,(216.53±48.175) pg/ml. The lung cancer patients were low remarkable. There was a significant difference between the two groups (P <0.01). There was a significant relation between the two groups (r =-0.349, P =0.006). Conclusion The expression of NKG2D and sMICA may provid one of the immune targets for diagnosing that can forecast the immune state and malignant metastasis of the lung cancer patients. The significant relation between NKG2D and sMICA may take on main role in the immune escaping of tumor. It may provide the suitable target of the patients for tumor organisms and immune treatment.