Alterations in circulating amino acid profiles have been observed in ischemic stroke patients; however, whether cerebral ischemia disrupts amino acid metabolism within brain tissue and whether this disruption contributes to cellular stress and cerebral injury remain unknown. This hypothesis-testing study investigates disrupted BCAA (branched-chain amino acid) catabolism as a key mechanism of ischemic brain damage and evaluates BCKDK (branched-chain α-keto acid dehydrogenase kinase) as a novel therapeutic target.

Mouse primary cortical neurons subjected to oxygen-glucose deprivation and brain tissue from a mouse acute ischemic stroke model were used as experimental systems. Untargeted metabolomics and metabolic flux analysis were used to characterize BCAA metabolism in both models. In vivo pharmacological inhibition or in vitro knockdown of BCKDK was performed using BT2 treatment or RNA interference. Primary outcome variables included infarct volume, BCKDH (branched-chain α-keto acid dehydrogenase) enzyme activity, neuronal viability, and markers of energy metabolism and glutamate excitotoxicity. Between-group differences were evaluated using 1-way ANOVA; data are presented as mean ± SD with 95% CIs and corresponding P values.

Metabolomics analysis of oxygen-glucose deprivation-exposed primary neurons revealed impaired BCAA catabolism and significant BCAA accumulation compared with normoxic controls. In ischemic mouse brain tissue, BCKDH activity was significantly suppressed, and BCKDK expression was markedly upregulated relative to sham-operated animals. Both pharmacological and genetic suppression of BCKDK substantially reduced cerebral ischemic injury, as evidenced by decreased infarct volume and improved neuronal survival (95% CI and P values per comparison). Mechanistically, ischemia-induced BCKDK expression via HIF-1α (hypoxia-inducible factor 1α)-mediated transcriptional activation, which inhibited BCAA conversion to tricarboxylic acid cycle substrates, thereby potentiating energy deficiency and glutamate excitotoxicity.

These data identify BCKDK as a novel hypoxia-responsive factor whose upregulation drives disrupted BCAA catabolism as a key mechanism of ischemic neuronal injury. BCKDK represents a promising therapeutic target for cerebral ischemia, directly supported by both in vitro and in vivo experimental evidence presented here.

Thyroid disorders (TDs) remain the second-most common endocrine disease after diabetes mellitus worldwide. However, there is a paucity of data on the prevalence and pattern of TDs in northern Nigeria. The study aimed to document the baseline spectrum of thyroid disorders as seen in the endocrinology, diabetes, and metabolism (EDM) outpatient clinic, Department of Internal Medicine of Rasheed Shekoni Federal University Teaching Hospital (RSFUTH), Dutse, over a four-year period.

A retrospective hospital-based descriptive study design was used to review the medical records of all patients seen in the EDM outpatient clinic between September 2020 and August 2024. All endocrinology diagnoses classified according to the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) were recorded. Information on demographic, source of referral, baseline clinical, and biochemical indices were analysed using SPSS version 20, and descriptive statistics were presented.

During the study period, a total of 30 patients' records who met the inclusion criteria were analysed. The mean age was 34.8 ± 10.2. The majority of the patients were female, contributing 76.7%, while males contributed 23.3%. The pattern of thyroid disorders was: Graves's disease among 14 (46.7%) of the patients, followed by toxic multinodular goitre (13%), nodular goitre (13.3%), simple goitre (13.3%), hypothyroidism (6.7%) and subclinical hypothyroidism (6.7%) respectively.

The most common thyroid disorder seen in RSFUTH was hyperthyroidism. Both sexes are affected, but with a female preponderance. There is a need for identifying the underlying risk factors from the identified areas with high burden of the condition, screening for early detection of cases and health education on thyroid disorders for early health-seeking behaviour, to prevent complications.

Chronic pulmonary aspergillosis (CPA) is a recognized complication in patients with pulmonary tuberculosis, particularly in high TB burden regions. Misdiagnosis and inappropriate treatment occur due to overlapping clinicoradiological features, leading to increased morbidity and mortality. Data on CPA occurrence and its association with PTB in tertiary care settings remain limited in resource-constrained countries.

