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Objective To explore the clinical prognostic value of rapid detection for plasma NT-proBNP levels on admission in patients with acute myocardial infarction.Methods 56 patients with AMI were measured plasma NT-proBNP imediately in hospital,and then they were divided into A,B and C group according to NT-proBNP levels (A group:< 500ng/L,B group:500-2 000ng/L,C group:> 2 000ng/L).The incidence of major adverse cardiac events (MACE including congestive heart failure,malignant arrhythmia,cardiogenic shock and sudden cardiac death) in subjects were observed respectively during hospitalisation and 30 days.Results The three group subjects with different NT-proBNP levels presented different incidence of MACE(A group:1,0;B group:3,1;C group:8,6) at duration of hospital stay,30days (x2 =6.705,P =0.035 ; x2 =7.957,P =0.008).With the NT-proBNP levels rising in AMI paitents,the inciedence of MACE increased.The incidence of MACE in A,B and C group were 6.6%,18.18% and 73.69% respectively.Conclusion In AMI patients,plasma NT-proBNP levels could predict early MACE incidence,which has an important value to evaluate the early clinical prognosis.
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Objective To study the clinical significance of plasma N-teminal pro brain natriuretic peptide (NT-pro-BNP) level in diagnosis and evaluation prognosis of patients with different heart failure.Methods Plasma NT-pro-BNP level was detected and compared in all patients at the first day and a week after the patients' condition turn better.Results The level of plasma NT-pro-BNP for the high blood pressure's heart disease and the chronic heart failure of coronary heart disease and the chronic heart failure of cor pulmonale were significantly higher than normal (t =2.98,t =2.98,t =2.98,P < 0.01).The level of plasma NT-pro-BNP was reduced after treatment (t =2.56,t =2.75,t =2.88,P < 0.05,P < 0.01,P < 0.01).The level of plasma NT-pro-BNP was gradually increased by the increased degree of the heart failure(t =2.78,P < 0.05).Conclusion The levels of plasma NT-pro-BNP at acute stage for the high blood pressure's heart disease and the chronic heart failure of coronary heart disease and the chronic heart failure of cor pulmonale were increased obviously and descend by the patients' condition return.The level of plasma NT-pro-BNP can monitor patients' condition and estimate the heart failure patients' prognosis.
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Objective To investigate the role of ghrelin promoting proliferation of pancreatic β cells and the mechanism of it. Methods Mouse pancreatic β cells(NIT-1)were treated with different concentrations of ghrelin.NIT-1 cells proliferation was measured by MTT incorporation assay,and the cell cycle was measured by Flow Cytometry,and the expression of ERK1/2 and the level of ERK1/2 phosphorylation were determined by Western blot assay.Results With the increase of concentration and the time of treatment,ghrelin promotes cell survival of pancreatic β cells.The S-phase portion was changed after treatment of ghrelin on NIT-1 for 48 hours.The S-phase percentage in the groups where ghrelin concention change from 0 tO 10-9,10-8,10-7 mol/L were(34.5±6.5)%,(42.1±7.4)%,(50.6±5.8)%,(71.4±9.4)%,respectively.Ghrelin also induces phesphorilation of ERK1/2 in NIT-1 cell,and a doseeffect relationship was demonstrated.Conclusion Ghrelin could promote proliferation of pancreatic β cells through activating the MAPK/ERK1/2 signaling pathway and changing the cell cycle.
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Objective To investigate the effect of ghrelin on PAI-1 secretion in HepG2 cells induced by TNF-αand the effect of p-38 MAPK.Methods HepG2 cells were cultured.The concentration of TNF-α used to treat the HepG2 cells wag selected.The effect of ghrelin on PAI-1 secretion induced by TNF-α was detected by ELISA,the p-38 MAPK expression was investigated by Western blot.Results The concentration of PAI-1 was increased when cells were exposed to different concentration of TNF-α.The p-p38 MAPK expression was increased when the cells were exposed to TNF-α,ghrelin could inhibit the increase of PAI-1 secretioN induced by TNF-α.The expression of p-p38 MAPK was decreased when the cells were pretreated with ghrelin.Conclusion PAI-1 secretion were increased after TNF-α in-creasing.Ghrelin could inhibit PAI-1 secretion via p38 MAPK.
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O tabagismo é a principal causa de morte prevenível na maioria dos países, inclusive no Brasil. Parar de fumar é uma estratégia importante para reduzir a morbidade e mortalidade associada às doenças tabaco-relacionadas. Sabe-se da relação inversa entre uso de nicotina e peso corporal, onde o índice de massa corporal tende a ser menor em fumantes quando comparados aos não fumantes. Além disso, abstinência tabágica resulta em aumento de peso, sendo que ex-fumantes geralmente aumentam de 5 a 6 kg, mas cerca de 10 por cento adquirem mais de 10 kg. O tratamento farmacológico para a cessação do tabagismo pode atenuar este ganho de peso. O aumento de peso na cessação do tabagismo como contributório à epidemia de obesidade é pouco estudado. Nos EUA, calcula-se que a fração do problema atribuível à cessação do tabagismo seja de 6 por cento para homens e 3,2 por cento para mulheres. Os mecanismos não são claros, mas há evidências mostrando que a dopamina e serotonina diminuem a ingestão alimentar. A administração de nicotina por qualquer via eleva agudamente os níveis destes neurotransmissores no cérebro, causando menor necessidade de ingestão energética e diminuindo o apetite. Além disso, a nicotina tem efeito direto no metabolismo do tecido adiposo, influenciando a taxa de ganho ponderal após a cessação do tabagismo. A leptina, grelina e neuropeptídio Y são peptídeos que podem contribuir para esta relação inversa entre nicotina e índice de massa corporal, em um papel ainda não determinado como conseqüente ou causador das variações ponderais.
