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学者姓名:袁祖贻

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Association of Blood Pressure Trajectories in Early Life with Subclinical Renal Damage in Middle Age SCIE
期刊论文 | 2018 , 29 (12) , 2835-2846 | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
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Background Although high BP is one of the most important factors affecting renal function, whether longitudinal BP trajectories in early life course are associated with renal function damage in later life is unclear. Methods To investigate the correlation between BP trajectories from childhood to adulthood and renal function in middle age, we used group-based trajectory models to identify BP trajectories in 2430 individuals (aged 6-15 years old at baseline) participating in the ongoing Hanzhong Adolescent Hypertension Cohort. We tested the association between these trajectories and subclinical renal damage in middle age, adjusting for several covariates. Results We identified four distinct systolic BP trajectories among 2430 subjects: low stable, moderate stable, high stable, and moderate increasing on the basis of systolic BP levels at baseline and during the 30-year follow-up period. The urinary albumin-to-creatinine ratio (uACR) was higher in moderate stable, high stable, and moderate increasing groups compared with the low stable group. A total of 228 individuals had subclinical renal disease by 2017. Compared with the low stable trajectory group, the other groups had increasingly greater odds of experiencing subclinical renal disease in middle age. These associations were not altered after adjustment for other covariates, except for in the moderate stable group. Analyzed results were similar for the mean arterial pressure and diastolic BP trajectory groups. Conclusions Higher BP trajectories were correlated with higher of uACR levels and risk of subclinical renal disease in middle age. Identifying long-term BP trajectories from early age may assist in predicting individuals' renal function in later life.

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GB/T 7714 Zheng, Wenling , Mu, Jianjun , Chu, Chao et al. Association of Blood Pressure Trajectories in Early Life with Subclinical Renal Damage in Middle Age [J]. | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY , 2018 , 29 (12) : 2835-2846 .
MLA Zheng, Wenling et al. "Association of Blood Pressure Trajectories in Early Life with Subclinical Renal Damage in Middle Age" . | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 29 . 12 (2018) : 2835-2846 .
APA Zheng, Wenling , Mu, Jianjun , Chu, Chao , Hu, Jiawen , Yan, Yu , Ma, Qiong et al. Association of Blood Pressure Trajectories in Early Life with Subclinical Renal Damage in Middle Age . | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY , 2018 , 29 (12) , 2835-2846 .
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Combination of the CYP2C19 metabolizer and the GRACE risk score better predicts the long-term major adverse cardiac events in acute coronary syndrome undergoing percutaneous coronary intervention SCIE PubMed Scopus
期刊论文 | 2018 , 170 , 142-147 | THROMBOSIS RESEARCH
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Introduction: Both Global Registry of Acute Coronary Events (GRACE) risk score and CYP2C19 metabolizer status can independently predict major adverse cardiac events (MACEs) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). We investigated whether their combination could better predict MACE occurrence in patients with ACS undergoing PCI. Materials and methods: This retrospective cohort study included 548 consecutive patients with ACS undergoing PCI. A cumulative MACE curve was calculated using the Kaplan-Meier method. Multivariate Cox regression was used to identify MACE predictors. The predictive value of GRACE risk score alone and CYP2C19 metabolizer status was estimated by the area under the receiver operating characteristic curve (AUC), net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Results: In a median of 28.58 months, 17 patients (3%) were lost to follow-up, and 62 (11.3%) experienced MACEs. Multivariate Cox regression analysis showed that both GRACE score and CYP2C19 metabolizer status were independent MACE predictors (hazard ratio 1.019, 95% CI 1.011-1.027, p < 0.001; hazard ratio 2.383, 95% CI 1.601-3.547, p < 0.001, respectively). Kaplan-Meier analysis showed that CYP2C19 PM increased the MACE risk (log rank test= 10.848, p= 0.004). The GRACE score adjustment by CYP2C19 metabolizer status enhanced the predictive value (AUC increased from 0.682 for GRACE score alone to 0.731 for GRACE score plus CYP2C19 metabolizer). This result was further verified by IDI and NRI. Conclusions: CYP2C19 metabolizer status and GRACE score are readily available predictive approaches for MACEs, and their combination derives a more accurate long-term MACE prediction in clopidogrel-treated patients with ACS undergoing PCI.

