Diabetes prevalence is increasing in Thailand, creating growing demands on the health system. Understanding the spatial distribution of diabetes risk and its association with socioeconomic and healthcare system factors among the diabetes risk population is critical for designing targeted prevention and intervention strategies. We examined the distribution of diabetes risk groups across provinces in Thailand with reference to the spatial association between economic, social and public health service factors based on data from the Ministry of Public Health's Health Data Center (HDC) for the year 2021. The dataset included 22,491,934 individuals across the 76 provinces as well as social, economic and public health services. The methods included Local Indicators of Spatial Association (LISA), Ordinary Least Squares (OLS), Spatial Lag Model (SLM) and Spatial Error Model (SEM). Explanatory variables included average night-time light intensity, average monthly income, hospital-to-population ratio and proportion of the population with health insurance. Major clusters of High-High (HH) diabetes risk were identified by LISA mainly located in the North of Thailand. In all models, the direction and significance of the associations were consistent (p<0.001 for all variables investigated and p<0.01). R2=0.47. The SLM gave the best fit, capturing spatial spill-over effects. Higher night-time light intensity (coefficient = -85.70, p<0.05) and higher monthly income (coefficient = -0.079, p<0.001) were negatively associated with diabetes risk. These inverse relationships implied that greater urbanization and higher socio-economic standing may protect against diabetes risk, possibly through improved access to health infrastructure, improved health education and preventive services. Conversely, the higher hospital-to-population ratios (coefficient = 572.28, p<0.001) and the larger proportions of Civil Servant Medical Benefits Scheme (CSMBS) coverage (coefficient = 226.46, p<0.001) the higher diabetes risk. These counterintuitive findings likely reflect reverse causation, in which provinces with higher disease burden or poor health attract more resources of health care and have increased insurance coverage, a pattern consistent with healthcare service distribution responding to existing health needs rather than preventing occurrence of disease.

To characterize longitudinal impaired fasting glucose (IFG) evolution patterns and evaluate their associations with the risk of incident cardio-kidney-metabolic (CKM) multimorbidity.

In this prospective cohort study, 43,073 adults from the Kailuan Study who underwent examinations in 2006 and 2010 and were free of cardiovascular disease, type 2 diabetes, and chronic kidney disease at baseline were included. IFG status was classified as sustained normal, progression, recovery, or persistent IFG. Participants were followed through 2021. The primary outcome was multimorbidity, defined as ≥2 of the following: cardiovascular disease, type 2 diabetes, or chronic kidney disease. Multivariable Cox models estimated adjusted hazard ratios (HRs).

Over a median follow-up of 11.0 years, 1,795 participants developed CKM multimorbidity. Compared with sustained normal fasting glucose, adjusted HRs (95% CIs) were 1.93 (1.72-2.17) for IFG progression, 1.69 (1.44-1.98) for IFG recovery, and 3.10 (2.74-3.52) for persistent IFG. Using IFG recovery as the reference, risks remained lower for sustained fasting glucose health (HR 0.59; 95% CI 0.51-0.69), whereas persistent IFG remained associated with a higher risk (HR 1.84; 95% CI 1.55-2.18). The association for IFG progression was attenuated and no longer statistically significant (HR 1.14; 95% CI 0.97-1.35).

Individuals who recover from IFG have a lower risk than those with persistent or progressive IFG, yet their risk remains higher than that of individuals with sustained fasting glucose health. These findings highlight that preventing the onset of IFG should be the optimal strategy, followed by timely intervention after its occurrence to mitigate long-term multisystem damage.

Hypoglycemia is a major safety concern for drivers with diabetes. Continuous glucose monitoring (CGM) improves detection of low glucose levels while driving, yet evidence regarding real-world use remains limited. We conducted a national survey of 1209 Australian drivers with diabetes treated with glucose-lowering medication (mean age 55, standard deviation15 years; 47% using CGM; 39% with type 1 diabetes). Twenty-eight percent of participants reported hypoglycemia while driving in the past 12 months. CGM use was associated with higher odds of reporting hypoglycemia while driving (adjusted odds ratio 3.61 [95% confidence interval: 2.19-5.68]), likely reflecting greater detection. Two-thirds of CGM users relied on CGM vibration or audio alerts, and fewer than one in five adjusted alert thresholds for driving. Difficulty using CGM while driving (50%) and legal uncertainty (43%) were the most frequent barriers. Drivers expressed strong interest in safer in-car CGM integration and clearer legal guidance to support glucose monitoring while driving.

