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BackgroundBans on tobacco advertising, promotion and sponsorship (TAPS) have the potential to influence smoking behaviour. However, many countries are yet to implement such strategies.ObjectiveThis study aimed to synthesise contemporary evidence on the effectiveness of TAPS bans on smoking prevalence, initiation and cessation.Data sourcesMedline, EMBASE, Scopus, Cochrane Library and Web of Science databases were searched up to 11 April 2024. Sixteen eligible studies were included.Data selection and extractionTwo reviewers independently screened each study and extracted relevant data. Quality assessment was performed in duplicate using the ROBINS-I tool. Discrepancies were resolved via consensus or a third reviewer. Random effects meta-analyses were conducted for reasonably comparable studies.Data synthesisThe meta-analyses showed that TAPS bans were associated with a lower prevalence of current smoking (pooled OR= 0.80, 95% CI 0.68 to 0.95, I 2=98.7%) and a reduced risk of smoking initiation (pooled HR=0.63, 95% CI 0.48 to 0.82, I 2=95%). There was no association between TAPS bans and smoking cessation (pooled OR=1.10, 95% CI 0.86 to 1.40, I2 =58.5%). Subgroup analyses revealed the effects of TAPS bans on smoking prevalence differed by duration of evaluation (p<0.01).ConclusionsThis review showed that TAPS bans were associated with a 20% lower odds of current smoking and a 37% reduced risk of smoking initiation. The available evidence suggests that TAPS bans influence smoking behaviour, which strengthens calls for the implementation and enforcement of these policies.

Idiopathic membranous nephropathy (iMN) is the major cause of end-stage renal disease (ESRD). Recent guidelines suggest limiting immunosuppressants only to high risk patients for ESRD. The present study is aimed at identifying new predictors for the renal outcome of iMN patients. We conducted a retrospective cohort study covering a period from January 2003 to December 2013. We enrolled participants who had received their first renal biopsy at our medical center in Taiwan with the diagnosis of iMN. Clinical, pathological and laboratory data were collected from medical records. Analyses with Mann–Whitney U test was used for continuous variables and Chi-square test for categorical variables. The Kaplan-Meier curve was used for the analyses of patient survival and renal survival. Youden index was used for evaluating the performance of a dichotomous diagnostic test for renal and patient outcomes. Cox proportional hazard regression was used to determine factors affecting renal survival.A total of 99 patients with renal biopsy-confirmed idiopathic iMNs were enrolled. C3 level ≤114 mg/dl predicted patient outcome (p < 0.001) with good predictive power (AUC = 0.736). The univariate analysis showed that risk factors for poor renal outcome were older age (HR = 1.04, p = 0.002), high BUN (HR = 1.03, p < 0.001), poor baseline renal function (HR = 1.30 and p < 0.001 for higher serum creatinine; HR = 0.97 and p < 0.001 for higher eGFR; HR = 1.06 and p < 0.001 for urine PCR), C3 ≤ 93.4 mg/dl (HR = 2.15, p = 0.017), NLR > 3.34 (HR = 3.30, p < 0.001) and PLR > 14.48 (HR = 2.54, p = 0.003). Stage of iMN did not fully account for the risk of ESRD. This is the first evidence that serum levels of C3 ≤ 93.4 mg/dl predicted poor renal outcomes with good predictive power. Easily obtained markers, NLR > 3.34 also predicted poor renal outcomes.

