Publications by authors named "M J Kafina"

Central retinal artery occlusion (CRAO) is a rare and visually debilitating vascular condition characterized by sudden and severe vision loss. CRAO is a compelling target for intravenous alteplase (tPA) and endovascular mechanical thrombectomy (MT) due to pathophysiological similarities with acute ischemic stroke; however, the utility of these interventions in CRAO remains dubious due to limited sample sizes and potential risks. To assess usage and outcomes of tPA and MT in CRAO, we queried the National Inpatient Sample database using International Classification of Disease, Ninth and Tenth edition for patients with CRAO and acute ischemic stroke between 2010 and 2019.

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Background: Previous literature has identified a survival advantage in acute ischemic stroke (AIS) patients with elevated body mass indices (BMIs), a phenomenon termed the "obesity paradox."

Objective: The aim of this study was to evaluate the independent association between obesity and clinical outcomes following AIS.

Methods: Weighted discharge data from the National Inpatient Sample were queried to identify AIS patients from 2015 to 2018.

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Article Synopsis
  • Erythropoietin (EPO) signaling is crucial for the final stages of red blood cell development, but how it affects iron metabolism remains unclear.
  • Research identified a protein called FAM210B that plays a key role in processes like hemoglobin formation and cell division during this maturation stage.
  • FAM210B is not directly an iron transporter but helps in iron import to mitochondria, which is necessary for producing heme and iron-sulfur clusters essential for red blood cell function.
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The zebrafish, Danio rerio, is a powerful model for the study of erythropoiesis and defining the genetic basis of hematological diseases. The mechanisms of erythroid differentiation are highly conserved in the zebrafish, permitting translational research studies and the modeling of erythropoiesis in higher vertebrates. An advantage of the system is the ability to manipulate gene expression and observe the effect on erythroid development in vivo, with relative ease and rapidity.

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Loss-of-function mutations in genes for heme biosynthetic enzymes can give rise to congenital porphyrias, eight forms of which have been described. The genetic penetrance of the porphyrias is clinically variable, underscoring the role of additional causative, contributing, and modifier genes. We previously discovered that the mitochondrial AAA+ unfoldase ClpX promotes heme biosynthesis by activation of δ-aminolevulinate synthase (ALAS), which catalyzes the first step of heme synthesis.

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