202 research outputs found

    Awareness of hypertension and depressive symptoms: a cross-sectional study in a primary care population

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    Objective: To investigate the association of hypertension awareness and depressive symptoms, and to analyse factors predisposing aware hypertensives to depressive symptoms.Design: Cross-sectional study in a primary care population.Setting: Cardiovascular risk factor survey in two semi-rural towns in Finland.Subjects: Two thousand six hundred seventy-six middle-aged risk persons without an established cardiovascular or renal disease or type 2 diabetes.Main outcome measures: Depressive symptoms, previous and new diagnosis of hypertension.Results: Hypertension was diagnosed in 47.9% of the subjects, of whom 34.5% (442/1 282) had previously undetected hypertension. Depressive symptoms were reported by 14% of the subjects previously aware of their hypertension, and by 9% of both unaware hypertensives and normotensive subjects. In the logistic regression analysis, both the normotensive (OR 0.62, 95% CI 0.45–0.86) (p = 0.0038) and the unaware hypertensive subjects (OR 0.54, 95% CI 0.35–0.84) (p = 0.0067) had lower risk for depressive symptoms than the previously diagnosed hypertensives. Among these aware hypertensives, female gender (OR 3.61, 95% CI 2.06–6.32), harmful alcohol use (OR 2.55, 95% CI 1.40–4.64) and obesity (OR 2.50, 95% CI 1.01–6.21) predicted depressive symptoms. Non-smoking (OR 0.57, 95% Cl 0.33–0.99) and moderate leisure-time physical activity compared to low (OR 0.53, 95% CI 0.33–0.84) seemed to buffer against depressive symptoms.Conclusion: Depressive symptoms are common in hypertensive persons even without comorbidities, if the person is already aware of his/her hypertension. Many modifiable, lifestyle associated factors may contribute to the association of hypertension and depressive symptoms.</p

    Normal levels of p27Xic1 are necessary for somite segmentation and determining pronephric organ size

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    The Xenopus laevis cyclin dependent kinase inhibitor p27Xic1 has been shown to be involved in exit from the cell cycle and differentiation of cells into a quiescent state in the nervous system, muscle tissue, heart and retina. We show that p27Xic1 is expressed in the developing kidney in the nephrostomal regions. Using over-expression and morpholino oligonucleotide (MO) knock-down approaches we show normal levels of p27Xic1 regulate pronephros organ size by regulating cell cycle exit. Knock-down of p27Xic1 expression using a MO prevented myogenesis, as previously reported; an effect that subsequently inhibits pronephrogenesis. Furthermore, we show that normal levels of p27Xic1 are required for somite segmentation also through its cell cycle control function. Finally, we provide evidence to suggest correct paraxial mesoderm segmentation is not necessary for pronephric induction in the intermediate mesoderm. These results indicate novel developmental roles for p27Xic1, and reveal its differentiation function is not universally utilised in all developing tissues

    Xenopus as a Model System for the Study of GOLPH2/GP73 Function: Xenopus golph2 Is Required for Pronephros Development

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    GOLPH2 is a highly conserved protein. It is upregulated in a number of tumors and is being considered as an emerging biomarker for related diseases. However, the function of GOLPH2 remains unknown. The Xenopus model is used to study the function of human proteins. We describe the isolation and characterization of Xenopus golph2, which dimerizes and localizes to the Golgi in a manner similar to human GOLPH2. Xenopus golph2 is expressed in the pronephros during early development. The morpholino-mediated knockdown of golph2 results in edema formation. Additionally, Nephrin expression is enhanced in the glomus, and the expression of pronephric marker genes, such as atp1b1, ClC-K, NKCC2, and NBC1, is diminished in the tubules and duct. Expression patterns of the transcription factors WT1, Pax2, Pax8, Lim1, GATA3, and HNF1ÎČ are also examined in the golph2 knockdown embryos, the expression of WT1 is increased in the glomus and expanded laterally in the pronephric region. We conclude that the deletion of golph2 causes an increase in the expression of WT1, which may promote glomus formation and inhibit pronephric tubule differentiation

    Predictors of clinical outcomes after periodontal treatment of aggressive periodontitis: 12-month randomized trial

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    Abstract Little is known about the factors that may be used in clinical practice to predict the therapeutic response of aggressive periodontitis patients. The aim of this study was to determine predictors of clinical outcomes after non-surgical treatment of aggressive periodontitis. A total of 24 patients (aged 13-26 years) received oral hygiene instructions, as well as subgingival scaling and root planing. Twelve subjects received systemic azithromycin at random. Clinical variables were assessed at baseline, 3, 6, 9, and 12 months. Baseline microbiological assessment was performed by checkerboard DNA-DNA hybridization. Multivariable models used generalized estimating equations. There were significant improvements in the entire sample in regard to pocket depth, clinical attachment level and bleeding on probing. Significant predictors of a reduction in mean pocket depth were: use of azithromycin, non-molar teeth, generalized disease and baseline pocket depth. Absence of plaque predicted a 0.22 mm higher attachment gain, whereas a baseline pocket depth ≄7 mm predicted a 1.36 mm higher attachment loss. Azithromycin, plaque, and baseline pocket depth were significant predictors of bleeding on probing. The concomitant presence of all three red complex species predicted a 0.78 mm higher attachment loss. It may be concluded that dental plaque, tooth type, disease extent, baseline pocket depth, and use of azithromycin were significant predictors of the clinical response to treatment for aggressive periodontitis in young individuals. Moreover, the presence of multiple periodontal pathogens may predict challenges in achieving a favorable outcome for aggressive periodontitis
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