Type 2 diabetes mellitus (T2DM) has been associated with higher perioperative risks in coronary artery bypass grafting (CABG). This study examines preoperative characteristics, surgical factors, and postoperative outcomes of diabetic and nondiabetic patients undergoing CABG to identify differences in clinical profiles and complications.

A retrospective analysis was conducted on 425 patients (214 nondiabetic, 211 diabetic) using SPSS 21. Continuous variables were compared using the Student t-test, whereas categorical variables were compared using the chi-squared test.

Diabetic patients had higher BMI (30.1 vs. 28.4 kg/m², p < 0.001), worse glycemic control (HbA1c 7.9 vs. 5.6, p < 0.001), and higher rates of hypertension (84.4% vs. 62.6%, p < 0.001) and CHF (73% vs. 64%, p = 0.03). They also exhibited lower hemoglobin levels (12.8 vs. Thirteen.6 g/dL, p < 0.001), higher INR (1.0 vs. 0.9, p < 0.001), and higher rates of STEMI (13.3% vs. 5.1%, p = 0.003). Sex distribution also differed, with fewer males in the diabetic group (147 vs. 172, p = 0.007). Surgically, they required more urgent/emergent procedures (27% vs. 7.4%, p < 0.001) and longer bypass times (147.5 vs. 135.2 min, p = 0.024). Postoperatively, diabetics had higher mortality (5.2% vs. 0.5%, p = 0.003), stroke (13.3% vs. 2.8%, p < 0.001); cardiovascular events such as MI or stroke (9% vs. 0.5%, p < 0.001); infections (36.5% vs. 2.3%, p < 0.001); renal failure (20.4% vs. 2.8%, p < 0.001); gastrointestinal events (17.5% vs. 4.7%, p < 0.001); postoperative cardiac arrest (33.6% vs. 22%, p = 0.005); reoperation for bleeding (9.5% vs. 1.4%, p < 0.001); and longer hospital stays (9.2 vs. 6.3 days, p < 0.001). After adjustment for baseline demographic and clinical characteristics, diabetes mellitus was independently associated with significantly worse postoperative outcomes.

Diabetic patients undergoing CABG had worse preoperative health, challenging surgical procedures, and much worse postoperative outcomes. These findings highlight the importance of targeted perioperative interventions for reducing hazards in this high-risk population.

Diabetic nephropathy (DN) is a serious microvascular complication of type 2 diabetes mellitus (T2DM).Single-nucleotide polymorphisms (SNPs) in long non-coding RNAs MALAT1 and ANRIL may influence their expression and function, potentially affecting T2DM and DN risk.

To investigate the association of MALAT1 SNPs rs619586 and rs3200401 and ANRIL SNPs rs10965215 and rs10738605 with T2DM and/or DN susceptibility and clinical correlates in an Egyptian population.

This case-control study included 64 T2DM patients, 75 DN patients, and 70 healthy controls from Fayoum University Hospital. Genomic DNA was extracted from peripheral blood, and SNP genotyping was performed using TaqMan real-time PCR. All analyses were adjusted for age and sex. The study had 80% power to detect associations based on expected differences in allele frequencies.

MALAT1 rs619586 GG genotype and G allele were associated with reduced T2DM risk (adjusted odds ratio (AOR) 0.31, P = 0.004 and DN risk (AOR 0.32, P = 0.003). Conversely, MALAT1 rs3200401 CT/TT genotypes increased T2DM risk (AOR 4.69, P<0.001) and DN risk (AOR 5.41, P<0.001). ANRIL rs10965215 GA/AA and rs10738605 CG genotypes were also associated with increased T2DM and DN risk versus controls. Notably, none of the SNPs were associated with DN progression among T2DM patients. This study is the first report of ANRIL SNPs in DN susceptibility.

MALAT1 rs619586 appears protective against T2DM and DN, while MALAT1 rs3200401 and ANRIL rs10965215/rs10738605 increase susceptibility. These SNPs may serve as early risk markers pending validation in larger cohorts.

Eruptive xanthomas are a rare manifestation of severe hypertriglyceridemia and are commonly associated with uncontrolled diabetes mellitus and an increased risk of acute pancreatitis. We report the case of a 41-year-old man who presented with diffuse papular skin lesions and neuropathic symptoms. He had no previous diagnosis of diabetes; however, initial investigations revealed a markedly elevated glycated hemoglobin (HbA1c) of 13.8%, and he was subsequently diagnosed with diabetes mellitus. Further testing showed severe hypertriglyceridemia (85.6 mmol/L), elevated cholesterol, and widespread eruptive xanthomas on examination. Despite the markedly raised triglyceride level, he remained clinically stable and reported no abdominal pain, nausea, or vomiting, with no abdominal tenderness on examination to suggest acute pancreatitis. He was managed as an outpatient with insulin therapy, a statin, a fibrate, and lifestyle modification. This led to a rapid improvement in triglyceride levels, glycemic control, and cutaneous lesions, with no development of pancreatitis. This case highlights eruptive xanthomas as a potential initial presenting feature of previously undiagnosed diabetes mellitus with severe hypertriglyceridemia, and illustrates that carefully selected clinically stable patients may be managed in the outpatient setting with early recognition and prompt metabolic optimisation.