Validation of the Oxford classification (MEST and MEST-C) for Immunoglobulin A nephropathy (IgAN) in the Taiwanese population is lacking. Our study aimed to validate this classification and assess individual lesion impact. We conducted a retrospective cohort study at Taichung Veterans General Hospital, Taiwan (Jan 2011–Jul 2023). Composite renal outcomes were evaluated using clinical conditions and estimated glomerular filtration rate (eGFR). We used Kaplan–Meier, univariable/multivariable logistic regression and ROC curves. Subgroup analysis considered eGFR < or ≥ 30.0 ml/min/1.73 m 2 . In 366 renal biopsies, serum creatinine was 1.34 mg/dl, eGFR 53.8 ml/min/1.73 m 2 , urine protein–creatinine ratio 1159 mg/g. T1/T2 lesions had lowest baseline eGFR (39.6/11.5 ml/min/1.73 m 2 ), correlating with poorest renal survival (median survival 54.7/34.4 months). Univariable analysis linked all individual variables to worse renal outcomes. Multivariable analysis (MEST/MEST-C) showed only T1/T2 linked to worse outcomes. T score had highest predictive power (AUC 0.728, sensitivity 60.2%, specificity 83.6%), with MEST having high AUC (0.758). No extra predictive power was seen transitioning MEST to MEST-C. Subgroup analysis (eGFR < 30.0 ml/min/1.73 m 2 ) associated C1 with improved renal outcomes (odds ratio 0.14, 95% CI 0.03–0.65). T lesion correlated with worse outcomes across subgroups. The T lesion consistently correlated with worse renal outcomes across all groups and baseline statuses. Integrating the C lesion into the transition from MEST to MEST-C did not enhance predictive power. Importantly, the C1 lesion was linked to improved renal outcomes in the eGFR < 30.0 ml/min/1.73 m 2 subgroup, likely due to treatment effects.

Background Transient progressive weakness and disability of lower limb during the early stage after TKR will increase the risk of fall, but the superior postoperative strength training mode have not been elucidated for functional restoration. This study aimed to compare whether the isokinetic lower limb training is superior to either isotonic or home isometric exercise during early stage after TKR in older people. Methods A total of 43 recruited old participants (mean age, 68.40 years old) receiving TKR were divided randomly based on the different four-week training modes into three groups including isokinetic, isotonic, and home isometric exercise (control group). The primary outcome was set as functional performance in terms of Timed Up and Go (TUG) test and the secondary outcomes include the peak torque of knee at 60 and 120 degree/ second, Short-Form 36 Health Survey (SF-36), and Western Ontario and McMaster Universities Arthritis index (WOMAC). Results All of the peak torque measurements of the knee improved significantly in both the isokinetic and the isotonic group, but not in the control group. Although isotonic training resulted in more strength gains, a significant enhancement in TUG test was observed in the isokinetic group only ( p  = 0.003). However, there were no significantly improvement of TUG test after training in other two groups. SF-36 and WOMAC improved after training in all three groups, with no significant difference in the degree of improvement between groups. Conclusion Isokinetic training for 4 weeks following TKR effectively improved all the outcome parameters in this study, including the TUG test, lower limb strength, and functional scores. However, both isokinetic and isotonic training modes could be recommended after TKR because of no significant difference in the degree of improvement between these two groups. Trial registration Clinical trial registration number: NCT02938416. Level of evidence I

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a major genetic contributor to end-stage kidney disease (ESKD). Current evidence on tolvaptan primarily focuses on slowing estimated glomerular filtration rate (eGFR) decline and kidney volume growth. However, direct confirmation of its effectiveness in reducing the need for hemodialysis in ESKD remains limited. We included ADPKD patients aged ≥18 years using TriNetx data from Sep 2, 2018, to Sep 3, 2023. Propensity score matching (PSM) ensured baseline comparability (standardized mean difference (SMD) <0.1). Hazard ratios (HRs) with 95% confidence intervals (CIs) evaluated outcomes, and subgroup analyses were performed. After 1:1 PSM, both groups comprised 673 patients. The average age was 45, with generally good health (3-5% diabetes, 2-3% ischemic heart disease). Baseline eGFR averaged ∼55 ml/min/1.732m . Post-matching, all SMDs were <0.1, indicating successful matching. Tolvaptan users exhibited lower eGFR (51.45 ± 30.09 vs. 57.37 ± 33.65,  < 0.001) and higher risk of stage 4-CKD (HR: 2.436, 95% CI:1.649, 3.599) compared to non-users. However, tolvaptan users showed significantly reduced chances of initiating hemodialysis (HR:0.362, 95%CI:0.176, 0.745), experiencing urinary tract infections (HR:0.581, 95%CI:0.354, 0.956), and all-cause mortality (HR:0.355, 95% CI:0.180, 0.700). Kaplan-Meier curves for hemodialysis initiation indicated higher survival rates among tolvaptan users across age and number of medication refill subgroups. This real-world study, employing precise matching, reveals tolvaptan's role in reducing hemodialysis initiation risk in ADPKD, despite initial hemodynamic-induced lower eGFR.

