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Blood pressure (BP) control is the most established practice for preventing the progression and complications of chronic kidney disease (CKD). We examined the influence of BP patterns on target organ damage in hypertensive patients with CKD by using long-term follow-up data of the APrODiTe-2 study.We collected 5 years of data of APrODiTe-2 study (1 year longitudinal study) participants after the enrollment on the progression of estimated glomerular filtration (eGFR), renal outcomes (doubling of serum creatinine, 50% decrease of eGFR, maintenance dialysis, and kidney transplantation), cerebro-cardiovascular (CCV) accidents, and all-cause mortality (n=378) to evaluate the long-term influence of BP patterns on target organ damages.Initially, more than 2/3 of patients showed masked (50.0%) and sustained uncontrolled (30.6%) BP control states as well as non- (31.3%) and reverse-dipping (35.0%) states. Only 18.8% and 20.8% of participants showed a better change in BP control patterns and a dipping pattern change to dippers over 1 year, respectively. Composite of new CCV accidents occurred in 43 patients (11.4%), and no BP patterns were associated with the occurrence of new CCV accidents. A worse change in BP control categories over 1 year was associated with increased occurrence of composites of renal outcomes after adjustment for age, sex, and the cause of CKD (HR 5.997 [1.454-24.742], P = .013 and HR 4.331 [1.347-13.927], P = .014, respectively). Patients with a worse initial BP control category, a worse change in BP control categories over 1 year, and higher clinic systolic BP and pulse pressure (PP) (> median level) were more likely to have faster eGFR progression (absolute eGFR and eGFR ratio).Higher BP burden (a worse change in BP control categories, higher initial clinic systolic BP and PP) was associated with faster eGFR progression and increased occurrence of renal outcomes.AIM Adequate bowel preparation is essential to the quality of colonoscopy. We performed a meta-analysis to determine the efficacy and safety of the addition of lubiprostone to the bowel preparation process prior to colonoscopy. METHODS Online databases, namely, PubMed, MEDLINE and Cochrane Library, were searched for randomized controlled trials that assessed the additive effect of lubiprostone on the quality of colon preparation in patients undergoing colonoscopy. Each included study was evaluated by the Jadad score to assess the quality of the study. The primary outcome was bowel preparation efficacy, defined as the proportion of patients with an excellent or poor preparation. The secondary outcomes included the length of the colonoscopy, polyp detection, and any adverse effects. RESULTS In total, 5 articles published between 2008 and 2016 fulfilled the selection criteria. The addition of lubiprostone to the bowel cleansing process significantly increased the proportion of patients with an excellent preparation (risk ratio [RR] = 1.68, 95% confidence interval (CI) 1.40-2.02, P less then .00001) but did not decrease the procedural time or increase the polyp detection rate (mean difference = -0.52, 95% CI -3.74-2.69, P = .75; RR = 1.16, 95% CI 0.96-1.42, P = .13, respectively). There was no significant difference in the proportion of patients with any adverse events. CONCLUSION The addition of lubiprostone to the bowel preparation regimen prior to colonoscopy is effective and safe.Cigarette smoking is associated with thicker carotid intima-media thickness (IMT), probably partly through inflammatory pathways. However, to what extent does inflammation mediate the smoking-carotid atherosclerosis association is unclear. We investigated the mediating effect of inflammation on the association between cigarette smoking and carotid IMT, and quantified the respective contributions of inflammatory markers to this association.A total of 1752 participants from Guangzhou Biobank Cohort Study-Cardiovascular Disease Sub-cohort (GBCS-CVD) were included. Using causal mediation analysis under the counterfactual framework, we decomposed total effects of cigarette smoking on IMT into indirect effects (through inflammatory response) and direct effects (not through inflammatory response).After adjusting for traditional risk factors, the indirect effects of per 10/L increment in leukocyte and granulocyte, per mg/L increment in high-sensitivity C-reactive protein (hs-CRP), and per mg/dL increment in fibrinogen on carotid IMT was 0.0028 mm (95% confidence interval [CI], 0.0011-0.0047), 0.0019 mm (95% CI, 0.0006-0.0034), 0.0017 mm (95% CI, 0.0006-0.003), and 0.001 mm (95% CI, 0.0001-0.0021), respectively. No evidence for a mediating role of lymphocyte was found. The proportion of the smoking-IMT association mediated by leukocyte, granulocyte, hs-CRP, and fibrinogen was 12.57% (95% CI, 8.50%-22.11%), 8.50% (95% CI, 5.76%-15.09%), 7.64% (95% CI, 5.20%-13.79%), and 4.48% (95% CI, 3.04%-8.03%), respectively. Restricting data analysis to men showed similar results.The effects of cigarette smoking on IMT were partly mediated by leukocyte, hs-CRP, and fibrinogen. The mediating role of leukocyte was likely mainly driven by higher granulocyte.The present study aimed to investigate the potential use of T2-weighted sequences with diffusion weighted imaging (DWI) in magnetic resonance (MR) enterography instead of conventional contrast-enhanced MR imaging (MRI) sequences for the evaluation of active inflammation in Crohn disease.Two-hundred thirteen intestinal segments of 43 patients, who underwent colonoscopy within 2 weeks before or after MR enterography were evaluated in this retrospective study. DWI sequences, T2-weighted sequences, and contrast-enhanced T1-weighted sequences were acquired in the MR enterography scan after cleaning of the bowel and using an oral contrast agent. https://www.selleckchem.com/products/sodium-phenylbutyrate.html First, the intestinal segments that had active inflammation in MR enterography were qualitatively evaluated in T2-weighted and contrast-enhanced T1-weighted sequences and then MR activity index (MRAI 1) and MRAI 2 were formed with and without contrast-enhanced sequences in 2 separate sessions.The correlation coefficient between contrast enhanced and DWI MR enterography scores (MRAI 1 and MRAI 2) of intestinal inflammation was 0.
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