Tobacco use is the leading preventable cause of death in most countries, including Brazil. Smoking cessation is an important strategy for reducing the morbidity and mortality associated with tobacco-related diseases. An inverse relationship between nicotine use and body weight has been reported, in which body weight tends to be lower among smokers than among nonsmokers. Smoking abstinence results in an increase in body weight for both males and females. On average, sustained quitters gain from 5 to 6 kg, although approximately 10 percent gain more than 10 kg. Pharmacological treatment for smoking cessation attenuates weight gain. The importance of smoking cessation as a contributing cause of the current obesity epidemic has been little studied. In the USA, the rate of obesity attributable to smoking cessation has been estimated at approximately 6.0 and 3.2 percent for males and females, respectively. Although the mechanisms are unclear, there is evidence that dopamine and serotonin are appetite suppressants. The administration of nicotine, regardless of the delivery system, acutely raises the levels of these neurotransmitters in the brain, reducing the need for energy intake and consequently suppressing appetite. In addition, nicotine has a direct effect on adipose tissue metabolism, influencing the rate of weight gain following smoking cessation. Leptin, ghrelin and neuropeptide Y are substances that might constitute factors involved in the inverse relationship between nicotine and body mass index, although their roles as determinants or consequences of this relationship have yet to be determined.
Sujets)
Femelle , Humains , Mâle , Poids , Nicotine/effets indésirables , Arrêter de fumer , Fumer/physiopathologie , Régulation de l'appétit/effets des médicaments et des substances chimiques , Régulation de l'appétit/génétique , Régulation de l'appétit/physiologie , Indice de masse corporelle , Poids/effets des médicaments et des substances chimiques , Poids/génétique , Poids/physiologie , Ghréline/génétique , Ghréline/métabolisme , Faim/effets des médicaments et des substances chimiques , Faim/physiologie , Leptine/génétique , Leptine/métabolisme , Neuropeptide Y/génétique , Neuropeptide Y/métabolisme , Obésité/étiologie , Obésité/prévention et contrôle , Polymorphisme génétique/effets des médicaments et des substances chimiques , Polymorphisme génétique/génétique , Prise de risque , Facteurs sexuels , Fumer/effets indésirables , Fumer/traitement médicamenteux , Prise de poids/effets des médicaments et des substances chimiques , Prise de poids/génétique , Prise de poids/physiologieRésumé
Objective:To investigate whether ghrelin, a novel endogenous ligand of growth hormone secretagogue receptor ( GHS-R) , was expressed in the thyroid tissues of different thyroid diseases, and its implication. Methods:The paraffin-embedded specimens of thyroid tissues from 2000 to 2004 were obtained from 57 patients with different thyroid diseases, including 5 subacute thyroiditis, 8 Hashimoto' s thyroiditis, 7 hyperthyroidism (Graves disease) , 8 nodular goiter, 5 thyroid adenoma, 3 thyroid lympho-ma, 8 papillary carcinoma, 3 follicular carcinoma, 5 medullary carcinoma and 5 undifferentiated carcinoma cases. The specimens of normal peri-adenoma thyroid tissues served as controls. Immunohistochemi-cal staining was used to detect ghrelin expression. Results:(1) ghrelin expression was undetectable in the thyroid tissues of normal control, subacute thyroiditis, Hashimoto' s thyroiditis and Graves disease. (2) ghrelin expression was also undetected in the tissues of nodular goiter, thyroid adenoma and thyroid lymphoma. (3 ) ghrelin-positive staining was found in the tumor cells of different types of thyroid carcin-moma. Five cases were positive within 8 cases in papillary carcinoma, 2 cases were positive within 3 cases in follicular carcinoma, 3 cases were positive within 5 cases in medullary carcinoma, 3 cases were positive within 5 cases in undifferentiated carcinoma. Conclusion:Ghrelin is expressed in malignant epithelial thyroid neoplasmas, but not in autoimmune or inflammatory thyroid diseases and benign nodular thyroid diseases. The results indicate that ghrelin expression may play an important role in the occurrence and development of thyroid carcinoma.
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Objective: To explore the exact role of ghrelin in glyco-and lipo-metabolism.Methods: We compared the levels of ghrelin mRNA in gastric tissue,ghrelin in gastric tissue and plasma among LETO rats(non diabetes,n=10),OLETF rats(type 2 diabetes,n=10),OLETF/M rats(OLETF rats managed with Metformin at the dose of 100 mg/kg weight,n=10) and OLETF/F rats(OLETF rats managed with Fenofibrate at the dose of 20 mg/kg weight,n=10).The levels of ghrelin mRNA were tested by Northern blotting,and the ghrelin content in gastric tissue and plasma detected by RIA.Results: At the age of 30 weeks,the ghrelin fasting plasma levels of OLETF rats were lower than those of LETO rats(37.49?6.42 vs 58.52?5.85,P0.05).However,the fasting blood plasma ghrelin levels of OLETF/F group were more than those that of the untreated OLETF rats(62.02?7.35 vs 37.49?6.42,P