Accurate estimation of meal composition from food images can support safer and more reliable insulin bolus decision-making for individuals with Type 1 diabetes. Existing food recognition and nutrition estimation systems are often designed for general dietary logging and do not directly integrate food analysis with personalized insulin therapy parameters.

This study presents an image-based nutrition estimation and insulin decision-support module developed within the AI-assisted Diabetes Care (AIDCARE) platform. The proposed system uses a convolutional neural network (CNN) to classify food items from a single meal image, and retrieves reference nutritional values from a food composition database. A separate multimodal large language model (MLLM)-based estimation component is then used to estimate portion size, allowing carbohydrate and nutrient values to be scaled according to the observed serving.

A curated food image dataset containing 40 food categories was used to evaluate three CNN architectures: ResNet50, Inception V3, and EfficientNet-B0. EfficientNet-B0 achieved the best classification performance, with 94.91% validation accuracy, 95.55% precision, 94.87% recall, and 94.90% F1-score. The portion-estimation component achieved an MAE of 12.27 g and an RMSE of 15.11 g. The estimated carbohydrate value is combined with user-specific clinical parameters, including the insulin-to-carbohydrate ratio and insulin sensitivity factor, to generate advisory bolus guidance. To support safety, the system requires user confirmation or correction of the recognized food category and estimated portion before insulin guidance is displayed.

The proposed system is intended for advisory decision support only and is not designed to replace clinical judgment or autonomous insulin delivery systems.

Young adulthood is a socially and biographically formative life stage, yet young adults from ethnic-national minority groups remain underrepresented in psycho-oncology research. This study examined how Arab young adults (YA) from East Jerusalem make meaning of cancer while receiving treatment in predominantly Jewish-Israeli hospitals.

Guided by a context-informed, constructivist qualitative framework, we conducted semi-structured, in-depth interviews with 15 Arab YA (aged 23-45) who were undergoing active cancer treatment. Interviews were conducted in Arabic, transcribed verbatim, and analyzed using reflexive thematic analysis to capture culturally and developmentally embedded meanings of illness and care.

Two interrelated sets of lived meanings emerged. First, participants described cancer through culturally embedded frameworks shaped by stigma, secrecy, family responsibility, and faith-based interpretations that provided meaning and emotional containment. These meanings were closely tied to the future-oriented concerns and relational obligations of young adulthood. Second, participants experienced Israeli hospitals as ambivalent institutional spaces: often perceived as safe, compassionate, and politically neutral yet at times marked by cultural misattunement, language barriers, and subtle inequality. Together, the findings show that cancer was experienced not only as a medical condition but as a deeply contextualized social and developmental experience.

The experience of cancer among Arab YA from East Jerusalem is shaped by the intersection of developmental stage, minority positioning, and institutional context. These findings highlight the importance of context-informed and culturally responsive psycho-oncology care for young patients from socially and politically marginalized backgrounds.

Restrained eating has been recognized as a maladaptive behavior linked to various adverse health outcomes, such as eating disorders and anxiety, which can significantly impact both physical and mental well-being. However, little is known about how perceived sociocultural pressures correlate with restrained eating. Therefore, based on the Tripartite Influence Model and Objectification Theory, we investigated the association between perceived sociocultural pressure and restrained eating as well as the potential mediating role of self-objectification and body-esteem in this association.

Participants were 1774 students aged 16-33 years (M_age = 19.28 years, 65.80% female) who completed assessments of perceived sociocultural pressure, self-objectification, body-esteem, and restrained eating.

The results indicated that after controlling for body mass index and sex, perceived sociocultural pressure was positively correlated with restrained eating. Self-objectification and body-esteem were serial mediators of the association between perceived sociocultural pressure and restrained eating.

These correlational results suggest that body-esteem may serve as a promising intervention target for programs designed to prevent and reduce restrained eating. In addition, these correlational findings shed light on the prevention and intervention of restrained eating and provide a new theoretical perspective on mental health. In addition, implications and directions for future research were also discussed.

The health consequences of being underweight are less well-studied than obesity. We aimed to examine the association between body mass index (BMI) and mortality from a wide range of diseases across the full BMI spectrum, with particular focus on how low BMI may affect premature and nonpremature death.

