Browsing by Author "Blessing C. Ukibe"

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    Advances in Laboratory Diagnosis and Clinical Management of Gilbert Disease
    (IAA Journal of Scientific Research, 2024) Nkiruka R Ukibe; Chioma Theresa Onwe; C.E. Onah; Ezinne G. Ukibe; Blessing C. Ukibe; Victory Ezennia Ukibe; Emmanuel Ifeanyi Obeagu
    Gilbert’s syndrome (GS) is an extensively mild condition characterized by periods of elevated levels of bilirubin in the blood. The bilirubin is an orange yellowish tinted molecule which is produced when red blood cells are broken down and this substance is eliminated from the body only after it undergoes bio-transformation in the liver which converts unconjugated bilirubin to conjugated bilirubin. When the level of unconjugated bilirubin increases beyond a determined point, the bilirubin pigment starts to discolour the cornea of the eyes (making them to appear light yellow) and with higher levels the skin may also turn to yellow (jaundice). Gilbert’s syndrome also known as constitutional hepatic dysfunction and familial non haemolytic jaundice. People with Gilbert’s syndrome have an inherited abnormality that causes reduced production of an enzyme involved in processing of bilirubin. A presumptive diagnosis of Gilbert’s syndrome is made when unconjugated hyperbilirubinemia is noted on several occasions.
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    Advances in Laboratory Diagnosis and Clinical Management of Gilbert Disease: A Comprehensive Review
    (Journal of Scientific Research, 2024) Nkiruka R Ukibe; Chioma Theresa Onwe; C.E. Onah1 Ezinne G. Ukibe; Blessing C. Ukibe; Victory Ezennia Ukibe; Emmanuel Ifeanyi Obeagu
    Gilbert’s syndrome (GS) is an extensively mild condition characterized by periods of elevated levels of bilirubin in the blood. The bilirubin is an orange yellowish tinted molecule which is produced when red blood cells are broken down and this substance is eliminated from the body only after it undergoes bio-transformation in the liver which converts unconjugated bilirubin to conjugated bilirubin. When the level of unconjugated bilirubin increases beyond a determined point, the bilirubin pigment starts to dis colour the cornea of the eyes (making them to appear light yellow) and with higher levels the skin may also turn to yellow (jaundice). Gilbert’s syndrome also known as constitutional hepatic dysfunction and familial non hemolytic jaundice. People with Gilbert’s syndrome have an inherited abnormality that causes reduced production of an enzyme involved in processing of bilirubin. A presumptive diagnosis of Gilbert’s syndrome is made when unconjugated hyper bilirubin anemia is noted on several occasions
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    Deciphering the Molecular Mechanisms Governing Autophagy: A Comprehensive Overview
    (IAA Journal of Scientific Research, 2024) Nkiruka R Ukib; Mmesoma Jessica Nwankwo; Onah C. E; Ezinne G. Ukibe; Blessing C. Ukibe; Victory Ezennia Ukibe; Emmanuel Ifeanyi Obeagu
    Autophagy, an evolutionarily conserved cellular process, intricately regulates the degradation and recycling of cellular components, ensuring cellular homeostasis. The molecular orchestration of autophagy involves a sophisticated network of signaling pathways and key molecular players. Key initiation steps involve nutrient-sensing pathways, including mTOR and AMPK, converging on the ULK1 complex, triggering autophagosome formation. Subsequent stages encompass the role of the PI3K complex, recruitment of ATGs, and autophagosome expansion, leading to cargo recognition and closure. The selectivity in autophagy is achieved through cargo-specific adaptors and receptors like p62/SQSTM1, NIX/BNIP3L, and NDP52, ensuring targeted degradation of damaged organelles, misfolded proteins, and pathogens. Upon fusion with lysosomes, autolysosomes are formed, culminating in the breakdown of engulfed cargo via lysosomal hydrolases. Autophagy's intricate interplay with cellular processes, including metabolism, immunity, and cell death pathways, underscores its multifaceted roles in physiological and pathological conditions. Dysregulated autophagy is implicated in neurodegenerative disorders, cancer, metabolic diseases, and infections, highlighting its clinical relevance. Understanding the molecular mechanisms of autophagy offers promising prospects for therapeutic interventions by targeting autophagic pathways. This overview provides insights into the molecular intricacies of autophagy, offering potential avenues for therapeutic modulation in various disease contexts.