Tumor patients with type 2 diabetes mellitus (T2DM) have a more immunosuppressive tumor microenvironment and weaker T-cell immune response to tumors within the tumor compared to non-T2DM patients when treated with immune checkpoint inhibitors (ICIs).In addition, high blood glucose levels may promote tumor immune escape. These factors may lead to a poor response to ICIs treatment in tumor patients with T2DM, affecting treatment prognosis. Although some studies have explored the association between tumor patients with T2DM and the prognosis of ICIs treatment, there is still controversy. Therefore, this study systematically evaluated the impact of T2DM on the prognosis of ICIs treatment in tumor patients through a meta-analysis, aiming to provide more accurate guidance for clinical practice and optimize the treatment strategy for tumor patients with T2DM.

We systematically searched PubMed, Embase, Web of Science, CNKI, and Wanfang Database to collect studies published from the database establishment to January 2026 that investigated the association between tumor patients with T2DM and the prognosis of ICIs treatment. The Risk Of Bias In Non-randomized Studies - of Interventions (ROBINS-I) was used to evaluate the risk of bias. The pooled hazard ratio (HR) and 95% confidence interval (CI) were calculated to assess the association between tumor patients with T2DM and the prognosis of ICIs treatment. The primary outcomes included overall survival (OS) and progression-free survival (PFS). Meta-analysis was conducted using RevMan 5.3 software.

A total of six studies were included, involving 1,225 participants. The meta-analysis showed that patients with T2DM who received ICIs treatment had poorer OS (HR = 1.49, 95%CI:1.25-1.77, P < 0.00001) and PFS(HR = 1.38, 95%CI:1.04-1.83, P = 0.03).Subgroup analyses indicated that regardless of sample size (<200 vs >200) or type of survival analysis (univariate vs multivariate), patients with tumors and T2DM who received ICI treatment were consistently associated with poorer OS. Regarding PFS, a worse outcome was observed in T2DM patients when the sample size was less than 200 or when univariate analysis was applied. However, no significant statistical difference in PFS was found between non-T2DM and T2DM patients treated with ICIs when the sample size exceeded 200 or when multivariate analysis was performed.

Based on the current limited evidence, this meta-analysis suggests that T2DM may be associated with poor OS in lung cancer patients treated with ICIs. However, due to the small number of included studies, limited sample size, inherent bias risks of the retrospective design, heterogeneity of tumor types, and the instability of PFS results. The conclusion of this study belongs to the 'put forward hypothesis' level and is not yet sufficient to support clinical practice recommendations. The current evidence cannot determine whether glycemic control can improve the efficacy of ICIs. Future studies need to verify this finding through large-sample, prospective cohort studies and clarify the independent impact of glycemic control levels on the efficacy of ICIs.

While a limited-scale study in Turkey identified an association between the cholesterol, high-density lipoprotein, and glucose (CHG) index and diabetic nephropathy, evidence on the relationship between the CHG index and chronic kidney disease (CKD) is lacking in Chinese general population. This study aimed to investigate the association of CHG index with CKD in this specific demographic.

A total of 9,095 Chinese participants aged ≥40 years were recruited from five regional communities of Luzhou city between May 2011 and December 2011. CHG index was calculated, and its possible relationships with CKD were evaluated by multivariate logistic regression analyses. Receiver operating characteristic (ROC) analysis was conducted to identify the predictive performance, and subgroup analysis evaluated its applicability in different populations.

The subjects with higher CHG index quartiles had significantly higher prevalence of CKD compared to those with lower quartiles (P for trend < 0.01). Multivariate logistic regression analysis demonstrated that per Standard deviation (SD) increase in CHG index remains significantly associated with a 57.7% increased risk of CKD [odds ratios (OR) = 1.577; 95% confidence intervals (CI) 1.301-1.911; P < 0.01], and subjects in the highest quartile of CHG index were significantly associated with a 32.8% increased risk of CKD when compared to those in the lowest quartile (OR = 1.328; 95% CI = 1.069-1.648; P < 0.01). Stratified analysis revealed that the associations between CHG index quartiles and CKD risk were observed only in subjects who were men, non-smoker, non-drinker, aged ≥60 years, receiving a less than high school education, having overweight/obesity, type 2 diabetes mellitus, dyslipidemia, normal blood pressure, and no atherosclerotic cardiovascular disease (P for trend < 0.01 or P for trend < 0.05). The optimal cutoff point for CHG index to distinguish patients with CKD from those without was 0.601, with a sensitivity of 73.6% and a specificity of 40.6%.

The CHG index was closely associated with CKD, and might be a potential biomarker for CKD in Chinese community adults.

To investigate the diagnostic value of serum APOC2 in patients with diabetes mellitus combined with pyogenic liver abscess.

From April 2023 to July 2023, 77 type 2 diabetes mellitus patients were included which divided into two groups: diabetes mellitus (n=55) and diabetes mellitus combined with pyogenic liver abscess (n=22). Additionally, 27 healthy individuals served as the control group. Serum APOC2 levels were detected and compared among the groups. ROC curve and logistic regression analysis were performed to evaluate the diagnostic value of serum APOC2.

Serum APOC2 levels were significantly higher in diabetes mellitus patients compared to the healthy control group (P=0.008). In diabetes mellitus combined with pyogenic liver abscess patients, APOC2 levels were significantly reduced (P<0.001) while increased post-treatment (P<0.001). ROC curve analysis showed high diagnostic accuracy for serum APOC2 in diabetes mellitus combined with pyogenic liver abscess (AUC=0.945). Logistic regression analysis revealed that reduced serum APOC2 levels were a risk factor for diabetes mellitus combined with pyogenic liver abscess (OR=0.02, 95% CI=0.01~0.16, P=0.012). The diabetes mellitus combined with pyogenic liver abscess patients with lower APOC2 levels had higher ALT (P=0.038) and AST levels (P=0.007), suggesting that reduced serum APOC2 levels were associated with liver damage.

Serum APOC2 levels are significantly decreased in patients with diabetes mellitus combined with pyogenic liver abscess, serving as a potential marker for predicting the occurrence of this condition. Lower levels of APOC2 are strongly linked to liver function impairment.

The immune system is a dynamic, complex network of interacting cells, molecules, and signals central to health. Immune digital twins - virtual representations of the immune system that evolve in tandem with their biological counterparts - offer a path toward predictive, patient-specific simulations, but their realization requires mechanistic frameworks that generalize across multiple cell types and disease contexts.

We constructed a logic-based mechanistic model of the human immune system built exclusively on human experimental data extracted from 449 publications. The model integrates 51 innate (e.g., NK cells, macrophages) and 37 adaptive (e.g., Th1/2/17, B cells) immune cell types and subtypes, together with 37 secretory factors and 1,450 regulatory interactions across 11 disease conditions, including nine pathogens, type 1 diabetes, and lung transplantation. Model predictions were validated against independent in vitro, ex vivo, and clinical observations not used during construction.

Across 38 validation experiments, agreement with published literature ranged from 75% to 90% across pathogens. The model reproduced pathogen-specific cytokine signatures for nine infections, captured synergistic and antagonistic effects in four coinfection scenarios (MTB-HIV, MTB-Helminth, SARS-CoV-2-EBV, and Plasmodium falciparum-Helminth), and resolved competing rejection and tolerance signals in lung transplantation challenged by CMV, EBV, and SARS-CoV-2.

This reference model unifies multiple immune contexts within a single simulatable model and generates a structured catalog of falsifiable predictions for experimental follow-up. The model is openly available on Cell Collective and as an SBML file, representing a step toward a clinically integrated immune digital twin for patient-specific applications.

Perioperative neurocognitive disorders (PND) include postoperative delirium within 7 days after surgery, delayed neurocognitive recovery up to 30 days, and postoperative neurocognitive disorder up to 12 months. These outcomes are related, but they are not the same. They arise from the interaction of baseline brain vulnerability and perioperative stress, including inflammation, vascular instability, blood-brain barrier injury, metabolic strain, and reduced neural reserve. Preoperative genetic profiling is useful because it can estimate latent susceptibility before surgery. Among current signals, APOE is the strongest and most biologically relevant locus. At the same time, Alzheimer's disease polygenic risk scores (AD-PRS) can capture non-APOE common-variant burden across lipid transport, endosomal trafficking, innate immune signaling, complement activity, microglial regulation, mitochondrial stress, and neurovascular integrity. Recent perioperative cohort studies have begun to test preoperative APOE-based and polygenic neurocognitive risk in surgical patients. Large delirium genetics studies also show a strong signal at the APOE locus and support overlap between delirium risk and Alzheimer's disease-related common-variant architecture. These findings support an APOE-aware framework in which APOE genotype is modeled separately from non-APOE AD-PRS. In clinical use, this genomic layer should be combined with baseline cognition, frailty, vascular comorbidity, surgery-related risk, and circulating biomarkers such as neurofilament light chain. This review summarizes the loci, molecular pathways, and translational model designs that can move preoperative genomic profiling from association to perioperative risk stratification.

Tumor necrosis factor-alpha (TNF-α) inhibitors are widely used in rheumatologic diseases but may increase the risk of primary tuberculosis (TB) infection or reactivation. Purified protein derivative (PPD) conversion is an important indicator of latent TB in immunosuppressed patients. This study aimed to determine the rate of PPD conversion and associated factors in patients receiving anti-TNF therapy.

This prospective study included adults with rheumatologic diseases who initiated anti-TNF therapy between March 2021 and September 2023. Patients with prior TB, previous anti-TNF exposure, or a positive baseline PPD were excluded. A PPD test was performed before treatment and repeated one year later. An induration ≥5 mm at follow-up was considered conversion.

Sixty patients completed the study (mean age 44.29 ± 14.70 years; 56.7% male). Six patients (10.0%) demonstrated PPD conversion after one year of anti-TNF therapy. Most conversions occurred in individuals with psoriatic arthritis (66.6%). No cases of active TB were detected clinically or radiologically. Statistical analysis showed no significant association between PPD conversion and age, sex, disease duration, anti-TNF type, methotrexate or corticosteroid use, diabetes mellitus, or hypertension. Psoriatic arthritis was the only factor significantly associated with conversion (P = 0.03).

Ten percent of patients receiving anti-TNF therapy developed PPD conversion, indicating new latent TB infection. Psoriatic arthritis was significantly associated with conversion, while medication type and other clinical factors were not. These findings support routine annual TB screening in anti-TNF recipients, particularly in regions with moderate or high TB prevalence.

Delayed Villous Maturation (DVM) is a histological hallmark in Gestational Diabetes Mellitus (GDM) pregnancies commonly observed after 36 weeks of gestation. It is associated with perinatal morbidity and mortality. Our study aims to assess DVM in the term placentas of GDM pregnancies and its association with its perinatal outcomes compared to normal pregnancies.

A total of 120 term placentae from GDM and normal pregnancies were collected from the Obstetrics and Gynaecology Department for one year and subjected to histopathological examination to evaluate DVM and its association with placental morphology and perinatal outcomes.

The current study found statistically significant increased presence of DVM in GDM placentas and its association with placental weight, diameter, maternal weight, glycated haemoglobin and foetal weight. The present study also observed presence of DVM with chorangiosis in a GDM placenta.

The present study has found a statistically significant association of DVM in GDM pregnancies with its perinatal outcomes compared to normal pregnancies. There is no antenatal ultrasound marker to detect placental DVM and adverse foetal outcomes caused due to it. Since there is risk of reoccurrence of DVM and type 2 diabetes in future pregnancies, identification of DVM in GDM pregnancies and its clinical association with foetal outcomes should be considered clinically important. This may explain the cause of intrauterine foetal deaths and adverse neonatal outcomes in the current pregnancy and indicating a need for comprehensive maternal care in future pregnancies to prevent perinatal outcomes by implementing Rescue by birth.

Individuals with type 1 diabetes (T1D) have increased mortality from cardiovascular disease (CVD) compared to general population, where hypertension is a major risk factor. The aim of this study was to evaluate blood pressure (BP) and arterial stiffness in young adults with childhood-onset T1D compared to healthy control subjects.

The atherosclerosis and childhood diabetes (ACD) study is a prospective population-based cohort study, with follow-up every fifth year on early atherosclerosis development and other cardiovascular risk factors in childhood-onset T1D compared to healthy controls. At baseline the cohort was recruited among children with T1D in a defined health-region in Norway along with their friends as healthy control subjects. The original T1D cohort was found to be representative of all children with T1D in Norway at that time. At the 10-year follow-up a cross-sectional analysis of 24-h ambulatory blood pressure measurements (ABPM), including arterial stiffness, was performed, along with an assessment of other CVD risk factors.

One hundred and twenty-three participants were included in the analysis (T1D n = 82, controls n = 41). The T1D group had mean ± SD age of 24 ± 3 years, diabetes duration of 15 ± 4 years and present HbA1c of 64 ± 14 mmol/mol (8.0 ± 1.3%). None of the T1D participants had previously known hypertension or were on antihypertensive treatment. Females with T1D had significantly higher mean weight, BMI, waist circumference, LDL-cholesterol, and apolipoprotein B than female controls. In females, almost all parameters of ABPM were significantly increased compared to their controls, whereas in males only nighttime blood pressure (BP) was significantly increased compared to controls. In the (stage 2) hypertensive group with T1D, LDL-c (3.1 ± 0.08; ρ = 0.038) was significantly increased. Arterial stiffness was significantly increased in the T1D group (24-h PWV was 8.0 ± 1.0 m/s vs. 7.2 ± 0.6 m/s; ρ = 0.011) compared to controls.

Young adults with childhood-onset T1D had significantly increased BP and arterial stiffness compared to controls, especially females.

To investigate the effects of liraglutide on cardiac structure and function in a mouse model of diabetic nephropathy at the massive proteinuria stage.

Twenty 12-week-old male spontaneous type 2 diabetic KKAy mice were fed a high-fat diet for 10 weeks to establish diabetic models with massive proteinuria, which were then randomly divided into diabetic model group and liraglutide treatment group, with 10 age-matched C57BL/6J mice fed a standard chow diet serving as the normal control group. After 8 weeks of intervention, cardiac structural and functional parameters of the mice were evaluated using echocardiography, and myocardial histopathological changes were observed with HE staining, Masson's trichrome staining, Sirius red staining, and transmission electron microscopy. Serum levels of cardiac-related indicators were measured, and the mRNA and protein levels of collagen I and collagen III were determined using RT-qPCR and Western blotting, respectively.

The diabetic mouse models showed significantly elevated blood glucose and increased body weight (P<0.05) with disordered myocardial fibers, severe interstitial and perivascular fibrosis, and markedly upregulated myocardial expressions of collagen I and collagen III. Echocardiography revealed significantly increased left ventricular wall thickness, interventricular septal thickness, and left ventricular mass, reduced left ventricular internal diameter, decreased LVEF, FS, FAC, and the E/A ratio, and prolonged IVRT in the mouse models. Liraglutide treatment significantly improved these pathologies and alleviated cardiac functional impairment in the diabetic mice.

Mice with diabetic nephropathy and massive proteinuria exhibit left ventricular hypertrophy and reduced cardiac function, accompanied by prominent myocardial interstitial fibrosis and inflammatory responses. Liraglutide improves cardiac structural and functional impairments in these mice possibly by alleviating myocardial fibrosis and inflammatory responses.

Mucormycosis, triggered by fungi of the order Mucorales, represents a potentially fatal invasive mycosis, with death rates over 50% despite intensive therapy. The COVID-19 pandemic brought a sharp increase in cases, especially in individuals with diabetes mellitus and those undergoing immunosuppressive treatment, emphasizing significant gaps in our comprehension of disease pathogenesis. Emerging molecular studies have highlighted key virulence factors, such as the CotH family of invasins that facilitate endothelial invasion via interaction with glucose-regulated protein 78 (GRP78), complex iron acquisition systems necessary for fungal growth, and the release of mucoricin, a ricin-like toxin that impairs vascular integrity. Host defense depends mainly on innate immunity, with neutrophils and macrophages working as critical effector cells, while adaptive Th1 and Th17 responses aid in the fungal removal. Mucorales use a variety of immune evasion techniques, such as pathogen-associated molecular pattern (PAMP) masking via cell wall transformations, resistance to phagocytic death, and metabolic utilization of host factors including hyperglycemia and increased free iron in diabetic ketoacidosis (DKA). This review summarizes current evidence of the molecular processes underlying mucormycosis pathogenesis, underscoring host-pathogen interactions at the cellular and molecular levels, immune evasion tactics, and translational potential for new diagnostic and therapeutic approaches. Comprehending these molecular processes is crucial for creating efficient therapies against mucormycosis in an era of growing immunocompromised patients and expanding infectious disease synergies.