Base de dados : MEDLINE
Pesquisa : D12.644.456.073.070 [Categoria DeCS]
Referências encontradas : 3248 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 325 ir para página                         

  1 / 3248 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29390444
[Au] Autor:Pan YH; Huang YM; Qiao YC; Ling W; Geng LJ; Xiao JL; Zhang XX; Zhao HL
[Ad] Endereço:Center for Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence.
[Ti] Título:Family history and renin-angiotensin system gene polymorphisms in Chinese patients with type 2 diabetes mellitus.
[So] Source:Medicine (Baltimore);96(51):e9148, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A positive family history is recognized as an important risk factor for type 2 diabetes mellitus (T2DM), but the association of family history with rennin-angiotensin system (RAS) gene polymorphisms has not been reported yet, thus we aim to investigate it.Family history records, clinical and biochemical data were obtained from 1239 T2DM patients. Polymerase chain reaction (PCR) was performed for angiotensin-converting enzyme (ACE) genotyping and PCR-restricted fragment length polymorphism was used for angiotensinogen (AGT) genotyping.Patients with a negative family history had higher level of triglyceride and blood pressure, whereas those with a positive family history showed younger onset age and lower body mass index value (All P < .05), these findings were age-dependent. The percentage of hypertension was lower with a higher percentage of overweight among the patients with a positive family history (All P < .05). Patients with a positive family history and those with a negative family history had comparable genotype and allele distribution of ACE gene insertion/deletion polymorphisms and AGT gene M/T polymorphisms.A positive family history of diabetes was not associated with the RAS gene polymorphisms.
[Mh] Termos MeSH primário: Angiotensinogênio/genética
Diabetes Mellitus Tipo 2/epidemiologia
Peptidil Dipeptidase A/genética
Polimorfismo de Fragmento de Restrição
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Grupo com Ancestrais do Continente Asiático
Pressão Sanguínea
Índice de Massa Corporal
China/epidemiologia
Estudos Transversais
Feminino
Frequência do Gene
Genótipo
Seres Humanos
Masculino
Meia-Idade
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Triglycerides); 11002-13-4 (Angiotensinogen); EC 3.4.15.1 (ACE protein, human); EC 3.4.15.1 (Peptidyl-Dipeptidase A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009148


  2 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28903744
[Au] Autor:Simonyte S; Kuciene R; Medzioniene J; Dulskiene V; Lesauskaite V
[Ad] Endereço:Institute of Cardiology of Medical Academy, Lithuanian University of Health Sciences, Sukileliu 15, LT-50161, Kaunas, Lithuania. sandritos@gmail.com.
[Ti] Título:Renin-angiotensin system gene polymorphisms and high blood pressure in Lithuanian children and adolescents.
[So] Source:BMC Med Genet;18(1):100, 2017 Sep 13.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Epidemiological studies have demonstrated the influence of environmental factors on HBP in the population of Lithuanian children, although the role of genetic factors in hypertension has not yet been studied. The aim of this study was to assess the distribution of AGTR1, AGT, and ACE genotypes in the Lithuanian child population and to determine whether these genotypes have an impact on HBP in childhood. METHODS: This cross-sectional study enrolled 709 participants aged 12-15 years. The subjects were genotyped for AGT (M235 T, rs699), AGTR1 (A1166C, rs5186), and ACE (rs4340) gene polymorphisms using real-time and conventional polymerase chain reactions. Blood pressure and anthropometric parameters were measured. RESULTS: The prevalence of HBP was 38.6% and was more frequently detected in boys than in girls (47.9% vs. 29.5%; p < 0.001). No significant differences in the frequencies of the AGT or AGTR1 genotypes or alleles between boys and girls were observed, except for ACE genotypes. The mean SBP value was higher in HBP subjects with ACE ID genotype compared to those with ACE II homozygotes (p = 0.04). No significant differences in BP between different AGT and AGTR1 genotype groups were found. Boys who carried the ACE ID + DD genotypes had higher odds of having HBP than carriers of the ACE II genotype did (controlling for the body mass index (BMI): OR = 1.83; 95% CI, 1.11-3.02, p = 0.024; and controlling for waist circumference (WC): OR = 1.76; 95% CI, 1.07-2.92, p = 0.035). These associations were not significant among girls. The same trend was observed in the multivariate analysis - after adjustment for BMI and WC, only boys with ACE ID genotype and ACE ID + DD genotypes had statistically significantly increased odds of HBP (aOR = 2.05; 95% CI, 1.19-3.53 (p = 0.01) and aOR = 1.82; 95% CI, 1.09-3.04 (p = 0.022), respectively). CONCLUSIONS: The evaluated polymorphisms of the AGT and AGTR1 genes did not contribute to the presence of HBP in the present study and may be seen as predisposing factors, while ACE ID genotypes were associated with significantly increased odds for the development of HBP in the Lithuanian child and adolescent population - especially in boys.
[Mh] Termos MeSH primário: Hipertensão/epidemiologia
Hipertensão/genética
Polimorfismo Genético
Sistema Renina-Angiotensina/genética
[Mh] Termos MeSH secundário: Adolescente
Alelos
Angiotensinogênio/genética
Pressão Sanguínea
Índice de Massa Corporal
Criança
Estudos Transversais
Feminino
Técnicas de Genotipagem
Seres Humanos
Lituânia/epidemiologia
Masculino
Peptidil Dipeptidase A/genética
Receptor Tipo 1 de Angiotensina/genética
Fatores de Risco
Análise de Sequência de DNA
Circunferência da Cintura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGT protein, human); 0 (AGTR1 protein, human); 0 (Receptor, Angiotensin, Type 1); 11002-13-4 (Angiotensinogen); EC 3.4.15.1 (ACE protein, human); EC 3.4.15.1 (Peptidyl-Dipeptidase A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-017-0462-z


  3 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28716988
[Au] Autor:Mullick AE; Yeh ST; Graham MJ; Engelhardt JA; Prakash TP; Crooke RM
[Ad] Endereço:From the Ionis Pharmaceuticals, Inc, Carlsbad, CA. amullick@ionisph.com.
[Ti] Título:Blood Pressure Lowering and Safety Improvements With Liver Angiotensinogen Inhibition in Models of Hypertension and Kidney Injury.
[So] Source:Hypertension;70(3):566-576, 2017 Sep.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uncontrolled hypertension is an important contributor to cardiovascular disease. Despite the armamentarium of antihypertensive treatments, there remains a need for novel agents effective in individuals who cannot reach acceptable blood pressure levels. Inhibitors targeting the renin-angiotensin-aldosterone system (RAAS) are widely used but may not optimally inhibit RAAS and demonstrate an acceptable safety profile. Experiments were conducted to characterize a series of AGT (angiotensinogen) antisense oligonucleotides (ASOs) and compare their efficacy and tolerability to traditional RAAS blockade. AGT ASOs which target multiple systemic sites of AGT versus an N-acetylgalactosamine-conjugated AGT ASO that targets the liver were compared with captopril and losartan. Spontaneously hypertensive rats fed an 8% NaCl diet, a model of malignant hypertension resistant to standard RAAS inhibitors, demonstrated robust and durable blood pressure reductions with AGT ASO treatments, which was not observed with standard RAAS blockade. Studies in rat models of acute kidney injury produced by salt deprivation revealed kidney injury with ASO treatment that reduced kidney-expressed AGT, but not in animals treated with the N-acetylgalactosamine AGT ASO despite comparable plasma AGT reductions. Administration of either captopril or losartan also produced acute kidney injury during salt deprivation. Thus, intrarenal RAAS derived from kidney AGT, and inhibited by the standard of care, contributes to the maintenance of renal function during severe RAAS challenge. Such improvements in efficacy and tolerability by a liver-selective AGT inhibitor could be desirable in individuals not at their blood pressure goal with existing RAAS blockade.
