Brian J. Prendergast, Ph.D. - US grants
Affiliations: | Psychology | University of Chicago, Chicago, IL |
Area:
Behavioral Neuroendocrinology, Seasonality, Circadian biology, PsychoneuroimmunologyWe are testing a new system for linking grants to scientists.
The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, Brian J. Prendergast is the likely recipient of the following grants.Years | Recipients | Code | Title / Keywords | Matching score |
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2001 — 2002 | Prendergast, Brian J | F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Neuroendocrine Regulation of Biological Timing @ Ohio State University DESCRIPTION (provided by applicant): The goal of the proposed research is to evaluate neuroendocrine mechanisms that coordinate seasonal reproduction in deer mice (Peromyscus maniculatus). Individuals of this long-day breeding species display reproductive involution in short days, followed by photorefractoriness and spontaneous gonadal recrudescence, the onset of which is regulated by an endogenous interval timer (IT). Whereas many studies have addressed factors mediating autumnal regression, little is known about neuroendocrine changes that permit accurate timing of photorefractoriness. These studies assess the functional significance of biological clocks by testing whether latitudinal differences in the onset of vernal breeding are associated with differences in the period of the IT in wild rodents. Deer mice will be housed in winter photoperiods to trigger reproductive regression. The timing of refractoriness will be compared between groups of mice derived from different northern latitudes. Follow-up experiments will specify the relevant photoperiodic experiences that determine the duration of the IT, whether the IT has a heritable genetic basis, and the response of the IT to artificial selection. A related set of experiments will address the physiological bases of photorefractoriness. Immunocytochemical techniques will be used to quantify the number, size, and density of GnRH-immunoreactive neurons after photorefractoriness has been triggered in short days, and patterns of GnRH mRNA expression will be compared between photorefractory and photoresponsive individuals via in situ hybridization. Experiments will determine whether changes in subpopulations of hypothalamic GnRH neurons mediate photorefractoriness, or alternatively whether photorefractoriness is a sequence of changes in pituitary responsiveness to GnRH. These studies will combine ecological and molecular techniques to assess neuroendocrine mechanisms governing reproductive variation and seasonal timekeeping. |
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2005 — 2008 | Prendergast, Brian J | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Processing Photoperiod Information by the Immune System @ University of Chicago DESCRIPTION (provided by applicant): Seasonal changes in immune function, health and disease are ubiquitous in humans, and contribute to annual patterns of mortality. The overall goal of the proposed research is to specify mechanisms by which endogenous and environmental factors control seasonal changes in the immune system of mammals. Analogies between photoperiodic control of the reproductive system and the immune system are critically examined at a formal level, and neural pathways are investigated at a mechanistic level. The point of departure for this work is the observation that exposure to short photoperiods alters several measures of immunity in Siberian hamsters; these changes occur entirely independently of the concurrent regression of the reproductive system. The formal properties and physiological substrates of the mechanism that perceives change in day length and communicates this information to the immune system remain unknown. These experiments will use in vivo and ex vivo measures of immune function to: (1) document the impact of natural changes in photoperiod on the immune system, (2) determine whether photoperiodic changes in immunity are dependent on pineal melatonin secretion and whether the duration of nocturnal melatonin secretion is the critical parameter for imparting seasonal information into the immune system, (3) identify the thalamic and hypothalamic melatonin target tissues that mediate the effects of photoperiod on the immune system, and (4) determine whether photoperiod-induced changes in sensitivity to inflammatory cytokine production participate in physiological and behavioral changes evident in the immune responses of mammals at different stages of their seasonal cycles. |
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2011 — 2015 | Prendergast, Brian J | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Biological Rhythms and Immune Function @ University of Chicago DESCRIPTION (provided by applicant): The immune system and the central nervous system interact in a bidirectional manner. Activity of the central nervous system can direct marked changes in immune function. Likewise, peripheral inflammation is associated with pathological changes in motivational states and behavior, mood and cognition. Circadian and seasonal clocks in the hypothalamus yield high-amplitude rhythms in immune function and afford direct investigation of mechanisms mediating brain-to-immune interactions. Daily and seasonal rhythms in morbidity in response to inflammation are directly relevant to survival of numerous illnesses. Understanding how biological clocks engage changes in the immune system has implications for the treatment and management of chronic diseases (e.g., cancer, obesity) and acute bacterial and viral infections. The overall goal of the proposed research is to identify the mechanisms by which daily (circadian) and seasonal time information is communicated from the brain to the immune system. Siberian hamsters will be used as a model species specifically because they exhibit robust seasonal and circadian rhythms in innate and adaptive immune function