After excluding ever-smokers and those with pre-existing major diseases, this study included 262 704 women aged 30-79 from the China Kadoorie Biobank. The baseline BMI (kg/m²) was calculated using measured height and weight and classified into six groups: < 18.5, 18.5-19.9, 20.0-22.4, 22.5-23.9 (reference), 24.0-27.9 and ≥ 28.0. Long-term follow-up was conducted by linking to the local death registry. Cox regression was used to estimate the hazard ratios (HRs) of BMI with all-cause and cause-specific mortality, after adjusting for waist circumference and potential confounders.

At baseline, 3.9%, 7.8% and 11.4% of participants had BMIs (kg/m²) of < 18.5, 18.5-19.9 and ≥ 28.0, respectively. During a median follow-up of 17.1 years, 29 531 deaths were recorded, including 11 455 premature deaths (under the age of 70) and 18 076 nonpremature deaths. The risk of all-cause mortality significantly increased at the lower extreme of BMI, reached a nadir around 23.5 kg/m² estimated from restricted cubic splines and showed a modest increase at the upper extreme. Participants with BMI < 18.5, 18.5-19.9 and 20.0-22.4 had higher risks of premature death (HRs) of 1.91 (1.73-2.10), 1.24 (1.14-1.34) and 1.16 (1.11-1.21), respectively. The corresponding HRs for nonpremature death were 1.46 (1.36-1.56), 1.17 (1.10-1.23) and 1.04 (1.01-1.08). The analysis of premature death involved 33 diseases from eight ICD-10 chapters, and nonpremature death involved 40 diseases from nine chapters. Underweight was linked to an increased risk of premature death in seven chapters and 10 diseases, including neoplasms (HR = 1.36, 95% CI: 1.16-1.59), endocrine-metabolic (6.03, 4.13-8.82), circulatory (1.85, 1.56-2.20), respiratory (5.85, 3.89-8.80), digestive (5.64, 3.13-10.18), genitourinary (2.61, 1.20-5.69) and external causes (2.06, 1.55-2.72). Underweight was also associated with an increased risk of nonpremature death in four chapters and seven diseases. In contrast, obesity was only associated with increased risks of premature and nonpremature death in two and one chapters, respectively.

Among Chinese female healthy never-smokers, underweight was an important risk factor for all-cause and multiple cause-specific mortality, especially the risk of premature death. While addressing the global obesity epidemic, the negative health consequences of low weight should not be ignored.

To evaluate crowd-management strategies used at mass public gatherings and to identify the evidence gaps and priorities that reduce the risk of stampedes.

Following PRISMA 2020 and PRISMA-S guidelines, the paper searched PubMed, Scopus, Web of Science, Google Scholar (gray literature), and the WHO Global Health Library (gray literature) published between January 1, 2010 and December 30, 2025. Eligible studies included observational, quasi-experimental, and simulation-based evaluations of crowd-safety interventions. Two reviewers independently screened records, extracted data, and appraised study quality using ROBINS-I and JBI checklist. A narrative (thematic) synthesis grouped interventions into engineering, operational, technology, and communication approaches.

Of 833 unique records identified, 13 studies met the inclusion criteria. Included studies were mainly observational analyses, simulation/modeling studies, or quasi-experiments from diverse settings (pilgrimages, festivals, sports events). Multi-modal strategies combining environmental design (one-way flows, barriers), operational controls, real-time monitoring, and trained personnel were consistently associated with improved crowd-flow indicators (shorter evacuation times).

Integrated crowd-management approaches can mitigate stampede risks, but require high-quality empirical evaluations and standardized outcome metrics to strengthen evidence for policy and practice.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420251142906, identifier CRD420251142906.

Evidence on the burden and clustering of metabolic non-communicable disease risks and on data-driven risk profiles remains limited. This study assessed trends in the clustering of metabolic risk factors in Viet Nam from 2015 to 2021 and identified behavioral-metabolic profiles in 2021.

A repeated cross-sectional design was used, using national STEPS data from 2015 (n = 3,074) and 2021 (n = 3,712), both of which included participants who completed all survey components. Behavioral risk factors (smoking, alcohol use, physical inactivity, and low fruit and vegetable intake) and metabolic risk factors (elevated blood pressure, fasting glucose, body mass index (BMI), and total cholesterol) were defined using Asian-calibrated cutoffs. Clustering was defined as the co-occurrence of two or more metabolic risk factors within an individual. Weighted analyses estimated prevalence and clustering, and latent class analysis (LCA) identified behavioral-metabolic profiles.