This study enrolled 143 adults from outpatient and inpatient departments. Newly and previously diagnosed PTB patients were included. The CPA diagnosis was based on symptoms lasting over three months, radiological findings, and microbiological/immunological evidence using Aspergillus IgG and BAL galactomannan testing. Data were analyzed using STATA 14.0. Descriptive statistics summarized demographic and clinical data, and comparative analyses between CPA and non-CPA groups used chi-square or Fisher's exact tests for categorical variables and Student's t-test for continuous variables.

CPA was diagnosed in 34.3% (49/143) of PTB patients. The CPA cohort showed male predominance (male-to-female ratio, 4:1), with associations with diabetes mellitus (70.8%, p=0.038) and post-tuberculosis lung disease (61.4%, p=0.040). Radiological features, including cavitation (47.4%, p=0.009), aspergilloma (55.9%, p=0.009), and infiltrates (72.3%, p=0.10) were more frequent in CPA patients. Aspergillus-specific IgG was positive in 69.4% (p<0.001) and BAL galactomannan in 43.9% (p<0.001) of CPA patients.

CPA is prevalent among PTB patients, especially those with TB history and comorbidities like diabetes. Integrated diagnostic approaches, including immunological and antigen testing, are recommended to improve differentiation and management in resource-limited settings.

Acute coronary syndrome (ACS) is increasingly recognized across sub-Saharan Africa due to rising cardiometabolic risk factors. However, contemporary data from Northwestern Nigeria remain limited. This study aimed to determine the prevalence, clinical characteristics, and risk factors of ACS among patients admitted to Aminu Kano Teaching Hospital (AKTH) in Kano, Northern Nigeria.

A hospital-based, cross-sectional study was conducted over 13 months. Consecutive adult patients diagnosed with ACS according to ACC/AHA criteria were enrolled. Data on demographics, risk factors, presentation, and laboratory findings were collected using a semi-structured questionnaire. Prevalence was calculated with 95% confidence intervals (CI). Continuous variables were expressed as mean ± standard deviation or median [interquartile range], and compared using Student's t-test or Mann-Whitney U test. Categorical variables were expressed as frequencies (percentages) and compared using Chi-square or Fisher's exact test. Statistical analysis was performed using SPSS software version 18.0, and a P-value <0.05 was considered significant.

Among 2001 general medical admissions and 564 cardiovascular admissions, 55 patients had ACS, yielding prevalence rates of 2.8% (95% CI: 2.1-3.6%) and 9.8% (95% CI: 7.5-12.5%), respectively. The mean age was 60.5±12.2 years, and 61.8% were male. Females were older than males (65.6±11.2 vs. 57.4±11.8 years, P=0.014). The predominant risk factors were hypertension (87.3%), physical inactivity (81.8%), dyslipidaemia (74.5%), and diabetes mellitus (40.0%). ST-segment elevation myocardial infarction (STEMI) was the commonest subtype (60%). Diabetes mellitus was associated with STEMI, while obesity was associated with unstable angina (P<0.05). Most patients (83.6%) presented beyond 12 hours after symptom onset.

ACS represents a significant proportion of cardiovascular admissions in Northwestern Nigeria, dominated by hypertension and metabolic disorders. There is an urgent need for public health interventions targeting modifiable risk factors and strategies to reduce pre-hospital delays.

Cardiovascular disease is the leading cause of morbidity and mortality among individuals with type 2 diabetes mellitus (T2DM). In Nigeria, the burden of diabetes-related cardiovascular disease is rising, yet data on the prevalence and clustering of cardiovascular risk factors remain limited. The study objective is to determine the prevalence and clustering of major cardiovascular risk factors among adults with T2DM in Northwestern Nigeria.

We retrospectively reviewed medical records of 396 adults with T2DM at Ahmadu Bello University Teaching Hospital, Zaria, to assess hypertension, dyslipidaemia, obesity, proteinuria, and renal function.

The mean age was 53.3 ± 11.3 years, and 49.2% were male. Dyslipidaemia (80.1%), hypertension (69.7%), and truncal obesity (61.9%) predominated. General obesity occurred in 32.6%, proteinuria in 26.3%, and reduced estimated glomerular filtration rate in 33.1%. Women had higher prevalences of hypertension, truncal obesity, and metabolic syndrome, whereas dyslipidaemia was more common in men. Renal abnormalities increased with age. High-risk clustering (≥4 factors) occurred in 64.7% of women and 40.0% of men. Truncal obesity predicted high-risk clustering, while older age and longer diabetes duration predicted reduced renal function.