Background Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a rare disease seen in the general population and has been reported as showing an increased incidence in the peritoneal dialysis (PD) population, as documented in case reports. Methods We conducted a case-control study using data from the Taichung Veterans General Hospital electric medical record database from the years 2010 to 2023. We defined cases as CIDP with End-stage kidney disease (ESKD) and controls as without CIDP. A logistic regression analysis was used to investigate the association between CIDP and dialysis modality, age, gender, dialysis duration, plasma potassium > 5.5 mEq/L and < 2.5 mEq/L, and intact parathyroid hormone (i-PTH) > 613 pg/mL. Results Our findings suggest that PD may be a risk factor in the ESKD population (Odds ratio: 5.125, C.I.: 1.078 ~ 24.372, p  = 0.040) according to logistic regression analysis. Dialysis duration, gender, diabetes mellitus, HbA1c > 7%, hypokalemia, hyperkalemia, and hyperparathyroidism did not show an association with CIDP. Conclusion There seems to be an association between PD and CIDP in this case-control study. Possible mechanisms may involve systemic inflammation induced by peritoneal dialysate exchange or the content of the dialysate. Further studies are still needed.

Data for the risk of any solid cancer in patients with polycystic kidney disease are scarce. Therefore, we did a nationwide cohort study in Taiwan to establish the risk of cancer in patients with polycystic kidney disease without either chronic kidney disease or end-stage renal disease. From inpatient claims of the Taiwan National Health Insurance Research Database, we included patients aged 20 years and older and diagnosed with polycystic kidney disease between January, 1998 and December, 2010, in the polycystic kidney disease cohort. Patients with a history of cancer, a history of chronic kidney disease or of end-stage renal disease (recorded from the Registry of Catastrophic Illness Patient Database) were excluded. For each patient with polycystic kidney disease, one patient aged older than 20 years with no history of polycystic kidney disease or cancer was randomly selected from the National Health Insurance Research Database, matched 1:1 on the basis of the propensity score calculated by logistic regression, and was included in the control non-polycystic kidney disease cohort. The follow-up period for each patient was estimated from the index date to the date of diagnosis of cancer, or the patient was censored due to withdrawal from the insurance programme (eg, death, immigration, or imprisonment) or on Dec 31, 2011. The primary outcome of interest was a diagnosis of cancer during a 14-year follow-up period. The risk of cancer was represented as a hazard ratio (HR) calculated in Cox proportional hazard regression models. 4346 patients with polycystic kidney disease and 4346 without were enrolled in the study. The median follow-up period in the polycystic kidney disease cohort was 3·72 years (IQR 1·25–7·31) and in the non-polycystic kidney disease cohort was 4·96 years (2·29–8·38). The overall incidence of cancer was higher in the polycystic kidney disease cohort than in the control cohort (20·1 [95% CI 18·3–21·9] per 1000 person-years vs 10·9 [10·1–11·8] per 1000 person-years; crude hazard ratio (HR) 1·77 [95% CI 1·52–2·07]; HR adjusted for age, sex, frequency of medical visits, and comorbidities was 1·83 [1·57–2·15]). The specific risks (adjusted subhazard ratios) were significantly higher in the polycystic kidney disease cohort than that in the non-polycystic kidney disease cohort for liver cancer (1·49 [95% CI 1·04–2·13]; p=0·030), colon cancer (1·63 [1·15–2·30]; p=0·006), and kidney cancer (2·45 [1·29–4·65]; p=0·006). To our knowledge, this is the first report of the association of polycystic kidney disease without end-stage renal disease with the risk of liver, colon, and kidney cancer. Health-care professionals should be aware of this risk, when treating patients with polycystic kidney disease. Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence, Academia Sinica Taiwan Biobank, Stroke Biosignature Project, NRPB Stroke Clinical Trial Consortium, Tseng-Lien Lin Foundation, Taiwan Brain Disease Foundation, Katsuzo and Kiyo Aoshima Memorial Funds, China Medical University Hospital, and Taiwan Ministry of Education.

