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O O Komolafe - One of the best experts on this subject based on the ideXlab platform.

  • some aspects of the biology of tilapia zillii gervais pisces cichlidae in opa reservoir ile ife nigeria
    2008
    Co-Authors: O O Komolafe
    Abstract:

    Some aspects of the biology of Tilapia zillii were examined between October 1997 and February 2000. Fish specimens were collected using a graded set of gillnets and castnets. Out of 1486 fish specimens, 867 were males while 619 were females. Regardless of their sex a significantly high number of fish were caught inshore (69.57%) than in the offshore areas (30.43%). In addition 48.65% of all fish specimens were caught in the middle segment of the reservoir. A wide range of fish sizes were caught and the species was not spatially distributed ( χ 2 cal. 27.39< χ 2 tab. 67.51; df. 820). The species fed on a variety of food substances predominantly shoreline aquatic macrophytes, algae and plankton. The feeding rhythm which started around 6.00am reached a peak by 3.00pm in the afternoon and it declined gradually until 6.00pm.

  • reproductive aspects of a cichlid fish tilapia zillii gervais pisces cichlidae in opa reservoir ile ife nigeria
    Ife Journal of Science, 2005
    Co-Authors: O O Komolafe
    Abstract:

    A total of 1486 specimen of the fish Tilapia zillii was collected by gillnetting and analysed for aspect of its reproductive biology in Opa reservoir, between October 1991 and February 1994. Sex ratio was approximately 1:1 (male: female). Fish total length at maturity was 15.1cm (males) and 13.2cm (females). The fecundity was 4329 ± 1153.9eggs, n = 685 with an egg diameter of 1.06mm ± 0.67mm, n = 619. The mean gonado-somatic index was 0.39±0.234.1, n = 865 (males) and 1.05±1.011.2, n = 619 (females). The relationship between fish length and fecundity relationship gave a statistically significant correlation (r = 0.5722, P Key Words: Fecundity, sex ratio, gonado-somatic index, substratum brooder Ife Journal of Science Vol.6(2) 2004: 119-122

  • the age and growth of tilapia zillii gervais in opa reservoir ile ife nigeria
    Ife Journal of Science, 2005
    Co-Authors: O O Komolafe
    Abstract:

    Specimens of Tilapia zillii (Gervais) were collected from Opa reservoir in Ile-Ife, Nigeria, between October 1991 and February 1994. The fishing methods employed were castnetting and gillnetting. Annular rings were formed on the scales of 1310 specimens of the species between December and February of each year of study. Male fish specimens grew faster and bigger than the female fish irrespective of age. Fish length at maturity was 11.0cm (male) and 9.7cm (female). Allometric growth was observed in the species and the relationship between fish length and scale length gave a statistically significant correlation r = 0.681; P Key Words: Tilapia zillii , annular ring, growth, age, condition-factor Ife Journal of Science Vol.6(1) 2004: 14-18

Bert Wouters - One of the best experts on this subject based on the ideXlab platform.

Stuart G Tangye - One of the best experts on this subject based on the ideXlab platform.

  • hyper ige syndrome due to an elusive novel intronic homozygous variant in dock8
    Journal of Clinical Immunology, 2021
    Co-Authors: Stuart G Tangye, Paul Gray, Bethany Pillay, Jin Yan Yap, William A Figgett, John Reeves
    Abstract:

    Rare, biallelic loss-of-function mutations in DOCK8 result in a combined immune deficiency characterized by severe and recurrent cutaneous infections, eczema, allergies, and susceptibility to malignancy, as well as impaired humoral and cellular immunity and hyper-IgE. The advent of next-generation sequencing technologies has enabled the rapid molecular diagnosis of rare monogenic diseases, including inborn errors of immunity. These advances have resulted in the implementation of gene-guided treatments, such as hematopoietic stem cell transplant for DOCK8 deficiency. However, putative disease-causing variants revealed by next-generation sequencing need rigorous validation to demonstrate pathogenicity. Here, we report the eventual diagnosis of DOCK8 deficiency in a consanguineous family due to a novel homozygous intronic deletion variant that caused aberrant exon splicing and subsequent loss of expression of DOCK8 protein. Remarkably, the causative variant was not initially detected by clinical whole-genome sequencing but was subsequently identified and validated by combining advanced genomic analysis, RNA-seq, and flow cytometry. This case highlights the need to adopt multipronged confirmatory approaches to definitively solve complex genetic cases that result from variants outside protein-coding exons and conventional splice sites.

