Charles E Wood
University Of Florida
Project start date: 1996-05-03
Project end date: 2017-01-31
Sponsored Links Excellgen http://Excellgen.com
Fetal Cardiovascular And Endocrine Reflex Responses
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 2R01HD033053-10A1 from National Institute Of Child Health And Human Development IRG: ZRG1
Abstract: Baroreceptor and chemoreceptor reflexes are actively involved in the control of fetal blood pressure and in the maintenance of blood flow to the placenta and to the metabolizing tissues. The present project is an investigation into the mechanism of the baro- and chemoreflexes. In the first two funding periods of this project, we discovered and explored the interaction between changes in fetal blood pressure and prostaglandin generation in the fetal brain. In the immediate past funding period, we found that prostaglandin synthase -1 (PGHS-1) activity in the fetal brain augments reflex activity and that PGHS-2 activity decreases reflex activity. We found that denervation of the arterial baroreceptor/chemoreceptors does not, by itself, alter the expression of these enzymes in the fetal brain; PGHS-2 expression (and likely subsequent activity) is unregulated by transient hypotension. We have also initiated the use of a cell culture model to make significant progress in understanding the molecular mechanism of the PGHS-2 response to oxygen and glucose deprivation. These discoveries suggest that the immediate response to hypotension in the fetus is dependent upon PGHS-1 activity, but that the more delayed increase in PGHS-2 may bias subsequent responses and predispose the fetus to hypoxic damage. These findings have led us to propose the following specific aims, to propose to answer the following questions 1) is there an association of glutaminergic pathways and prostanoids in the mediation of the reflex responses to cerebral hypoperfusion? 2) Is the ability of the fetus to maintain blood pressure and blood gases during hypovolemia impaired by blockade of prostaglandin biosynthesis or NMDA receptors? 3) What is the molecular and cellular basis of the upregulation of PGHS-2 in response to hypotension? In the proposed 5-year continuation of this project, the answers to these questions will significantly enhance our understanding of the mechanism by which prostanoids act within the brain to alter cardiovascular function. We will answer all of these questions using in vivo as well as cellular and molecular techniques. The results will build on our previous discoveries to significantly improve our understanding of the mechanism of the fetal stress response during hypotension. The results will identify the processes within the reflex pathway that can be manipulated pharmacologically and therefore enhance fetal survival during hypotensive stress.
Project start date: 1996-05-03
Project end date: 2011-11-30
2R01HD033053-10A1 (2007): $267969
2R01HD033053-05A1 (2001): $257870
Grants awarded to Charles E Wood
Short-Term Research Training For Minority Students
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 5T35HL007930-09 from National Heart, Lung, And Blood Institute IRG: ZHL1
Abstract: This is an application for competitive renewal of the NHLBI Short-Term Research Training for Minority Students program which has been in place at the University of Florida since 1999. The purpose of this training program is to offer minority undergraduate students and students in health professional schools ten week experience in an active research laboratory, to offer them didactic material covering topics of interest to, and needed by, young scientists. The proposed renewal of this training program is planned as a broad-based exposure to research in cardiovascular, pulmonary, and hematologic research in three colleges of the University of Florida Health Science Center. The faculty listed in the proposed renewal of this training program span three colleges within the HSC (Medicine, Pharmacy, and Veterinary Medicine). We want this program to capture the diversity of interests and approaches to cardiovascular science, to offer a snapshot of professors in three colleges with overlapping research interests but different academic missions, to offer to our trainees a wealth of possibilities in science beyond what are sometimes naive notions of medical practice, The program director is Charles E. Wood, Ph.D., a well-known developmental cardiovascular physiologist. Dr. Wood will direct the relevant activities in the office of the department chairman s office as well as the Office of Minority Affairs (OMA). OMA will provide the staff for the recruiting and mentormatching process. Selection of trainees is done by a committee consisting of four faculty members, two from OMA and two from the basic science faculty. Selection and oversight of lectures and training seminars offered during the training program will be done by Dr. Wood in his role as program director. At the end of the program, the trainees are tracked by the OMA. Tracking occurs via contact with the student at their home (permanent) addresses. When appropriate, individual students are encouraged to apply to the various graduate programs at the University of Florida, especially to the Interdisciplinary Program in Biomedical Sciences, but also to Ph.D. graduate programs in the College of Pharmacy or the College of Veterinary Medicine. Students interested in becoming clinician scientists are encouraged to apply to the University of Florida College of Medicine. The emphasis of this training program in the next five years will be to significantly expand the students horizons and to recruit students into basic biomedical science.
