Concentrated Growth Factor (CGF) is a third-generation autologous platelet concentrate utilized for its high density of bioactive molecules. However, the influence of chronic hyperglycemia on the specific growth factor composition of CGF remains underexplored. This study aimed to quantify and compare the concentrations of IGF-1, VEGF-A, and TGF-β1 in CGF derived from individuals with uncontrolled type 2 diabetes mellitus (T2DM) versus non-diabetic controls.

A cross-sectional study was conducted involving 80 participants: 40 with uncontrolled T2DM (HbA1c > 7%) and 40 non-diabetic controls (HbA1c < 6%). CGF was isolated via a standardized variable-speed centrifugation protocol (Medifuge MF200). Growth factor levels were quantified using validated, high-sensitivity enzyme-linked immunosorbent assays (CV < 10%). Data were analyzed using independent t-tests and Pearson's correlation (P < 0.05), adjusting for age and BMI.

CGF from uncontrolled diabetics exhibited significantly lower mean concentrations of all measured factors compared to controls: IGF-1 (0.42 ± 0.15 vs. 1.58 ± 0.06 ng/mL; P< 0.001), VEGF-A (0.11 ± 0.02 vs. 0.21 ± 0.03 ng/mL; P< 0.001), and TGF-β1 (2.52 ± 0.36 vs. 2.76 ± 0.15 ng/mL;P < 0.001). The largest reduction was observed in IGF-1 (~72%), followed by VEGF-A (~46.7%) and TGF-β1 (~8.7%). Correlation analysis indicated that these reductions were significantly associated with hyperglycemic status (HbA1c) rather than demographic variables such as age or BMI.

Uncontrolled hyperglycemia is associated with a significant quantitative depletion of key regenerative growth factors within CGF, particularly IGF-1 and VEGF-A. These findings suggest that the intrinsic regenerative potential of autologous CGF may be compromised in diabetic patients, indicating a need for optimized glycemic control or adjunctive strategies in clinical regenerative procedures.

The present study investigated the effect of selenium-enriched eggs (SE egg) vs. zeaxanthin-enriched eggs (ZE egg) on glycemic and lipid metabolism in patients with diabetes.

Fifty-eight patients with type 2 diabetes were recruited and randomly divided into group SE egg (27 subjects) and ZE egg (31 subjects). The two groups of participants consumed either SE egg or ZE egg twice a day for a total of 12 weeks of intervention. Fasting blood samples were collected before and after the intervention to detect changes in blood glucose and lipid levels.

After the intervention, the fasting blood glucose, homeostatic model assessment of insulin resistance, and triglyceride-glucose index of both SE and ZE groups of subjects significantly decreased (p < 0.05). Among subjects with a baseline glycosylated hemoglobin A1c (HbA1c) < 8.9%, eggs from both groups showed an enhanced improvement in glucose and lipid metabolism. The ZE egg group showed a significant decrease in triglycerides (p = 0.0007) and an increase in homeostatic model assessment of β-cell function (p = 0.06). There was no significant difference in HbA1c between the two groups after the intervention.

This study demonstrates that SE egg and ZE eggs have comparable effects on improving glucose metabolism profiles in diabetic patients, with an improved efficacy observed in subjects with lower baseline HbA1c levels. Furthermore, ZE eggs suggest potential benefits in lowering TG levels.

https://www.chictr.org.cn/index.html, Identifer, ChiCTR2300077522.

This case describes an uncommon presentation of a hypoglycemia-related stroke mimic in a patient with poorly controlled type 2 diabetes, in whom acute neurological symptoms developed despite a blood glucose level above the conventional hypoglycemic threshold. A 72-year-old woman presented with acute fatigue, drowsiness, and dysarthria after initiation of an intensified glucose-lowering regimen. Her blood glucose level was 4.1 mmol/L at symptom onset and increased after glucose administration; however, her neurological symptoms persisted. Because acute ischemic stroke could not be confidently excluded during the emergency evaluation, intravenous alteplase was administered. Her symptoms subsequently improved approximately 9.5 hours after symptom onset. Comprehensive neurovascular and brain imaging, including computed tomography, computed tomography angiography, magnetic resonance imaging, and transcranial Doppler ultrasonography, showed no evidence of acute ischemic lesions or significant vascular occlusion. After adjustment of her glucose-lowering therapy, her neurological condition remained stable, and no permanent neurological deficits were observed. This case highlights the diagnostic challenge of distinguishing hypoglycemia-related stroke mimic from acute ischemic stroke, particularly in patients with poorly controlled diabetes and fluctuating glucose levels. It also suggests that relative or rapidly declining glucose levels may contribute to stroke-like neurological symptoms even when absolute glucose values do not meet the conventional definition of hypoglycemia. Careful clinical assessment, timely glucose measurement, and urgent stroke evaluation remain essential when acute ischemic stroke cannot be reliably excluded.

