Ezekiel Damilare Jacobs

Mr. Ezekiel Damilare Jacobs

orcid

Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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24 February 2022 in Bulletin of the National Research Centre
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EJEzekiel Damilare Jacobs
Ezekiel Damilare Jacobs
MOMalachy Okeke
Malachy Okeke
Background: The first wave of the Coronavirus Disease 2019 (COVID-19) pandemic began when the first index case was reported in Nigeria on the 27th of February 2020, and since then, more than 68,000 cases of the disease were confirmed, with 1173 deaths as of November 30, 2020. Main body: Daily situation reports from the Nigeria Centre for Disease Control spanning February 27–November 30, 2020, were fully considered in this review. Further literature search was performed using PubMed and Google Scholar databases for articles related to response measures adopted by Nigeria. The instantaneous reproduction number (R) was then estimated as a metric to investigate the non-pharmaceutical intervention measures. Nigeria responded to COVID-19 pandemic by implementing anti-COVID-19 mitigation strategies in travel restrictions, social distancing, source control, contact tracing, self-isolation, and quarantine, as well as in clinical interventions. Our epidemiological model estimated the R-value of more than 1.0 in Nigeria and in each of all the 36 states and the Federal Capital Territory. Conclusion: Nigeria implemented containment and mitigation measures in response to the first wave of COVID-19 and these measures may have contributed to the mild COVID-19 outcome in Nigeria compared to the global trend. However, inadequate PCR testing capacity, lack or suboptimal utilization of epidemic metrics like the virus reproduction number (R) to inform decision making, and premature easing of lockdown measures among others were major challenges to the effective implementation of the COVID-19 response measures.

22 May 2025 in medRxiv
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EJEzekiel Damilare Jacobs
Ezekiel Damilare Jacobs
AAAdeyemi Timothy Akinade
Adeyemi Timothy Akinade
COChucks Marvellous Obere
Chucks Marvellous Obere
Background Amyotrophic lateral sclerosis (ALS) is a rare, progressive neurodegenerative disorder causing motor neuron degeneration, muscle paralysis, and death within 3–5 years, with a rising global prevalence. While thyroid dysfunction is implicated in the pathology of other neurodegenerative diseases, its role in ALS remains unclear due to conflicting reports from observational studies. To address this, we aimed to investigate the causal relationship between thyroid function and ALS using two-sample Mendelian Randomization (MR). Method We performed a two-sample MR study to evaluate the bidirectional causal relationship between thyroid function traits (TSH, FT4, autoimmune hyperthyroidism, autoimmune hypothyroidism) and ALS. We used SNPs from GWAS data (TSH and FT4: n=271,040; autoimmune hyperthyroidism: n=1,828 cases/279,855 controls; autoimmune hypothyroidism: n=40,926 cases/274,069 controls; ALS: n=27,205 cases/110,881 controls). We applied the inverse-variance weighted (IVW) method as the primary analysis, with sensitivity analyses (MR-Egger, weighted median, weighted mode, MR-PRESSO) to assess pleiotropy and heterogeneity. Results We identified a causal effect of autoimmune hyperthyroidism on reducing ALS risk (IVW OR = 0.96; 95% CI: 0.93–0.99; P = 0.03), but no associations for TSH (IVW OR = 0.99; 95% CI: 0.94–1.04; P = 0.71), FT4 (IVW OR = 1.03; 95% CI: 0.96–1.12; P = 0.36), or autoimmune hypothyroidism (IVW OR = 1.01; 95% CI: 0.98–1.05; P = 0.39) with ALS. Bidirectional analysis of genetic liability to ALS showed no causal effect on TSH (IVW OR = 0.98; 95% CI: 0.96–1.01; P = 0.65), FT4 (IVW OR = 0.98; 95% CI: 0.94–1.02; P = 0.46), autoimmune hypothyroidism (IVW OR = 0.93; 95% CI: 0.76–1.13; P = 0.59), or autoimmune hyperthyroidism (IVW OR = 1.01; 95% CI: 0.76–1.33; P = 0.78). Conclusion We found that genetic predisposition to autoimmune hyperthyroidism may reduce ALS risk. Our findings expand the knowledge of its genetic underpinnings and lay a foundation for future research into therapeutic strategies targeting thyroid function to mitigate ALS risk.

16 November 2025 in Sclerosis
Verified
Journal Article
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AAAdeyemi Timothy Akinade
Adeyemi Timothy Akinade
EJEzekiel Damilare Jacobs
Ezekiel Damilare Jacobs
COChucks Marvellous Obere
Chucks Marvellous Obere
VOVictor Omeiza Ogaji
Victor Omeiza Ogaji
EAEmmanuel Alakunle
Emmanuel Alakunle
OAOlaitan I Awe
Olaitan I Awe
Background: Very few case reports have explored a potential link between ankylosing spondylitis (AS), an autoimmune disorder, and amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative condition. We aimed to investigate whether genetic liability to AS causally influences the risk of ALS, and vice versa, using a bidirectional two-sample Mendelian randomization (MR) framework. Methods: We performed a two-sample MR study to evaluate the bidirectional causal relationship between genetic liability to ankylosing spondylitis and ALS risk. We used 6 valid single nucleotide polymorphisms (SNPs) from genome-wide association study (GWAS) data (AS: 1462 cases and 164,682 controls; ALS: 27,205 cases and 110,881 controls). We used the inverse-variance weighted (IVW) approach as the primary statistical method for causal estimation, with sensitivity analyses (including MR-Egger, weighted median, weighted mode, Mendelian Randomization Pleiotropy Residual Sum and Outlier (MR-PRESSO), leave-one-out, and single SNP analysis) to assess pleiotropy and heterogeneity. Results: There was no evidence of a causal association between genetic predispositions to ankylosing spondylitis (AS) and amyotrophic lateral sclerosis (ALS) (IVW OR = 1.01; 95% CI: 0.99–1.02; p = 0.10). The results from the weighted median, weighted mode, MR-Egger, and simple mode methods were consistent and nonsignificant. In the reverse analysis, genetic liability to ALS showed no causal effect on AS (IVW OR = 0.88; 95% CI: 0.70–1.12; p = 0.33), with similar null findings across all sensitivity methods. Conclusions: Overall, our bidirectional two-sample MR analyses provided no evidence supporting a causal relationship between AS and ALS.

18 January 2022 in Research Square
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EJEzekiel Damilare Jacobs
Ezekiel Damilare Jacobs
Background The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) which caused about 80,000 Coronavirus Disease 2019 (COVID-19) incidences during its first wave in Nigeria is an enveloped virus, with infective properties that make it susceptible to inactivation, upon exposure to harsh conditions, including temperature. Moreover, temperature has been reported to influence the spread and viability of most known human coronaviruses. The aim of this study is to examine the impact of temperature variables on the transmission of COVID-19 in Nigeria during its first wave in the country. Methods Daily COVID-19 incidences for 300 days of the virus presence in Nigeria were obtained from the Nigeria Centre for Disease Control, and used in the estimation of the instantaneous reproduction number (R). In this study, R was used to determine COVID-19 transmissibility, while the daily incidences reflected the spread rate of the virus in Nigeria. Meteorological data from the Nigerian Meteorological Agency, and World Bank Climate Projection Data, were matched with each of R and COVID-19 incidences, to determine the correlation between them, using Spearman’s correlation coefficient (rs) test. Results R estimation of 1.4 reflects the prevailing transmissibility of COVID-19 in Nigeria. No significant and positive relationship was observed between COVID-19 incidences and temperature variables. However, Minimum temperature (℃) showed strongest association with R (rs = 0.9273; p = 0.001). Conclusion The strong relationship observed between R and minimum temperature, suggests that temperature could be a driver modulating the transmission routes of COVID-19 in Nigeria.