Project start date: 1999-05-01
Project end date: 2009-04-30
5T35HL007930-09 (2007): $101833
5T35HL007930-08 (2006): $101833
5T35HL007930-07 (2005): $64818
2T35HL007930-06 (2004): $101833
SHORT-TERM TRAINING IN BIOMEDICAL RESEARCH FOR UNDER-REPRESENTED MINORITIES
Charles E Wood, Professor
University Of Florida, 219 Grinter Hall, Gainesville, Fl 32611-5500
Grant 1R25HL103181-01 from National Heart, Lung, And Blood Institute
Abstract: This is a revised application for competitive renewal of the NHLBI Short-Term Research Training for Minority Students program which has been in place at the University of Florida since 1999. The purpose of this training program is to offer undergraduate students and students in health professional schools a ten week experience in an active research laboratory, to offer them didactic material covering topics of interest to, and needed by, young scientists. The students recruited into this program will be underrepresented in medical science (under-represented minorities, disabled, or disadvantaged students). The proposed renewal of this training program is planned as a broad- based exposure to research in cardiovascular, pulmonary, and hematologic research in three colleges of the University of Florida Health Science Center. The faculty for this proposed training program spans several departments. We want this program to capture the diversity of interests and approaches to cardiovascular science, to offer a snapshot of professors in three colleges (Medicine, Pharmacy, and Veterinary Medicine) with overlapping research interests but different academic missions, to offer to our trainees a wealth of possibilities in science beyond what are sometimes naive notions of medical practice. Most of the faculty are directly involved in research which is easily identifiable as cardiovascular, pulmonary, or cardiorenal research. The program director is Charles E. Wood, Ph.D., a well-known developmental cardiovascular physiologist who has made fundamental contributions to the understanding of the reflex control of the fetal cardiovascular system. Dr. Wood will direct the relevant activities in the office of the department chairman´s office as well as the Office of Minority Affairs (OMA). Selection of trainees is done by a committee consisting of four faculty members, all leading members of the U.F. College of Medicine faculty. Selection and oversight of lectures and training seminars offered during the training program will be done by Dr. Wood in his role as program director. The structure of the program is designed to be an 8-10 week mentored laboratory experience with an overarching weekly lecture series that will is designed to inform students about the structure of academic science and doctoral training programs. The students will also be required to attend a short course in the Responsible Conduct of Research. A plan for evaluation of program effectiveness is proposed that will assess career goals, perceived barriers, knowledge of academic research careers, and knowledge of higher education in research. The evaluation plan will be used as the basis of a report, after 5 years, of effectiveness of this modality of research training for undergraduates. At the end of the program, the trainees are tracked by the OMA. Students are encouraged to apply for a second summer in this program. When appropriate, individual students are encouraged to apply to the various graduate programs at the University of Florida, especially to the Interdisciplinary Program in Biomedical Sciences, but also to Ph.D., M.D., D.V.M., and Pharm.D. programs. We want to make our trainees aware of the power of basic research, especially in the cardiovascular sciences, so that they will be motivated to choose careers in research and to successfully initiate graduate-level training. We will be a success if we improve recruitment and success of under-represented minorities in academic science. This program is designed to increase the number of students from under-represented populations (minorities, students with disabilities, and students from disadvantaged backgrounds) choosing careers in biomedical science. The long-term goal is to strengthen the effectiveness and relevance of biomedical science by increasing the diversity of the scientists who are performing hypothesis-driven research. (End of )
Keywords: Basic Research; Basic Science; Biomedical Research; Cardiovascular; Cardiovascular Body System; Cardiovascular system; Cardiovascular system (all sites); Chair; Chairman; Chairperson; Chairwoman; D.V.M.; DVM; Development; Disabled Persons; Disabled Population; Disadvantaged; Doctor of Medicine; Doctor of Pharmacy; Doctor of Philosophy; Doctor of Veterinary Medicine; Education; Educational Achievement; Educational Status; Educational aspects; Effectiveness; Evaluation; Exposure to; Faculty; Florida; Funding; Goals; Grant; Handicapped; Health Care Professional; Health Professional; Health Sciences; Health profession; Healthcare professional; Healthcare worker; Individual; Instruction; Knowledge; Laboratories; Laboratory Research; Lectures; Lectures (PT); Lectures [Publication