Immunoglobulin A Nephropathy (IgAN) is the most common type of glomerulonephritis with variable renal outcome. The association between IgAN and patient survival is limited. The effect of crescents on patient survival was never studied. We conducted a retrospective cohort study between January 2003 and December 2013. All patients with the biopsy-proved IgAN was enrolled for the analysis of patient survival and renal survival. Cox regression model was used analyze the associated factors for patient survival. All 388 participants with IgAN were enrolled, in which 45 patients with crescents. The mean percentage of glomeruli involvement was 23±18.9%. After long-term follow-up, crescents group had both worse renal (p = 0.034) and patient survivals (p = 0.016). In univariate Cox regression model, the age (HR = 1.08, 95% CI = 1.05-1.12, p<0.001), crescents (HR = 3.93, 95% CI = 1.18-13.07, p = 0.025), serum albumin (HR = 0.023, 95%CI = 0.11-0.50, p<0.001), blood total protein (HR = 0.46, 95%CI = 0.28-0.75, p = 0.002), HDL (HR = 0.95, 95%CI = 0.91-0.99, p = 0.009), daily urine protein (HR = 1.14, 95%CI = 1.01-1.29, p = 0.038), urine PCR (HR = 1.07, 95%CI = 1.02-1.12, p = 0.003), serum IgM (HR = 0.98, 95%CI = 0.96-1.00, p = 0.036), BUN (HR = 1.02, 95%CI = 1.01-1.02, p = 0.005), and eGFR (HR = 0.097, 95%CI = 0.94-0.99, p = 0.0011) were associated with patient survival. After multivariate Cox regression analysis, age (HR = 1.08, 95%CI = 1.01-1.13, p = 0.013), crescents (HR = 5.57, 95%CI = 1.14-29.05, p = 0.034), and HDL (HR = 0.94, 95%CI = 0.90-0.99, p = 0.026) were associated with patient survival. Crescents IgAN is with the highest risk (up to 5.75 of HR) for patient mortality. The major strengths of the present study is that crescents IgAN had worse patient survival compared to non-crescents IgAN. Clinicians should be more careful to care patients with crescents IgAN.

Developmental processes extend beyond embryogenesis to support lifelong tissue adaptations. Avian feather follicles, with their resident stem cells and capacity for cyclic regeneration, provide a dynamic model for postnatal tissue remodeling. Here, we propose the Mandarin duck ( Aix galericulata ) as an ideal model to study lifelong developmental modulation, focusing on the sexually dimorphic “sail feather”—a secondary flight feather in males that undergoes seasonal transformation into a strikingly asymmetric, ornamented phenotype during the breeding season. We identified asymmetric morphogen expression in regenerating male sail feathers and used transcriptome and H3K27ac ChIP-seq to uncover male and female signaling pathways and regulatory elements. Comparative epigenomic profiling reveals enriched estrogen receptor binding motifs in females. Hormone profiling shows seasonal variation, with a marked rise in female estrogen levels preceding the mating season. These results imply Mandarin duck sail feathers integrate local morphogenetic programs, epigenetic regulation, and systemic hormonal cues to orchestrate sexually dimorphic and seasonally dynamic feather morphogenesis. This work establishes a framework for further mechanistic study of the interplay between regeneration, regional identity, and hormonal plasticity in a vertebrate integumentary system.

Chronic kidney disease-mineral bone disorder is a common complication in patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD), and it increases the risk of osteoporosis and fractures. This study aimed to develop predictive machine-learning (ML) models to identify osteoporosis risk in patients with CKD stages 3–5 and ESKD. We retrospectively analyzed a de-identified osteoporosis database from a Taiwanese hospital, including 6614 patients with CKD stages 3–5 and ESKD who underwent bone mineral density (BMD) scans between January 2011 and June 2022. Nine ML algorithms were applied to predict osteoporosis: logistic regression, XGBoost, LightGBM, CatBoost, SVM, decision tree, random forest, k-nearest neighbors, and an artificial neural network (ANN). The ANN model achieved the highest predictive performance, with an area under the curve (AUC) of 0.940 on the validation and 0.930 on the test datasets. The receiver operating characteristic curve, confusion matrix, and predictive probability histogram revealed that the ANN model performed well in terms of discrimination. Calibration and decision curve analyses further demonstrated the reliability and applicability of the ANN model. The ANN model demonstrated the potential for clinical implementation in screening high-risk patients for osteoporosis.