Joseph Breen - Academia.edu (original) (raw)

Papers by Joseph Breen

AMIA ... Annual Symposium proceedings. AMIA Symposium, 2021

After the emergence of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in 2019, iden... more After the emergence of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in 2019, identification of immune correlates of protection (CoPs) have become increasingly important to understand the immune response to SARS-CoV-2. The vast amount of preprint and published literature related to COVID-19 makes it challenging for researchers to stay up to date on research results regarding CoPs against SARS-CoV-2. To address this problem, we developed a machine learning classifier to identify papers relevant to CoPs and a customized named entity recognition (NER) model to extract terms of interest, including CoPs, vaccines, assays, and animal models. A user-friendly visualization tool was populated with the extracted and normalized NER results and associated publication information including links to full-text articles and clinical trial information where available. The goal of this pilot project is to provide a basis for developing real-time informatics platforms that can inform re...

The International Journal of Neuropsychopharmacology, 2001

Neuropsychiatric diseases such as schizophrenia and bipolar disorder are major causes of morbidit... more Neuropsychiatric diseases such as schizophrenia and bipolar disorder are major causes of morbidity throughout the world. Despite extensive searches, no single gene, RNA transcript, or protein has been found which can, on its own, account for these disorders. Recently, the availability of genomic tools such as cDNA microarrays, serial analysis of gene expression (SAGE) and large-scale sequencing of cDNA libraries has allowed researchers to assay biological samples for a large number of RNA transcripts. Similarly, proteomic tools allow for the quantitation of a large number of peptides and proteins. These methods include two-dimensional electrophoresis and surface-enhanced laser desorption\ionization (SELDI). We have initiated experiments which apply these techniques to the comparison of RNAs and proteins expressed in clinical samples obtained from individuals with psychiatric diseases and controls. These methods have the potential to identify pathways that are involved in the pathogenesis of complex psychiatric disorders. The characterization of these pathways may allow for the development of new methods for the diagnosis and treatment of schizophrenia, bipolar disorder, and other human psychiatric diseases.

The Journal of Nutritional Biochemistry, 1997

The activity of the enzyme lecithin; retinol acyltransferase (LRAT) is extremely low in the liver... more The activity of the enzyme lecithin; retinol acyltransferase (LRAT) is extremely low in the liver of vitamin A-deficient rats, but is rapidly induced after administration of retinoic acid (RA). The nuclear receptors for RA are closely related to the receptors for thyroid hormone, and molecular cross-talk between these receptors has been observed in vitro and in cultured cells. Therefore we

Journal of Biological Chemistry, 1998

Endocrinology, 1995

T3 inhibits transcription of the rat TSH beta gene, and two T3 response elements have been identi... more T3 inhibits transcription of the rat TSH beta gene, and two T3 response elements have been identified that bind T3 receptors and that share sequence homology with the consensus sequence that is also recognized by retinoic acid receptors (RARs). We, therefore, asked whether RA was a regulator of TSH beta gene expression in vivo. Using RNase protection analysis, we found that vitamin A deficiency led to a 2-fold increase in rat pituitary TSH beta messenger RNA (mRNA) levels, which returned to normal 18 h after treatment with RA (20 micrograms/rat). Vitamin A deficiency had no effect on TSH beta mRNA levels in hypothyroid rats. Coadministration of RA and T3 (10 micrograms/100g body wt) to either vitamin A-deficient or vitamin A-deficient, hypothyroid animals caused decreases in TSH beta mRNA content that were indistinguishable from those seen with T3 alone. Surprisingly, vitamin A deficiency had no significant effect on GH mRNA levels in euthyroid or hypothyroid rats. Furthermore, treatment of vitamin A-deficient, hypothyroid animals with RA for either 18 or 72 h had no effect on GH mRNA levels, whereas T3 caused 11-fold and 18-fold increases in GH mRNA, respectively, at these times. We also used transient transfection to test for direct, retinoid receptor-mediated regulation of TSH beta gene transcription by RA. A plasmid TSH beta luciferase, containing 0.8 kilobases of rat TSH beta gene 5&amp;amp;amp;amp;amp;amp;amp;#39;-flanking sequences, exon 1, and 150 base pairs of intron 1, was transfected into CV-1 cells. Cotransfection with RAR alpha and retinoid X receptor-beta induced TSH beta expression by 3.5-fold, and treatment with RA suppressed this induction by 46%. These results show that vitamin A levels play a significant role in regulating the expression of the TSH beta gene, but not the GH gene, in vivo and suggest that RA may suppress TSH beta gene transcription directly by an RAR-retinoid X receptor heterodimer-mediated mechanism.