Sleep disorders-including sleep deprivation, obstructive sleep apnea (OSA), and circadian rhythm disruption-and metabolic diseases such as obesity and type 2 diabetes represent major, interconnected public health challenges. This review aims to synthesize current evidence on the bidirectional crosstalk between these conditions, with a focus on the mediating role of dysregulated adipokine secretion.

We elaborate a mechanistic framework wherein specific sleep disturbances disrupt circadian rhythms and alter the secretory profiles of key adipokines, including leptin, adiponectin, interleukin-6 (IL-6), and angiopoietin-like protein 4 (ANGPTL4). Sleep deprivation and fragmentation promote a state of leptin dysregulation and reduce adiponectin levels, while OSA-driven intermittent hypoxia potently upregulates IL-6 and ANGPTL4. These alterations collectively contribute to insulin resistance, dyslipidemia, and chronic low-grade inflammation, thereby elevating metabolic disease risk. Conversely, obesity and diabetes exacerbate sleep disorders through pathways involving visceral adiposity, neuroendocrine dysfunction (e.g. HPA-axis activation), and diabetes-related symptoms (e.g. nocturia, neuropathic pain), forming a vicious cycle. Clinical and preclinical evidence underscores that the synchronization of sleep-circadian biology is fundamental to maintaining adipokine homeostasis and metabolic health.

The evidence positions sleep and circadian health as critical, modifiable determinants of metabolic risk. Integrating sleep assessment and evidence-based interventions (e.g. CPAP for OSA, sleep extension, circadian realignment) into standard preventive and clinical frameworks for metabolic diseases is a promising strategy. Public health initiatives should elevate 'quality sleep' as a pillar of health alongside nutrition and physical activity to mitigate the intertwined epidemics of metabolic and sleep disorders.

Recent studies suggest first-trimester maternal haemoglobin (Hb) may be linked to gestational diabetes mellitus (GDM), but evidence remains limited. This study examined the association between high first-trimester haemoglobin and GDM risk.

This prospective study included 18 484 singleton pregnant women with a gestational age of ≤14 weeks in the Fujian Birth Cohort Study. Haemoglobin of the first trimester is divided into low (<110 g/L), normal (110-130 g/L) and high (≥130 g/L). Multivariate logistic regression and restricted cubic spline (RCS) models were used to explore the association between Hb level and GDM risk, and to gradually adjust sociodemographics, lifestyle and metabolic factors. Stratified and combined analysis was performed according to maternal age, pre-pregnancy body mass index and mode of conception.

Mean early Hb was 127.3 ± 9.6 g/L. The crude GDM incidence was 17.7%, 19.6%, and 25.3% in the low, normal, and high Hb groups, respectively. High Hb was significantly associated with increased GDM risk in crude (odds ratio (OR) = 1.40; 95% confidence interval (CI) = 1.30-1.50, P < 0.001), Model 2 (OR = 1.31; 95% CI = 1.22-1.41, P < 0.001), and Model 3 (OR = 1.24; 95% CI = 1.15-1.34, P < 0.001), with only 5.3% attenuation after adjusting for metabolic markers. Restricted cubic spline analyses showed a linear positive dose-response relationship between Hb and GDM risk (P for nonlinearity = 0.274). The association was stronger in non-advanced maternal age (non-AMA), overweight/obese, and spontaneously conceiving women, and combined effects were observed for high Hb with AMA, overweight/obesity, and assisted reproductive technology (ART).

Early pregnancy haemoglobin is significantly associated with GDM risk, modified by age, pre-pregnancy BMI, and conception mode. Haemoglobin screening in early pregnancy may help identify high-risk women. Further studies are needed to clarify related mechanisms and evaluate interventions.