Metabolic diseases, including type 2 diabetes mellitus (T2DM), obesity, dyslipidemia, Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), and obstructive sleep apnoea (OSA), are characterized by a complex and interconnected pathophysiological syndrome. These conditions involve insulin resistance, chronic inflammation, and disturbances in energy homeostasis. Typically, they affect multiple organs and require comprehensive treatment.

This narrative review examines the multi-organ effects of tirzepatide, a new dual agonist of the glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) receptors. Tirzepatide possesses innovative therapeutic properties and targets multiple metabolic pathways. The review incorporates peer-reviewed sources, including clinical trials, preclinical studies, and specialist reviews. Emphasis is placed on tirzepatide's physiological effects on pancreatic β-cells, adipose tissue, the liver, the gastrointestinal tract, the cardiovascular system, the kidneys, the brain, and gut microbiota.

Tirzepatide is a dual receptor agonist that increases insulin levels, decreases glucagon levels, slows gastric emptying, and promotes feelings of fullness, contributing to significant weight loss. Recent preclinical studies have shown that tirzepatide can also alter gut microbiota composition, leading to increased Bacteroidetes and decreased Firmicutes. Additionally, tirzepatide has been shown to enhance intestinal barrier integrity. Clinical trial programs, such as SURPASS and SURMOUNT, have demonstrated that tirzepatide provides improved glycemic control and weight loss compared to current treatments. Other benefits include improvements in lipid profiles, reduced hepatic steatosis, and potential protection for the heart and kidneys.

Tirzepatide is a multi-organ integrator with a therapeutic effect extending beyond glucose regulation. It can influence bowel hormones, improve metabolic parameters, and facilitate communication between different organs, making it a promising treatment for metabolic disorders. However, its broader clinical applications need to be confirmed through additional real-life studies and extended evaluations.

Klebsiella quasipneumoniae is a member of the Klebsiella pneumoniae complex that is difficult to distinguish from K. pneumoniae using conventional laboratory methods, and information on its clinical manifestations is limited. We describe the first known case of invasive infection with hypervirulent K. quasipneumoniae subsp. similipneumoniae in Japan. A 65-year-old woman with pancreatogenic diabetes mellitus presented with fever and nausea. Computed tomography revealed a liver abscess and multiple pulmonary nodules with cavitation suggestive of septic pulmonary emboli. Blood cultures yielded an isolate identified as K. pneumoniae complex. Whole-genome sequencing (WGS) subsequently identified the isolate as K. quasipneumoniae subsp. similipneumoniae, sequence type 367 (ST367) and capsular type K1 (KL1). The isolate exhibited a hypermucoviscous phenotype and harbored the virulence-associated genes iroBCDN, iucABCD/iutA, rmpA/A2, and peg-344. The patient improved following antimicrobial therapy with meropenem for 10 days, followed by cefmetazole for 13 days, and was discharged home after a hospital stay of 81 days. This case highlights the potential for invasive infection caused by hypervirulent K. quasipneumoniae, the usefulness of WGS for species identification, and the need for ongoing clinical and genomic surveillance to monitor the emergence of this pathogen.

The impact of increasingly prevalent cardiovascular-kidney-metabolic (CKM) multimorbidity on absolute survival remains unclear. We aimed to assess the association of CKM multimorbidity with mortality and life expectancy in US adults.

We included 46,543 adults (mean age 50.0 years) from NHANES (1999-2018). CKM conditions included type 2 diabetes (T2DM), chronic kidney disease (CKD), and cardiovascular disease (CVD). Over a 9.2-year median follow-up, mortality risk increased sequentially with the number of CKM conditions. Compared to participants without CKM conditions, adjusted hazard ratios for all-cause mortality were 2.59 (95% CI: 2.30-2.92) for T2DM + CKD, 2.27 (1.90-2.72) for T2DM + CVD, 2.69 (2.39-3.04) for CKD + CVD, and 3.57 (3.08-4.14) for all three conditions. Using life table methods, we estimated corresponding reductions in life expectancy at age 50. Compared to the reference group, life expectancy losses were 9.2, 8.8, 13.2, and 17.0 years for individuals with T2DM + CKD, T2DM + CVD, CKD + CVD, and all three conditions, respectively. These profound reductions were predominantly attributable to increased CVD deaths, even among those without baseline CVD.