Type]; Lung; M.D.; Medical; Medicine; Mentors; Minority; Mission; Modality; National Heart, Lung, and Blood Institute; Organ System, Cardiovascular; Outcome; People with Disabilities; Persons with Disabilities; Ph.D.; PhD; Pharm.D.; PharmD; Pharmacies; Pharmacy facility; Population; Program Effectiveness; Programs (PT); Programs [Publication Type]; Qualifying; Recruitment Activity; Reflex control; Reporting; Research; Research Training; Respiratory System, Lung; Role; Schools; Science; Science of Medicine; Scientist; Series; Structure; Students; Training; Training Programs; Underrepresented Minority; Universities; Vascular, Heart; Veterinary Medicine; Wood; Wood material; ing; base; career; circulatory system; college; conference; design; designing; disability; disabled; disabled people; educational level; experience; fetal; improved; interest; lectures; member; professor; programs; public health relevance; pulmonary; recruit; responsible research conduct; social role; success; symposium; training achievement; training level; training status; under-represented minority; underserved minority
Relevance: This program is designed to increase the number of students from under-represented populations (minorities, students with disabilities, and students from disadvantaged backgrounds) choosing careers in biomedical science. The long-term goal is to strengthen the effectiveness and relevance of biomedical science by increasing the diversity of the scientists who are performing hypothesis-driven research
Project start date: 2010-06-01
Project end date: 2015-05-31
Budget start date: 1-JUN-2010
Budget end date: 31-MAY-2011
PFA/PA: RFA-HL-10-013
1R25HL103181-01 (2010): $118276
TRAINING IN ENDOCRINE, METABOLIC, AND PRENATAL BASIS OF CHRONIC KIDNEY DISEASE
Charles E Wood, Professor
University Of Florida, 219 Grinter Hall, Gainesville, Fl 32611-5500
Grant 5T32DK076541-03 from National Institute Of Diabetes And Digestive And Kidney Diseases
Abstract: This is a revised application for a training program in Endocrine, Metabolic, and Perinatal Basis of Chronic Kidney Disease to support 3 predoctoral trainees. The overall goal is to produce top quality independent investigators with a strong translational approach who can develop and sustain outstanding research programs. The training faculty consists of 23 mentors from 6 departments in the Colleges of Medicine, Pharmacy, and Veterinary Medicine. The faculty consists of basic scientists and clinician-scientists with a wide range of interests and expertise, much of which is focused on endocrine-cardiorenal interactions. The predoctoral trainees will be recruited and trained through the College of Medicine´s Interdisciplinary Program in Biomedical Sciences (IDP). The pool of trainee grant eligible candidates from the entire US has averaged 170/year during the past 3 years with ~ 50/year entering the training program. These trainees enter with an average combined verbal plus quantitative GRE scores of ~1200-1250, and undergraduate GPAs of ~3.5. The IDP provides comprehensive lecture and laboratory courses as well as laboratory rotations and advanced course work in specialized disciplines. Subsequent training focuses on independent research in the laboratory of choice as well as supplemental training in development of communication skills and ethical aspects of research. A core curriculum for this training program has been designed with the intent of providing the students with the knowledge appropriate for researchers working on the endocrine, metabolic, and prenatal basis of chronic kidney disease. The predoctoral training usually takes ~ 5 years with the first year provided by the respective college, an average of 3-4 years support anticipated from the training grant and additional funds supplied by the mentors research grants
Keywords: Chronic Kidney Failure; Chronic Renal Disease; Endocrine; Kidney Failure, Chronic; Metabolic; Renal Failure, Chronic; Training; base; chronic kidney disease; prenatal; unborn
Project start date: 2008-06-01
Project end date: 2013-05-31
Budget start date: 1-JUN-2010
Budget end date: 31-MAY-2011
5T32DK076541-03 (2010): $67870
5T32DK076541-02 (2009): $67462
RENAL TRANSPORTERS AND FETAL NEUROENDOCRINOLOGY
Charles E Wood, Professor
University Of Florida, 219 Grinter Hall, Gainesville, Fl 32611-5500
Grant 5R01HD057561-02 from Eunice Kennedy Shriver National Institute Of Child Health & Human Development