Keyword :

Prognosis Risk factor GRACE score CYP2C19 metabolizer Acute coronary syndrome

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GB/T 7714 Bai, Xiao-Fang , Zhang, Ya-Ping , Zhou, Juan et al. Combination of the CYP2C19 metabolizer and the GRACE risk score better predicts the long-term major adverse cardiac events in acute coronary syndrome undergoing percutaneous coronary intervention [J]. | THROMBOSIS RESEARCH , 2018 , 170 : 142-147 .
MLA Bai, Xiao-Fang et al. "Combination of the CYP2C19 metabolizer and the GRACE risk score better predicts the long-term major adverse cardiac events in acute coronary syndrome undergoing percutaneous coronary intervention" . | THROMBOSIS RESEARCH 170 (2018) : 142-147 .
APA Bai, Xiao-Fang , Zhang, Ya-Ping , Zhou, Juan , Wu, Yue , Li, Rui-Feng , Sun, Li-Zhe et al. Combination of the CYP2C19 metabolizer and the GRACE risk score better predicts the long-term major adverse cardiac events in acute coronary syndrome undergoing percutaneous coronary intervention . | THROMBOSIS RESEARCH , 2018 , 170 , 142-147 .
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Prognostic significance and dynamic change of plasma macrophage migration inhibitory factor in patients with acute ST-elevation myocardial infarction Scopus SCIE
期刊论文 | 2018 , 97 (43) | Medicine
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Macrophage migration inhibitory factor (MIF) has been reported as an inflammatory cytokine in many inflammatory diseases, including rheumatoid arthritis and ischemic diseases. However, dynamic changes of MIF within the first 24 hours on admission and potential prognostic significance following ST-elevation myocardial infarction (STEMI) have been little known. In this study, we examined the dynamic change of MIF level and its potential diagnostic and prognostic value after the onset of STEMI. Plasma MIF levels were evaluated in symptomatic subjects who received coronary angiogram with a median 27 months follow-up for the development of major adverse cardiovascular events (MACEs).Of all 993 subjects, patients with STEMI showed a significantly higher MIF levels than in patients with non-ST elevation acute coronary syndrome, stable angina, and normal coronary artery, respectively (P < .01). Plasma MIF levels elevated as early as 12 hours post-onset of STEMI and peaked rapidly within 24 hours, and remained elevated from about day 5 till day 9 during hospitalization. In multivariate analysis, MIF was associated with a decreased risk of MACEs occurrence in STEMI patients after adjustment for traditional cardiovascular risk factors [hazard ratio 0.81, (0.72-0.90), P < .001]. The ROC curve for MACEs was 0.72 (95% CI 0.62-0.80, P < .001) and 0.85 (95% CI 0.80-0.90, P < .001) using Framingham risk factors only and combined with MIF, individually.Measurement of MIF adds potential information for the early diagnosis of acute STEMI and significantly improves risk prediction of MACEs when added to a prognostic model with traditional Framingham risk factors.