[Mh] Termos MeSH primário: Lesão Renal Aguda
Angiotensinogênio/metabolismo
Hipertensão
Oligonucleotídeos Antissenso
Sistema Renina-Angiotensina
[Mh] Termos MeSH secundário: Lesão Renal Aguda/etiologia
Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/fisiopatologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Modelos Animais de Doenças
Resistência a Medicamentos/fisiologia
Hipertensão/tratamento farmacológico
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Rim/metabolismo
Rim/fisiopatologia
Oligonucleotídeos Antissenso/metabolismo
Oligonucleotídeos Antissenso/farmacologia
Ratos
Ratos Endogâmicos SHR
Sistema Renina-Angiotensina/efeitos dos fármacos
Sistema Renina-Angiotensina/fisiologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Antihypertensive Agents); 0 (Oligonucleotides, Antisense); 11002-13-4 (Angiotensinogen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09755


  4 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28490451
[Au] Autor:Agassandian K; Grobe JL; Liu X; Agassandian M; Thompson AP; Sigmund CD; Cassell MD
[Ad] Endereço:Department of Anatomy and Cell Biology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa.
[Ti] Título:Evidence for intraventricular secretion of angiotensinogen and angiotensin by the subfornical organ using transgenic mice.
[So] Source:Am J Physiol Regul Integr Comp Physiol;312(6):R973-R981, 2017 Jun 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Direct intracerebroventricular injection of angiotensin II (ANG II) causes increases in blood pressure and salt and water intake, presumably mimicking an effect mediated by an endogenous mechanism. The subfornical organ (SFO) is a potential source of cerebrospinal fluid (CSF), ANG I, and ANG II, and thus we hypothesized that the SFO has a secretory function. Endogenous levels of angiotensinogen (AGT) and renin are very low in the brain. We therefore examined the immunohistochemical localization of angiotensin peptides and AGT in the SFO, and AGT in the CSF in two transgenic models that overexpress either human AGT (A mice), or both human AGT (hAGT) and human renin (SRA mice) in the brain. Measurements were made at baseline and following volumetric depletion of CSF. Ultrastructural analysis with immunoelectron microscopy revealed that superficially located ANG I/ANG II and AGT immunoreactive cells in the SFO were vacuolated and opened directly into the ventricle. Withdrawal of CSF produced an increase in AGT in the CSF that was accompanied by a large decline in AGT immunoreactivity within SFO cells. Our data provide support for the hypothesis that the SFO is a secretory organ that releases AGT and possibly ANG I/ANG II into the ventricle at least under conditions when genes that control the renin-angiotensin system are overexpressed in mice.
[Mh] Termos MeSH primário: Angiotensina II/metabolismo
Angiotensina I/metabolismo
Angiotensinogênio/metabolismo
Ventrículos Cerebrais/metabolismo
Sistema Renina-Angiotensina
Órgão Subfornical/metabolismo
[Mh] Termos MeSH secundário: Angiotensina I/líquido cefalorraquidiano
Angiotensina I/secreção
Angiotensina II/líquido cefalorraquidiano
Angiotensina II/secreção
Angiotensinogênio/líquido cefalorraquidiano
Angiotensinogênio/genética
Animais
Ventrículos Cerebrais/secreção
Ventrículos Cerebrais/ultraestrutura
Genótipo
Seres Humanos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Renina/genética
Renina/metabolismo
Sistema Renina-Angiotensina/genética
Órgão Subfornical/secreção
Órgão Subfornical/ultraestrutura
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGT protein, human); 11002-13-4 (Angiotensinogen); 11128-99-7 (Angiotensin II); 9041-90-1 (Angiotensin I); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00511.2016


  5 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28396529
[Au] Autor:van Thiel BS; Góes Martini A; Te Riet L; Severs D; Uijl E; Garrelds IM; Leijten FPJ; van der Pluijm I; Essers J; Qadri F; Alenina N; Bader M; Paulis L; Rajkovicova R; Domenig O; Poglitsch M; Danser AHJ
[Ad] Endereço:From the Division of Vascular Medicine and Pharmacology, Department of Internal Medicine (B.S.v.T., A.G.M., L.t.R., D.S., E.U., I.M.G., F.P.J.L., A.H.J.D.), Department of Vascular Surgery (B.S.v.T., L.t.R., I.v.d.P., J.E.), Department of Molecular Genetics, Cancer Genomics Center Netherlands (B.S.v.
