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Biomedical subjects

Muhammad Naeem

Publications and source records attributed to Muhammad Naeem.

3 recordsLinked to original sources

Artificial intelligence-derived myocardial fibrosis on cardiac magnetic resonance for prognosis in cardiomyopathy: A systematic review of a sparse evidence base.

BACKGROUND: Myocardial fibrosis on cardiovascular magnetic resonance (CMR), assessed by late gadolinium enhancement (LGE) and parametric mapping, is an established predictor of adverse events in cardiomyopathy. We assessed whether artificial intelligence (AI) quantification of fibrosis adds independent prognostic value. METHODS: We searched six databases, a clinical-trials register, and a preprint server from inception to 13 June 2026. Eligible studies used AI to generate a fibrosis marker in adults with ischemic or nonischemic cardiomyopathy, with covariate-adjusted outcomes over ≥12 months. Risk of bias was assessed using PROBAST, PROBAST+AI, and QUIPS. Fewer than three comparable studies precluded meta-analysis; certainty was rated using GRADE. RESULTS: Of 448 records (381 after de-duplication), 18 full texts were reviewed and two included, one peer-reviewed and one preprint. In an ischemic-cardiomyopathy registry (Ghanbari et al.; n = 216 analytic, 26 events), AI-derived dense LGE scar predicted arrhythmic events (univariable hazard ratio [HR] 2.35, 95% CI 1.33-4.15), and AI-derived but not manual scar improved discrimination beyond guideline criteria (area under the curve 0.63 to 0.68; p = 0.02). In a nonischemic dilated-cardiomyopathy preprint (Kim et al.; n = 347, 119 events), automated extracellular volume ≥30% predicted cardiovascular death or heart-failure hospitalization (adjusted HR 2.00, 95% CI 1.32-3.03). Both were at high risk of bias, with data-derived thresholds and no external validation. CONCLUSIONS: Across only two studies, AI-derived fibrosis was independently associated with adverse cardiovascular events, but its added value over manual quantification remains unproven. Certainty was very low. The evidence base is sparse and not yet ready for clinical use.

Humans

Molecular epidemiology and antimicrobial resistance determinants of Corynebacterium diphtheriae causing infections in Karachi, Pakistan, 2023-2024.

OBJECTIVES: Diphtheria remains endemic in Pakistan, with cases increasing following the COVID-19 pandemic despite ongoing vaccination programs. This study analyzes the genomic diversity, virulence, and antimicrobial resistance patterns of pharyngeal diphtheria strains collected during the Karachi outbreak. METHODS: Corynebacterium diphtheriae isolates from a tertiary care hospital laboratory in Karachi (August 2023-October 2024) were included. Antimicrobial susceptibility testing and whole-genome sequencing of phenotypically confirmed isolates were performed. Phylogenetic and bioinformatics analyses were performed using diphtOscan and AMRFinderPlus tools. RESULTS: A total of 47 pharyngeal C. diphtheriae isolates were included. The median age of patients was 7 years, and the male-to-female ratio was 1.6:1. The tox gene was present in 89.4% of isolates, while only 29% (n = 13/45) demonstrated toxin production. Genomic analysis identified 10 sequence types; ST384 and ST698 were most prevalent. Phenotypically, 34% (n = 16) were resistant to both erythromycin and penicillin, and 49% (n = 23) were multidrug-resistant. The most prevalent resistance genes were sul1 (100%), erm(X) (76.6%), and pbp2m (51.1%). CONCLUSION: Circulation of diverse C. diphtheriae strains with alarming antimicrobial resistance underscores the need for genomic surveillance to evaluate transmission trends. We further highlight the limitations of the Elek test in detecting toxin production and the need for improved diagnostics in low- and middle-income countries.

Antimicrobial resistance

Hypoxia-activated scleraxis a mediates epicardial progenitor differentiation into a unique cardiac perivascular cell type.

The epicardium provides progenitor cells and paracrine signals essential for heart development and regeneration, yet the mechanisms regulating epicardial cell fate remain poorly understood. Here, we identify the transcription factor Scleraxis a (scxa) as a key regulator of epicardial progenitor differentiation in zebrafish. Single-cell transcriptomics, genetic lineage tracing, and cardiac injury models reveal transient scxa expression in activated epicardial progenitor cells (aEPCs) during developmental coronary angiogenesis and heart regeneration. scxa+ epicardial cells predominantly differentiate into a previously uncharacterized col18a1a+ perivascular population, termed epicardial-derived perivascular mesenchymal cells (Epi-PMCs), which is distinct from pericytes, vascular smooth muscle cells, and mammalian adventitial fibroblasts. Epi-PMCs closely associate with coronary vessels and may contribute to vascular stabilization and remodeling, potentially through collagen XVIII. Loss of scxa increases coronary vessel density. Hypoxia and Hif signaling induce scxa expression, identifying a hypoxia-responsive mechanism that promotes epicardial differentiation toward a vascular-supportive fate during heart development and regeneration.

Animals