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Transitioning from pediatric to adult sickle cell disease (SCD) care is challenging for emerging adults (aged 17-25 years). This period is marked by a 7-fold increase in mortality rates and has the highest rates of hospitalizations, emergency room visits, and hospital readmissions compared with children living with SCD. These challenges are exacerbated by fragmented care coordination, difficulty navigating adult health care systems, and increased self-management responsibilities. This study aims to compare the effectiveness of 2 interventions designed to support emerging adults living with SCD during this transition: a mobile health (mHealth) app and community health worker (CHW) support to standard care. The Community Health Workers and Mobile Health for Emerging Adults Transitioning Sickle Cell Disease Care (COMETS) trial is an ongoing multicenter, 3-arm, open-label randomized controlled trial; 375 emerging adults (aged 17-25 years) are being enrolled and randomized 1:1:1 to (1) a 6-month CHW intervention focused on self-management skills, symptom tracking, care coordination, and transition planning; (2) a 6-month mHealth self-management program (enhanced iManage application) with tailored SMS text messaging (THRIVE [Texting Health-Related Resources to Inform, Motivate, and Engage] 2.0); or (3) enhanced usual care (control). Participants are followed for 18 months. The primary outcome is the change in self-reported health-related quality of life assessed using the PedsQL SCD module. Secondary outcomes include acute care use (hospitalizations and emergency department visits), patient activation, self-management behavior, and successful transfer to adult hematology care. The institutional review board at Children's Hospital of Philadelphia approved this study in June 2018. Recruitment began in January 2019 and ended in December 2022; we completed data collection in November 2024. We have enrolled a total of 405 participants. This trial addresses a critical gap in transition intervention research for young adults with SCD. It will provide evidence on the comparative effectiveness of 2 promising interventions (CHW and mHealth) and inform the development of scalable and sustainable transition support programs. Findings will have implications for improving health-related quality of life, reducing acute care use, and promoting successful transition to adult-centered SCD care for this vulnerable population. ClinicalTrials.gov NCT03648710; https://clinicaltrials.gov/study/NCT03648710. DERR1-10.2196/69239.

Background Obesity is associated with an aggressive subtype of breast cancer called basal-like breast cancer (BBC). BBC has no targeted therapies, making the need for mechanistic insight urgent. Reducing adiposity in adulthood can lower incidence of BBC in humans. Thus, this study investigated whether a dietary intervention to reduce adiposity prior to tumor onset would reverse HFD-induced BBC. Methods Adult C3(1)-Tag mice were fed a low or high fat diet (LFD, HFD), and an obese group initially exposed to HFD was then switched to LFD to induce weight loss. A subset of mice was sacrificed prior to average tumor latency to examine unaffected mammary gland. Latency, tumor burden and progression was evaluated for effect of diet exposure. Physiologic, histology and proteomic analysis was undertaken to determine mechanisms regulating obesity and weight loss in BBC risk. Statistical analysis included Kaplan–Meier and log rank analysis to investigate latency. Student’s t tests or ANOVA compared variables. Results Mice that lost weight displayed significantly delayed latency compared to mice fed HFD, with latency matching those on LFD. Plasma leptin concentrations significantly increased with adiposity, were reduced to control levels with weight loss, and negatively correlated with tumor latency. HFD increased atypical ductal hyperplasia and ductal carcinoma in situ in mammary gland isolated prior to mean latency—a phenomenon that was lost in mice induced to lose weight. Importantly, kinome analysis revealed that weight loss reversed HFD-upregulated activity of PKC-α, PKD1, PKA, and MEK3 and increased AMPKα activity in unaffected mammary glands isolated prior to tumor latency. Conclusions Weight loss prior to tumor onset protected against the effects of HFD on latency and pre-neoplastic lesions including atypical ductal hyperplasia and DCIS. Using innovative kinomics, multiple kinases upstream of MAPK/P38α were demonstrated to be activated by HFD-induced weight gain and reversed with weight loss, providing novel targets in obesity-associated BBC. Thus, the HFD-exposed microenvironment that promoted early tumor onset was reprogrammed by weight loss and the restoration of a lean phenotype. Our work contributes to an understanding of underlying mechanisms associated with tumor and normal mammary changes that occur with weight loss.

According to the Brazilian Society of Nephrology, 12 million Brazilians have some degree of renal alteration and 52 million present risk factors for the development of CKD, among them, aging, obesity, AH and diabetes mellitus (DM) [4]. Some factors corroborate for increased albumin excretion, including central obesity, increased systolic blood pressure, renal dysfunction, hypertriglyceridemia, decreased HDL-cholesterol, and insulin resistance [11]. The following biochemical tests were performed: analysis of hematocrit and hemoglobin parameters; serum glucose, triglycerides, LDL-cholesterol, HDL-cholesterol, albumin, uric acid, creatinine, urea, serum sodium. Results The majority of AH patients evaluated were female (77.6%), aged 60 years or older (67.2%), without spouse (58.4%), overweight (65.8%), with schooling up to complete primary school (54.4%), followed by the illiterate population (26.1%), with family income between one and three minimum wages (84.6%), systolic blood pressure lower than 140 mmHg (76.3%) and diastolic blood pressure lower than 90 mmHg (78.6%).