Publications by authors named "A J Vine"

A surgeon was among the teams caring for critically-ill patients with COVID-19 infection during the height of the pandemic in March and April 2020 in Brooklyn. He recorded his experiences and thoughts as events unfolded, a chronicle of the landmark public health event of the century. Working to exhaustion alongside his colleagues from Mount Sinai Hospital, he encountered tragedy and inspiration.

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As early endosomes mature, the SAND-1/CCZ-1 complex acts as a guanine nucleotide exchange factor (GEF) for RAB-7 to promote the activity of its effector, HOPS, which facilitates late endosome-lysosome fusion and the consumption of AP-3-containing vesicles. We show that CCZ-1 and the HOPS complex are essential for the biogenesis of gut granules, cell type-specific, lysosome-related organelles (LROs) that coexist with conventional lysosomes in Caenorhabditis elegans intestinal cells. The HOPS subunit VPS-18 promotes the trafficking of gut granule proteins away from lysosomes and functions downstream of or in parallel to the AP-3 adaptor.

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Article Synopsis
  • Hermansky-Pudlak syndrome is a human disease linked to defective lysosome-related organelles (LROs) caused by mutations in the BLOC-1 complex, which includes proteins like Pallidin and Snapin.
  • Research shows that the C. elegans genes glo-2 and snpn-1 encode homologues of these BLOC-1 subunits, with their functions being conserved, as mutations in these genes led to issues in gut granule formation.
  • The study suggests that the BLOC-1 complex in C. elegans retains functions that are independent of the AP-3 complex and highlights the potential for using C. elegans to further explore the role of BLOC-1 in cellular processes.
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Acute lung injury (ALI) is mediated by an early proinflammatory response resulting from either a direct or indirect insult to the lung mediating neutrophil infiltration and consequent disruption of the alveolar capillary membrane ultimately leading to refractory hypoxemia. The mitogen-activated protein kinase (MAPK) pathways are a key component of the molecular response activated by those insults triggering the proinflammatory response in ALI. The MAPK pathways are counterbalanced by a set of dual-specific phosphatases (DUSP) that deactivate the kinases by removing phosphate groups from tyrosine or threonine residues.

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While most carriers of human T-cell leukemia virus type 1 (HTLV-1) remain asymptomatic throughout their lifetime, infection is associated with the development of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The exact parameters that determine these outcomes are unknown but are believed to include host genetic factors that control the immune response to infection. Host response to fellow retroviridae member HIV is influenced by the expression of members of the Killer Immunoglobulin Receptor (KIR) family including KIR3DS1.

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