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GB/T 7714 Deng, Fuxue , Zhao, Qiang , Deng, Yangyang et al. Prognostic significance and dynamic change of plasma macrophage migration inhibitory factor in patients with acute ST-elevation myocardial infarction [J]. | Medicine , 2018 , 97 (43) .
MLA Deng, Fuxue et al. "Prognostic significance and dynamic change of plasma macrophage migration inhibitory factor in patients with acute ST-elevation myocardial infarction" . | Medicine 97 . 43 (2018) .
APA Deng, Fuxue , Zhao, Qiang , Deng, Yangyang , Wu, Yue , Zhou, Dong , Liu, Weimin et al. Prognostic significance and dynamic change of plasma macrophage migration inhibitory factor in patients with acute ST-elevation myocardial infarction . | Medicine , 2018 , 97 (43) .
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Short-Term High-Salt Diet Increases Corin Level to Regulate the Salt-Water Balance in Humans and Rodents SCIE PubMed Scopus
期刊论文 | 2018 , 31 (2) , 253-260 | AMERICAN JOURNAL OF HYPERTENSION
WoS CC Cited Count: 2
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BACKGROUND Dietary sodium and potassium affect the fluctuation in blood pressure (BP) and renal function. Corin, with its enzymatic activity to convert proatrial natriuretic peptide (pro-ANP) to biologically active ANP, regulates BP, cardiac, and renal functions. We investigated whether corin expression responds to a high-salt (HS) diet to regulate salt and water balance. METHODS Forty-two volunteers followed 3 sequential diets for 7 days each: a low-salt (LS) diet (3.0 g/day NaCl), a HS diet (18.0 g/day NaCl), followed by an HS diet with K+ supplementation (HS + K+) (18.0 g/day NaCl and 4.5 g/day KCl). RESULTS Corin level was higher with the HS diet than the LS and HS + K+ diets and was positively correlated with systolic BP (SBP) and 24-hour urinary Na+ and microalbumin (U-mALB) excretion. In rodents, serum and renal levels of corin were transiently increased with the HS diet and were decreased if the HS diet was continued for up to 7 days. HS loading increased SBP, 24-hour urinary Na+, U-mALB excretion, and the expression of proprotein convertase subtilisin/kexin-6 (PCSK6), a corin activator. Knockdown of PCSK6 or corin in high salt-treated M1-cortical collecting duct (M1-CCD) cells increased the expression of aquaporin 2 (AQP2) and beta-epithelial Na+ channel (beta-ENaC). CONCLUSIONS Short-term HS may induce the PCSK6-corin-ANP-AQP2/beta-ENaC pathway in the kidney. Enhanced serum corin level in humans and rodents is positively correlated with HS-induced SBP and 24-hour urinary Na+ and U-mALB excretion, which suggests that corin is involved in the saltwater balance in response to HS intake.

Keyword :

blood pressure potassium PCSK6 corin hypertension high-salt diet

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GB/T 7714 Zhang, Jiao , Yin, Yanjun , Chen, Lili et al. Short-Term High-Salt Diet Increases Corin Level to Regulate the Salt-Water Balance in Humans and Rodents [J]. | AMERICAN JOURNAL OF HYPERTENSION , 2018 , 31 (2) : 253-260 .
MLA Zhang, Jiao et al. "Short-Term High-Salt Diet Increases Corin Level to Regulate the Salt-Water Balance in Humans and Rodents" . | AMERICAN JOURNAL OF HYPERTENSION 31 . 2 (2018) : 253-260 .
APA Zhang, Jiao , Yin, Yanjun , Chen, Lili , Chu, Chao , Wang, Yang , Lv, Yongbo et al. Short-Term High-Salt Diet Increases Corin Level to Regulate the Salt-Water Balance in Humans and Rodents . | AMERICAN JOURNAL OF HYPERTENSION , 2018 , 31 (2) , 253-260 .
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Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians SCIE PubMed Scopus
期刊论文 | 2018 , 119 (2) , 228-237 | BRITISH JOURNAL OF NUTRITION
WoS CC Cited Count: 2 SCOPUS Cited Count: 3
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Salt, promoting oxidative stress, contributes to insulin resistance, whereas K, inhibiting oxidative stress, improves insulin sensitivity. Oxidative stress activation of NLRP3 inflammasome is a central player in the induction of insulin resistance. Therefore, we hypothesised that NLRP3 inflammasome may mediate the effects of salt and K on insulin resistance. In all, fifty normotensive subjects were recruited from a rural community of Northern China. The protocol included a low-salt diet for 7 d, then a high-salt diet for 7 d and a high-salt diet with K supplementation for another 7 d. In addition, THP-1 cells were cultured in different levels of Na with and without K. The results showed that salt loading elevated fasting blood glucose, insulin and C-peptide levels, as well as insulin resistance, whereas K supplementation reversed them. Meanwhile, additional K reversed the active effects of high salt on NLRP3 inflammasome in both the subjects and THP-1 cells, and the change of insulin resistance index notably related with the alteration of plasma IL-1 beta, the index of NLRP3 inflammasome activation, during intervention in the subjects. Additional K ameliorated oxidative stress induced by high salt in both the subjects and cultured THP-1 cells, and the change of oxidative stress related with the alteration of plasma IL-1 beta during intervention in the subjects. In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.