Cardiovascular risk factors are highly prevalent and clustered among adults with T2DM in Northwestern Nigeria. Truncal obesity is a key driver of clustering, underscoring the need for integrated cardiovascular risk assessment and targeted interventions.

ST resolution (STR) is associated with improved cardiac outcomes after primary percutaneous coronary intervention (PPCI) and is a marker of success. In this study, we aimed to determine the relationship between the STR degree and outcomes after coronary bifurcation PPCI.

This cohort study was conducted at Sina Hospital, Tehran, Iran, from January 11, 2017, to March 20, 2022. Studied variables included age, sex, diabetes mellitus, hypertension, smoking, dyslipidemia, bifurcation type, bifurcation classification, PPCI strategy, type of MI, culprit vessel, door to device time, contrast volume, post PPCI thrombolysis in myocardial infarction, cardiac death, major adverse cardiovascukar events, type of stent, ejection fraction (EF), and STR. Follow-up was performed for every patient from the PPCI date until November 2022 to 2022 November, with a 34 ± 25 (median ± IQR) months. STR was calculated as maximum ST elevation (max STE) from the 90 -min ECG after PPCI.

EF in the low-risk group was higher than in the medium- and high-risk groups. Patients with inferior MI were at lower risk than those with anterior MI. The right coronary artery and left circumflex as the culprit vessels had a lower STR than the left anterior descending artery (LAD). Multiple logistic regression showed that PPCI in the main vessel (MV)/side branch (SB) increased cardiac death 6.43 times more than intervention in MV [OR: 4.637, 95% CI (1.021-21.055), p = 0.047]. Additionally, high-risk STR increased the chance of cardiac death 5.83 times more than low-risk [OR: 5.833, 95% CI (1.215-28.006), p = 0.028]. Medium-risk STR and LAD as a culprit vessel were predictors of EF less than 50% [OR: 3.462, 95% CI (1.345-8.91), p = 0.01], [OR: 5.237, 95% CI (1.091-25.143), p = 0.039], respectively.

In bifurcation lesions, in addition to the STR, the MV/SB intervention strategy was another predictor of cardiac death. Also, STR was a predictor of EF.

Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea in the United States. Gut dysbiosis and chronic inflammation are key contributors to CDI susceptibility and severity. Metabolic syndrome (MetS)-defined by central obesity, hypertriglyceridemia, low HDL cholesterol, hypertension, and type 2 diabetes mellitus (T2DM)-is increasingly prevalent worldwide and is characterized by chronic immune dysregulation and alterations in gut microbiota. These pathophysiologic features may overlap with mechanisms that predispose individuals to CDI and its complications.

Using a large electronic health record database encompassing 102 health care organizations, we examined the association between metabolic conditions (MetS, obesity, and T2DM) and the risk of CDI diagnosis and severe clinical outcomes. Individuals with a diagnosis of each metabolic condition were compared with matched controls.

All 3 metabolic conditions were associated with an increased risk of CDI. The strongest association was observed in patients with MetS (odds ratio [OR], 1.94), followed by obesity (OR, 1.14) and T2DM (OR, 1.11). The impact of metabolic disorders on CDI severity varied based on the specific condition. Patients with MetS and obesity were more likely to develop sepsis, leukocytosis, and neutrophilia and to require ICU admission; however, they had lower risk of hypoalbuminemia, recurrent CDI, and all-cause mortality. In contrast, patients with T2DM had greater odds of developing all of the CDI-associated complications.

MetS, obesity, and T2DM were all associated with an increased likelihood of CDI diagnosis. However, their effects on CDI severity varied among the 3 conditions examined-patients with T2DM had the greatest risk of adverse outcomes, including sepsis, ICU admission, recurrent CDI, and mortality.

Type 1 diabetes is characterized by autoimmune destruction of pancreatic β‑cells, whereas type 2 diabetes involves chronic low‑grade systemic inflammation. Stem cell therapy, through both direct cell replacement and immunomodulation, holds great promise for treating diabetes. However, a comprehensive bibliometric analysis systematically mapping the knowledge structure, evolutionary trajectory, and immunological landscape of this field is currently lacking.