CKM multimorbidity is independently associated with remarkably reduced life expectancy. Because these life years lost are largely driven by CVD mortality, integrated prevention strategies are urgently needed.

Complex anal fistulas pose a significant surgical challenge because of high recurrence rates and the risk of fecal incontinence. Fistulotomy with primary sphincteroplasty has been proposed as a single-stage treatment that combines fistula eradication with sphincter reconstruction. However, concerns regarding postoperative continence have limited its widespread adoption. This study aimed to evaluate the long-term clinical and functional outcomes of fistulotomy with primary sphincteroplasty in patients with complex anal fistulas.

A retrospective, single-center cohort study was conducted at the University Hospital of Mersin, Turkey. The study included 382 patients with complex cryptoglandular anal fistulas who underwent fistulotomy with primary sphincteroplasty between January 2013 and January 2023. All procedures were performed by 3 experienced colorectal surgeons using a standardized technique. Primary outcomes were healing rates, recurrence, and continence status assessed by the Wexner score over a mean follow-up of 52.5 months.

The cohort consisted of 277 male (72.5%) and 105 female (27.5%) patients, with a mean age of 42.1 ± 13.7 years. Primary healing after fistulotomy with primary sphincteroplasty was achieved in 91.9% (351 of 382) of patients. Recurrence occurred in 31 patients (8.1%), of whom 19 were successfully treated with redo fistulotomy with primary sphincteroplasty. The final persistent recurrence rate was 3.1% (12 of 382), resulting in an overall success rate of 96.9%. No cases of major fecal incontinence were reported. Minor incontinence was observed in 4.9% of patients. Multivariate analysis identified female gender, diabetes mellitus, active smoking, body mass index >28 kg/m², and operative time >60 minutes as independent predictors of recurrence.

Fistulotomy with primary sphincteroplasty demonstrates excellent long-term efficacy as a single-stage procedure for complex cryptoglandular anal fistulas, providing durable healing with minimal impact on continence when performed by experienced surgeons.

Obesity represents a growing concern in the aviation environment due to its association with cardiovascular disease, diabetes mellitus, and obstructive sleep apnea, conditions that may compromise aeromedical certification and long-term medical fitness for flight duties. Although bariatric surgery (BS) effectively reduces obesity-related comorbidities, its long-term implications for pilots remain insufficiently characterized from an aeromedical perspective. This systematic review evaluates long-term health outcomes following BS relevant to flight personnel performance, safety, and aeromedical decision-making.

This PRISMA-compliant systematic review included studies published between 2013-2024. Long-term postoperative outcomes following BS were evaluated in relation to aeromedical certification and fitness-for-duty standards established by the Federal Aviation Administration, European Union Aviation Safety Agency, and International Civil Aviation Organization.

Of 3201 records identified, 38 studies met inclusion criteria. BS demonstrated substantial long-term benefits, including sustained weight loss, improved glycemic control, and reduced cardiovascular events. However, several aeromedically relevant risks were identified. Chronic micronutrient deficiencies-particularly vitamin B12, iron, copper, and vitamin D-were frequently reported and may result in anemia and potential in-flight incapacitation. Neurological complications were reported in 5-16% of patients and altered pharmacokinetics may impair absorption. Notably, no long-term aviation-specific postoperative surveillance guidelines were identified.

Given the absence of aviation-specific guidance, aeromedical certification following BS should be based on individualized, risk-oriented assessments rather than early postoperative outcomes alone. This approach should emphasize lifelong monitoring of nutritional status and neurocognitive function, while recognizing that evidence highlights the need for further research to better define aeromedical implications. Mendoza Mantilla DA, Serna AZ, Delgado AM, Mathers CH. Long-term post-bariatric surgical outcomes for aeromedical certification consideration. Aerosp Med Hum Perform. 2026; 97(7):524-533.