Keyword :

NLRP3 inflammasome Oxidative stress Insulin resistance Potassium Sodium

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GB/T 7714 Wan, Zhaofei , Wen, Wen , Ren, Keyu et al. Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians [J]. | BRITISH JOURNAL OF NUTRITION , 2018 , 119 (2) : 228-237 .
MLA Wan, Zhaofei et al. "Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians" . | BRITISH JOURNAL OF NUTRITION 119 . 2 (2018) : 228-237 .
APA Wan, Zhaofei , Wen, Wen , Ren, Keyu , Zhou, Dong , Liu, Junhui , Wu, Yue et al. Involvement of NLRP3 inflammasome in the impacts of sodium and potassium on insulin resistance in normotensive Asians . | BRITISH JOURNAL OF NUTRITION , 2018 , 119 (2) , 228-237 .
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AMP-activated Protein Kinase Phosphorylation of Angiotensin-Converting Enzyme 2 in Endothelium Mitigates Pulmonary Hypertension SCIE PubMed Scopus
期刊论文 | 2018 , 198 (4) , 509-520 | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
WoS CC Cited Count: 1 SCOPUS Cited Count: 2
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Rationale: Endothelial dysfunction plays an integral role in pulmonary hypertension (PH). AMPK (AMP-activated protein kinase) and ACE2 (angiotensin-converting enzyme 2) are crucial in endothelial homeostasis. The mechanism by which AMPK regulates ACE2 in the pulmonary endothelium and its protective role in PH remain elusive. Objectives: We investigated the role of AMPK phosphorylation of ACE2 Ser680 in ACE2 stability and deciphered the functional consequences of this post-translational modification of ACE2 in endothelial homeostasis and PH. Methods: Bioinformatics prediction, kinase assay, and antibody against phospho-ACE2 Ser680 (p-ACE2 S680) were used to investigate AMPK phosphorylation of ACE2 Ser680 in endothelial cells. Using CRISPR-Cas9 genomic editing, we created gain-of-function ACE2 S680D knock-in and loss-of-function ACE2 knockout (ACE22/2) mouse lines to address the involvement of p-ACE2 S680 and ACE2 in PH. The AMPK-p-ACE2 S680 axis was also validated in lung tissue from humans with idiopathic pulmonary arterial hypertension. Measurements and Main Results: Phosphorylation of ACE2 by AMPK enhanced the stability of ACE2, which increased Ang (angiotensin) 1-7 and endothelial nitric oxide synthase-derived NO bioavailability. ACE2 S680D knock-in mice were resistant to PH as compared with wild-type littermates. In contrast, ACE2-knockout mice exacerbated PH, a similar phenotype found in mice with endothelial cell-specific deletion of AMPK alpha 2. Consistently, the concentrations of phosphorylated AMPK, p-ACE2 S680, and ACE2 were decreased in human lungs with idiopathic pulmonary arterial hypertension. Conclusions: Impaired phosphorylation of ACE2 Ser680 by AMPK in pulmonary endothelium leads to a labile ACE2 and hence is associated with the pathogenesis of PH. Thus, AMPK regulation of the vasoprotective ACE2 is a potential target for PH treatment.

Keyword :

converting enzyme 2 vascular endothelium AMP-activated protein kinase angiotensin pulmonary hypertension

