Hypertension is common in adults and often undiagnosed, and the prevalence of pre- and undiagnosed-hypertension remains unclear. We aimed to investigate the prevalence of pre- and undiagnosed-hypertension and their correlates among urban Chinese adults. A total of 7435 participants aged 20-79 were included in this study. Data on demographics, lifestyle and medical history were collected through a structured interview. Pre- and undiagnosed-hypertension was defined as systolic blood pressure/ diastolic blood pressure (SBP/DBP) of 120-139/80-89 mm Hg and SBP⩾140 mm Hg and/or DBP⩾90 mm Hg, respectively, in participants without a history of hypertension and use of antihypertensive medication. Prevalence rates were calculated and standardized using local age- and gender-specific census data. Data were analysed using multinomial logistic regression with adjustment for potential confounders. Of all the participants, 2726 (36.7%) were diagnosed with pre-hypertension and 919 (12.3%) with undiagnosed-hypertension. Undiagnosed-hypertension accounted for 37.3% of all participants with hypertension. The prevalence of pre-hypertension gradually decreased with age, while undiagnosed-hypertension increased, although presenting different changing patterns among men and women. In a fully adjusted multinomial logistic regression, age, male sex, low socio-economic status (SES), abdominal obesity, alcohol drinking, physical inactivity and type 2 diabetes mellitus (T2DM) were significantly associated with increased odds of pre- and undiagnosed-hypertension. In conclusions, the prevalence of pre- and undiagnosed-hypertension was ~50% among urban Chinese adults. Abdominal obesity, low SES, alcohol drinking, physical inactivity and T2DM may be indicators for pre- and undiagnosed-hypertension.
The epithelial-to-mesenchymal transition (EMT) program is crucial for the epithelial cancer progression and fibrotic diseases. Our previous work has demonstrated that p66Shc, a focal adhesion-associated adaptor protein, is frequently downregulated in lung cancers and its depletion promotes metastasis behavior through anoikis resistance. However, mechanism underlying loss of p66Shc and EMT response is not fully understood. Here, we showed that p66Shc deficiency enhanced the expression of ZEB1, the known mesenchymal transcription factor and consequently increased Vimentin, and decreased epithelial markers of E-cadherin and β-catenin. p66Shc depletion also increased cell invasion and migration. In addition, ChIP and luciferase assays showed that these effects were directly mediated by ZEB1 repression of p66Shc promoter. Thus, our findings define a critical role of p66Shc in the suppression of fibrotic EMT response with a negative feedback loop between p66Shc and ZEB1 in lung epithelial cancer cells.
This study was undertaken to clarify the role and mechanism of pyruvate dehydrogenase kinase isoform 2 (PDK2) in chondrogenic differentiation of mesenchymal stem cells (MSCs). MSCs were isolated from femurs and tibias of Sprague-Dawley rats, weighing 300-400 g (5 females and 5 males). Overexpression and knockdown of PDK2 were transfected into MSCs and then cell viability, adhesion and migration were assessed. Additionally, the roles of aberrant PDK2 in chondrogenesis markers SRY-related high mobility group-box 6 (Sox6), type ΙΙ procollagen gene (COL2A1), cartilage oligomeric matrix protein (COMP), aggrecan (AGC1), type ΙX procollagen gene (COL9A2) and collagen type 1 alpha 1 (COL1A1) were measured by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The expressions of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK) and extracellular regulated protein kinase (ERK) were measured. Overexpressing PDK2 promoted cell viability, adhesion and inhibited cell migration in MSCs (all P<0.05). qRT-PCR assay showed a potent increase in the mRNA expressions of all chondrogenesis markers in response to overexpressing PDK2 (P<0.01 or P<0.05). PDK2 overexpression also induced a significant accumulation in mRNA and protein expressions of JNK, p38MAPK and ERK in MSCs compared to the control (P<0.01 or P<0.05). Meanwhile, silencing PDK2 exerted the opposite effects on MSCs. This study shows a preliminary positive role and potential mechanisms of PDK2 in chondrogenic differentiation of MSCs. It lays the theoretical groundwork for uncovering the functions of PDK2 and provides a promising basis for repairing cartilage lesions in osteoarthritis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.