Vivek Patel

Bio: Vivek Patel is an academic researcher from Northwestern Polytechnical University. The author has contributed to research in topics: Medicine & Friction stir processing. The author has an hindex of 25, co-authored 136 publications receiving 2443 citations. Previous affiliations of Vivek Patel include University College West & Johns Hopkins University School of Medicine.

ZBP1 recognition of β-actin zipcode induces RNA looping

Abstract: ZBP1 (zipcode-binding protein 1) was originally discovered as a trans-acting factor for the ‘‘zipcode’’ in the 39 untranslated region (UTR) of the b-actin mRNA that is important for its localization and translational regulation. Subsequently, ZBP1 has been found to be a multifunctional regulator of RNA metabolism that controls aspects of localization, stability, and translation for many mRNAs. To reveal how ZBP1 recognizes its RNA targets, we biochemically characterized the interaction between ZBP1 and the b-actin zipcode. The third and fourth KH (hnRNP K homology) domains of ZBP1 specifically recognize a bipartite RNA element located within the first 28 nucleotides of the zipcode. The spacing between the RNA sequences is consistent with the structure of IMP1 KH34, the human ortholog of ZBP1, that we solved by X-ray crystallography. The tandem KH domains are arranged in an intramolecular anti-parallel pseudodimer conformation with the canonical RNA-binding surfaces at opposite ends of the molecule. This orientation of the KH domains requires that the RNA backbone must undergo an ~180° change in direction in order for both KH domains to contact the RNA simultaneously. The RNA looping induced by ZBP1 binding provides a mechanism for specific recognition and may facilitate the assembly of posttranscriptional regulatory complexes by remodeling the bound transcript.

Recent Development in Friction Stir Processing as a Solid-State Grain Refinement Technique: Microstructural Evolution and Property Enhancement

Abstract: Increasing demand of lightweight structures with exceptional properties elicits materials processing and manufacturing technologies to tailor blanks in order to achieve or enhance those pre...

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Optic Neuritis and Myelitis in COVID-19.

Abstract: T he outbreak of the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), was first reported in late December 2019 in Wuhan, China, (1) and has since transformed into a rapidly evolving global pandemic. As the number of infections grows, so does our knowledge of possible clinical symptoms, signs, and manifestations. The coronavirus family of viruses, including SARS coronavirus 1 (SARS-CoV-1) and Middle East respiratory syndrome coronavirus (MERS-CoV), is most well known for causing respiratory syndromes, with severe cases leading to acute respiratory distress syndrome (ARDS). There is an ever-growing body of literature describing other organs as sites of damage caused by this family of viruses, including cardiac (2), gastrointestinal (3), neurological (4–11), and ophthalmic (12–14) involvement. The neuroinvasive potential of SARS-CoV-1, MERS-CoV, and other coronaviruses has been described, and it has been hypothesized that SARS-CoV-2 may be able to directly access the central nervous system (CNS) through a transsynaptic route given considerable sequence homology, and that this may be a mechanism of respiratory failure in COVID-19 (5). Moreover, a recent report of SARS-CoV-2 preceding antiphospholipid antibody syndrome (9) leading to thrombus formation underscores the potential for this infectious agent to trigger autoantibody production. Additional reports of COVID-19 presenting as Miller Fisher syndrome (10), Guillain–Barré syndrome (11), and Kawasaki syndrome (13) offer specific examples of this virus’s ability to dysregulate the immune system. Herein, we describe a case of a young man presenting with bilateral severe optic neuritis and myelitis, determined to be simultaneously SARS-CoV2 and myelin oligodendrocyte glycoprotein (MOG) IgG antibody positive. We believe this is a unique neuroophthalmic manifestation of SARS-CoV-2 and the first such case to be reported in the literature. This report adheres to the tenets of the Declaration of Helsinki. Patient data were obtained through inpatient and outpatient encounters and medical records at Keck Medical Center, University of Southern California. Informed consent was obtained verbally as well as part of the patient agreement for use of clinical information and photographs for educational purposes. A 26-year-old Hispanic man presented for evaluation of bilateral, subacute, sequential vision loss first affecting the left eye, then the right eye 3 days later. Pain with eye movements preceded the vision symptoms in each eye. An ophthalmologist noted disc edema and urgently referred him to our practice for further evaluation. On review of systems, he reported a few days of progressive dry cough before the onset of eye pain and vision loss. He also endorsed numbness on the soles of his feet and neck discomfort with forward flexion but denied shooting, electric-like pain. He denied fevers, chills, sweats, shortness of breath, rhinorrhea, chest pain, or changes in taste or smell. There were no recent headaches, weakness, imbalance, bowel or bladder dysfunction, and cognitive or mood changes. He further denied personal or family history of demyelinating or autoimmune disorders. He had 4 dogs at home and denied cat exposure. He denied recent travel or sick contacts. Our examination revealed hand motion vision in the right eye and 20/250 in the left eye, with a right relative afferent pupillary defect. Ocular motor and remaining cranial nerve examinations were normal. Dilated fundus examination revealed bilateral disc edema and venous congestion, with retinal perivenous hemorrhages in the right eye (Fig. 1). His clinical picture of severe sequential bilateral optic neuritis with disc edema was highly suspicious for MOG antibody disease, but the broader differential diagnosis also included infectious, inflammatory, and infiltrative processes. Our initial workup included testing for QuantiFERON-TB Division of Neuro-Ophthalmology (SZ, VRP), USC Roski Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, California; Division of Infectious Disease (ECJ-L), Department of Internal Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California; and Division of Neuroimmunology (DJS, CJA), Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles, California.