[Ti] Título:Brain Renin-Angiotensin System: Does It Exist?
[So] Source:Hypertension;69(6):1136-1144, 2017 Jun.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Because of the presence of the blood-brain barrier, brain renin-angiotensin system activity should depend on local (pro)renin synthesis. Indeed, an intracellular form of renin has been described in the brain, but whether it displays angiotensin (Ang) I-generating activity (AGA) is unknown. Here, we quantified brain (pro)renin, before and after buffer perfusion of the brain, in wild-type mice, renin knockout mice, deoxycorticosterone acetate salt-treated mice, and Ang II-infused mice. Brain regions were homogenized and incubated with excess angiotensinogen to detect AGA, before and after prorenin activation, using a renin inhibitor to correct for nonrenin-mediated AGA. Renin-dependent AGA was readily detectable in brain regions, the highest AGA being present in brain stem (>thalamus=cerebellum=striatum=midbrain>hippocampus=cortex). Brain AGA increased marginally after prorenin activation, suggesting that brain prorenin is low. Buffer perfusion reduced AGA in all brain areas by >60%. Plasma renin (per mL) was 40× to 800× higher than brain renin (per gram). Renin was undetectable in plasma and brain of renin knockout mice. Deoxycorticosterone acetate salt and Ang II suppressed plasma renin and brain renin in parallel, without upregulating brain prorenin. Finally, Ang I was undetectable in brains of spontaneously hypertensive rats, while their brain/plasma Ang II concentration ratio decreased by 80% after Ang II type 1 receptor blockade. In conclusion, brain renin levels (per gram) correspond with the amount of renin present in 1 to 20 µL of plasma. Brain renin disappears after buffer perfusion and varies in association with plasma renin. This indicates that brain renin represents trapped plasma renin. Brain Ang II represents Ang II taken up from blood rather than locally synthesized Ang II.
[Mh] Termos MeSH primário: Amidas/farmacologia
Angiotensina II/farmacologia
Barreira Hematoencefálica/efeitos dos fármacos
Encéfalo/metabolismo
Fumaratos/farmacologia
Hipertensão/tratamento farmacológico
Sistema Renina-Angiotensina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Angiotensinogênio/metabolismo
Animais
Pressão Sanguínea/efeitos dos fármacos
Barreira Hematoencefálica/metabolismo
Encéfalo/efeitos dos fármacos
Acetato de Desoxicorticosterona/farmacologia
Modelos Animais de Doenças
Camundongos
Camundongos Knockout
Distribuição Aleatória
Ratos
Ratos Endogâmicos SHR
Valores de Referência
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Fumarates); 11002-13-4 (Angiotensinogen); 11128-99-7 (Angiotensin II); 502FWN4Q32 (aliskiren); 6E0A168OB8 (Desoxycorticosterone Acetate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.116.08922


  6 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28378551
[Au] Autor:Lee MJ; Kim SS; Kim IJ; Song SH; Kim EH; Seo JY; Kim JH; Kim S; Jeon YK; Kim BH; Kim YK
[Ad] Endereço:Department of Internal Medicine, Pusan National University Hospital, Busan, Korea.
[Ti] Título:Changes in Urinary Angiotensinogen Associated with Deterioration of Kidney Function in Patients with Type 2 Diabetes Mellitus.
[So] Source:J Korean Med Sci;32(5):782-788, 2017 May.