Objective: To summarize the clinical characteristics, diagnostic and therapeutic strategies, and prognostic factors in patients with pulmonary mucormycosis. Methods: The patients with pulmonary mucormycosis admitted to the Department of Respiratory and Critical Care Medicine and the Lung Transplantation Department of China-Japan Friendship Hospital from January 2016 to March 2023 were retrospectively evaluated. High-risk factors, clinical manifestations, imaging findings, microbiological tests, therapeutic interventions, and clinical outcomes were analyzed, and variables were compared between survivors and non-survivors. Intergroup statistical analyses were performed using the chi-squared test, or Fisher's exact test, etc. Results: Of the 47 patients (21 confirmed, 26 clinically diagnosed), 32 (68.1%) were male, and the mean age of the cohort was (48±17) years. High-risk factors were present in 87.2% (41/47) of patients, primarily diabetes mellitus (53.2%, 25/47) and immunosuppression (42.6%, 20/47); 53.2% (25/47) had a history of voriconazole exposure. Hemoptysis occurred in 57.4% (27/47) of patients, of whom 17.0% (8/47) experienced massive hemoptysis; 48.9%(23/47) required interventional or surgical management. Chest CT scans revealed large consolidative opacities (70.2%, 33/47) and thick-walled cavities (48.9%, 23/47), and contrast-enhanced CT identified vascular involvement. The positive rate for lower respiratory tract fungal culture was only 17.1% (6/35), and that of smear microscopy was 18.2% (6/33), whereas the positive rate of metagenomic next-generation sequencing (mNGS) reached 76.0% (19/25), with mNGS of bronchoalveolar lavage fluid reaching 85.0% (17/20). Overall, 34.0% (16/47) of patients were diagnosed exclusively via mNGS. Conventional amphotericin B formulations were administered to 68.1% (32/47) of patients (including 10 who received liposomal amphotericin B); these formulations were associated with an adverse drug reaction rate of 86.7% (26/30), which contributed to only 40.7% (11/27) of these treated patients receiving a full therapeutic dose. Azoles were administered to 91.5% (43/47) of patients (15 received azoles alone), and among those treated with posaconazole, 88.0% (22/25) achieved target plasma concentrations; 48.9% (23/47) received combination therapy consisting of an amphotericin B formulation plus an azole. The survival rate among patients who underwent surgical intervention combined with antifungal therapy was 11/12, which was higher than that of patients who received antifungal therapy alone (28/35). Compared with survivors, non-survivors demonstrated significantly higher incidences of dyspnea (8/8 vs. 14/39, P=0.001), uncontrolled fever (6/8 vs. 12/39, P=0.027), pleural effusion (8/8 vs. 17/39, P=0.003), atelectasis (5/8 vs. 6/39, P=0.016), and severe complications (7/8 vs. 13/39, P=0.015). Furthermore, a significantly lower proportion of non-survivors received adequate antifungal dosing (1/8 vs. 21/39, P=0.037). Conclusions: Pulmonary mucormycosis predominantly occurs in high-risk populations such as those with diabetes mellitus or immunosuppression. Hemoptysis is a prominent clinical manifestation, while imaging findings commonly include large areas of consolidation, thick-walled cavities, and signs of vascular invasion. Early execution of contrast-enhanced chest CT, along with bronchoscopy with bronchoalveolar lavage fluid mNGS, improves the diagnostic yield. Adequate antifungal therapy combined with aggressive surgical intervention may contribute to improved prognosis. Severe complications, dyspnea, uncontrolled fever, pleural effusion, atelectasis, and inadequate antifungal treatment are associated with a poor prognosis, underscoring the need for early recognition and management.

Gestational diabetes mellitus (GDM) is one of the most common metabolic disorders in pregnancy and is associated with significant maternal and fetal risks. The study aims to investigate lipid metabolism profiles associated with GDM to identify independent risk factors.

Clinical data from 17,452 women with singleton pregnancies who received regular prenatal care and nutritional assessment at Fujian Maternity and Child Health Hospital between December 2011 and December 2019 were analyzed. Participants were divided into GDM and control groups based on diagnosis. Gestational age was confirmed by first-trimester ultrasound, and lipid profiles were measured in early (10-13 weeks) and late pregnancy (28-32 weeks). GDM was diagnosed using either a two-step approach (2011-2014) or the International Association of Diabetes and Pregnancy Study Groups (IADPSG) one-step 75-g oral glucose tolerance test. Maternal characteristics, pregnancy outcomes, and lipid indicators-including total cholesterol (TC), triglycerides (TG), LDL-C, HDL-C, and apolipoproteins (Apo-A1, Apo-B)-were extracted. Feature selection was performed using LASSO regression and the Boruta algorithm.

Age, TG/HDL-C ratio, TG, pre-pregnancy BMI, and HDL-C were identified as independent risk factors for GDM. Levels of ALT, HGB, Apo-B, TC, TG, and TG/HDL-C ratio were significantly higher in the GDM group, while HDL-C was lower (P < 0.05). Threshold analysis indicated that first-trimester HDL-C and TG/HDL-C ratio critical cut-off points were 2.37 and 1.33, respectively.

Abnormal lipid metabolism is a hallmark of GDM and may serve as a predictive biomarker. Assessment of TG/HDL-C ratio and HDL-C in early pregnancy could improve risk stratification and facilitate early interventions.

Diabetic peripheral neuropathy is a disabling chronic complication of diabetes mellitus, associated with neuropathic pain, sensory dysfunction, and reduced quality of life. Because pharmacological treatments often provide only partial relief, photobiomodulation therapy (PBMT) has emerged as a promising non-pharmacological strategy with metabolic, anti-inflammatory, and neuromodulatory effects. To assess the feasibility of local PBMT, administered alone or combined with intravascular laser irradiation of blood (ILIB), and to explore preliminary short-term changes in neuropathic pain, neuropathic symptoms, and sensory responses in individuals with diabetic peripheral neuropathy. This prospective randomized controlled pilot trial included 26 participants allocated to three groups: local PBMT, local PBMT combined with ILIB, and sham control. All randomized participants completed 12 sessions over 23 days. Neuropathic pain intensity was assessed using the Visual Analog Scale, and neuropathic symptoms were evaluated using the Michigan Neuropathy Screening Instrument. Friedman and McNemar tests were used for exploratory within-group and paired analyses, and a linear mixed-effects model evaluated pain trajectory over time. Neuropathic pain intensity decreased across the five assessment points (p < 0.001), with significant intragroup reduction in the local PBMT group (p = 0.007). Improvements were observed in selected symptoms, including numbness, cramps, and dry skin with fissures. The mixed-effects model showed a significant effect of time on pain reduction (beta = -0.78; p = 0.001), although no significant group x time interaction was detected. Local PBMT, administered alone or combined with ILIB, was feasible in this outpatient pilot trial and was followed by preliminary short-term reductions in neuropathic pain and selected neuropathic symptoms. However, no definitive between-group superiority was demonstrated, and the findings should be interpreted cautiously because of the pilot design, small sample size, heterogeneity in baseline pain intensity, potential placebo effects, and short follow-up period.

To investigate the association and dose-response relationship between rate-pressure product (RPP) and prevalent diabetic retinopathy (DR), and to develop a nomogram for identifying DR in patients with type 2 diabetes mellitus (T2DM).

A total of 1,316 hospitalized patients with T2DM, including 464 with DR, were retrospectively enrolled. LASSO regression was used for variable selection. Correlation analyses, multivariable logistic regression, and restricted cubic spline (RCS) analyses were performed to evaluate the association and dose-response relationship between RPP and prevalent DR. Subgroup analyses were conducted to assess the stability of the association. A nomogram was constructed and evaluated using receiver operating characteristic (ROC) analysis, bootstrap validation, calibration assessment, Brier score, and decision curve analysis.

After full adjustment for confounders, RPP was independently and positively associated with prevalent DR. Per 1-SD increase in RPP was associated with higher odds of DR (OR = 1.292, 95% CI: 1.136-1.469; P < 0.001). RCS analysis showed a significant overall association without evidence of nonlinearity (P for nonlinear > 0.05), and a positive dose-response trend was observed (P for trend < 0.001). The association remained consistent across most subgroups without significant interactions. The nomogram incorporating disease duration, using insulin, HbA1c, and RPP demonstrated acceptable discrimination (AUC = 0.732; bootstrap-corrected AUC = 0.727), good calibration, and favorable clinical utility.

RPP is independently associated with prevalent DR in patients with T2DM. The RPP-based nomogram shows acceptable discrimination and calibration, suggesting clinical utility for DR identification.

This conceptual review provides a synthesising narrative of the interdependent regulation of intracellular pH (pHi), nitric oxide (NO), and adenosine-the pHi-NO-adenosine triad-in fetoplacental endothelial dysfunction associated with gestational diabetes mellitus (GDM). GDM is associated with fetoplacental endothelial dysfunction, involving altered nitric oxide (NO) synthesis, reduced adenosine uptake, and dysregulated intracellular pH (pHi). Human umbilical vein endothelial cells (HUVECs) from GDM pregnancies exhibit increased endothelial NO synthase activity and decreased adenosine transport via human equilibrative nucleoside transporters, processes modulated by NO and pHi. These changes converge in the ALANO (Adenosine/L-Arginine/Nitric Oxide) signalling pathway, which enhances NO synthesis through increased L-arginine uptake. Importantly, similar mechanisms are observed in both macrovascular and microvascular endothelial cells, suggesting widespread placental vascular involvement. Maternal pre-pregnancy body mass index stratification reveals further heterogeneity in these responses. Disruptions in this signalling triad, i.e. NO, adenosine, and pHi, may impair placental perfusion, nutrient delivery, and fetal development, with potential long-term cardiometabolic consequences. Understanding these interrelated mechanisms provides a framework for targeted interventions in GDM, emphasizing the need for personalized approaches in maternal-foetal medicine.