which can be readily driven and synchronized by changes in the light-dark cycle. In this species, the amplitude of the seasonal cycle in several measures of immunity encompasses a range that would be clinically diagnostic of an immunocompromised state, yet hamsters exhibit these changes in immunity in the absence of co-morbid illness and in response to little more than a few hours'change in the light-dark cycle. Understanding the mechanisms by which time information drives changes in immune function will identify novel endogenous mechanisms by which the brain affects the immune system. This is a fundamentally-important issue which will inform treatments for seasonally-recurring illnesses in humans, and the causes of robust circadian rhythms in morbidity. These experiments will assess redistribution of blood leukocyte phenotypes, alterations in adaptive T cell-mediated immune function (DTH reactions), and changes in the magnitude of infection-induced innate inflammatory responses in experiments that seek to: (1) identify the cellular mechanisms by which changes in day length and melatonin control immune cell activity, (2) specify the role of thyroid hormone signaling in the genesis of seasonal changes in the immune system, (3) characterize the influence of the hypothalamic circadian pacemaker on daily rhythms in the immune system and on organismal-level immunocompetence, and (4) identify the output mechanisms that mediate coupling between the circadian clock and the immune system. The proximate causes of human seasonal and circadian rhythms in health and immune function remain largely unknown. Together, the work will afford major and novel biological insights into the mechanisms by which the nervous and endocrine systems guide the activity of the immune system. PUBLIC HEALTH RELEVANCE: Biological clocks in the brain generate high-amplitude daily and seasonal rhythms in immune function and afford direct investigation of mechanisms by which the central nervous system modulates immunity. Daily and seasonal rhythms in morbidity in response to inflammation are directly relevant to survival of numerous illnesses, thus understanding how biological clocks engage changes in the immune system has implications for the treatment and management of chronic diseases and acute bacterial and viral infections. The proposed research seeks to identify the mechanisms by which circadian and seasonal time information is communicated from the brain to the immune system;the work will afford major and novel biological insights into neural and endocrine modulation of immunity. |
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2015 | Chang, Eugene [⬀] Jones, Dean Paul Prendergast, Brian J |
R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Diet Induced Obesity From Gut Microbial Disruption of Host Metabolic Networks @ University of Chicago ? DESCRIPTION (provided by applicant): The proposed multi-PI, multidisciplinary investigations will address the fundamental basis of diet-induced obesity (DIO) that currently afflicts one third of adult Americans and is projected to affect >90% of Americans by 2050. While genetics play a role, non-genetic factors introduced through changes in Western diet and lifestyle are the more likely causes for the alarming trends in human obesity. Recently, the role of the gut microbiome in mediating DIO has been suggested, a notion supported by our own preliminary data that show germ-free (GF) mice are protected from DIO and that dysbiosis induced by a high saturated fat diet disrupts the circadian clock (CC) networks of the suprachiasmatic nucleus (SCN) and liver. Circadian rhythms are essential to all life forms, whether human, a member of the animal kingdom, plant, or microbe. Circadian rhythms are endogenous and provide living organisms with the ability to entrain to external cues (zeitgebers) so that they can adapt to, and synchronize with, changes in the environment. We will test the hypothesis that the obesogenic effects of high saturated fat western diets are due to their effects on the chronobiology and function of the gut microbiota, resulting in the generation of specific microbial metabolites that perturb hepatic CC/NR regulatory networks and skew energy states towards the development of obesity. A collaborative approach will be undertaken that includes investigators from The University of Chicago and Emory University who have broad and extensive expertise in research of disease pathophysiology and state-of-the-art analytics for gut microbial metagenomic sequencing, metabolomics, nutritional studies, and relevant bioinformatics. Three specific aims are proposed: (1) to determine if the obesogenic effects of high saturated fat diets are due to their impact on gut microbial chronobiology, function, and metabolomes that specifically target hepatic and central CC regulatory networks, (2) Characterize mechanisms by which gut microbes provide feedback effects on the circadian system in the CNS and liver using classical chronobiological approaches in GF, CONV, and SPF mice. and (3) to identify specific microbe- dependent metabolites from the metabolome that mediate the effects of diet-induced regulation of hepatic CC gene networks and/or their downstream effector pathways using high throughput, hepatic organoid assay systems. Their effects in vivo on hepatic regulatory networks and metabolic/physiological functions will then be vetted in studies involving conventionalized (CONV) and GF mice. Collectively, these data will provide a wealth of novel and clinically-useful information to better understand the role, mechanisms, and mediators of western diet-induced gut dysbiosis in human obesity. This information will have direct relevance to the development of effective therapeutic compounds that can correct the imbalances in brain and hepatic regulatory networks caused by western-diet induced dysbiosis, thereby restoring host metabolic states to health. |
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