A 13-year-old neutered female domestic shorthair cat was referred for weight loss, polyphagia, polyuria, polydipsia and intermittent vomiting. Blood work demonstrated diabetes mellitus; abdominal ultrasonography revealed a hypoechoic, thickened pancreas with two large fluid-filled cavities within the body and right limb. Cytology of the aspirated fluid indicated suppurative inflammation with bacterial infection, which cultured Pasteurella multocida. Medical management for diabetes mellitus and pancreatic abscessation was initiated. After approximately 4 months of antimicrobial therapy and five percutaneous drainages, clinical signs improved; nevertheless, serial abdominal ultrasonography demonstrated persistent pancreatic abscessation, while repeated cultures and antibiograms documented progressively resistant bacterial infections. The condition culminated in abscess rupture and septic peritonitis, prompting surgical drainage and omentalisation. Histopathological examination of the pancreatic parenchyma revealed severe lymphoplasmacytic pancreatitis with glandular atrophy, while evaluation of the pancreatic tissue associated with the abscess demonstrated a suspected pancreatic exocrine neoplasm, most compatible with a well-differentiated adenocarcinoma.

This case highlights the need for earlier consideration of surgical intervention in cases of recurrent pancreatic abscessation and underscores the importance of including concurrent pancreatic neoplasia as a differential diagnosis in chronic, non-resolving presentations.

Type 1 diabetes mellitus (T1DM) is a multifactorial disease wherein a genetic predisposition, upon exposure to environmental factors, triggers seroconversion and subsequent beta-cell destruction. The global incidence of T1DM has risen in recent decades, underscoring the significant role environmental factors play in actuating inherent genetic risk. However, the absence of an identifiable unique triggering factor complicates the identification of risk groups. Advances in bioinformatics and epigenetic research are opening new opportunities for early diagnosis, prevention, and novel therapies for the condition. A comprehensive analysis of complex molecular pathways will make it possible to develop algorithms for the early diagnosis, disease course prediction, and therapy personalization based on a patient's genetic profile. This review systematizes current data on the genetic and epigenetic heterogeneity of autoimmune diabetes and its potential triggers. It assesses the regional and ethnic disparities in T1DM incidence globally and within the Russian Federation, and it discusses the potential of clinical-genetic models for disease prediction.

Cervicofacial necrotizing fasciitis is a rare, rapidly progressive and fatal polymicrobial necrotizing infection of the fascial and subcutaneous tissue of the head and neck resulting from the vascular thrombosis and ischemia within the fascial plane.

The aim of this study was to evaluate the clinical presentations and management outcomes of patients managed for cervicofacial necrotizing fasciitis at the University College Hospital, Ibadan.

The data of patients managed for cervicofacial necrotizing fasciitis between January 2018 and December 2023 were extracted from case notes obtained from the medical records. All patients were admitted and those with comorbidities were co-managed with the physicians. Antibiotics were administered empirically after samples for microbiology culture and sensitivity were taken. Patients had extraction of offending teeth, serial debridement and honey dressing until no visible sign of infection and wounds epithelized. SPSS was used for data analysis.

During this period, seventeen patients with cervicofacial necrotizing fasciitis were managed. The male to female ratio was 1.8:1 with mean age of 57.65 (+17.674) years. Most (88.2%) of the patients were of low socio-economic status. Anaemia was the commonest underlying systemic condition while about half (47.1%) of the patients were diagnosed with diabetes mellitus. The only identified aetiology was odontogenic infection among all patients. Seventyfive percent of patients with diabetes presented with features of sepsis. The Chi-test test showed statistical significance association between the diagnosis of diabetes mellitus and sepsis at presentation (P-value=0.030) . Submandibulocervical region was the commonest affected site and average hospital stay was 13.59 (+8.382) days. The major complication encountered was scar formation with no mortality recorded.

Cervicofacial necrotizing fasciitis is a rare but debilitating disease which is usually associated with poverty and presence of comorbidities. Its non-specific symptoms make late presentations common. Hence, the need for high index of suspicion for prompt management.

To report a rare case of concurrent Gitelman syndrome (GS) and Turner syndrome (TS) and explore their interplay in driving a complex clinical phenotype.

A single-case report with literature review.

A 34-year-old woman was evaluated via clinical history, laboratory tests (electrolytes, glucose, thyroid function), and genetic analysis (karyotyping, SLC12A3 sequencing).

The patient presented with short stature, hypokalemia, and hyperglycemia. Genetic testing confirmed a 45, X/46, XX mosaic karyotype (TS) and compound heterozygous SLC12A3 mutations (GS). Associated conditions included diabetes mellitus, Hashimoto's thyroiditis, and hyperlipidemia. Insulin and potassium supplementation achieved short-term stabilization.

