Comparative Evaluation of Productivity and Cost Effectiveness of Catfish Fingerling Production in Earthen Pond and Recirculation System in Ibadan, Nigeria

Despite the popularity of the African catfish and its great market potentials, the production is still basically at subsistence level due majorly to inadequate supply of seed for stocking. This has been linked to the absence of reliable production techniques for the mass production and rearing of the species under practical farming conditions. The purpose of this study therefore, was to find a suitable culture system for the mass production of catfish (Clarias gariepinus) fingerlings. Protected earthen pond and a unit of recirculation system were used. Fertilized eggs fromfemale were divided into two equal halves and incubated under the same conditions. Forty-nine thousand frys each were stocked into the protected earthen pond and a unit recirculation system respectively. The frys in the two systems were raised for twenty one days and fed the same quantityand quality of feed throughout the period. The survival rate of the frys in the recirculation system was 79% as against 17% in the earthen pond. However, bigger sized (2.2 ± 0.23g) fingerlings were obtained from the earthen pond relative to those cultured in the recirculation system (0.9 ±0.07g). The cost of raising frys in a recirculation system (N34,000) was twice that needed for earthen pond (N17,000), but this was more than made up for in the profit from sales, which was N311,360 and N99,156 respectively. The main reason for fish farming is the expected return tobe, therefore, the choice of income-generating activities, amongst several options available, should be made on the grounds of their expected returns

The Differential Susceptibility of Yoruba Ecotype Nigerian Indigenous Chicken Varieties To Newcastle Disease

This experiment was conducted to assess and compare the susceptibility of the varieties of Yoruba indigenous chicken ecotype: Yoruba Smooth Feathered (YSF), Yoruba Frizzled Feathered (YFF) and Yoruba Naked Neck (YNN) to Newcastle disease. A total of sixty (60) 16 weeks old chickens were used comprising of twenty (20) chickens per variety. The assessmentof their susceptibility to Newcastle disease was by evaluation of clinical signs, humoral response, mortality, pathology following contact with Newcastle disease infected chickens. The experimental chickens developed clinical signs of Newcastle disease from day 9 after infection. Haemagglutination inhibition (HI) titre was determined on days 0, 21and28 post-infection. On day 0, the HI titre of the 3 genotypes were below 3log2, on day 21, there were significant differences within the group (P<0.05) where in YNN had the highest mean HI titre of 7.5. Therewas decrease in the mean HI titre in all on day 28 with the YNN having the least reduction (P<0.05). The antibody titre against Newcastle disease was higher in the YNN than all the other varieties. The mortality commenced on day 10 after infection with 70% mortality in YSF, 40% in YFF and 30% in YNN. The proventricular, enteric and caecal tonsilar haemorrhages associated with the disease were more frequent and severe in YSF.This finding indicated that YFF and YSF may possibly be more susceptible to Newcastle disease than the YNN. It was concluded that indigenous chickens of Yoruba ecotype in Nigeria differ in their susceptibility to ND with YNN being possibly the most resistant to Newcastle disease followed by YFF and the least, YSF.Keywords: Hemagglutination inhibition, Newcastle Disease, indigenous Chicken, Ecotype, Varietie

The comparative susceptibility of commercial and Nigerian indigenous chicken ecotypes to Salmonella gallinarum infection

This study was to evaluate the possible genetic resistance of exotic and indigenous chicks to Salmonella gallinarum. A total of 72 nine weeks-old chicks were used for the study. The Fulani ecotype (Fulani smooth feathers - FSF), Yoruba ecotype (Yoruba smooth feathers - YSF), and the Exotic  breed (Nera Black) chicks were infected with a dose of S. gallinarum (8.3 x 106 CFU) and were observed for 16 days. Evaluation of resistance was  based on clinical signs, mortality, pathology, leukocyte count, bacterial  count from liver and spleen of infected chicks. The highest peak for clinical signs in S. gallinarum infected chicks coincides with highest mortalities  recorded on day 11-12 dpi and bacterial count of both liver and spleen on day 8. The lymphocytes count declined on day 8 for all the experimental chicks except for the exotic breed. There was no significant difference between the bacterial counts of the different groups on day 8. In S. gallinarum infected chicks, 94.4% of all the chicks showed clinical signs after infection, the exotic breed showed a prolonged clinical signs while the Yoruba ecotype showed the least. 87.5%, 80.0% and 37.5% mortality were recorded in the exotic breed, Fulani and Yoruba ecotypes respectively. The study showed that the exotic chicken (Nera Black) was more susceptible to Salmonella gallinarum infection. It also indicated that within the ecotypes in Nigeria, Fulani ecotype was more susceptible to Salmonella gallinarum infection than the Yoruba ecotype. The lower clinical signs and mortality observed in Yoruba ecotype indicated a resistance of the ecotype to S. gallinarum infection.Keywords: Ecotypes, Nigerian Indigenous chicken, Salmonella gallinarum infection

Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10−8) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10−8). The top IBC association for SBP was rs2012318 (P= 6.4 × 10−6) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10−6) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexit

Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

A Meta-analysis of Gene Expression Signatures of Blood Pressure and Hypertension

Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%–9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension

Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study.

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10(-8)) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10(-8)). The top IBC association for SBP was rs2012318 (P= 6.4 × 10(-6)) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10(-6)) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexity

Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction