We explored the associations between vitamin C intake and the risk of islet autoimmunity (IA) and/or type 1 diabetes in genetically at-risk children. Furthermore, we explored associations between vitamin C metabolism-related single nucleotide polymorphisms (SNPs) and type 1 diabetes outcomes.

The current study within Environmental Determinants of Diabetes in the Young (TEDDY) cohort included 8478 children followed up every 3-6 months for relevant autoantibodies and diet. Dietary vitamin C intake was assessed longitudinally throughout childhood using age-specific dietary assessment methods and analysed using repeated measurements. Cox regression was used for the primary analyses and Bayesian joint longitudinal-survival models as sensitivity analyses.

A total of 777 (9.2%) children developed IA, including 292 (3.4%) with IAA-first and 337 (4.0%) with GADA-first autoimmunity; 319 (41.0%) progressed to type 1 diabetes. Mean (SD) vitamin C intake was 60.7 (38.8) mg/1000 kcal. Higher vitamin C intake was associated with an increased risk of IAA-first autoimmunity (adjusted hazard ratio 1.04; 95% confidence interval 1.00-1.07, per 10 mg/1000 kcal increase) while lowest and highest tertiles of intake were associated with increased risk of GADA-first autoimmunity as compared to mid-tertile [(1.65; 1.20-2.27) and (1.42; 1.02-1.98), respectively]. Sensitivity analyses using Bayesian joint longitudinal-survival models supported the primary findings and suggested nonlinear associations between vitamin C intake and the risks of IA and multiple IA. Associations between vitamin C-related SNPs and study outcomes did not withstand correction for multiple testing.

Vitamin C intake was not consistently associated with IA or progression to type 1 diabetes. However, the observed nonlinear association, with lowest risk for moderate intakes, merits further investigation.

NCT00279318, 06/09/2004.

Accurate detection of exhaled acetone (ACE) and isopropanol (IPA) mixtures is critical for the non-invasive screening of diabetic ketoacidosis and the continuous monitoring of lipid metabolism in type 1 diabetes mellitus. However, the broad clinical application of this approach remains severely constrained by the inherent cross-sensitivity of metal oxide semiconductor (MOS) sensors. To address this, a microelectromechanical systems (MEMS) dual-sensor array integrating PdO-modified SnO2/ZnO and MoS2/ZIF-67 nanocomposites was developed for simultaneous gas identification and concentration regression. By pioneering the extraction of distinct transient thermokinetic responses of the materials, combined with a multi-task learning architecture featuring a 1D Convolutional Neural Network and a Bidirectional Long Short-Term Memory (CNN-BiLSTM) network, the system efficiently analyzed dynamic sensing data using a sliding time window (K). At an optimal 15-s window, the model demonstrated robust real-time predictive capabilities, achieving 95.4% classification accuracy and a regression mean absolute error (MAE) of 0.625 ppm across clinical IPA/ACE ratios. This deep learning-enabled framework circumvents traditional steady-state limitations, providing a scalable, low-power solution for precise clinical breathomics and metabolic disease screening.

We describe a case of concurrent metformin-associated lactic acidosis (MALA) and euglycemic diabetic ketoacidosis (EDKA) in a 64-year-old woman with type 2 diabetes mellitus (T2DM) treated with metformin and tirzepatide who presented with shock, encephalopathy, and severe high anion gap metabolic acidosis after two weeks of markedly reduced oral intake following tirzepatide dose escalation. While incretin-based therapies, including dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 receptor agonists (GIP/GLP-1 RAs) such as tirzepatide, are highly effective for glycemic control and weight management, gastrointestinal (GI) adverse effects may lead to prolonged caloric restriction and starvation physiology. In this patient, starvation ketosis progressed to EDKA, while concurrent dehydration and acute kidney injury (AKI) impaired metformin clearance, resulting in MALA with markedly elevated lactate. The patient required endotracheal intubation, vasopressor support, and continuous renal replacement therapy (CRRT), with rapid clinical and metabolic improvement following discontinuation of metformin and tirzepatide. This case highlights the potential for severe overlapping metabolic complications involving starvation-related ketoacidosis, dehydration, AKI, and impaired metformin clearance when incretin-based therapies are continued during prolonged poor oral intake.

