Progeny trial of Prosopis africana in Benue State, Nigeria

Progeny trial of Prosopis africana in Benue State, Nigeria was carried out in a pot culture experiment over a period of three months. The State was stratified into three zones and one Local Government Area was randomly selected from each zone for seed collection. The seeds were assessed for germination in the laboratory, and seedling emergence, bi-monthly height and numbers of leaves were taken on the field for three months. At the end of 90 days after sowing, seedling total dry matter weight was taken. Tetraoxosulphate (VI) acid (H2SO4) seed scarification gave the best germination (100%), followed by hot water (20%), while ordinary water led to no seed germination (0%). Seeds collected from zone A (derived savannah) showed the best performance in seedling height, leaf number and total biomass. Whereas, seeds from Zone B (Southern Guinea Savannah) gave the least. Based on the studies, Katsina-Ala (zone A) can be regarded as the best place for collection of seeds of Prosopis africana for plantation establishment.Keywords: Prosopis africana, progeny, seed germination, seedling emergence, seed

Generating GBX1 anitbodies: A useful tool in determining developmental mechanisms regulated by GBX1 [abstract]

Abstract only availableInactivation of Gbx1 in mice results in a locomotor phenotype specifically affecting hind-limb motion. GBX1 is a DNA-binding transcription factor that regulates the expression of its direct target genes. We are trying to create antibodies, which can be used as a reagent to identify target genes directly regulated by GBX1, in addition, these antibodies will be used for immunohistochemical analysis. The results from these studies will provide insight into the clarification of regulatory mechanisms controlling locomotion in mammals. In order to generate antibodies to GBX1, we will generate protein, which can be used elicit an immune response in chickens. To do this we have cloned the Gbx1 open reading frame (ORF) into the pBluescript II KS (+/-) vector, which allows for DNA sequencing. We then transformed the construct into DH5 cells. After sequencing, the Gbx1 ORF was subcloned into the protein expression vector pRSET B and transformed into BL21 bacterial cells. Protein expression was induced using Isopropyl -D-1-thiogalactopyranoside (IPTG). GBX1 protein will then be analyzed by SDS-PAGE and Western blot analysis. Upon confirmation of protein expression, GBX1 will be purified and used to elicit an immune response in chickens to generate GBX1 antibodies. Once antibodies have been generated, characterization will be carried out by analyzing the antibodies using Western blot analysis and immunohitochemistry

Can Crude Oil Exploration Influence the Phytochemicals and Bioactivity of Medicinal Plants? : A Case of Nigerian Vernonia amygdalina and Ocimum gratissimum.

Acknowledgments The authors also thank Ruangelie Edrada- Ebel of the Faculty of Pharmaceutical Sciences, The Natural Products Metabolomics Group, Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde for her contribution to the methodology. Funding The authors recognise the financial support of the Schlumberger Faculty for the Future Foundation Scholarship to conduct the present study.Peer reviewedPublisher PD

Transactivation of EGFR by LPS induces COX-2 expression in enterocytes

Necrotizing enterocolitis (NEC) is the leading cause of gastrointestinal morbidity and mortality in preterm infants. NEC is characterized by an exaggerated inflammatory response to bacterial flora leading to bowel necrosis. Bacterial lipopolysaccharide (LPS) mediates inflammation through TLR4 activation and is a key molecule in the pathogenesis of NEC. However, LPS also induces cyclooxygenase-2 (COX-2), which promotes intestinal barrier restitution through stimulation of intestinal cell survival, proliferation, and migration. Epidermal growth factor receptor (EGFR) activation prevents experimental NEC and may play a critical role in LPS-stimulated COX-2 production. We hypothesized that EGFR is required for LPS induction of COX-2 expression. Our data show that inhibiting EGFR kinase activity blocks LPS-induced COX-2 expression in small intestinal epithelial cells. LPS induction of COX-2 requires Src-family kinase signaling while LPS transactivation of EGFR requires matrix metalloprotease (MMP) activity. EGFR tyrosine kinase inhibitors block LPS stimulation of mitogen-activated protein kinase ERK, suggesting an important role of the MAPK/ERK pathway in EGFR-mediated COX-2 expression. LPS stimulates proliferation of IEC-6 cells, but this stimulation is inhibited with either the EGFR kinase inhibitor AG1478, or the selective COX-2 inhibitor Celecoxib. Taken together, these data show that EGFR plays an important role in LPS-induction of COX-2 expression in enterocytes, which may be one mechanism for EGF in inhibition of NEC

Dataset on noise level measurement in Ota metropolis, Nigeria

Datasets contained in this article are noise level measurementcarried out at 41 different locations in Ota metropolis, Nigeria. Thenoise readings were measured at a time interval of 30 min for eachsite considered using a precision grade sound level meter. Theanalysis was based on the noise descriptors LAeq,L10,L90,LD, TNIand NEI. Results from the study reflects that the highest and lowestequivalent noise levels (LAeq) were recorded at commercial areas(96 dB (A)) and residential areas (52 dB (A)), respectively, thebackground noise level (L90) has the highest and lowest values atcommercial areas (77 dB (A)) and residential areas (44 dB (A)),respectively and the peak value (L10) has the highest value andlowest value at the commercial areas (96 dB (A)) and residentialareas (56 dB (A)). Based on the WHO recommendations and stan-dards, only 2 out of the 41 locations considered are under normallyacceptable situation while the noise levels of other areas are notacceptable. Noise map developed in this study provides enoughinformation for technical controls and interim legislation againstenvironmental noise pollution in the metropolis. Moreover, con-sidering the noise emission standards, planning and promoting thecitizens awareness about the high noise risk could help to mitigatethe effect of noise in Ota, Metropolis. The noise data in this study are useful as reference and guideline for future regulations onnoise limit to be implemented for urban areas in Nigeria anddeveloping countries at large

A GIS – based method for assessment and mapping of noise pollution in Ota metropolis, Nigeria

A detailed method used for assessing and mapping noise pollution levels in Ota metropolis, Nigeria using ArcGIS 10.5 Software is presented in this paper. Noise readings were measured at a time interval of 30 min for each site considered using a precision grade soundlevel meter. The noise map developed was based on the computed values of average equivalent noise (LAeq) for the selected locations. Results of this study show that the A weighted sound level (LAeq), the background noise level (L10) and the peak noise level (L90) vary with location and period of the day due to traffic characteristics especially traffic volume, vehicle horns, vehicle mounted speakers, and unmuffled vehicles at road Junctions, major roads, motor parks and commercial centres. Based on the U.S. Department of Housing and Urban Development (HUD) recommendations and standards, only one (1) out of the 41 locations considered is under normally acceptable situation, while 12 locations are under normally unacceptable and the noise levels of the rest locations are clearly unacceptable. Results of this study are useful as reference and guideline for future planning and regulations on noise limit to be implemented for urban areas like Ota Metropolis

Factors associated with delayed presentation to healthcare facilities for Lassa fever cases, Nigeria 2019: a retrospective cohort study.

BACKGROUND: Large outbreaks of Lassa fever (LF) occur annually in Nigeria. The case fatality rate among hospitalised cases is ~ 20%. The antiviral drug ribavirin along with supportive care and rehydration are the recommended treatments but must be administered early (within 6 days of symptom onset) for optimal results. We aimed to identify factors associated with late presentation of LF cases to a healthcare facility to inform interventions. METHODS: We undertook a retrospective cohort study of all laboratory confirmed LF cases reported in Nigeria from December 2018 to April 2019. We performed descriptive epidemiology and a univariate Cox proportional-hazards regression analysis to investigate the effect of clinical (symptom severity), epidemiological (age, sex, education, occupation, residential State) and exposure (travel, attendance at funeral, exposure to rodents or confirmed case) factors on time to presentation. RESULTS: Of 389 cases, median presentation time was 6 days (IQR 4-10 days), with 53% attending within 6 days. There were no differences in presentation times by sex but differences were noted by age-group; 60+ year-olds had the longest delays while 13-17 year-olds had the shortest. By sex and age, there were differences seen among the younger ages, with 0-4-year-old females presenting earlier than males (4 days and 73% vs. 10 days and 30%). For 5-12 and 13-17 year-olds, males presented sooner than females (males: 5 days, 65% and 3 days, 85% vs. females: 6 days, 50% and 5 days, 61%, respectively). Presentation times differed across occupations 4.5-9 days and 20-60%, transporters (people who drive informal public transport vehicles) had the longest delays. Other data were limited (41-95% missing). However, the Cox regression showed no factors were statistically associated with longer presentation time. CONCLUSIONS: Whilst we observed important differences in presentation delays across factors, our sample size was insufficient to show any statistically significant differences that might exist. However, almost half of cases presented after 6 days of onset, highlighting the need for more accurate and complete surveillance data to determine if there is a systemic or specific cause for delays, so to inform, monitor and evaluate public health strategies and improve outcomes

HLA-DQA1*05 carriage associated with development of anti-drug antibodies to infliximab and adalimumab in patients with Crohn's Disease

Anti-tumor necrosis factor (anti-TNF) therapies are the most widely used biologic drugs for treating immune-mediated diseases, but repeated administration can induce the formation of anti-drug antibodies. The ability to identify patients at increased risk for development of anti-drug antibodies would facilitate selection of therapy and use of preventative strategies.This article is freely available via Open Access. Click on Publisher URL to access the full-text

Mechanisms and management of loss of response to anti-TNF therapy for patients with Crohn's disease: 3-year data from the prospective, multicentre PANTS cohort study

This is the final version. Available from Elsevier via the DOI in this record. Background We sought to report the effectiveness of infliximab and adalimumab over the first 3 years of treatment and to define the factors that predict anti-TNF treatment failure and the strategies that prevent or mitigate loss of response. Methods Personalised Anti-TNF therapy in Crohn’s disease (PANTS) is a UK-wide, multicentre, prospective observational cohort study reporting the rates of effectiveness of infliximab and adalimumab in anti-TNF-naive patients with active luminal Crohn’s disease aged 6 years and older. At the end of the first year, sites were invited to enrol participants still receiving study drug into the 2-year PANTS-extension study. We estimated rates of remission across the whole cohort at the end of years 1, 2, and 3 of the study using a modified survival technique with permutation testing. Multivariable regression and survival analyses were used to identify factors associated with loss of response in patients who had initially responded to anti-TNF therapy and with immunogenicity. Loss of response was defined in patients who initially responded to anti-TNF therapy at the end of induction and who subsequently developed symptomatic activity that warranted an escalation of steroid, immunomodulatory, or anti-TNF therapy, resectional surgery, or exit from study due to treatment failure. This study was registered with ClinicalTrials.gov, NCT03088449, and is now complete. Findings Between March 19, 2014, and Sept 21, 2017, 389 (41%) of 955 patients treated with infliximab and 209 (32%) of 655 treated with adalimumab in the PANTS study entered the PANTS-extension study (median age 32·5 years [IQR 22·1–46·8], 307 [51%] of 598 were female, and 291 [49%] were male). The estimated proportion of patients in remission at the end of years 1, 2, and 3 were, for infliximab 40·2% (95% CI 36·7–43·7), 34·4% (29·9–39·0), and 34·7% (29·8–39·5), and for adalimumab 35·9% (95% CI 31·2–40·5), 32·9% (26·8–39·2), and 28·9% (21·9–36·3), respectively. Optimal drug concentrations at week 14 to predict remission at any later timepoints were 6·1–10·0 mg/L for infliximab and 10·1–12·0 mg/L for adalimumab. After excluding patients who had primary non-response, the estimated proportions of patients who had loss of response by years 1, 2, and 3 were, for infliximab 34·4% (95% CI 30·4–38·2), 54·5% (49·4–59·0), and 60·0% (54·1–65·2), and for adalimumab 32·1% (26·7–37·1), 47·2% (40·2–53·4), and 68·4% (50·9–79·7), respectively. In multivariable analysis, loss of response at year 2 and 3 for patients treated with infliximab and adalimumab was predicted by low anti-TNF drug concentrations at week 14 (infliximab: hazard ratio [HR] for each ten-fold increase in drug concentration 0·45 [95% CI 0·30–0·67], adalimumab: 0·39 [0·22–0·70]). For patients treated with infliximab, loss of response was also associated with female sex (vs male sex; HR 1·47 [95% CI 1·11–1·95]), obesity (vs not obese 1·62 [1·08–2·42]), baseline white cell count (1·06 [1·02–1·11) per 1 × 10⁹ increase in cells per L), and thiopurine dose quartile. Among patients treated with adalimumab, carriage of the HLA-DQA1*05 risk variant was associated with loss of response (HR 1·95 [95% CI 1·17–3·25]). By the end of year 3, the estimated proportion of patients who developed anti-drug antibodies associated with undetectable drug concentrations was 44·0% (95% CI 38·1–49·4) among patients treated with infliximab and 20·3% (13·8–26·2) among those treated with adalimumab. The development of antidrug antibodies associated with undetectable drug concentrations was significantly associated with treatment without concomitant immunomodulator use for both groups (HR for immunomodulator use: infliximab 0·40 [95% CI 0·31–0·52], adalimumab 0·42 [95% CI 0·24–0·75]), and with carriage of HLA-DQA1*05 risk variant for infliximab (HR for carriage of risk variant: infliximab 1·46 [1·13–1·88]) but not for adalimumab (HR 1·60 [0·92–2·77]). Concomitant use of an immunomodulator before or on the day of starting infliximab was associated with increased time without the development of anti-drug antibodies associated with undetectable drug concentrations compared with use of infliximab alone (HR 2·87 [95% CI 2·20–3·74]) or introduction of an immunomodulator after anti-TNF initiation (1·70 [1·11–2·59]). In years 2 and 3, 16 (4%) of 389 patients treated with infliximab and 11 (5%) of 209 treated with adalimumab had adverse events leading to treatment withdrawal. Nine (2%) patients treated with infliximab and two (1%) of those treated with adalimumab had serious infections in years 2 and 3. Interpretation Only around a third of patients with active luminal Crohn’s disease treated with an anti-TNF drug were in remission at the end of 3 years of treatment. Low drug concentrations at the end of the induction period predict loss of response by year 3 of treatment, suggesting higher drug concentrations during the first year of treatment, particularly during induction, might lead to better long-term outcomes. Anti-drug antibodies associated with undetectable drug concentrations of infliximab, but not adalimumab, can be predicted by carriage of HLA-DQA1*05 and mitigated by concomitant immunomodulator use for both drugs.Guts UKCrohn’s and Colitis UKCure Crohn’s ColitisAbbVieMerck Sharp and DohmeNapp PharmaceuticalsPfizerCelltrion Healthcar