Browsing by Author "Rotimi, Solomon Oladapo"

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Association between CYP17A1 and HSD3B1 gene polymorphisms and testosterone levels in Nigerian prostate cancer patients
(Scientific Reports, 2025) Ekenwaneze, Christogonus Chichebe; Zakari, Suleiman; Amadi, Emmanuel Chimuebuka; Okesola, Mary; Rotimi, Solomon Oladapo; Oyekan, Ademola; Fatiregun, Olamijulo; Iweala, Emeka Eze Joshua; Odedina, Folakemi T.; Ogunlana, Olubanke Olujoke
Prostate cancer (PCa) is a primary global health concern and the leading cause of cancer-related deaths in men. Genetic variation in androgen pathways is essential in PCa development and progression. Cytochrome P450 17A1 (CYP17A1) gene encodes a critical metabolic enzyme involved in testosterone (TT) synthesis, as it converts cholesterol into androstenedione. Similarly, the 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) gene encodes an enzyme that catalyses the conversion of dehydroepiandrosterone (DHEA) to androstenedione, a critical precursor for TT production. The case-control study was conducted on 40 PCa patients and 40 healthy males with matching ages. Detection of CYP17A1 and HSD3B1 polymorphisms was done using the TaqMan genotyping assay, and estimation of TT levels in serum was done using the enzyme-linked immunosorbent assay technique. Detected genotypes were AA, AG, and GG for CYP17A1, and AA and CA for HSD3B1; the adrenalpermissive CC genotype of HSD3B1 was absent. The TT levels were significantly lower in PCa patients (p = 0.00148). No significant associations were found between polymorphisms in CYP17A1, HSD3B1 and TT levels. The HSD3B1 CA genotype showed a non-significant trend toward increased PCa risk (OR = 2.39, p = 0.183) that requires validation in larger studies before any clinical relevance can be established.
Association between CYP17A1 and HSD3B1 gene polymorphisms and testosterone levels in Nigerian prostate cancer patients
(Scientific reports, 2025) Ekenwaneze, Christogonus Chichebe; Zakari, Suleiman; Amadi, Emmanuel Chimuebuka; Okesola, Mary; Rotimi, Solomon Oladapo; Oyekan, Ademola; Fatiregun, Olamijulo; Iweala, Emeka Eze Joshua; Odedina, Folakemi T.; Ogunlana, Olubanke Olujoke
Prostate cancer (PCa) is a primary global health concern and the leading cause of cancer-related deaths in men. Genetic variation in androgen pathways is essential in PCa development and progression. Cytochrome P450 17A1 (CYP17A1) gene encodes a critical metabolic enzyme involved in testosterone (TT) synthesis, as it converts cholesterol into androstenedione. Similarly, the 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) gene encodes an enzyme that catalyses the conversion of dehydroepiandrosterone (DHEA) to androstenedione, a critical precursor for TT production. The case-control study was conducted on 40 PCa patients and 40 healthy males with matching ages. Detection of CYP17A1 and HSD3B1 polymorphisms was done using the TaqMan genotyping assay, and estimation of TT levels in serum was done using the enzyme-linked immunosorbent assay technique. Detected genotypes were AA, AG, and GG for CYP17A1, and AA and CA for HSD3B1; the adrenalpermissive CC genotype of HSD3B1 was absent. The TT levels were significantly lower in PCa patients (p = 0.00148). No significant associations were found between polymorphisms in CYP17A1, HSD3B1 and TT levels. The HSD3B1 CA genotype showed a non-significant trend toward increased PCa risk (OR = 2.39, p = 0.183) that requires validation in larger studies before any clinical relevance can be established.
Disparities in Allostatic Load Among Different Races: A Comprehensive Scoping Review
(Journal of Racial and Ethnic Health Disparities, 2025-10-01) Olowokere, Olanike Gloria; Olasehinde, Olutola Esther; Bisi‑Adeniyi, Titilayo Ifeoluwa; Onyia, Abimbola F.; De Campos, Opeyemi Christiana; Rotimi, Oluwakemi Anuoluwapo; Rotimi, Solomon Oladapo
Background Allostatic load measures the cumulative stress, and it varies across populations. Its accurate measurement among racial groups is essential for understanding the effects of chronic stress on health. This review is aimed at investigating disparities in allostatic load between races and exploring the underlying mechanisms driving these disparities. Methods A systematic search of literature was conducted, resulting in the inclusion of 296 relevant studies. These studies investigated a wide range of allostatic load biomarkers from the cardiovascular, metabolic, neuroendocrine, and immune systems. They involved diverse racial and ethnic populations with variations in age, gender, socioeconomic status (SES), and stress exposure. Results The review revealed disparities in allostatic load biomarkers across different population groups. The extensive examination of a wide range of biomarkers in the selected studies showed systolic and diastolic blood pressure (DBP), heart rate/pulse rate, high-density lipoprotein cholesterol, glycosylated hemoglobin (HbA1c), body mass index, total cholesterol (TC), C-reactive protein, and interleukin-6 (IL-6)/IL-6 receptor as the most frequently used biomarkers across populations. Socioeconomic status, age, racial discrimination, stressful life events, and adverse health outcomes were associated with allostatic load across different racial groups. Conclusion Disparities exist in previous studies on allostatic load due to differences in biomarker inclusion, calculation methods, study types, and populations studied. In addition, the roles of factors like social determinants of health, discrimination, and constitutive factors like genetics and age were discussed.
