This study aimed to identify symptom clusters in hospitalized patients with type 2 diabetes mellitus (T2DM), construct a symptom network, and determine core symptoms.

A cross-sectional study was conducted among 331 hospitalized patients with type 2 diabetes mellitus recruited by convenience sampling from the Department of Endocrinology at a tertiary Grade A hospital in Sanya City. Demographic and clinical data were collected using a self-designed questionnaire, and symptoms were assessed with the Diabetes Symptom Checklist-Revised. Exploratory factor analysis was used to extract symptom clusters, and a Gaussian graphical model with graphical LASSO regularization was applied in R to construct the symptom network and calculate centrality indices.

Five clinically meaningful symptom clusters were identified. Network analysis showed strong symptom interconnections, particularly between reduced appetite and drowsiness or fatigue, polydipsia and polyuria, abnormal sensations in the legs or feet and blurred vision, and chest tightness and shortness of breath. Reduced appetite, polydipsia, and abnormal sensations in the legs or feet had the highest strength centrality, whereas reduced appetite, abnormal sensations in the legs or feet, and constipation showed relatively high betweenness centrality, suggesting potential bridging roles. Palpitations and shortness of breath had high positive expected influence values, indicating that they may serve as influential symptoms within the network.

The clinical symptoms of hospitalized T2DM patients do not exist in isolation but co-occur in specific symptom clusters. In clinical practice, healthcare providers can use symptom clusters and core symptoms as key focal points for rapid assessment and intervention. Identifying these clusters and their core symptoms may allow clinicians to streamline assessment and target interventions more efficiently.

This study provides a novel framework for understanding symptom interconnections in T2DM patients through network analysis. These findings are intended to provide theoretical guidance for stratified management and comprehensive interventions in clinical practice.

This systematic review and three-level meta-analysis evaluated the effects of exercise interventions on glycemic control, lipid metabolism, body composition/fat distribution, and liver function in patients with type 2 diabetes mellitus (T2DM) complicated by non-alcoholic fatty liver disease (NAFLD), and examined potential sources of heterogeneity relevant to individualized exercise prescription.

Randomized controlled trials were searched in Web of Science, PubMed, Cochrane Library, EBSCO, Embase, and CNKI from database inception to February 2026. The review followed PRISMA 2020 and used a three-level meta-analytic model to account for dependent effect sizes extracted from the same study. A priori subgroup analyses were conducted by exercise modality, and meta-regression was used to explore heterogeneity.

Twenty-four studies involving 2,578 participants were included. Overall, exercise reduced BMI (Hedges' g = -0.36, p < 0.001), FPG (Hedges' g = -0.42, p < 0.001), HbA1c (Hedges' g = -0.52, p < 0.001), HOMA-IR (Hedges' g = -0.48, p < 0.001), LDL-C (Hedges' g = -0.36, p = 0.001), TG (Hedges' g = -0.45, p < 0.001), ALT (Hedges' g = -0.41, p < 0.001), AST (Hedges' g = -0.38, p < 0.001), and GGT (Hedges' g = -0.40, p < 0.001), and increased HDL-C (Hedges' g = 0.28, p = 0.009). Modality-specific analyses suggested that MICT may be more favorable for FPG, LDL-C, VAT, and HFC, whereas HIIT showed larger effects for HbA1c, HOMA-IR, TG, ALT, and GGT. Heterogeneity was substantial for TG, ALT, AST, HbA1c, and GGT in the primary analyses; however, sensitivity analyses reduced I ² below 50% without materially altering the pooled effects. Evidence for resistance training was limited by the small number of studies and should be interpreted cautiously. Meta-regression suggested that medication status and exercise frequency may be potential contributors to between-study heterogeneity.

Exercise, particularly aerobic exercise, appears to be a beneficial adjunctive strategy for improving metabolic and liver-related outcomes in patients with T2DM and NAFLD. Because clinical heterogeneity, medication use, dietary co-interventions, and study quality may influence the estimates, modality-specific conclusions should be applied cautiously and individualized according to patients' metabolic profile, comorbidities, and exercise tolerance.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420261327724, identifier CRD420261327724.

Many patients with neovascular age-related macular degeneration (nAMD), diabetic macular edema (DME), or retinal vein occlusion who have lost copay assistance from the DBA Good Days national charity fund have been forced to switch treatment from branded intravitreal antivascular endothelial growth factor (anti-VEGF) therapy to bevacizumab. This study sought to characterize the short-term impact of these changes on clinical outcomes.

This retrospective study included 89 eyes of 69 patients with nAMD, DME, or retinal vein occlusion who transitioned from receiving branded anti-VEGF therapy (aflibercept 2.0 mg or 8.0 mg; faricimab) to bevacizumab. The primary endpoint was changes from baseline in central subfield thickness (CST) after 1, 2, and 3 injections. Secondary endpoints included changes in best-corrected visual acuity (BCVA), intraocular pressure, intraretinal fluid, subretinal fluid, pigment epithelial detachment, injection intervals, predictors of poor outcome (BCVA loss of ≥15 Early Treatment Diabetic Retinopathy Study letters or CST increase of ≥50 µm), and switchback to branded therapy.

From baseline to after the third bevacizumab injection, the CST increased from a mean (±SD) 228.7 ± 52.3 µm to 271.3 ± 40.0 µm in the overall cohort (P = .004), and from 224.1 ± 50.6 µm to 268.6 ± 38.5 µm among nAMD eyes (P = .007). The injection interval decreased from a median 8.6 weeks (interquartile range [IQR], 7.0-10.9 weeks) preswitch to 7.5 weeks (IQR, 5.3-9.5 weeks) after 3 injections (P < .001). Fourteen eyes (15.7%) met the criteria for poor outcome, and 15 (16.9%) were switched back to branded therapy. Worsening intraretinal fluid was an early indicator of suboptimal response, and shorter preswitch injection intervals were a predictor of switching back to branded therapy.

Switching from branded anti-VEGF therapy to bevacizumab was associated with anatomic worsening and shorter injection intervals. Shorter preswitch intervals and early postswitch intraretinal fluid changes may help identify patients at risk for poor outcomes.

Platelet-rich fibrin has shown regenerative potential in periodontal treatments; nonetheless, patients with Type 2 diabetes mellitus (T2DM) may experience altered biological activities. Therefore, this study aimed to evaluate the regenerative potential and growth factor release profiles of advanced platelet-rich fibrin (A PRF) and injectable platelet-rich fibrin (i-PRF) derived from participants with controlled and uncontrolled T2DM.

This study compared n = 87 (29 per group) participants-controlled T2DM, uncontrolled T2DM, and Healthy non-diabetic groups-analysing blood samples for HbA1c, platelet count, and growth factors like Vascular endothelial growth factor (VEGF), Platelet-derived growth factor-BB (PDGF-BB), Insulin-like growth factor-1 (IGF-1), Transforming growth factor-beta 1 (TGF-β1), Transforming growth factor-beta 2 (TGF-β2) via Enzyme-linked immunosorbent assay (ELISA), assessing cytocompatibility with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, and employing statistical methods like Analysis of variance (ANOVA) correlation, and regression.

PRF derived from participants with uncontrolled T2DM demonstrated significantly reduced PDGF-BB and TGF-β2 release compared with healthy participants in both A-PRF (P = 0.016), i-PRF (P = 0.033), and A-PRF (P = 0.002) and i-PRF (P = 0.0034. VEGF release was significantly lower in uncontrolled T2DM than in well-controlled T2DM in both A-PRF (P = 0.0096) and i-PRF (P = 0.0023). Compared with the uncontrolled T2DM group, well-controlled T2DM exhibited significantly higher VEGF release in both A-PRF (P = 0.0096) and i-PRF (P = 0.0023), and significantly higher IGF-1 (P < 0.05) and TGF-β2 (P = 0.033) levels in i-PRF. Platelet counts were comparable across the study groups, whereas cell viability was highest in PRF from healthy participants. HbA1c was not independently associated with the evaluated growth factor concentrations in multivariable analyses.

A-PRF and i-PRF derived from participants with well-controlled T2DM exhibited biological properties comparable to those of healthy non-diabetic individuals, whereas uncontrolled T2DM was associated with reduced release of key growth factors, indicating compromised healing potential. These findings suggest that achieving good glycaemic control may optimize the biological performance of PRF for periodontal regenerative therapy. However, the present findings are based on in vitro analyses; confirmation through well-designed prospective clinical studies remains essential before these findings can be translated into routine clinical practice.

Type 2 diabetes mellitus (T2DM) is a major risk factor for pulmonary tuberculosis (PTB), exacerbates disease severity and reduces the efficacy of anti-tuberculosis therapy. Previous studies have shown that T2DM is associated with exacerbated metabolic disturbances in patients with PTB. However, metabolic differences between PTB patients with comorbid T2DM (PTB-DM) and those with PTB after anti-TB therapy remain unclear.

Untargeted metabolomic analysis was conducted on plasma samples collected from April 2024 to November 2025 at Tianjin Haihe Hospital, China. A total of 75 participants were enrolled, including healthy controls, patients with newly diagnosed drug-sensitive PTB, patients with PTB-DM, as well as two independent post-treatment groups sampled after 6 months of standard anti-TB therapy: patients with PTB and patients with PTB-DM.

Patients with PTB exhibited marked metabolic disturbances, particularly in tyrosine metabolism and steroid hormone biosynthesis. Patients with PTB-DM showed broader metabolic reprogramming, including changes in arginine and proline metabolism, steroid hormone biosynthesis, cAMP signaling, and taurine and hypotaurine metabolism. After 6 months of standard therapy, the PTB_6M group showed treatment-associated metabolic differences, especially in bile acid metabolism, suggesting partial normalization of several metabolic features. In contrast, patients with PTB-DM after treatment showed persistent metabolic abnormalities involving sphingolipid, purine and biotin metabolism. Notably, 12-HETE and 12-HHTrE showed elevated levels in active PTB, decreased levels after treatment, but remained relatively higher in PTB-DM after treatment.

This study offers an integrated assessment of metabolic alterations in PTB and PTB-DM, suggesting that comorbid T2DM is associated with broader metabolic dysregulation during active PTB and persistent post-treatment metabolic abnormalities.

Diabetic kidney disease (DKD) is a prevalent microvascular complication of type 2 diabetes mellitus (T2DM) and contributes substantially to end-stage renal disease. The atherogenic index of plasma (AIP) has exhibited biomarker utility. However, its relationship with DKD remains uncertain.

This cross-sectional investigation included 10,112 T2DM subjects from the National Metabolic Management Center of Yuhuan Second People's Hospital between September 2017 and February 2025 and 5,573 individuals in NHANES cohort (1999-2020). AIP values were calculated and categorized into quartiles. Multivariable logistic regression, restricted cubic spline, and stratified subgroup analyses were applied for assessing the link between AIP and DKD. The area under the curve (AUC), net reclassification improvement (NRI) and integrated discrimination improvement (IDI) was used to assess the discriminative ability of AIP.

After adjustment for confounding factors, each one-unit AIP rise resulted in a 72% higher likelihood of DKD (OR: 1.72, 95% CI: 1.51-1.96, p < 0.001). Relative to the lowest AIP quartile, the highest quartile showed a 54% higher odds DKD (OR: 1.54, 95% CI: 1.36-1.75, p < 0.001), with a clear dose-response effect (P for trend <0.001). Spline modeling indicated a positive linear link between AIP and DKD, which was apparent in all examined subgroups (all P for interaction >0.05) and externally validated in NHANES. Incorporating AIP into the baseline model modestly improved discrimination, increasing the area under the curve from 68.42 to 68.76%, with a continuous NRI of 0.118 (95% CI: 0.079-0.157, p < 0.001) and an IDI of 0.006 (95% CI: 0.004-0.007, p < 0.001).

AIP shows an independent positive association with DKD in individuals with T2DM, demonstrating a linear dose-response relationship, but the incremental predictive value is limited. The association between AIP and DKD still needs to be further validated by larger-scale prospective studies.

Surgically treated oral cancer patients often face velopharyngeal insufficiency, which adversely impacts their quality of life (QOL). Our past investigations revealed noticeable MR signal shifts in velopharyngeal-related muscles during water deglutition on CMR among healthy individuals. We hypothesized that analyzing these distinct signal fluctuations could offer a novel visual perspective for detecting deglutition anomalies in surgical oral cancer cases. This feasibility study aimed to assess velopharyngeal-related muscular performance via CMR in post-operative oral cancer patients.

Nineteen patients with oral malignancies were prospectively evaluated pre- and post-operatively. Twelve quantitative CMR metrics alongside subjective dysphagia scores were investigated. We analyzed whether signal intensity (SI) ratio alterations in these muscles correlated with dysphagia severity and clinical parameters.

Although three specific CMR parameters significantly worsened post-operatively, muscle MR signal values increased during deglutition without significant variation between pre- and post-surgical states. Subjective swallowing assessments remained entirely normal across all subjects.

This preliminary investigation indicates that CMR can visualize stable velopharyngeal-related muscle activity after surgery in oral cancer patients maintaining adequate swallowing status. Nevertheless, confirmation via larger, symptomatic patient cohorts alongside gold-standard techniques remains mandatory.

To evaluate associations between shrinkage of ablated liver area on computed tomography (CT) over time after radiofrequency ablation (RFA) and clinical parameters related to liver function and fibrosis.

Patients with hepatocellular carcinoma who underwent RFA and follow-up CT were retrospectively reviewed. The ablated area volume (AAV) on CT obtained within 1 week and around 6 months after RFA was measured, and reduction rate of AAV was calculated. The AAV reduction rate was compared among Child-Pugh classification, modified albumin-bilirubin (mALBI) grades, FIB-4 index categories, and lesion locations using generalized estimating equations (GEE). Univariable and multivariable GEE analyses were performed to evaluate associations between the AAV reduction rate and clinical parameters.

Fifty-three lesions in 41 patients (median age, 76 [range, 38-88] years, 24 men) were evaluated. The AAV reduction rate was significantly lower in Child-Pugh class B than class A (p < 0.001) and in mALBI grade 2b than grade 1 (p < 0.001) or grade 2a (p = 0.004). Significant differences were also observed among FIB-4 index groups (p < 0.001) and among lesion locations, with lower AAV reduction rates in medial and anterior segments than in lateral (p < 0.001) and posterior (p = 0.017) segments. Univariable GEE analyses showed significant associations between AAV reduction rate and cholinesterase, albumin, total bilirubin (T-Bil), prothrombin time, platelet count, and FIB-4 index (p < 0.05). Multivariable GEE analysis demonstrated that both albumin and T-Bil remained independently associated with AAV reduction rate (p < 0.001).

The AAV reduction rate tended to be lower in patients with impaired liver function and advanced liver fibrosis.

Background/Objectives: Lifestyle interventions may alleviate treatment-related toxicity and improve patient-centered outcomes during radiotherapy (RT). This scoping review mapped randomized evidence on lifestyle interventions delivered during RT, summarized reported outcomes, and identified evidence gaps. Methods: PubMed and Web of Science were searched for randomized controlled trials (RCTs) published from April 2016 to April 2026. Eligible studies included adults who received exercise, nutritional, psychological, combined, or multimodal lifestyle interventions during their RT treatment. Study characteristics, intervention details, and outcomes were charted and narratively synthesized. Results: Twenty-three RCTs were included. Exercise interventions were evaluated in 12 studies, nutrition in five, psychological in one, combined exercise-and-nutrition in two, combined nutrition-and-psychological in two, and multimodal interventions comprising all three components in one study. Breast, head and neck, and prostate cancers were most frequently represented. QoL, fatigue, and functional capacity were the most commonly assessed outcomes. Exercise interventions were most consistently associated with improvements in fatigue and functional capacity, whereas effects on QoL were less consistent. Nutritional interventions showed favorable findings for nutritional status and treatment-related toxicity. Psychological, combined, and multimodal interventions showed favorable findings for selected QoL, fatigue, nutritional, and psychological outcomes. Key evidence gaps included heterogeneous intervention protocols and outcomes assessment, limited evidence for non-exercise interventions and underrepresentation of several cancer populations. Conclusions: Lifestyle interventions delivered during RT may improve selected patient-centered and treatment-related toxicity outcomes. Exercise comprised the largest body of evidence, whereas other intervention types were less frequently evaluated. Heterogeneity across studies limits conclusions regarding optimal approaches. Further RT-specific studies using standardized intervention programs and comparable outcome measures are required to inform supportive-care delivery.

Melanoma survivors may develop additional primary malignancies, but data from Eastern European hospital cohorts are scarce. We aimed to estimate the observed incidence of second primary cancers (SPCs) within a Romanian referral-centre cohort, identify associated factors, and explore the association of SPC occurrence with overall survival.

We conducted a retrospective, hospital-based cohort study of 394 patients with histopathologically confirmed cutaneous melanoma followed at two referral centres in Cluj-Napoca. Additional malignancies were counted as new primaries only when clinical and/or histopathological documentation distinguished them from recurrence or metastasis. Incidence density was expressed per 1000 person-years. Multivariable logistic regression assessed age, sex, residence, and Breslow thickness. Fixed-covariate Cox and Kaplan-Meier analyses were considered exploratory because of immortal-time and competing-risk limitations.

Over 1848 person-years, 79 patients (20.1%) developed at least one SPC (131 events; observed incidence 70.9/1000 person-years), most frequently cutaneous (53.6/1000 person-years). SPC occurrence increased with age (Cochran-Armitage Z = 5.63, p < 0.001); the Kaplan-Meier complement estimate reached 20.7% at five years. Age independently predicted SPC (OR 1.86 per decade, p < 0.001), whereas greater Breslow thickness was inversely associated (OR 0.86, p = 0.008). Actinic keratosis showed a strong unadjusted association (OR 6.64, p < 0.001) but was not included in the adjusted model. The fixed-status Cox model showed lower mortality among patients with an SPC (HR 0.36, p < 0.001), a finding vulnerable to detection and immortal-time bias.

SPCs were frequent in this hospital cohort and predominantly cutaneous. Older age was an independent predictor, while actinic keratosis was a strong unadjusted marker. Prospective, population-based validation is needed before surveillance intensity is individualised.