  • deficiency of th17 cells in hyper ige syndrome due to mutations in stat3
    Journal of Experimental Medicine, 2008
    Co-Authors: Cindy S, Gary Y J Chew, Nicholas Simpson, Archana Priyadarshi, Melanie Wong, Bodo Grimbacher, David A Fulcher, Stuart G Tangye, Matthew C Cook
    Abstract:

    Hyper-immunoglobulin E syndrome (HIES) is a primary immune deficiency characterized by abnormal and devastating susceptibility to a narrow spectrum of infections, most commonly Staphylococcus aureus and Candida albicans. Recent investigations have identified mutations in STAT3 in the majority of HIES patients studied. Despite the identification of the genetic cause of HIES, the mechanisms underlying the pathological features of this disease remain to be elucidated. Here, we demonstrate a failure of CD4+ T cells harboring heterozygous STAT3 mutations to generate interleukin 17-secreting (i.e., T helper [Th]17) cells in vivo and in vitro due to a failure to express sufficient levels of the Th17-specific transcriptional regulator retinoid-related orphan receptor t. Because Th17 cells are enriched for cells with specificities against fungal antigens, our results may explain the pattern of infection susceptibility characteristic of patients with HIES. Furthermore, they underscore the importance of Th17 responses in normal host defense against the common pathogens S. aureus and C. albicans.

John Reeves - One of the best experts on this subject based on the ideXlab platform.

  • hyper ige syndrome due to an elusive novel intronic homozygous variant in dock8
    Journal of Clinical Immunology, 2021
    Co-Authors: Stuart G Tangye, Paul Gray, Bethany Pillay, Jin Yan Yap, William A Figgett, John Reeves
    Abstract:

    Rare, biallelic loss-of-function mutations in DOCK8 result in a combined immune deficiency characterized by severe and recurrent cutaneous infections, eczema, allergies, and susceptibility to malignancy, as well as impaired humoral and cellular immunity and hyper-IgE. The advent of next-generation sequencing technologies has enabled the rapid molecular diagnosis of rare monogenic diseases, including inborn errors of immunity. These advances have resulted in the implementation of gene-guided treatments, such as hematopoietic stem cell transplant for DOCK8 deficiency. However, putative disease-causing variants revealed by next-generation sequencing need rigorous validation to demonstrate pathogenicity. Here, we report the eventual diagnosis of DOCK8 deficiency in a consanguineous family due to a novel homozygous intronic deletion variant that caused aberrant exon splicing and subsequent loss of expression of DOCK8 protein. Remarkably, the causative variant was not initially detected by clinical whole-genome sequencing but was subsequently identified and validated by combining advanced genomic analysis, RNA-seq, and flow cytometry. This case highlights the need to adopt multipronged confirmatory approaches to definitively solve complex genetic cases that result from variants outside protein-coding exons and conventional splice sites.

Matthew C Cook - One of the best experts on this subject based on the ideXlab platform.

  • deficiency of th17 cells in hyper ige syndrome due to mutations in stat3
    Journal of Experimental Medicine, 2008
    Co-Authors: Cindy S, Gary Y J Chew, Nicholas Simpson, Archana Priyadarshi, Melanie Wong, Bodo Grimbacher, David A Fulcher, Stuart G Tangye, Matthew C Cook
    Abstract:

    Hyper-immunoglobulin E syndrome (HIES) is a primary immune deficiency characterized by abnormal and devastating susceptibility to a narrow spectrum of infections, most commonly Staphylococcus aureus and Candida albicans. Recent investigations have identified mutations in STAT3 in the majority of HIES patients studied. Despite the identification of the genetic cause of HIES, the mechanisms underlying the pathological features of this disease remain to be elucidated. Here, we demonstrate a failure of CD4+ T cells harboring heterozygous STAT3 mutations to generate interleukin 17-secreting (i.e., T helper [Th]17) cells in vivo and in vitro due to a failure to express sufficient levels of the Th17-specific transcriptional regulator retinoid-related orphan receptor t. Because Th17 cells are enriched for cells with specificities against fungal antigens, our results may explain the pattern of infection susceptibility characteristic of patients with HIES. Furthermore, they underscore the importance of Th17 responses in normal host defense against the common pathogens S. aureus and C. albicans.