[Is] ISSN:1598-6357
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Urinary angiotensinogen (AGT) is potentially a specific biomarker for the status of the intrarenal renin-angiotensin system (RAS) in patients with diabetes mellitus. We explored whether changes in urinary AGT excretion levels were associated with the deterioration of kidney function in type 2 diabetes patients with preserved kidney function. Urinary baseline AGT levels were measured in 118 type 2 diabetic patients who were not taking RAS blockers and who had estimated glomerular filtration rates (eGFRs) ≥ 60 mL/min/1.73 m². A total of 91 patients were followed-up for 52 months. Changes in urinary levels of AGT (ΔAGT) were calculated by subtracting urinary AGT/creatinine (Cr) at baseline from urinary AGT/Cr after 1 year. ΔAGT was significantly inversely correlated with annual eGFR change (ß = -0.29, P = 0.006; ß = -0.37, P = 0.001 after adjusting for clinical factors). RAS blockers were prescribed in 36.3% of patients (n = 33) during follow-up. The ΔAGT values were lower in the RAS blockers users than in the non-RAS blockers users, but the differences were not statistically significant (7.37 ± 75.88 vs. 22.55 ± 57.45 µg/g Cr, P = 0.081). The ΔAGT values remained significantly correlated with the annual rate of eGFR change (ß = -0.41, P = 0.001) in the patients who did not use RAS blockers, but no such correlation was evident in the patients who did. ΔAGT is inversely correlated with annual changes in eGFR in type 2 diabetes patients with preserved kidney function, particularly in RAS blocker-naïve patients.
[Mh] Termos MeSH primário: Angiotensinogênio/urina
Diabetes Mellitus Tipo 2/diagnóstico
Insuficiência Renal Crônica/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Albuminúria/complicações
Albuminúria/patologia
Antagonistas de Receptores de Angiotensina/farmacologia
Antagonistas de Receptores de Angiotensina/uso terapêutico
Creatinina/urina
Diabetes Mellitus Tipo 2/complicações
Ensaio de Imunoadsorção Enzimática
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Masculino
Meia-Idade
Insuficiência Renal Crônica/complicações
Insuficiência Renal Crônica/tratamento farmacológico
Insuficiência Renal Crônica/fisiopatologia
Sistema Renina-Angiotensina/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 11002-13-4 (Angiotensinogen); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.3346/jkms.2017.32.5.782


  7 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28367083
[Au] Autor:Lin CH; Liao CC; Huang CH; Tung YT; Chang HC; Hsu MC; Huang CC
[Ad] Endereço:Physical Education Office, Yuan Ze University, Taoyuan 32003, Taiwan.
[Ti] Título:Proteomics Analysis to Identify and Characterize the Biomarkers and Physical Activities of Non-Frail and Frail Older Adults.
[So] Source:Int J Med Sci;14(3):231-239, 2017.