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GB/T 7714 Zhang, Jiao , Dong, Jianjie , Martin, Marcy et al. AMP-activated Protein Kinase Phosphorylation of Angiotensin-Converting Enzyme 2 in Endothelium Mitigates Pulmonary Hypertension [J]. | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE , 2018 , 198 (4) : 509-520 .
MLA Zhang, Jiao et al. "AMP-activated Protein Kinase Phosphorylation of Angiotensin-Converting Enzyme 2 in Endothelium Mitigates Pulmonary Hypertension" . | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE 198 . 4 (2018) : 509-520 .
APA Zhang, Jiao , Dong, Jianjie , Martin, Marcy , He, Ming , Gongol, Brendan , Marin, Traci L. et al. AMP-activated Protein Kinase Phosphorylation of Angiotensin-Converting Enzyme 2 in Endothelium Mitigates Pulmonary Hypertension . | AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE , 2018 , 198 (4) , 509-520 .
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Pioglitazone stabilizes atherosclerotic plaque by regulating the Th17/Treg balance in AMPK-dependent mechanisms SCIE PubMed Scopus
期刊论文 | 2017 , 16 | CARDIOVASCULAR DIABETOLOGY | IF: 5.235
WoS CC Cited Count: 1
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Background: Pioglitazone (PIO), a thiazolidinediones drug, is a well-known anti-diabetic medicine, but its anti-atherosclerotic effects remain controversial. Thus it is important to investigate the effects of PIO on atherogenesis and the relevant mechanisms. Methods: For in vitro studies, primary cultured or AMP-activated protein kinase (AMPK) inhibited splenocytes were treated with oxidized low density lipoprotein (ox-LDL) or ox-LDL plus PIO. Percentage of T helper 17 (Th17) and regulatory T (Treg) cells were determined by flow cytometry. Expression of AMPK, interleukin-17 (IL-17) and forkhead box P3 (FoxP3) were detected by Western blots. For in vivo studies, apolipoprotein E-deficient (apoE-/-) mice fed with western diet were treated with PIO or vehicle for 8 weeks respectively. Percentage of Th17 and Treg cells in spleen were measured by immunohistochemical analysis. The atherosclerotic lesions were analyzed using oil red O staining, and collagen types I and III in atherosclerotic lesions were stained by Sirius red. Expression of IL-17 and FoxP3 were determined by quantitative polymerase chain reaction. Results: In cultured primary splenocytes, PIO dramatically inhibited Th17 and raised Treg. Intriguingly, pharmacological and genetic AMPK inhibitions abolished PIO-induced Treg elevation and Th17 inhibition. Moreover, PIO significantly induced AMPK phosphorylation, decreased IL-17(+) and increased - FoxP3(+) cells in spleen of apoE-/- mice. Finally, PIO did not alter plaque area, but intriguingly, stabilized atherosclerotic plaque through collagen induction in apoE-/- mice. PIO treatment also improved Th17/Treg balance in atherosclerotic lesions. Conclusions: PIO exhibits anti-atherosclerotic effects for stabilization of atherosclerotic plaque through regulating the Th17/Treg balance in an AMPK-dependent manner.

Keyword :

AMPK Atherosclerosis Pioglitazone T cell Signaling

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GB/T 7714 Tian, Yuling , Chen, Tao , Wu, Yan et al. Pioglitazone stabilizes atherosclerotic plaque by regulating the Th17/Treg balance in AMPK-dependent mechanisms [J]. | CARDIOVASCULAR DIABETOLOGY , 2017 , 16 .
MLA Tian, Yuling et al. "Pioglitazone stabilizes atherosclerotic plaque by regulating the Th17/Treg balance in AMPK-dependent mechanisms" . | CARDIOVASCULAR DIABETOLOGY 16 (2017) .
APA Tian, Yuling , Chen, Tao , Wu, Yan , Yang, Lin , Wang, Lijun , Fan, Xiaojuan et al. Pioglitazone stabilizes atherosclerotic plaque by regulating the Th17/Treg balance in AMPK-dependent mechanisms . | CARDIOVASCULAR DIABETOLOGY , 2017 , 16 .
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IFN-gamma aggravates neointimal hyperplasia by inducing endoplasmic reticulum stress and apoptosis in macrophages by promoting ubiquitin-dependent liver X receptor-alpha degradation SCIE PubMed Scopus
期刊论文 | 2017 , 31 (12) , 5321-+ | FASEB JOURNAL | IF: 5.595
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Neointimal hyperplasia is the main cause of restenosis after percutaneous coronary interventions (PCIs). Both IFN-gamma and macrophages play nonredundant roles in the pathogenesis of vascular intimal hyperplasia; however, the underlying mechanisms remain elusive and must be further investigated. In mouse peritoneal macrophages, IFN-gamma significantly accelerated degradation and up-regulated polyubiquitination of liver X receptor (LXR)-alpha. Signal transducer and activator of transcription 1 (STAT1) inhibitor, fludarabine, and PIAS1 knockdown reduced ubiquitination and increased the expression of LXR-alpha in IFN-gamma-treated macrophages. IFN-gamma also increased the expression of endoplasmic reticulum (ER) stress-related proteins, including p-PERK, p-eIIF2 alpha, and CCAAT-enhancer-binding protein homologous protein (CHOP), as well as apoptosis of macrophages. Treatment with ER stress inhibitor, 4-phenylbutyric acid (4-PBA), and LXR agonist, T0901317 (T0), alleviated IFN-gamma-induced apoptosis in macrophages. Neointimal hyperplasia was significant after carotid ligation for 4 wk in ApoE(-/-) mice. IFN-gamma mAb, T0, and 4-PBA treatment not only significantly attenuated neointimal hyperplasia but also decreased CD68(+)TUNEL(+) double-positive macrophages in the hyperplastic neointima. Moreover, after 4-PBA or T0 administration, the number of CD68(+)p-eIIF2 alpha(+) and CD68(+)CHOP(+) double-positive cells in neointimal was also apparently decreased. Taken together, these results defined an unexpected role of IFN-gamma and LXR-alpha in the development of neointimal hyperplasia. The PIAS1/STAT1-dependent LXR-alpha degradation induced by IFN-gamma promoted ER stress and apoptosis in macrophages, which leads to aggravated neointimal hyperplasia. LXR agonist efficiently improved neointimal hyperplasia, which may be a promising new strategy to ameliorate restenosis and vascular remodeling after PCI.

Keyword :

restenosis inflammation ER stress

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GB/T 7714 Zhao, Qiang , Zhou, Dong , You, Hongjun et al. IFN-gamma aggravates neointimal hyperplasia by inducing endoplasmic reticulum stress and apoptosis in macrophages by promoting ubiquitin-dependent liver X receptor-alpha degradation [J]. | FASEB JOURNAL , 2017 , 31 (12) : 5321-+ .
MLA Zhao, Qiang et al. "IFN-gamma aggravates neointimal hyperplasia by inducing endoplasmic reticulum stress and apoptosis in macrophages by promoting ubiquitin-dependent liver X receptor-alpha degradation" . | FASEB JOURNAL 31 . 12 (2017) : 5321-+ .
APA Zhao, Qiang , Zhou, Dong , You, Hongjun , Lou, Bowen , Zhang, Yan , Tian, Yuling et al. IFN-gamma aggravates neointimal hyperplasia by inducing endoplasmic reticulum stress and apoptosis in macrophages by promoting ubiquitin-dependent liver X receptor-alpha degradation . | FASEB JOURNAL , 2017 , 31 (12) , 5321-+ .
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Potassium supplementation ameliorates increased plasma homocysteine induced by salt loading in normotensive salt-sensitive subjects SCIE PubMed Scopus
期刊论文 | 2017 , 39 (8) , 769-773 | CLINICAL AND EXPERIMENTAL HYPERTENSION | IF: 1.367
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The mechanism by which high-salt and low-potassium diet contributes to hypertension remains poorly understood. Plasma homocysteine (Hcys) is recognized as a primary mediator of blood pressure (BP) response to some diets. Therefore, the present study tried to investigate whether plasma Hcys and BP could be regulated by salt loading in normotensive salt-sensitive (SS) persons, and further explored whether potassium supplementation could reverse the effect. We enrolled 47 normotensive subjects, aged 29-65 years. The protocol included 7 days on a low-salt diet (3g/day, NaCl), 7 days on a high-salt diet (18g/day), and then a high-salt diet with potassium supplementation (4.5g/day) for 7 days. After high-salt intake, BP was significantly increased and potassium supplementation lowered it in the SS group. Plasma Hcys were higher in SS subjects than in salt-resistant (SR) subjects after salt loading (34.4 +/- 17.0 mol/L versus 19.16 +/- 6.4 mol/L, P < 0.01). Plasma Hcys in SS subjects was increased on a high-salt diet than on a low-salt diet (34.4 +/- 17.0 mol/L versus 16.5 +/- 8.3 mol/L, P < 0.01), but plasma Hcys was ameliorated by potassium supplementation (34.4 +/- 17.0 mol/L versus 20.9 +/- 10.4 mol/L, P < 0.01). In SS subjects, the change of mean arterial blood pressure (MBP) correlated significantly and positively with the alteration of plasma Hcys during low-salt to high-salt intake and high-salt to high-salt with potassium supplementation (r = 0.75, P < 0.001; r = 0.74, P < 0.001, respectively). Our results indicate that Hcys may partly mediate the impact of high-salt intake and potassium supplementation on BP in SS subjects.

