Foreign Bodies ; complications ; diagnosis ; Glottis ; Hoarseness ; diagnosis ; etiology ; Humans ; Male ; Middle Aged

Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; Apoptosis ; drug effects ; Cyclin-Dependent Kinases ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Gene Expression ; drug effects ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Neoplasms ; drug therapy ; metabolism ; Protein-Tyrosine Kinases ; metabolism ; Signal Transduction

Air Pollutants, Occupational ; analysis ; Cyanamide ; analysis ; Spectrophotometry ; Workplace

AIM: To investigate the effect of Ginsenoside Rb1(G-Rb1) on transcription of glucocorticoid receptor ? (GR?) mRNA and expression of its protein in a acute promyelocytic leukemia cell line. METHODS: Antiproliferation effects of G-Rb1 on HL60 cells were determined by MTT. The transcription of GR mRNA and expression of GR were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot, respectively. RESULTS: G-Rb1 inhibited the growth of HL-60 cell line in a time-dependent and dose-dependent manner. After 36 hours treatment with 80 mg/L G-Rb1, the expression of GR? mRNA and GR protein increased. CONCLUSION: G-Rb1 exhibits the inhibitory effects on cell growth in HL60 cells, and increases the expression of GR? mRNA and protein. [

Objective To understand the changes of cardiac systolic and diastolic function in human immunodeficiency virus (HIV)-infected patients without evidence of cardiac disease in China.Methods Forty-two HIV-infected patients who were followed up in the Department of Infectious Diseases at Peking Union Medical College Hospital without cardiac involvement were recruited.All the HIV-infected patients had received highly active antiroviral therapy (HAART) for more than 12 months with viral suppression.And 30 age and sex matched healthy subjects without cardiac disease manifestations were enrolled as controls.Every group members underwent transthoracic echocardiography evaluation.The indexes of cardiac systolic and diastolic function between HIV-infected patients and healthy controls were compared.Results Diastolic abnormality occurred in 20 cases in HIV-infected group and 6 cases in control group, with statistically significant difference (χ2=5.79, P=0.007).The E wave deceleration time (EDT) in HIV-infected patients were significantly decreased than healthy controls ([161.87±21.64] ms vs.[190.34±37.22], t=-3.20, P=0.002).There were no significant differences of E/A ratio ([1.16±0.35] vs.[1.19±0.26]), E/Ea ratio ([5.43±1.99] vs.[5.78±0.91]), isovolumic relaxation time (IVRT), ([93.18±20.34] ms vs.[93.57±18.55]ms), Ea ([10.18±2.80] cm/s vs.[11.45±2.75] cm/s) between HIV-infected patients and controls (t=1.13,1.53,0.67 and 0.29, respectively, all P>0.05).Among cardiac systolic function markers, left ventricular ejection fractions in HIV-infected patients and control group were (66.7±6.4)% and (68.7±4.2)%, respectively.And left ventricular shortening rates were (37.08±4.79)% and (38.17±3.96)%, respectively.Both showed no significant difference between the two groups (t=-1.51 and-1.00, respectively, both P>0.05).Conclusions Compared with control group, subclinical cardiac diastolic dysfunction is more frequently observed in HIV-infected patients.However, there are no significant differences of cardiac systolic function markers between HIV-infected patients and controls.

Animals ; Arrestins ; metabolism ; Liver ; pathology ; Liver Cirrhosis, Experimental ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred ICR ; beta-Arrestins

Child ; Congresses as Topic ; Humans ; Pediatrics

The records of 25 psychiatric patients ( clients ) who received case management from November 2009 to July 2010 were retrospectively analyzed.The factors related to the quality of professional relationship established between case managers and the clients were evaluated.The study revealed that timely supports, encourage and affirmation from case managers ( 40%) , the successful coordinate service (40%) , the active care for clients (24%) and helping to build up confidence and hope for clients (24%) were favourable factors for professional relationship establishment, while lack of desire to receive service and change from clients (24%) was adverse factor.