[Is] ISSN:1449-1907
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Globally, the proportion of older adults is increasing. Older people face chronic conditions such as sarcopenia and functional decline, which are often associated with disability and frailty. Proteomics assay of potential serum biomarkers of frailty in older adults. Older adults were divided into non-frail and frail groups ( = 6 each; 3 males in each group) in accordance with the Chinese-Canadian Study of Health and Aging Clinical Frailty Scale. Adults were measured for grip power and the 6-min walk test for physical activity, and venous blood was sampled after adults fasted for 8 h. Ultra-high-performance liquid chromatography-tandem mass spectrometry was used for proteomics assay. The groups were compared for levels of biomarkers by test and Pearson correlation analysis. Non-frail and frail subjects had mean age 77.5±0.4 and 77.7±1.6 years, mean height 160.5±1.3 and 156.6±2.9 cm and mean weight 62.5±1.2 and 62.8±2.9 kg, respectively. Physical activity level was lower for frail than non-frail subjects (grip power: 13.8±0.4 26.1±1.2 kg; 6-min walk test: 215.2±17.2 438.3±17.2 m). Among 226 proteins detected, for 31, serum levels were significantly higher for frail than non-frail subjects; serum levels of Ig kappa chain V-III region WOL, COX7A2, and albumin were lower. The serum levels of ANGT, KG and AT were 2.05-, 1.76- and 2.22-fold lower (all < 0.05; Figure 1A, 2A and 3A) for non-frail than frail subjects and were highly correlated with grip power (Figure 1B, 2B and 3B). Our study found that ANGT, KG and AT levels are known to increase with aging, so degenerated vascular function might be associated with frailty. In total, 226 proteins were revealed proteomics assay; levels of angiotensinogen (ANGT), kininogen-1 (KG) and antithrombin III (AT) were higher in frail than non-frail subjects (11.26±2.21 5.09±0.74; 18.42±1.36 11.64±1.36; 22.23±1.64 9.52±0.95, respectively, < 0.05). These 3 factors were highly correlated with grip power ( < 0.05), with higher correlations between grip power and serum levels of ANGT (r = -0.89), KG (r = -0.90), and AT (r = -0.84). In conclusion, this is the first study to demonstrate a serum proteomic profile characteristic of frailty in older adults. Serum ANGT, KG and AT levels could be potential biomarkers for monitoring the development and progression of frailty in older adults.
[Mh] Termos MeSH primário: Envelhecimento/sangue
Biomarcadores/sangue
Idoso Fragilizado
Proteômica
Sarcopenia/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Envelhecimento/patologia
Angiotensinogênio/sangue
Antitrombina III/metabolismo
Exercício
Feminino
Força da Mão/fisiologia
Seres Humanos
Cininogênios/sangue
Masculino
Sarcopenia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Kininogens); 11002-13-4 (Angiotensinogen); 9000-94-6 (Antithrombin III)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.7150/ijms.17627


  8 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28356296
[Au] Autor:Massmann GA; Zhang J; Seong WJ; Kim M; Figueroa JP
[Ad] Endereço:Perinatal Research Laboratory, Department of Obstetrics and Gynecology, Center for Research in Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
[Ti] Título:Sex-dependent effects of antenatal glucocorticoids on insulin sensitivity in adult sheep: role of the adipose tissue renin angiotensin system.
[So] Source:Am J Physiol Regul Integr Comp Physiol;312(6):R1029-R1038, 2017 Jun 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exposure to glucocorticoids in utero is associated with changes in organ function and structure in the adult. The aims of this study were to characterize the effects of antenatal exposure to glucocorticoids on glucose handling and the role of adipose tissue. Pregnant sheep received betamethasone (Beta, 0.17 mg/kg) or vehicle 24 h apart at 80 days of gestation and allowed to deliver at term. At 9 mo, male and female offspring were fed at either 100% of nutritional allowance (lean) or ad libitum for 3 mo (obese). At 1 yr, they were chronically instrumented under general anesthesia. Glucose tolerance was evaluated using a bolus of glucose (0.25 g/kg). Adipose tissue was harvested after death to determine mRNA expression levels of angiotensinogen (AGT), angiotensin-converting enzyme (ACE) 1, ACE2, and peroxisome proliferator-activated receptor γ (PPAR-γ). Data are expressed as means ± SE and analyzed by ANOVA. Sex, obesity, and Beta exposure had significant effects on glucose tolerance and mRNA expression. Beta impaired glucose tolerance in lean females but not males. Superimposed obesity worsened the impairment in females and unmasked the defect in males. Beta increased ACE1 mRNA in females and males and AGT in females only ( < 0.05 by three-way ANOVA). Obesity increased AGT in females but had no effect on ACE1 in either males or females. PPAR-γ mRNA exhibited a significant sex ( = 42.8; < 0.01) and obesity ( = 6.9; < 0.05) effect and was significantly higher in males ( < 0.01 by three-way ANOVA). We conclude that adipose tissue may play an important role in the sexually dimorphic response to antenatal glucocorticoids.