Balance impairment and postural instability represent critical challenges for the aging population, serving as primary precursors to falls and functional decline in individuals with Type 2 Diabetes Mellitus. While traditional clinical models have largely separated these conditions, attributing balance loss in T2DM to peripheral neuropathy and in AD to central cortical atrophy, mounting evidence suggests a convergence of multi-system impairments driven by a shared central pathophysiology. This narrative review proposes an integrative framework centered on a vicious, self-reinforcing cycle involving metabolic dysfunction, chronic neuroinflammation, and mitochondrial failure as the core mechanistic link driving balance impairment. We detail how systemic and cerebral insulin resistance, coupled with glucotoxicity, trigger the activation of the NLRP3 inflammasome and the subsequent release of pro-inflammatory cytokines. This inflammatory environment exacerbates mitochondrial bioenergetic failure and oxidative stress, selectively targeting high-energy motor circuits such as the striatum and basal ganglia while simultaneously contributing to musculoskeletal sarcopenia and peripheral nerve demyelination. By synthesizing the intricate interplay between these molecular pathways, this review moves beyond disease-specific silos to offer a novel perspective on the shared pathophysiology of postural instability. Furthermore, we explore the therapeutic potential of metabolic modulators, such as GLP-1 receptor agonists, and mitochondrial-targeted antioxidants, alongside multimodal rehabilitation strategies. Ultimately, this unified model provides a foundation for developing precision-based interventions to mitigate fall risk and preserve functional independence in vulnerable aging populations.

We investigated the characteristics of typical adult-onset type 1 diabetes (T1D) and insulin-dependent latent autoimmune diabetes in adults (LADA) in Thailand.

This retrospective chart review enrolled typical T1D and insulin-dependent LADA patients diagnosed at age ≥30 years, and who were followed up at Siriraj Hospital, Thailand, during 2014-August 2024. Potential patients were searched from the Type 1 Diabetes Registry of Siriraj Diabetes Center and electronic medical record.

Among 84 patients, 32 were typical T1D and 52 LADA. At diagnosis, both groups had normal body mass index (20.9 ± 4.5 kg/m²), significant weight loss (13.3 ± 6.4%), short duration of hyperglycemic symptoms (1 [1-2] months), and high fasting blood glucose (259 [174-345] mg/dL). Diabetic ketoacidosis (DKA) was the first presentation in 76.7% of typical T1D and in 2.6% of LADA. Anti-glutamic acid decarboxylase (anti-GAD) was tested in 91.7% of patients (positive: T1D 72%, LADA 100%). Almost 70% of patients with LADA were initially misdiagnosed as T2D and were ultimately diagnosed at 7.6 [2.6-17.5] years later. Patients with LADA had a higher incidence of recurrent DKA. At latest follow-up, patients with LADA had significantly higher systolic blood pressure (SBP), glycated hemoglobin (HbA_1c), and insulin resistance compared to typical T1D.

We found a higher proportion of LADA than typical T1D, and 70% of LADA were initially misdiagnosed as T2D. Both groups were characterized by a normal BMI, significant weight loss, and a short duration of hyperglycemic symptoms. However, LADA rarely presented with DKA and had higher HbA_1c and insulin resistance during follow-up.

Atrial fibrillation (AF) increases thromboembolic risk, and oral anticoagulants (OACs) substantially reduce this risk; however, their safe and effective use requires adequate patient knowledge. We aimed to assess AF- and OAC-related awareness among Turkish patients and to identify predictors of knowledge.

This single-center, cross-sectional survey was conducted between July 1, 2024 and January 1, 2025, and included consecutive adults with non-valvular AF receiving warfarin or direct OACs for at least three months. A structured questionnaire collected data on demographic characteristics, comorbidities, medication use, adherence, and knowledge across six domains: arrhythmia name, treatment indication, dosing schedule, side effects, drug and food interactions, and consequences of dose modification. A composite knowledge score (range, 0���6) was calculated. Multivariable linear regression was used to evaluate predictors of knowledge, including age, sex, and education level. Ethics approval was obtained, and all participants provided written informed consent.

