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Collaborating Across Private, Public, Community, and Federal Hospital Systems: Lessons Learned from the Covid-19 Pandemic Response in NYC

Schaye, Verity E; Reich, Jenna A; Bosworth, Brian P; Stern, David T; Volpicelli, Frank; Shapiro, Neil M; Hauck, Kevin D; Fagan, Ian M; Villagomez, Seagram M; Uppl, Amit; et al
ORIGINAL:0015308
ISSN: n/a
CID: 5000222

Don't Be So Rash: A Case Of Infective Endocarditis With Skin Manifestations

Nagpal, Neha; Shontz, Edward; Martinez-Velazquez, Luis; Prasad, Prithiv; Shvartsbeyn, Marianna; Villagomez, Seagram
ORIGINAL:0015202
ISSN: 1553-5606
CID: 4937222

Central nervous system burkitt variant post-transplant lymphopro life rative disorder (PTLD) [Meeting Abstract]

Lo, M; Villagomez, S M
Learning Objective #1: Recognize that PTLD as part of the differential when post transplant individuals present with unexplained pain, fever, or organ dysfunction. Learning Objective #2: Burkitt Lymphoma subtype as well as CNS involvement represent more aggressive manifestations of PTLD and should be managed more aggressively. CASE: 72 year-old man with end stage renal disease secondary to diabetic nephropathy status post living donor renal transplant on tacro-limus presents with headache, diplopia, and blurry vision found to have CNIII palsy on neurologic examination. Facial CT and Gadolinium enhanced Brain MRI showed complete bilateral maxillary sinus opacification and leptomeningeal enhancement. He was started on broad spectrum antibiotics, but given continuous headache and concern for meningitis a lumbar puncture was performed. CSF studies showed atypical lymphocytes of predominantly monoclonal B cells. CSF FISH showed rearrangement of c-myc oncogene negative for rearrangement of bcl6 or bcl2. Serum LDH was elevated and peripheral EBV PCR was positive. Bone marrow biopsy was negative for malignancy. Further CT imaging revealed thickening of the small bowel and mesenteric lymph-adenopathy. Patient was started on dexamethasone, intrathecal metho-trexate, and R-Hyper CVAD with interval regression of abdominal LAD, mass, improvement in ptosis, and decrease in LDH. IMPACT: The case represents an uncommon manifestation of an rare variant of disease that should warrant a different approach to diagnosis and treatment. DISCUSSION: PTLD is a well recognized, heterogenous group of disorders. The mechanism of PTLD involves EBV-induced B cell proliferation and antigen mediated T cell activation which upregulate pro-growth factors such as c-Myc. The result of which ranges from early mononucleosis-like illness, polyclonal lymphoid infiltrates, to lymphomas. Therapy involves immune reconstitution, local surgical excision, corticosteroids, antiviral agents, radiation and chemotherapy. Burkitt Lymphoma (BL) is a distinct form of PTLD. BL is an aggressive, mature B cell lymphoma composed of a monomorphic population of lymphoid cells with high mitotic and proliferation rates. Monoclonality is shown as isolated c-myc rearrangement as opposed to rear-rangements in c-myc, bcl6, and bcl2 seen in diffuse large B cell lymphoma, the most common form of PTLD. BL represents a distinct monomorphic PTLD and should be managed more aggressively with lymphoma specific chemotherapy rather than simply decreasing immunosuppression. CNS involvement of PTLD is rare, reportedly in 7-15% of all PTLD, when present is predictive of inferior survival. Compared to non-PCNS PTLD, primary CNS PTLD has a higher incidence of monomorphic EBV related disease, and late involvement with poor survival. Prior kidney transplant were also more frequent in primary CNS PTLD compared to other forms of PTLD. As a parallel, in systemic non hodgkins lymphoma, renal localization is also associated with high rates of CNS involvement
EMBASE:622328981
ISSN: 1525-1497
CID: 3138032

ASYMPTOMATIC PROSTATITIS, AN UNCOMMON MANIFESTATION OF BRUCELLOSIS [Meeting Abstract]

Selden, Elizabeth; Innes, Lindsay; Villagomez, Seagram M.
ISI:000331939301465
ISSN: 0884-8734
CID: 883262

Bone strength and related traits in HcB/Dem recombinant congenic mice

Yershov, Y; Baldini, T H; Villagomez, S; Young, T; Martin, M L; Bockman, R S; Peterson, M G; Blank, R D
Fracture susceptibility depends jointly on bone mineral content (BMC), gross bone anatomy, and bone microarchitecture and quality. Overall, it has been estimated that 50-70% of bone strength is determined genetically. Because of the difficulty of performing studies of the genetics of bone strength in humans, we have used the HcB/Dem series of recombinant congenic (RC) mice to investigate this phenotype. We performed a comprehensive phenotypic analysis of the HcB/Dem strains including morphological analysis of long bones, measurement of ash percentage, and biomechanical testing. Body mass, ash percentage, and moment of inertia each correlated moderately but imperfectly with biomechanical performance. Several chromosome regions, on chromosomes 1, 2, 8, 10, 11, and 12, show sufficient evidence of linkage to warrant closer examination in further crosses. These studies support the view that mineral content, diaphyseal diameter, and additional nonmineral material properties contributing to overall bone strength are controlled by distinct sets of genes. Moreover, the mapping data are consistent with the existence of pleiotropic loci for bone strength-related phenotypes. These findings show the importance of factors other than mineral content in determining skeletal performance and that these factors can be dissected genetically.
PMID: 11393796
ISSN: 0884-0431
CID: 158416