All metabolic risks increased between 2015 and 2021, most sharply for raised fasting glucose (12.0% → 37.7%). This increase was a major contributor to intensified clustering, with the prevalence of ≥2 risk factors increasing from 27.6% to 46.6% and ≥3 risk factors increasing from 8.7% to 20.1%. LCA revealed three profiles: "Health-Conscious" (38.1%, low behavioral and metabolic risks), "Metabolic Risk-Aware" (34.6%, low behavioral but high metabolic risks, linked to older age), and "High Behavioral Risk with Moderate Metabolic Comorbidity" (27.3%, characterized by high smoking and alcohol use together with moderate metabolic abnormalities, concentrated among socioeconomically disadvantaged men).

Metabolic risks in Viet Nam increased markedly between 2015 and 2021, with elevated glucose levels playing an important role in multi-risk clustering. These distinct profiles underscore the need for integrated, multi-risk screening and management in primary care, especially targeting older adults and socioeconomically disadvantaged men.

Male fertility has declined globally. Diabetes and aging are major contributors to the reduced sperm production and testicular dysfunction. Elevated glucagon signaling leads to diabetic complications, yet its impact on male reproductive function remains unclear.

Streptozotocin-induced type 1 diabetic mice, naturally aged mice, and healthy young male mice were treated with a glucagon receptor (GCGR) monoclonal antibody or control. Sperm quality and testicular outcomes, including histology, oxidative stress, and apoptosis, were assessed. We then generated global Gcgr knockout mice and compared their sperm parameters and testicular outcomes with those of wild-type mice. Mouse spermatogonia cells, spermatocyte cells, Leydig cells, and Sertoli cells were treated with different concentrations of glucagon, and cell proliferation was evaluated. In Sertoli cells, maturation markers and blood-testis barrier (BTB)-associated genes were examined. The histology and function of Sertoli cells were further measured in diabetic or aged mice after GCGR antibody treatment. To investigate the underlying mechanism, we treated Sertoli cells with glucagon, a GCGR antibody, or a GLP-1R antagonist, and measured the lactate content, lactate dehydrogenase activity, and the expression of glucose transporters, glycolysis-associated genes, and lactate dehydrogenase isoforms. We focused on the glycolytic regulator 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3). The lactate production and PFKFB3 level were further determined in diabetic or aged mice. Next, by using over-expression or knockdown of Pfkfb3 in glucagon-treated Sertoli cells and constructing Pfkfb3 heterozygous knockout mice, we confirmed the role of PFKFB3 in lactate production and Sertoli-cell function.

In diabetic mice, the GCGR antibody increased sperm concentration (P < 0.001) and reduced testicular oxidative stress and apoptosis. In aged mice, the GCGR antibody improved progressive motility (P = 0.004), with minimal effects on reproductive hormone levels, testicular oxidative stress, and apoptosis. In healthy young mice, the GCGR antibody increased sperm concentration (P = 0.003), progressive motility (P = 0.022), and total motility (P = 0.020). Global Gcgr knockout impaired spermatogenesis despite improved metabolic status, indicating the participation of GCGR signaling in embryonic testicular development and spermatogenesis. Glucagon did not directly alter isolated sperm motility or proliferation of testicular cell lines, but it suppressed Sertoli-cell maturation markers, BTB-associated genes, lactate production, and PFKFB3 expression. These effects were rescued by the GCGR antibody, whereas GLP-1R blockade showed partial or variable protection. Besides, these inhibitory effects of glucagon were rescued by Pfkfb3 overexpression while Pfkfb3 knockdown showed the similar effects with glucagon. In diabetic and aged mice, the GCGR antibody administration restored Sertoli-cell maturation markers and BTB markers, upregulated testicular lactate levels and increased the abundance of PFKFB3. Pfkfb3 heterozygous deletion reduced total motility (P = 0.007) and testicular lactate content (P = 0.013), accompanied by the lower Sertoli-cell markers and BTB-associated genes expression.

Pharmacological GCGR blockade reverses dysfunctional Sertoli cells and restores spermatogenesis in models of diabetes and aging, and PFKFB3-mediated lactate production participated this process. Our study presents a promising therapeutic strategy for male infertility.

