70 research outputs found
UC-36 Using Machine Learning Techniques to Predict RT-PCR Results for COVID-19 Patients.
With the COVID-19 pandemic still a threat, healthcare professionals and medical industries keep searching for better ways to mitigate the spread of COVID-19. While Machine Learning has been applied in many other domains, there is now a high demand for diagnosis systems that utilize Machine Learning techniques in the healthcare domain and in particular combating COVID-19. In this project, we explore the role of Machine Learning models in combating COVID-19, using WEKA as the main tool for analysis.Advisors(s): Dr. Ming Yang - IT 4983 Capstone Professor Dr. Seyedamin Pouriyeh - Project OwnerTopic(s): Data/Data AnalyticsIT 498
Urinary catecholamines and mitral valve prolapse in panic-anxiety patients
Free norepinephrine and epinephrine were measured in two consecutive 12-hour urine collections gathered during normal activity and sleep from 23 panic-anxiety patients and 9 normal subjects. Mitral value prolapse (MVP) was found in 7 of 20 patients who had echocardiograms. Mean nighttime norepinephrine and epinephrine excretion in panic-anxiety patients without MVP was significantly higher than that of control subjects, and was significantly higher than that of anxiety patients with MVP. In the daytime, all groups had higher catecholamine (CA) levels, but the differences between the groups were less pronounced. Medication significantly relieved symptoms and was associated with decreased CA levels. Elevated basal CA levels may characterize the subgroup of panic-anxiety patients who do not have MVP.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25817/1/0000380.pd
Systemic hormonal and physiological abnormalities in anxiety disorders
Among the studies of systemic hormonal and physiological abnormalities associated with anxiety disorders, the most consistent and extensive findings suggest (a) peripheral adrenergic hyperactivity (including increases in norepinephrine but not epinephrine) and functional dysregulation, (b) increased incidence of mitral valve prolapse in panic patients, and (c) normal suppressibility of the hypothalamic-pituitary-adrenal cortical endocrine system with dexamethasone in panic patients. Other less-certain findings include (a) increased circulating concentrations of plasma ACTH and/or cortisol, and prolactin, in panic patients, (b) increased platelet monoamine oxidase activity in generalized anxiety and/or panic patients, (c) decreased gonadal axis activity in some anxious individuals, (d) decreased nighttime melatonin plasma concentrations in panic patients, and (e) peripheral [alpha]2 and [beta]-adrenoreceptor down-regulation, with normal serotonin binding parameters. These findings, taken together, provide tentative support for dysfunction in adrenergic and GABAergic central nervous system mechanisms in people with anxiety disorders. Abnormal anxiety and normal stress both show evidence of adrenergic hyperactivity; however, there appear to be differences in hormonal profiles, especially the apparent lack of increase of epinephrine during panic attacks, as well as differences in the reactivity of the system, and in the "trigger" mechanisms which determine when the response occurs.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27526/1/0000570.pd
Cell-Specific ĂąâŹĆCompetition for CaloriesĂąâŹïżœ Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-human Animals
The mammalian body is a complex physiologic ĂąâŹĆecosystemĂąâŹïżœ in which cells compete
for calories (i.e., nutrient-energy). Axiomatically, cell-types with competitive advantages
acquire a greater number of consumed calories, and when possible, increase in
size and/or number. Thus, it is logical and parsimonious to posit that obesity is the
competitive advantages of fat-cells (adipocytes) driving a disproportionate acquisition
and storage of nutrient-energy. Accordingly, we introduce two conceptual frameworks.
Asymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specific
competition for calories that determines the partitioning of nutrient-energy to oxidation,
anabolism, and/or storage; and Effective Caloric Intake which describes the number
of calories available to constrain energy-intake via the inhibition of the sensorimotor
appetitive cells in the liver and brain that govern ingestive behaviors. Inherent in
these frameworks is the independence and dissociation of the energetic demands
of metabolism and the neuro-muscular pathways that initiate ingestive behaviors and
energy intake. As we demonstrate, if the sensorimotor cells suffer relative caloric
deprivation via asymmetric competition from other cell-types (e.g., skeletal muscle- or
fat-cells), energy-intake is increased to compensate for both real and merely apparent
deficits in energy-homeostasis (i.e., true and false signals, respectively). Thus, we
posit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesity
and metabolic diseases is engendered by apparent deficits (i.e., false signals) driven
by the asymmetric inter-cellular competition for calories and concomitant differential
partitioning of nutrient-energy to storage. These frameworks, in concert with our
previous theoretic work, the Maternal Resources Hypothesis, provide a parsimonious
and rigorous explanation for the rapid rise in the global prevalence of increased body
and fat mass, and associated metabolic dysfunctions in humans and other mammals
inclusive of companion, domesticated, laboratory, and feral animals
Deciphering colorectal cancer genetics through multi-omic analysis of 100,204 cases and 154,587 controls of European and east Asian ancestries
In the version of this article initially published, the author affiliations incorrectly listed âCandiolo Cancer Institute FPO-IRCCS, Candiolo (TO), Italyâ as âCandiolo Cancer Institute, Candiolo, Italy.â The change has been made to the HTML and PDF versions of the article
Defining the causes of sporadic Parkinson's disease in the global Parkinson's genetics program (GP2)
The Global Parkinsonâs Genetics Program (GP2) will genotype over 150,000 participants from around the world, and integrate genetic and clinical data for use in large-scale analyses to dramatically expand our understanding of the genetic architecture of PD. This report details the workflow for cohort integration into the complex arm of GP2, and together with our outline of the monogenic hub in a companion paper, provides a generalizable blueprint for establishing large scale collaborative research consortia
Multi-ancestry genome-wide association meta-analysis of Parkinson?s disease
Although over 90 independent risk variants have been identified for Parkinsonâs disease using genome-wide association studies, most studies have been performed in just one population at a time. Here we performed a large-scale multi-ancestry meta-analysis of Parkinsonâs disease with 49,049 cases, 18,785 proxy cases and 2,458,063 controls including individuals of European, East Asian, Latin American and African ancestry. In a meta-analysis, we identified 78 independent genome-wide significant loci, including 12 potentially novel loci (MTF2, PIK3CA, ADD1, SYBU, IRS2, USP8, PIGL, FASN, MYLK2, USP25, EP300 and PPP6R2) and fine-mapped 6 putative causal variants at 6 known PD loci. By combining our results with publicly available eQTL data, we identified 25 putative risk genes in these novel loci whose expression is associated with PD risk. This work lays the groundwork for future efforts aimed at identifying PD loci in non-European populations
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