The coexistence of GS and TS likely synergistically exacerbated metabolic and electrolyte derangements. This highlights the need for multidisciplinary, personalized long-term management in such overlapping genetic disorders.

Total pancreatectomy (TP) often leads to insulin-deficient diabetes, including unstable "brittle diabetes." Autologous islet transplantation during or after TP can prevent or treat diabetes by reinfusing functional islets into the portal vein. This case report details the perioperative nursing strategies for a patient undergoing image-guided planned autologous islet transplantation following TP.

A 64-year-old male with pancreatic cancer, type 2 diabetes, and hypertension underwent TP and initial autologous islet transplantation but required a second transplantation due to poor graft function. Preoperatively, he exhibited fluctuating blood glucose (8.9-14.5 mmol/L) and anxiety about surgical outcomes.

The patient was diagnosed with recurrent pancreatic cancer post-TP and chemotherapy, compounded by insulin-dependent diabetes and suboptimal islet function necessitating secondary transplantation.

A multidisciplinary approach included meticulous preoperative islet quality control, intraoperative portal vein catheterization under ultrasound guidance, and dynamic monitoring of portal pressure. Postoperative care featured anticoagulation (heparin/low-molecular-weight heparin), glycemic management via insulin micropump, and thromboprophylaxis using intermittent pneumatic compression. Psychological support and preoperative education alleviated patient anxiety.

Posttransplantation, blood glucose stabilized (3.9-7.7 mmol/L), enabling discontinuation of exogenous insulin. The patient was discharged on day 18 without complications such as thrombosis or hemorrhage.

Multidisciplinary collaboration, tailored nursing interventions, and rigorous complication prevention ensured successful outcomes. This case highlights the critical role of structured perioperative care in achieving insulin independence after complex islet transplantation.

Type 2 diabetes mellitus is characterized by systemic insulin resistance, chronic low-grade inflammation, and progressive metabolic dysfunction. Increasing evidence identifies the gut microbiota as a central regulator of host immunometabolism through a diet-microbiota-host axis. Gut microbiota-derived metabolites, including short-chain fatty acids, bile acids, branched-chain amino acids, and trimethylamine N-oxide, integrate endocrine signaling, intracellular metabolic pathways, and inflammatory responses across intestinal and systemic compartments, thereby shaping glucose homeostasis and metabolic balance. Diet acts as an upstream determinant by modulating microbial composition and metabolic activity. Beyond soluble metabolites, extracellular vesicles have emerged as an additional mode of intercellular communication. Vesicles derived from diet or microbiota carry bioactive cargos such as proteins, lipids, and small RNAs, enabling the transfer of functional signals that may influence both microbial ecology and host immunometabolic processes. This review summarizes metabolite-dependent and vesicle-mediated signaling pathways and highlights how these interconnected mechanisms position the gut microbiota as a signaling hub linking dietary inputs to host cellular regulation. This framework provides a conceptual basis for microbiota-targeted strategies in the prevention and treatment of type 2 diabetes.

IntroductionIn Mexico, delays in pediatric cancer diagnosis remain a major barrier to timely care and are partly driven by inefficiencies in referral pathways. This study aimed to evaluate the impact of a direct pathway on referral intervals for patients with suspected childhood cancer treated at a high-specialty hospital in Mexico.MethodsWe conducted a retrospective observational cohort study based on a comprehensive review of medical records of patients referred to a high-specialty hospital in Mexico between 2017 and 2022. Patients' characteristics, along with dates from symptom recognition to diagnosis, were collected. The exposure was the referral pathway: standard versus direct (Golden Code strategy) pathway, which enables access to pediatric oncology through a zero-rejection policy. The primary outcome was the time attributable to oncological referral (TAOR), analyzed as a continuous variable and a dichotomous outcome. Secondary intervals were calculated using standardized definitions. Regression models were used to evaluate factors associated with untimely (>7 days) referral.ResultsA total of 399 patients were included. The direct pathway was associated with a shorter TAOR compared to the standard pathway (median 2.0 vs. 7.0 days; p<0.001). The proportion of timely referrals was substantially higher in the direct pathway (91.3%) than in the standard (50.6%) and reduced the likelihood of an untimely referral (OR = 0.098, 95% CI: 0.055-0.173; p<0.001). No differences were observed in other diagnostic intervals.ConclusionThe direct referral pathway improves the timeliness and consistency of access to pediatric oncology care by reducing referral delays and increasing the proportion of patients evaluated within recommended referral intervals. However, the absence of changes in the secondary intervals, such as time to oncological diagnosis, highlights the need for complementary actions targeting downstream diagnostic processes. Strengthening referral systems represents a feasible and impactful strategy to address delays in pediatric cancer care in middle-income settings.