Early-onset colorectal cancer (EOCRC, < 50 years) is rising in the United States, whereas late-onset CRC (LOCRC, ≥ 50 years) is declining. Fewer studies have examined association between risk factors and age at colorectal (CRC) diagnosis by race. Hence, we investigated whether associations between lifestyle and clinical risk factors and age at CRC diagnosis differed by race.

Retrospective study conducted between 2010 and 2023 using data from a tertiary medical center in Alabama. Exposure included lifestyle factors-smoking status, and body mass index; clinical factors-type 2 diabetes (T2D), hypertension, and hyperlipidemia. Outcome was age at CRC diagnosis categorized as LOCRC and EOCRC. Multivariable logistic regression was used to examine association between lifestyle and clinical risk factors with age at CRC diagnosis after controlling for race, sex, and marital status. Race-stratified analyses were conducted.

Among 3,209 CRC patients, 54.1% were male, 71.4% White, and 55.8% were married. LOCRC was diagnosed in 81.2%. Patients who were former smokers (OR: 1.89; 95% CI: 1.50, 2.39), had T2D (OR: 1.92; 95% CI: 1.44, 2.57), hypertension (OR: 2.46; 95% CI: 1.65, 3.66), and hyperlipidemia (OR: 3.32; 95% CI: 2.35, 4.70) had higher odds of LOCRC, whereas obesity (OR: 0.61; 95% CI: 0.48, 0.77) had lower odds of LOCRC compared to EOCRC. Hypertension showed significant association with LOCRC in White patients. Hyperlipidemia showed stronger association with LOCRC in Black patients.

Obesity was more prevalent in EOCRC patients and hence these differences should be considered in development of age-stratified screening and prevention strategies.

Renal tubular senescence is a defining pathological feature of diabetic kidney disease (DKD) and a key driver of disease progression. While glucotoxic stress is recognized as a major contributor to tubular aging, the upstream regulatory mechanisms remain incompletely understood. Here, we investigated the role of C1q/TNF-related protein 1 (CTRP1) in DKD-associated tubular senescence and its mechanistic link to SGLT2-mediated glucose uptake. We conducted a retrospective observational case-control analysis of human renal biopsy specimens, complemented by mechanistic experiments in NRK-52E cells and a high-fat diet/streptozotocin/uninephrectomy (HFD-STZ-UNx) rat model. Renal cortical tissues from DKD patients and controls were analyzed via immunohistochemistry and Western blotting. CTRP1 expression increased progressively with DKD severity and was positively correlated with the senescence markers p21 (R = 0.498) and p16 (R = 0.494). Bioinformatic analysis of CTRP1-deficient mice revealed consistent SGLT2 downregulation, which was validated experimentally in NRK-52E cells, where CTRP1 overexpression increased SGLT2 expression and glucose uptake, particularly under hyperglycemic conditions. In HFD/STZ/UNx-induced DKD rats, dapagliflozin (0.1 mg/kg/day) improved metabolic abnormalities and renal dysfunction and attenuated tubular senescence. Dapagliflozin suppressed CTRP1-SGLT2 axis activation, reduced glucose uptake in renal tubular cells, and markedly decreased the proportion of CTRP1⁺SGLT2⁺ double-positive tubular cells. These findings support the presence of a previously unrecognized CTRP1-SGLT2 signaling axis associated with glucose-mediated tubular senescence in DKD and provide mechanistic insight into SGLT2 inhibitor-mediated renoprotection.

Inequities in diabetes diagnosis, management, and outcomes are deeply rooted in social determinants of health and structural racism. Historical policies such as redlining and concentrated poverty in low-income neighborhoods have shaped environments characterized by limited access to healthy food and proper healthcare, which ultimately led to a disproportionate burden of diabetes in these populations. The consequences of these disparities for racial and ethnic minoritized groups include a lower ability to achieve glycemic targets, receive novel glucose-lowering agents, and/or have access to diabetes technology. The downstream effect is that this population experiences worse health outcomes from complications (i.e., amputation, blindness, end-stage renal disease) and mortality. This narrative review synthesizes current literature on racial/ethnic inequities in diabetes care, highlighting differences in screening, glycemic control, complication rates, and mortality in people living with diabetes from diverse racial and ethnic backgrounds, but also identifies opportunities for intervention to ensure equitable access to evidence-based care.