[Mh] Termos MeSH primário: Tecido Adiposo/efeitos dos fármacos
Betametasona/análogos & derivados
Glicemia/efeitos dos fármacos
Glucocorticoides/administração & dosagem
Resistência à Insulina
Insulina/sangue
Sistema Renina-Angiotensina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Tecido Adiposo/fisiopatologia
Fatores Etários
Angiotensinogênio/genética
Angiotensinogênio/metabolismo
Animais
Betametasona/administração & dosagem
Biomarcadores/sangue
Glicemia/metabolismo
Feminino
Regulação da Expressão Gênica
Idade Gestacional
Masculino
Obesidade/sangue
Obesidade/genética
Obesidade/fisiopatologia
PPAR gama/genética
PPAR gama/metabolismo
Peptidil Dipeptidase A/genética
Peptidil Dipeptidase A/metabolismo
Gravidez
Efeitos Tardios da Exposição Pré-Natal
RNA Mensageiro/metabolismo
Sistema Renina-Angiotensina/genética
Carneiro Doméstico
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Glucocorticoids); 0 (Insulin); 0 (PPAR gamma); 0 (RNA, Messenger); 11002-13-4 (Angiotensinogen); 52081-45-5 (betamethasone acetate phosphate); 9842X06Q6M (Betamethasone); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00181.2016


  9 / 3248 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28324005
[Au] Autor:Ghosh A; Abdo S; Zhao S; Wu CH; Shi Y; Lo CS; Chenier I; Alquier T; Filep JG; Ingelfinger JR; Zhang SL; Chan JSD
[Ad] Endereço:Department of Medicine, Université de Montréal and Centre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
[Ti] Título:Insulin Inhibits Nrf2 Gene Expression via Heterogeneous Nuclear Ribonucleoprotein F/K in Diabetic Mice.
[So] Source:Endocrinology;158(4):903-919, 2017 04 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress induces endogenous antioxidants via nuclear factor erythroid 2-related factor 2 (Nrf2), potentially preventing tissue injury. We investigated whether insulin affects renal Nrf2 expression in type 1 diabetes (T1D) and studied its underlying mechanism. Insulin normalized hyperglycemia, hypertension, oxidative stress, and renal injury; inhibited renal Nrf2 and angiotensinogen (Agt) gene expression; and upregulated heterogeneous nuclear ribonucleoprotein F and K (hnRNP F and hnRNP K) expression in Akita mice with T1D. In immortalized rat renal proximal tubular cells, insulin suppressed Nrf2 and Agt but stimulated hnRNP F and hnRNP K gene transcription in high glucose via p44/42 mitogen-activated protein kinase signaling. Transfection with small interfering RNAs of p44/42 MAPK, hnRNP F, or hnRNP K blocked insulin inhibition of Nrf2 gene transcription. Insulin curbed Nrf2 promoter activity via a specific DNA-responsive element that binds hnRNP F/K, and hnRNP F/K overexpression curtailed Nrf2 promoter activity. In hyperinsulinemic-euglycemic mice, renal Nrf2 and Agt expression was downregulated, whereas hnRNP F/K expression was upregulated. Thus, the beneficial actions of insulin in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 and Agt gene transcription and preventing Nrf2 stimulation of Agt expression via hnRNP F/K. These findings identify hnRNP F/K and Nrf2 as potential therapeutic targets in diabetes.