Danggui Buxue Decoction (DBD), a classical Traditional Chinese Medicine (TCM) formula comprising Astragalus membranaceus (Fisch.) Bunge (Astragali Radix) and Angelica sinensis (Oliv.) Diels (Angelicae Sinensis Radix) in a 5:1 ratio, has been traditionally used to treat "Xiaoke" (wasting-thirst syndrome) and is increasingly applied as an adjunctive therapy for diabetic nephropathy (DN). DN is a major microvascular complication of diabetes mellitus for which effective curative therapies remain limited. Although DBD has demonstrated promising clinical efficacy in the prevention and management of DN, its pharmacologically active constituents and underlying mechanisms of action have yet to be fully elucidated.

This study aimed to comprehensively profile the blood-entering bioactive constituents of DBD, identify the core active compound through integrated UPLC-Q-TOF-MS/MS and network pharmacology analyses, and elucidate the molecular mechanisms by which the core constituent protects against high glucose-induced podocyte injury, with particular focus on the miR-223-3p/NLRP3 inflammasome axis.

UPLC-Q-TOF-MS/MS was employed to globally characterize the chemical constituents of Danggui Buxue Decoction (DBD), and the absorbed components and in vivo metabolites were identified in a DN rat model. Network pharmacology combined with target intersection analysis was used to identify the core active constituents. Subsequently, PPI network construction, GO functional annotation, and KEGG pathway enrichment analyses were performed to elucidate the underlying molecular mechanisms. In a high glucose-induced MPC5 podocyte model, CCK-8, TUNEL, and JC-1 assays were conducted to evaluate the cytoprotective effects of the major active constituents. Furthermore, Western blotting, qRT-PCR, and dual-luciferase reporter assays were performed to clarify the regulatory mechanism of the miR-223-3p/NLRP3 axis.

UPLC-Q-TOF-MS/MS identified a total of 1,584 chemical constituents in DBD, among which 249 absorbed components and 155 in vivo metabolites were detected in the plasma of DN model rats. Network pharmacology analysis identified senkyunolide A (SA) as the core active constituent, which targeted 33 NLRP3 inflammasome-related proteins, covering the entire activation cascade of this pathway. PPI network construction and enrichment analyses further revealed that SA-associated targets were involved in key biological processes at the systems level, including oxidative stress and PI3K-Akt/NF-κB signaling pathways. In vitro experiments demonstrated that SA at a concentration of 50 μmol/L significantly ameliorated high glucose-induced podocyte injury, apoptosis, and mitochondrial dysfunction. Mechanistically, SA upregulated miR-223-3p expression, thereby directly inhibiting NLRP3 inflammasome activation, which in turn suppressed Caspase-1 cleavage and GSDMD-mediated pyroptosis. Meanwhile, SA maintained mitochondrial dynamic homeostasis and energy metabolism by regulating DRP1 phosphorylation, upregulating OPA1 and MFN2, and activating the PGC-1α/MnSOD pathway, ultimately exerting multi-level protective effects on podocytes.

SA is identified as the core bioactive constituent of DBD responsible for its therapeutic effects in DN. SA exerts multi-level renoprotective effects by upregulating miR-223-3p, suppressing NLRP3 inflammasome activation and GSDMD-mediated pyroptosis, and maintaining mitochondrial dynamic homeostasis via the PGC-1α/MnSOD pathway. These findings provide a scientific basis for the rational application of DBD in the clinical prevention and treatment of diabetic nephropathy and highlight the miR-223-3p/NLRP3 axis as a promising therapeutic target.

Metabolic diseases, including type 2 diabetes mellitus, obesity, and metabolic dysfunction-associated steatotic liver disease, are major global health challenges, sharing features such as disrupted glucose-lipid homeostasis, mitochondrial dysfunction, and chronic low-grade inflammation. Among mammalian sirtuins, SIRT7, though poorly characterized, is important for chromatin state, metabolic flux, mitochondrial function, and inflammatory responses in metabolically active tissues. Clinical and preclinical studies link dysregulated SIRT7 to multiple metabolic diseases, with tissue-specific effects on hepatic lipogenesis, insulin signaling, adipose function, and even metabolism-related hepatocellular carcinoma. Despite advances in the development of SIRT7-targeted inhibitors, significant challenges remain, including the absence of selective activators, limited structural characterization, incomplete understanding of tissue-specific regulatory mechanisms, and potential dose-dependent effects. This review integrates current knowledge on SIRT7-mediated regulatory networks and discusses emerging efforts to develop selective SIRT7 modulators, including structural-guided approaches based on AlphaFold models.