A total of 261 patients were included (median age, 67 years; 50.2% women). Hypertension and diabetes mellitus were present in 64.8% and 32.2% of patients, respectively. Direct oral anticoagulants (DOACs) accounted for 72.4% of prescriptions, whereas 27.6% of patients received warfarin. Although 36% of participants had AF for more than six years, only 16.5% could correctly name their arrhythmia. While 92% knew they were taking an anticoagulant, 24% misunderstood its indication. Knowledge of side effects was limited, with 68% reporting no awareness. Awareness of interactions was poor: 88% reported no knowledge of drug���drug interactions, and 71% were unaware of food interactions. Most patients knew their dosing schedule (92.3%) and reported that they would not double a missed dose (99.6%). Self-reported adherence was high (94% 'always' and 4% 'often'), and taking medication with meals was associated with better adherence (���� = 17.0, P < 0.001). The mean knowledge score was 2.8 +- 1.3 (Cronbach's �� = 0.50). Higher educational attainment and female sex were associated with greater knowledge, whereas age was inversely associated with knowledge.

Despite high self-reported adherence, substantial knowledge gaps persist among patients receiving anticoagulation for AF, particularly regarding side effects and drug or food interactions. Targeted, health-literacy-sensitive educational strategies may improve medication safety and clinical outcomes in patients receiving anticoagulation for AF.

Intestinal Staphylococcus aureus colonization in type 2 diabetes mellitus (T2DM) remains poorly defined with respect to prevalence, clinical associations, and molecular characteristics. We investigated intestinal S. aureus colonization in 142 patients with T2DM and characterized the recovered isolates using antimicrobial susceptibility testing, resistance gene profiling, multilocus sequence typing, accessory gene regulator typing, spa typing, and whole-genome sequencing. Clinical and laboratory characteristics were compared between colonized and non-colonized patients, and siderophore production and biofilm formation were evaluated in major molecular types. S. aureus colonization was identified in 30 patients (21.1%, 95% confidence interval: 15.2%-28.6%) based on a single fecal sample per patient, including one methicillin-resistant isolate. Isolates remained highly susceptible to most tested antimicrobials, except penicillin. The β-lactamase gene blaZ was the most prevalent resistance determinant (83.3%). MLST revealed a polyclonal population dominated by ST15 (30.0%), ST1156 (26.7%), and ST5 (26.7%), with agr II (56.7%) and spa type t84 (43.3%) being the most common types. Whole-genome sequencing further demonstrated distinct plasmid architectures between methicillin-susceptible S. aureus and methicillin-resistant S. aureus (MRSA) isolates and identified an SCCmec IVc (2B) element in the MRSA isolate. Siderophore production was significantly higher in ST15 and ST1156 than in ST5, whereas biofilm formation did not. These findings provide a comprehensive characterization of the clinical and epidemiological profiles of intestinal S. aureus colonization in patients with T2DM and highlight the need for continued genomic surveillance and mechanistic studies to support infection prevention and therapeutic strategies.IMPORTANCEIntestinal Staphylococcus aureus colonization in type 2 diabetes mellitus (T2DM) has remained largely uncharacterized despite the well-documented heightened infection risk in this population. Here, we show that 21.1% (95% confidence interval: 15.2%-28.6%) of hospitalized T2DM patients harbor gut S. aureus (only 3.3% methicillin-resistant S. aureus [MRSA]). The isolates form a polyclonal population dominated by ST15, ST1156, and ST5, carry predominantly blaZ, and display lineage-specific differences in siderophore production-an iron-acquisition trait critical for gut persistence. These data establish the diabetic intestine as a clinically relevant reservoir, underscore the limitations of nares-only surveillance, and highlight the need for integrated genomic and mechanistic studies to guide infection prevention in T2DM.

This is a protocol for a Cochrane review (intervention). The objectives are as follows: To determine if lower blood pressure (BP) targets (i.e. ≤ 130/85 mmHg), compared with standard BP targets (i.e. ≤ 140 to 160/90 to 100 mmHg) are associated with reduction in mortality and morbidity in people with elevated BP and diabetes mellitus.