[Mh] Termos MeSH primário: Angiotensinogênio/genética
Diabetes Mellitus Tipo 1/genética
Ribonucleoproteínas Nucleares Heterogêneas Grupo F-H/genética
Ribonucleoproteínas Nucleares Heterogêneas Grupo K/genética
Insulina/farmacologia
Fator 2 Relacionado a NF-E2/genética
Transcrição Genética/efeitos dos fármacos
[Mh] Termos MeSH secundário: Angiotensinogênio/metabolismo
Animais
Diabetes Mellitus Tipo 1/tratamento farmacológico
Diabetes Mellitus Tipo 1/metabolismo
Nefropatias Diabéticas/tratamento farmacológico
Nefropatias Diabéticas/genética
Nefropatias Diabéticas/metabolismo
Expressão Gênica/efeitos dos fármacos
Ribonucleoproteínas Nucleares Heterogêneas Grupo F-H/metabolismo
Ribonucleoproteínas Nucleares Heterogêneas Grupo K/metabolismo
Insulina/uso terapêutico
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Camundongos Transgênicos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Regiões Promotoras Genéticas/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heterogeneous-Nuclear Ribonucleoprotein Group F-H); 0 (Heterogeneous-Nuclear Ribonucleoprotein K); 0 (Insulin); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 11002-13-4 (Angiotensinogen); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1576


  10 / 3248 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28283551
[Au] Autor:Sharma NM; Nandi SS; Zheng H; Mishra PK; Patel KP
[Ad] Endereço:Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and nsharma@unmc.edu.
[Ti] Título:A novel role for miR-133a in centrally mediated activation of the renin-angiotensin system in congestive heart failure.
[So] Source:Am J Physiol Heart Circ Physiol;312(5):H968-H979, 2017 May 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An activated renin-angiotensin system (RAS) within the central nervous system has been implicated in sympathoexcitation during various disease conditions including congestive heart failure (CHF). In particular, activation of the RAS in the paraventricular nucleus (PVN) of the hypothalamus has been recognized to augment sympathoexcitation in CHF. We observed a 2.6-fold increase in angiotensinogen (AGT) in the PVN of CHF. To elucidate the molecular mechanism for increased expression of AGT, we performed in silico analysis of the 3'-untranslated region (3'-UTR) of AGT and found a potential binding site for microRNA (miR)-133a. We hypothesized that decreased miR-133a might contribute to increased AGT in the PVN of CHF rats. Overexpression of miR-133a in NG108 cells resulted in 1.4- and 1.5-fold decreases in AGT and angiotensin type II (ANG II) type 1 receptor (AT R) mRNA levels, respectively. A luciferase reporter assay performed on NG108 cells confirmed miR-133a binding to the 3'-UTR of AGT. Consistent with these in vitro data, we observed a 1.9-fold decrease in miR-133a expression with a concomitant increase in AGT and AT R expression within the PVN of CHF rats. Furthermore, restoring the levels of miR-133a within the PVN of CHF rats with viral transduction resulted in a significant reduction of AGT (1.4-fold) and AT R (1.5-fold) levels with a concomitant decrease in basal renal sympathetic nerve activity (RSNA). Restoration of miR-133a also abrogated the enhanced RSNA responses to microinjected ANG II within the PVN of CHF rats. These results reveal a novel and potentially unique role for miR-133a in the regulation of ANG II within the PVN of CHF rats, which may potentially contribute to the commonly observed sympathoexcitation in CHF. Angiotensinogen (AGT) expression is upregulated in the paraventricular nucleus of the hypothalamus through posttranscriptional mechanism interceded by microRNA-133a in heart failure. Understanding the mechanism of increased expression of AGT in pathological conditions leading to increased sympathoexcitation may provide the basis for the possible development of new therapeutic agents with enhanced specificity.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/genética
MicroRNAs/genética
Sistema Renina-Angiotensina/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico
Angiotensinogênio/metabolismo
Animais
Linhagem Celular Tumoral
Insuficiência Cardíaca/fisiopatologia
Rim/inervação
Losartan/uso terapêutico
Masculino
MicroRNAs/biossíntese
Núcleo Hipotalâmico Paraventricular/fisiopatologia
Ratos
Ratos Sprague-Dawley
Receptor Tipo 1 de Angiotensina/biossíntese
Receptor Tipo 1 de Angiotensina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (MIRN133 microRNA, rat); 0 (MicroRNAs); 0 (Receptor, Angiotensin, Type 1); 11002-13-4 (Angiotensinogen); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00721.2016



página 1 de 325 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde