Type II Diabetes Mellitus (T2DM) and periodontitis present an independent bidirectional relationship. While T2DM is associated with a higher prevalence, incidence, and severity of periodontitis, periodontitis might worsen glycemic control and inflammatory biomarker levels in diabetics. Although there is no standardized therapy for the treatment of diabetic patients with periodontitis, different periodontal interventions report improvements in clinical and cardiometabolic parameters.

To summarize the current evidence regarding the clinical management of patients with T2DM and periodontitis, with a secondary focus on the impact of periodontal interventions on cardiometabolic biomarkers.

A literature search was conducted between 2010 and 2026. Information about the clinical management of periodontitis in individuals with T2DM and its impact on cardiometabolic biomarkers was classified and summarized.

A comprehensive periodontal examination and diagnosis should be performed, with close collaboration with the patient's physician. Prior dental treatment, capillary blood glucose between 70 and 180 mg/dL, and up to 240 mg/dL in emergency procedures are suggested. The EFP's stepwise treatment approach is recommended, considering periodontal therapy in multiple sessions. Antibiotic therapy or prophylaxis are not recommended in all cases, whereas periodontal maintenance may be required every 3-6 months. Periodontal interventions in diabetic individuals have been shown to decrease glycated hemoglobin (HbA1c) and C-reactive protein (CRP), together with other inflammatory and cardiometabolic biomarkers.

Patients with T2DM benefit from several periodontal treatment strategies, with a positive impact on inflammatory and cardiometabolic biomarkers associated with eventual reductions in diabetic control and systemic inflammation.

To compare weight-normalized tidal lung function trajectories from corrected 40 weeks to 6 months postmenstrual age (PMA) between preterm infants (28-36 + 6 weeks gestation, including 23 infants born <32 weeks) and term infants (≥37 weeks); identify independent perinatal-neonatal risk factors disrupting early pulmonary maturation; and validate the predictive value of term-equivalent lung indices for composite respiratory morbidity in Chinese preterm infants.

This single-center prospective cohort enrolled 111 infants (75 preterm, 36 term) from 2020 to 2024. Standardized tidal spirometry was conducted at corrected 40 weeks, 3 and 6 months PMA following ATS/ERS guidelines; weight-normalized tidal volume (VT/kg) was designated as the primary endpoint to eliminate confounding derived from somatic growth differences. Linear mixed models (LMM) with random infant intercepts were used to model longitudinal pulmonary developmental changes. Multivariate linear and logistic regression analyses were fully adjusted for gestational age, birth weight, bronchopulmonary dysplasia (BPD), total ventilation duration, antenatal glucocorticoid exposure and small-for-gestational age (SGA) status. Sample size calculation confirmed ≥33 participants per group was required to detect a 0.7 mL/kg intergroup VT/kg difference with 80% power; both cohorts exceeded this threshold.

A total of 19/111 infants (17.1%) developed composite respiratory morbidity (physician-diagnosed pneumonia combined with recurrent wheezing ≥2 episodes) by 6 corrected months, with a significantly higher burden among preterm infants (16/75, 21.3%) relative to term infants (3/36, 8.3%, P = 0.049). At corrected 40 weeks PMA, preterm infants displayed impaired expiratory function (lower TPEF/TE, TEF50) and elevated resting respiratory rate (RR, all P < 0.05), while intergroup disparities in raw tidal volume disappeared entirely after weight normalization. Preterm infants exhibited partial compensatory lung catch-up growth: moderate and late preterm infants (32-36 + 6 weeks) achieved lung function comparable to term infants by 6 months PMA, whereas infants born <32 weeks maintained persistent deficits in VT/kg and TEF50 (P < 0.05). Fully adjusted regression identified advanced maternal age, neonatal positive-pressure resuscitation and low 5-min Apgar score as independent factors hindering early lung maturation. Gestational diabetes mellitus showed no independent correlation with VT/kg after weight normalization; its crude positive association with raw tidal volume was fully explained by fetal macrosomia. Higher VT/kg (OR = 0.74, 95%CI 0.55-0.95, P = 0.030), TEF75 (OR = 0.93, 95%CI 0.85-0.99, P = 0.048) and TEF50 (OR = 0.89, 95%CI 0.78-0.98, P = 0.030) at corrected 40 weeks independently reduced the odds of subsequent composite respiratory morbidity.

Birth before 32 weeks gestation leads to sustained weight-standardized pulmonary dysfunction at 6 corrected months despite partial compensatory lung development. Multiple modifiable antenatal and neonatal exposures regulate infant pulmonary maturation. Weight-standardized tidal indices measured at term-equivalent age serve as practical screening biomarkers for respiratory risk stratification among preterm infants, supporting standardized routine pulmonary monitoring in neonatal clinical practice.

To investigate whether a single intraoperative dose of dexamethasone alters perioperative glycemic dynamics in older patients with type 2 diabetes undergoing thoracoscopic lung resection. Glycemic dynamics were captured using continuous glucose monitoring (CGM).

72 patients aged ≥ 60 years with type 2 diabetes who underwent elective thoracoscopic lung resection were randomly assigned to receive either 8 mg of dexamethasone or placebo (0.9% saline) intravenously during anesthesia induction. The primary outcome was the maximum change in intraoperative blood glucose from preoperative baseline. Key secondary outcomes included CGM-derived glycemic variability (GV) metrics, including standard deviation (SD), coefficient of variation (CV), blood glucose instability index (GLI) and time-in-range measures, assessed throughout the perioperative period. Multivariable linear regression was performed to assess the independent effect of dexamethasone on glycemic outcomes after adjusting for relevant covariates. The accuracy of CGM was assessed using mean absolute relative difference and Bland-Altman analysis.

The dexamethasone group exhibited greater median (IQR) maximum intraoperative glucose change: 3.6 (3.3-4.9) mmol/L vs. 3.1 (2.6-4.0) mmol/L; P = 0.009. Dexamethasone was also associated with higher intraoperative GV: SD (1.1 [1.0-1.4] mmol/L vs. 0.8 [0.7-1.0] mmol/L, P < 0.001), CV (21.9 [6.3] vs. 15.8 [6.1]; P < 0.001), and GLI (3.0 [1.7-4.1] mmol²/L²/h vs. 1.4 [0.9-2.4] mmol²/L²/h; P < 0.001). Multivariable analysis confirmed that dexamethasone independently predicted greater intraoperative glucose excursions and glycemic variability. Perioperative time-in-range metrics did not differ significantly between groups. CGM demonstrated acceptable accuracy in this surgical setting.

A single 8 mg intraoperative dose of dexamethasone increases maximum intraoperative glucose change and amplifies GV in older patients with diabetes. These findings reveal a previously uncharacterized dimension of dexamethasone-induced glycemic instability in this vulnerable population and highlight the need for glycemic monitoring strategies that capture transient fluctuations potentially missed by conventional intermittent measurements.

www.chictr.org.cn, identifier [ChiCTR2300077167].

The global epidemic of type 2 diabetes mellitus (T2D), along with its rising prevalence among younger populations, raises substantial public health concerns; severe hypertriglyceridemia (sHTG) is a major risk factor for acute pancreatitis. Insulin resistance in T2D often coincides with dyslipidemia, contributing to lipotoxicity, and insulin-resistant states may be linked to specific genetic variants.

This report presents a 27-year-old man with poor glycemic control, recurrent dizziness, extreme hypertriglyceridemia (TG > 37.87 mmol/L), insulin resistance, pancreatic fat infiltration, and early-stage diabetic nephropathy. Despite a family history of T2D, his clinical presentation far exceeded that of typical T2D. High-throughput sequencing revealed a heterozygous LRP6 variant (c.3107A>G, p.Asn1036Ser).

Multidisciplinary treatment-incorporating acute-phase plasma exchange, ω-3 fatty acid ethyl ester 90, inclisiran, subcutaneous insulin aspart pump therapy, metformin, insulin icodec, finerenone, and Huangkui capsules-led to improvements in the patient's metabolic indicators.

This case report describes a patient with type 2 diabetes mellitus presenting with extreme metabolic disorders, in whom a variant in the LRP6 gene was detected. Although the variant co-occurs with the observed phenotype, its pathogenicity cannot currently be established in the absence of functional validation. This case emphasizes that genetic variant screening should be considered in patients with unexplained severe metabolic disturbances, particularly those with early-onset disease. This case also provides a foundation for future functional studies and genetic confirmation.

To examine whether perceived social support mediates the relationship between perceived stress and self-management behaviors in patients with type 2 diabetes mellitus (T2DM) complicated by metabolic dysfunction-associated steatotic liver disease (MASLD), and to provide a theoretical basis for targeted psychosocial interventions in clinical practice.

By convenience sampling, patients with T2DM and MASLD were recruited from a tertiary hospital in Changsha between April 2024 and September 2025. Data were collected using a general information questionnaire, the Chinese Perceived Stress Scale, the Perceived Social Support Scale, and the Chronic Disease Self-Management Behavior Measurement Scale.

The mean scores for perceived stress, perceived social support, and self-management behaviors were 25.66 ± 8.02, 56.05 ± 10.28, and 27.63 ± 8.62, respectively. Pearson correlation analysis indicated that dimensions such as loss of control and tension were significantly associated with both social support and self-management behaviors (all P < 0.01). Perceived stress was negatively correlated with perceived social support (r = -0.534, P < 0.01) and self-management behaviors (r = -0.391, P < 0.01), whereas perceived social support showed a positive correlation with self-management behaviors (r = 0.471, P < 0.01). Mediation analysis demonstrated that perceived social support partially mediated the association between perceived stress and self-management behaviors, accounting for 50.2% of the total effect.

Perceived social support functions as a key mediator linking perceived stress and self-management behaviors in patients with T2DM and MASLD. These findings highlight the importance of integrating psychological assessment into routine nursing care. Interventions such as family-involved nursing care, peer support groups, and the utilization of community-based healthcare resources may help establish a coordinated support system that connects the hospital, family, and society. The proposed approach could mitigate the adverse impact of stress on self-management behaviors and ultimately improve patient outcomes.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as potential adjuncts to insulin therapy for type 1 diabetes mellitus (T1DM). However, interpretation of the available evidence is complicated by substantial primary-study overlap, methodological heterogeneity and variable certainty of evidence. Thus, we conducted an overlap-informed umbrella review to evaluate the efficacy and safety of GLP-1RAs as adjunctive therapy in T1DM.

We searched PubMed/MEDLINE, Embase, the Cochrane Central Register of Controlled Trials and OpenAlex from inception to 22 June 2026, and manually screened reference lists to identify systematic reviews with meta-analyses that included randomized controlled trials (RCTs), either alone or alongside nonrandomized studies, evaluating adjunctive GLP-1RA therapy in T1DM. Methodological quality was assessed using AMSTAR 2, and primary-study overlap was quantified using a citation matrix and corrected covered area (CCA). Outcome-specific representative meta-analyses were selected, and their primary-study data were independently reanalyzed using random-effects models. Continuous and dichotomous outcomes were summarized as mean differences (MDs) and risk ratios (RRs), respectively, with 95% confidence intervals (CIs). The certainty of evidence was assessed using GRADE.

Eighteen systematic reviews with meta-analyses encompassing 56 unique primary studies (35 RCTs and 21 nonrandomized studies) were included. The calculated CCA was 19.6%, indicating a very high degree of primary-study overlap, largely driven by the ADJUNCT ONE and ADJUNCT TWO trials. Adjunctive GLP-1RA therapy reduced HbA1c (MD, -0.23% [95% CI, -0.30 to -0.17]; moderate certainty), body weight (MD, -3.93 kg [-4.29 to -3.56]; moderate certainty) and total daily insulin dose (MD, -5.74 IU/day [-7.30 to -4.17]; low certainty). No significant improvement was observed in time in range (MD, 1.99% [95% CI, -1.17 to 5.15]; very low certainty). No statistically significant increases were observed in severe hypoglycemia (RR, 0.83 [95% CI, 0.36-1.91]; low certainty) or diabetic ketoacidosis (RR, 0.67 [95% CI, 0.16-2.86]; low certainty). However, GLP-1RAs increased the risks of nausea (RR, 2.88 [95% CI, 2.20-3.76]; high certainty), vomiting (RR, 3.11 [1.94-4.97]; high certainty), and withdrawal due to adverse events (RR, 2.10 [1.42-3.12]; high certainty), whereas the risk of diarrhoea was not significantly increased (RR, 1.88 [0.82-4.33]; low certainty).

Adjunctive GLP-1RA therapy was associated with a modest reduction in HbA1c and clinically relevant reductions in body weight and insulin requirements, without a significant improvement in time in range. Gastrointestinal adverse events were increased, whereas the risks of diabetic ketoacidosis and severe hypoglycemia remained uncertain. These findings do not support routine use but suggest a potential role in selected individuals for whom weight reduction and lower insulin requirements are therapeutic priorities.

Sodium-glucose co-transporter 2 inhibitors (SGLT2i) improve cardiovascular and renal outcomes in type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD) and chronic heart failure (CHF). Despite clinical guideline recommendations, SGLT2i uptake in UK primary care remains suboptimal and information on utilisation is limited. This study aims to quantify and describe the UK primary care population with T2DM, CKD and/or CHF who are eligible for but not currently prescribed an SGLT2i.

A cross-sectional study was conducted using routinely collected electronic health records from the Optimum Patient Care Research Database. Adults aged ≥ 18 years on 1 July 2024 were included. Descriptive analyses estimated disease prevalence (defined by morbidity-coded diagnosis), SGLT2i eligibility (defined using NICE clinical guidelines) and current SGLT2i treatment (defined as any SGLT2i prescription in the previous 2 months) by conditions and selected characteristics. Main results are based on diagnosed disease; in a separate CKD sensitivity analysis, indicative CKD (without a morbidity code) was defined using kidney function test results.

In the study population of 9.8 million adults, prevalence was 6.52% for T2DM, 4.95% for diagnosed CKD (6.07% including indicative CKD) and 1.40% for CHF. Among all SGLT2i-eligible individuals, 17.5% were currently prescribed an SGLT2i. Current SGLT2i treatment was lowest in CKD-only patients (3.8% treated among eligible) and highest in those meeting eligibility criteria for all three indications (32.9% treated). SGLT2i treatment was lower in women and older adults.

SGLT2i therapy is significantly underutilised in UK primary care, particularly for CKD. Equitable implementation of SGLT2i clinical guidelines is vital to improve cardio-renal-metabolic care.

Shoulder dystocia (SD) is rare, but it has serious consequences. Antepartum risk stratification for SD has demonstrated variability across populations, reflecting differences in assessment methodologies.

We conducted a retrospective analysis using a prospectively audited electronic database from a single center. All singleton vertex deliveries between January 2012 and December 2017 were reviewed. SD cases were identified by the recorded use of ancillary maneuvers during shoulder delivery. Case-control matching was informed by previously published odds ratios for key variables and evaluated using conditional logistic regression.

A total of 80,349 eligible delivery records were reviewed, of which 23,392 (29.11%) were Cesarean deliveries. Among the remaining 56,957 vaginal births, 58 cases of SD were identified, representing an incidence of 0.10%. An additional 880 gestational age-matched controls were selected, based on a conservative control-to-case ratio of 15:1. Maternal and neonatal birth injuries were documented in 5 SD cases (8.6%) and 6 control cases (0.7%), respectively (p < 0.001). Adjusted odds ratios (95% confidence intervals) for associated risk factors were as follows: fetal macrosomia (birthweight >/= 4000 g), 22.99 (8.49-62.25); maternal overweight (body mass index >/= 25 kg/m²), 3.44 (1.41-8.44); diabetes mellitus, 2.32 (1.12-4.78); and nulliparity, 1.62 (0.89-2.94), with statistical significance observed for all (p < 0.05) except nulliparity. Conditional logistic regression modeling revealed distortion in matching between parity and maternal age >/= 35 years, as well as fetal macrosomia, which attenuated statistical significance (p = 0.113).

Fetal macrosomia was the most robust independent predictor of SD. Maternal overweight and diabetes mellitus were contributory and modifiable risk factors. Parity did not independently predict SD events, likely due to a Type I statistical error.

Hypervirulent Klebsiella pneumoniae (hvKP) is an important cause of invasive community-acquired infection, particularly in individuals with diabetes mellitus. However, cerebrospinal fluid (CSF)-derived hvKP isolates, especially those belonging to the ST86-KL2 lineage, remain poorly characterized at the integrated clinical, genomic, and phenotypic levels.

A K. pneumoniae isolate, designated BP9811, was recovered from the CSF of a patient with meningitis and diabetes mellitus and identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and 16 S rRNA sequencing. Antimicrobial susceptibility testing and whole-genome sequencing were performed to define its resistance, virulence, sequence type (ST), capsular type, and plasmid content. Virulence was evaluated using the Galleria mellonella infection model. In addition, interaction with human cerebral microvascular endothelial cells was preliminarily assessed using adhesion, gentamicin protection, and transmission electron microscopy assays, together with measurement of relative ompA transcription by reverse transcription-quantitative polymerase chain reaction. Comparative phylogenetic analyses were performed using publicly available CSF-derived and KL2 K. pneumoniae genomes.

BP9811 was identified as a hypermucoviscous ST86-KL2 hvKP isolate that remained susceptible to all tested antimicrobial agents. Whole-genome sequencing revealed an IncHI1B virulence plasmid carrying canonical hvKP-associated determinants, including rmpA/rmpA2, peg-344, iucABCD, and iroBCD. In the Galleria mellonella model, BP9811 showed high virulence comparable to that of the hypervirulent reference strain NTUH-2044. In HCMEC/D3 cells, BP9811 exhibited increased adhesion and intracellular recovery under the tested conditions, and transmission electron microscopy confirmed bacterial internalization. BP9811 also showed higher ompA transcript levels than the control strain. Phylogenetic analysis indicated that BP9811 was genetically distinct from currently available CSF-derived isolates and occupied a related branch within the KL2 population.

This study provides an integrated clinical, genomic, and phenotypic characterization of BP9811, a CSF-derived ST86-KL2 hvKP isolate recovered from a patient with meningitis and diabetes mellitus. BP9811 carried a canonical hvKP virulence plasmid, displayed marked virulence-associated phenotypes, and showed enhanced interaction with human cerebral microvascular endothelial cells in vitro under the tested conditions. These findings expand the limited isolate-level evidence on central nervous system-associated hvKP and provide a basis for future comparative and mechanistic studies.

Diabetes mellitus is a prevalent chronic condition globally. A frequent complication is gastric motility disorder, which substantially impacts patients' quality of life and overall well-being. The SMC-ICC-PDGFRα⁺ (SIP) syncytium plays an important role in coordinating gastrointestinal (GI) motility. Auricular vagus nerve stimulation (aVNS) has demonstrated promising therapeutic efficacy against diabetic motility disorders, yet the underlying mechanism is not well understood. This study aims to evaluate whether low-frequency aVNS attenuates gastric dysmotility in diabetic rats through regulation of the SIP syncytium and its signaling pathways.

Male Sprague-Dawley rats were employed to induce a diabetic gastric motility disorder (DGMD) model using streptozotocin (STZ). The DGMD rats underwent treatment with aVNS, a combination of aVNS and body electroacupuncture (aVNS-EA), and sham aVNS. Gastric motility was evaluated by the solid gastric emptying rate (SGER). Gastric antrum pathology was assessed via hematoxylin and eosin (H&E) staining, SIP syncytium function was evaluated by immunofluorescence, and serum nitric oxide (NO) levels were measured with a Griess kit.

Low-frequency aVNS significantly enhanced SGER and upregulated the expression of interstitial cells of Cajal (ICCs) and platelet-derived growth factor receptor alpha-positive (PDGFRα⁺) cells in the antrum; the smooth muscle marker α-SMA was increased at the immunofluorescence and messenger RNA (mRNA) levels, but not significantly at the protein level. aVNS-EA exhibited similar effects, whereas sham aVNS showed no significant change. aVNS also upregulated neuronal nitric oxide synthase (nNOS), increased NO release, and activated the soluble guanylate cyclase-cyclic guanosine monophosphate-protein kinase G1 (sGC-cGMP-PKG1) pathway. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), the soluble guanylate cyclase (sGC) inhibitor, reversed the aVNS-induced improvements in SGER and SIP syncytium integrity.

In contrast, aVNS-EA benefits were only partially inhibited by ODQ. These results suggest that low-frequency aVNS improves gastric motility and SIP syncytium function in diabetic rats by activating the NO/sGC/cyclic guanosine monophosphate (cGMP)/protein kinase G1 (PKG1) pathway and that the aVNS-EA yields additional beneficial effects.