Objective To investigate the effects of ketogenic amino acid ( KAA) replacement diet on insulin resistance in mice fed with high fat diet(HFD) and to analyze the possible mechanism. Methods C57BL mice were fed with a control diet, HFD, and KAA-fortified HFD(HFDKAAR)from the age of 8 weeks, and 8 weeks after HFD initiation, the HFD-fed mice were divided into two groups:one group of mice were fed the same HFD, the other group were fed HFDKAAR ( HFD→HFDKAAR ) . The metabolic evaluations were performed at the end of 16 weeks. Blood glucose levels were measured at 0, 15, 30, 60, 90, and 120 min after the injection of glucose ( 1 g/kg BW intraperitoneal glucose tolerance test, ipGTT) . The insulin,β-hydroxybutyrate, and acetoacetate levels in the plasma were measured via ELISA. The insulin resistance index ( IRI) and area under curve ( AUC) were calculated. The expression of hepatic LKB1 ( liver kinase B1 ) , AMP-activated protein kinase ( AMPK ) , and mTOR ( Mammalian target of rapamycin ) protein, and mcp-1 mRNA were measured by western blot and real-time PCR respectively. Results HFD-fed group of mice displayed significantly heavier body weight,heavier intra-abdominal fat weight, and significant deterioration of glucose tolerance at the end of 16 weeks in addition to higher insulin levels( all P<0. 05), HFDKAAR-fed mice exhibited significantly ameliorated high fat diet-induced obesity and glucose intolerance compared to the HFD-fed mice, which was associated with decreased insulin levels, IRI, AUC, and mcp-1 mRNA expression (all P<0. 05). HFD suppressed hepatic LKB1 and AMPK phosphorylation expression, and increased mTOR phosphorylation levels compared to the control diet-fed mice(all P<0. 05). In contrast, treatment with the HFDKAAR diet increased LKB1and p-AMPK expression, which was associated with suppressed p-mTOR levels compared to the HFD-fed mice(all P<0. 05). Conclusion KAA may ameliorate high fat diet-induced obesity, glucose intolerance, via normalizing the hepatic LKB1-AMPK-mTOR nutritional signal passageway. KAA replacement diet seems to be a potential nutritional intervention for the treatment for patients with metabolic defects, such as obesity, glucose intolerance, as well as metabolic syndrome.

Objective To investigate the effect of Bunao capsule on learning,memory and antioxidative abilities of rats with Alzhheimer’s disease(AD)induced by D-galactose combined with amyloid β-protein(Aβ25-35 ),and provide experimental basis for the prevention and treatemtn of AD. Methods A total of 90 SD male rats were randomly divided into model control group,piracetam group,sham operated group,Bunao capsule(0.79,1.58,3.15 g·kg-1 )groups(n= 15 each).The rat models were established by intraperitoneal injection of D-galactose and injection of Aβ25-35 into the bilateral lateral cerebral ventricle.Then rats were given corresponding drugs by gavage in different groups for 8 weeks.The learning and memory abilities were meseured by Morris water maze test.The morphology of brain cells was observed by HE staining.The activities of glutathione peroxidase(GSH-Px)and superoxide dismutase( SOD),and the malondialdehyde( MDA)contents in the brain tissues were measured by spectrophotometry. Results The target quadrant residence time was(20.39±7.75)s and(20.82±5.09)s in Bunao capsule (1.58,3.15 g·kg-1 )groups,which were significantly increased as compared with that in model control group[(12. 35 ± 6.95)s](P<0.01).Brain nerve cell morphology in Bunao capsule(1.58,3.15 g·kg-1 )groups was obviously improved as compared with that in model control group,and was close to that in sham operated group.The activities of GSH-Px and SOD were significantly increased,and MDA contents decreased in Bunao capsule groups as compared with those in model control group (P<0.01). Conclusion Bunao capsule can dose-dependently improve the learning,memory and antioxidative abilities of AD rats.The mechanism may involve upregulation of antioxidative enzyme activities and removal of oxidative products.