Evaluation of Serum Myelin Basic Protein in POAGPatients at a Tertiary Institution in Lagos, Nigeria
(Research Square, 2025) Anikwenwa, Judith Ogechi; Adenekan, Adetunji Olusesan; Alabi, Adegboyega Sunday; Idowu, Oluwatobi Olalekan; Sule, Ademola Ayoda; Aribaba, Olufi sayo Temitayo; Rotimi, Solomon Oladapo; Onakoya, Adeola Olukorede
Abstract Purpose Glaucoma, a neurodegenerative disorder, causes retinal ganglion cell damage and loss of neurons in thevisual system up to the visual cortex. The loss of myelin sheath leads to the release of myelin sheathcomponents, including the myelin basic protein (MBP), into the bloodstream. While MBP has shownpromise as a biomarker for glaucoma in some Asian populations, data among individuals of Africandescent remain limited. This study evaluated the serum levels of MBP in primary open-angle glaucoma(POAG) patients compared to non-glaucoma controls, with the aim of reporting its usefulness as abiomarker for glaucoma detection in an African population. Methods This cross-sectional study compared serum MBP levels in treatment-naive primary open-angle glaucoma(POAG) patients and non-glaucoma controls. Blood samples were collected from 83 treatment-naivePOAG participants and 83 age and sex matched non-glaucoma participants and analyzed using enzyme-linked immunosorbent assay (ELISA). Results The mean age of POAG participants was 50.78 ± 17.3 years, with a male predilection. The meanintraocular pressure (IOP) was signifi cantly higher in POAG patients (18.22 ± 6.8 mmHg) than in controls(13.89 ± 2.5 mmHg). Serum MBP levels were signifi cantly elevated in POAG patients (1128.75 ng/L)compared to controls (963.75 ng/L; p < 0.001). There was no signifi cant correlation between MBP levelsand disease severity. MBP levels were higher in high-tension glaucoma and females; however, thedifference was not statistically signifi cant. Conclusion Findings supported the neurodegenerative state of POAG and the use of serum MBP levels as a potentialbiomarker for early POAG detection.
Exome sequencing in Nigerian children with early-onset epilepsy syndromes
(Epilepsia Open, 2024-10-31) Ademuwagun, Ibitayo Abigail; Adam, Yagoub; Rotimi, Solomon Oladapo; Syrbe, Steffen; Radtke, Maximilian; Hentschel, Julia; Lemke, Johannes R.; Adebiyi, Ezekiel
Objective: Nigeria, along with other Sub-Saharan African countries, bears the highest burden of epilepsy worldwide. This high prevalence is attributed to a combination of factors, including a significant incidence of infectious diseases, perinatal complications, and genetic etiologies. Genetic testing is rarely available and is not typically included in the routine diagnostic work-up for individuals with infantile and childhood epilepsy syndromes in these regions. Exome sequencing (ES) offers a diagnostic yield of 24%–62%, but these figures primarily reflect data from high-income countries (HICs) and may not be applicable to low-and middle-income countries (LMICs). In this study, we employed ES to investigate the genetic basis of early-onset epilepsy in 22 affected children from Nigeria. Methods: The study involved sampling of patients diagnosed with early-onset epilepsy syndromes at the Lagos State University Teaching Hospital (LASUTH) Neurology clinic. Venous blood samples were collected, and genomic DNA was isolated and purified. Molecular analysis included DNA fragmentation, ligation, target enrichment, library preparation, and whole-exome sequencing. Computational analysis involved variant calling, curation, and classification using specialized tools and databases. Results: Pathogenic variants were identified in 6 out of 22 individuals, equaling a diagnostic yield of 27.3% and comprising variants in BPTF, NAA15, SCN1A, TUBA1A and twice in CACNA1A. Significance: In this study, we present the first exome study on early-onset epilepsy syndromes from West Africa, facilitated by a Nigerian-German research collaboration. Our findings reveal a genetic diagnostic yield comparable to that of HICs. The integration of genomic medicine into epilepsy management in Nigeria holds promising prospects for improving patient care and reducing mortality rates