Keyword :

sodium potassium homocysteine salt sensitive Blood pressure

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GB/T 7714 Wan, Zhaofei , Ren, Keyu , Wen, Wen et al. Potassium supplementation ameliorates increased plasma homocysteine induced by salt loading in normotensive salt-sensitive subjects [J]. | CLINICAL AND EXPERIMENTAL HYPERTENSION , 2017 , 39 (8) : 769-773 .
MLA Wan, Zhaofei et al. "Potassium supplementation ameliorates increased plasma homocysteine induced by salt loading in normotensive salt-sensitive subjects" . | CLINICAL AND EXPERIMENTAL HYPERTENSION 39 . 8 (2017) : 769-773 .
APA Wan, Zhaofei , Ren, Keyu , Wen, Wen , Zhou, Dong , Liu, Junhui , Fan, Yan et al. Potassium supplementation ameliorates increased plasma homocysteine induced by salt loading in normotensive salt-sensitive subjects . | CLINICAL AND EXPERIMENTAL HYPERTENSION , 2017 , 39 (8) , 769-773 .
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The Amelioration of Insulin Resistance in Salt Loading Subjects by Potassium Supplementation is Associated with a Reduction in Plasma IL-17A Levels SCIE PubMed Scopus
期刊论文 | 2017 , 125 (8) , 571-576 | EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES | IF: 1.623
WoS CC Cited Count: 1
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Background High dietary salt intake contributes to the development of autoimmune/inflammatory diseases including metabolic syndrome (MetS) which potassium supplementation can potentially reverse. T helper (Th) 17 cells as well as its production interleukin (IL)-17A are involved in the pathogenesis of MetS. The polarization of Th17 cells and enhanced IL-17A production induced by high salt might increase the risk of autoimmune/inflammatory diseases. Methods 45 normotensive subjects (aged 29 to 65 years) were enrolled from a rural community of Northern China at random. All of the participants were maintained on a low-salt (3 g/day) diet for 7 days, a high-salt (18 g/day) diet for 7 days, and then a high-salt diet with potassium supplementation (4.5 g/day, KCl) for another 7 days. Insulin resistance (IR) was determined based on the homeostasis model assessment index (HOMA-IR). Results Participants exhibited increased plasma insulin level, as well as progressed HOMA-IR, during a high-salt diet intervention, which potassium supplementation reversed. Moreover, after salt loading, the plasma IL-17A concentrations increased significantly (4.2 +/- 2.1 pg/mL to 9.7 +/- 5.1 pg/mL; P < 0.01), whereas dropped considerably when dietary potassium was supplemented (9.7 +/- 5.1 pg/mL to 2.0 +/- 0.9 pg/mL; P < 0.001). Statistically significant correlations were found between changes in HOMA-IR and changes in plasma IL-17A concentrations during the interventions (low-to high-salt: r = 0.642, P < 0.01; high-salt to potassium supplementation: r = 0.703, P < 0.01). Based on multivariate regression analysis, plasma IL-17A showed as an independent predictor of IR. Conclusions The amelioration of salt-loading-induced IR by potassium supplementation in participants may be related to the reduction in plasma IL-17A concentration.

Keyword :

IL-17A high salt consumption insulin resistance Th17 potassium supplementation

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GB/T 7714 Wen, Wen , Wan, Zhaofei , Zhou, Dong et al. The Amelioration of Insulin Resistance in Salt Loading Subjects by Potassium Supplementation is Associated with a Reduction in Plasma IL-17A Levels [J]. | EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES , 2017 , 125 (8) : 571-576 .
MLA Wen, Wen et al. "The Amelioration of Insulin Resistance in Salt Loading Subjects by Potassium Supplementation is Associated with a Reduction in Plasma IL-17A Levels" . | EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES 125 . 8 (2017) : 571-576 .
APA Wen, Wen , Wan, Zhaofei , Zhou, Dong , Zhou, Juan , Yuan, Zuyi . The Amelioration of Insulin Resistance in Salt Loading Subjects by Potassium Supplementation is Associated with a Reduction in Plasma IL-17A Levels . | EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES , 2017 , 125 (8) , 571-576 .
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