Using CiteSpace, VOSviewer, and the "bibliometrix" R package, we performed a comprehensive bibliometric analysis of 1,600 publications on stem cell therapy for diabetes retrieved from the Web of Science Core Collection (1995-2025). The analysis focused on the distribution of countries/regions, institutions, and authors, and examined research hotspots and development trends through co‑citation networks, keyword bursts, and cluster analysis.

The field has evolved through four developmental stages: concept validation (before 2007), clinical breakthrough of immune intervention (2007-2014), technological explosion of β‑cell differentiation (2014-2019), and optimization with complication‑oriented expansion (2019-present). Cell replacement and immunomodulation emerged as two core and increasingly prominent paradigms. Keyword burst analysis identified immunology‑related hotspots such as regulatory T cells, macrophage polarization, and exosomes. Mesenchymal stem cells and their exosomes exhibit great potential in immunomodulation and regeneration, opening broad prospects for the treatment of diabetes and its complications.

The field is moving toward more refined cell engineering, with notable progress in understanding the mechanisms of β‑cell maturation and differentiation. Future research will place greater emphasis on the development of immune evasion technologies, including the design of novel biocompatible encapsulation materials and the exploration of local immunomodulatory strategies. This will require deep integration of cell biology, immunology, genetic engineering, and clinical medicine to address fundamental issues related to cell function, immune rejection, and long‑term safety, thereby providing safer, more effective, and more universally applicable therapeutic strategies for diabetes.

Chronic pancreatitis (CP) progressively destroys pancreatic parenchyma and predisposes patients to pancreatogenic type 3c diabetes mellitus (T3cDM).

We conducted a systematic review and meta-analysis of cohort studies enrolling adults with clinically and/or instrumentally confirmed CP and no pre-existing diabetes at baseline.

Systematic review and meta-analysis of cohort studies.

Scopus, Web of Science Core Collection, and PubMed were searched from inception to August 2025. Random-effects models estimated pooled incidence of new-onset diabetes and the proportion requiring insulin. Prespecified subgroup analyses were stratified by follow-up duration (<60 months, 60-120 months, >120 months). Meta-regression explored demographic, behavioral, and clinical moderators.

Nineteen studies met the inclusion criteria and contributed to the primary meta-analysis of incident diabetes after CP. The pooled incidence of diabetes was 30% (95% CI: 27-34; I² = 94.8%), with a prediction interval of 15%-49%. Exploratory follow-up-stratified analysis suggested a time-dependent increase: 18% (95% CI: 14-22) at <60 months, 25% (95% CI: 15-35) at 60-120 months, and 44% (95% CI: 24-66) at >120 months (p for subgroup differences = 0.0184). Among patients who developed diabetes, 59% (95% CI: 46-71; 7 studies; I² = 91.7%) required insulin therapy. Meta-regression did not identify statistically significant study-level moderators, although pancreatic calcification showed a non-significant positive trend.

CP is associated with a substantial and time-dependent incidence of diabetes; however, the pooled estimates should be interpreted cautiously because the included studies were observational and highly heterogeneous. These findings support long-term glycemic monitoring and careful classification of pancreatogenic diabetes in patients with CP, while optimal screening intervals and treatment timing require further prospective evidence.

PROSPERO CRD420251136931.

Prediabetes increases the risk of type 2 diabetes mellitus (T2DM). Accurate prediction is crucial for early prevention, but evidence on prediction models has not been comprehensively synthesized. This study systematically evaluated the accuracy of such models in predicting prediabetes-to-T2DM progression.

Databases including Cochrane Library, Embase, PubMed, and Web of Science were searched up to June 2, 2025. PROBAST was applied to evaluate the risk of bias. STATA 15.0 was employed to analyze the pooled concordance index (C-index) with 95% CI, to conduct subgroup and sensitivity analyses, and to assess publication bias.

Sixteen studies were included, covering 1,368,130 prediabetic individuals with 187,225 progressing to T2DM. Pooled incidence was 42.3‰ (95% CI: 27.2‰-60.4‰). Pooled C-indices of the training and validation sets were 0.76 (0.71-0.80) and 0.84 (0.82-0.86), respectively. Logistic regression and random forest yielded C-indices of 0.81 and 0.86, respectively.

Prediction models show promising accuracy for predicting progression from prediabetes to T2DM, although the evidence remains limited, particularly due to the lack of external validation. Future research should strengthen model development, external validation, and reporting quality to improve the robustness and clinical applicability of prediction models for the progression of prediabetes.

https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251104222.