Abstract: The overall goal of the experiments performed in this laboratory are to identify the mechanisms controlling the activity of the hypothalamus-pituitary-adrenal (HPA) axis in fetal sheep. Providing a more complete understanding of the activity of the HPA axis will be key to understanding fetal stress, homeostasis, and (in sheep and perhaps in other species) the control of parturition. In past years, we have investigated several of the physiological and endocrine mechanisms controlling the activity of the ovine fetal HPA axis. We have reported that estrogen potently stimulates the fetal HPA axis, that the major circulating form of estradiol is estradiol-3-sulfate, and that exogenous estradiol-3-sulfate effectively stimulates fetal HPA axis activity. We have hypothesized that estradiol-3-sulfate could be taken up by the fetal brain directly through one or more organic anion transporters (OAT´s), transporters that are known to transport sulfoconjugated estrogens. We have also hypothesized that the estradiol-3- sulfate might be deconjugated prior to both uptake and action. The proposed experiments are designed to test these hypotheses mechanistically. Specifically, we propose three specific aims 1) to elucidate the roles of Organic Anion Transporters (OAT´s) and steroid sulfatase (STS) in the uptake of sulfoconjugated estrogens by the fetal brain; 2) to test OAT´s as mediators of estradiol-3-sulfate action in the fetal HPA axis; and 4) to test the physiological roles of estrogen receptors in HPA Axis responses to estradiol-3-sulfate. To achieve these aims, we will perform experiments using a combination of in vivo, pharmacological, biochemical, and molecular techniques. Together, these techniques will allow us to quantify estradiol-3-sulfate secretion and clearance kinetics and brain uptake in vivo, and use specific blockers of OAT and STS activity to test the roles played by these transport and deconjugation systems in vivo. Using physiological, biochemical, and molecular techniques well established in this laboratory, we will also be able to test the roles of these systems in the HPA axis response to estradiol-3-sulfate. We anticipate that the results of these studies will lead to the design of pharmacologic strategies for manipulating fetal HPA activity in utero. Fetal stress is a prevalent cause of fetal death and morbidity in utero. Nevertheless, little is known about the mechanisms controlling the fetal stress hormones and we lack safe and effective ways of manipulating fetal stress hormone secretion. This proposal is aimed at providing a novel understanding of fetal stress hormones and novel approaches towards manipulating the fetal stress response
Keywords: 3 Beta-Hydroxysteroid Sulfate Sulfatase; ADRGND; Adrenal Glands; Adrenals; Aeroseb-HC; Applications Grants; Aquadiol; Arylsulphatase C; Autoregulation; Binding; Binding (Molecular Function); Biochemical; Birth; Blood; Blood - brain barrier anatomy; Blood Plasma; Blood-Brain Barrier; Body Tissues; Brain; Brain region; Cells; Cetacort; Chemotherapy-Hormones/Steroids; Cholesterol Sulfatase; Cholesterol Sulfate Sulfatase; Cort-Dome; Cortef; Cortenema; Cortisol; Cortispray; Cortril; DHEA Sulfatase; DNA; Data; Dehydroepiandrosterone Sulfate Sulfatase; Deoxyribonucleic Acid; Dermacort; Dimenformon; Diogyn; Diogynets; Eldecort; Encephalon; Encephalons; Endocrine; Endocrine Gland Secretion; Environment; Estra-1, 3, 5(10)-triene-3, 17-diol (17beta)-; Estrace; Estradiol; Estradiol-17 beta; Estradiol-17beta; Estraldine; Estrogen Receptors; Estrogenic Agents; Estrogenic Compounds; Estrogens; Estrone Sulfate Sulfatase; Estrone Sulfate Sulfohydrolase; Family; Fetal Activity; Fetal Death; Fetal Movement; Fetus; Gene Transcription; Genetic Transcription; Gestation; Goals; Grant Proposals; Grants, Applications; Hemato-Encephalic Barrier; Homeostasis; Hormones; Hydrocortisone; Hydrocortone; Hypophysis; Hypophysis Cerebri; Hypothalamic structure; Hypothalamus; Hytone; Infusion; Infusion procedures; Isoforms; Kidney; Kinetic; Kinetics; Laboratories; Lead; Mediating; Mediator; Mediator of Activation; Mediator of activation protein; Membrane Transport Proteins, Organic Anion; Methods and Techniques; Methods, Other; Modeling; Molecular; Molecular Interaction; Morbidity; Morbidity - disease rate; Nervous System, Brain; Nervous System, Pituitary; Neuroendocrinology; Nutracort; Organic Anion Transporters; Ovis; Ovocyclin; Ovocylin; Parturition; Pb element; Physiologic; Physiological; Physiological Homeostasis; Pituitary; Pituitary Gland; Pituitary-Adrenal System; Plasma; Play; Pregn-4-ene-3, 20-dione, 11, 17, 21-trihydroxy-, (11beta)-; Pregnancy; Pregnant Women; Preparation; Process; Proctocort; Progynon; Protein Isoforms; RNA Expression; Reporting; Reticuloendothelial System, Blood; Reticuloendothelial System, Serum, Plasma; Role; Serum, Plasma; Sheep; Source; Staging; Steroid Compound; Steroid Sulfohydrolase; Steroid Sulphatase; Steroids; Sterol Sulfatase; Steryl-sulfatase; Sterylsulfatase; Stress; Sulfatases; System; System, LOINC Axis 4; Techniques; Testing; Therapeutic Estradiol; Therapeutic Estrogen; Therapeutic Hormone; Therapeutic Hydrocortisone; Time; Tissues; Transcription; Transcription, Genetic; Urinary System, Kidney; Viscera; biological adaptation to stress; design; designing; estradiol-3-sulfate; experiment; experimental research; experimental study; fetal; fetal stress; fetus death; heavy metal Pb; heavy metal lead; hypothalamic; in utero; in vivo; lung maturation; member; new approaches; novel; novel approaches; novel strategies; novel strategy; pituitary adrenal axis; prenatal stress; public health relevance; reaction; crisis; renal; research study; response; social role; stress response; stress; reaction; suprarenal gland; uptake
Relevance: Fetal stress is a prevalent cause of fetal death and morbidity in utero. Neverthless, little is known about the mechanisms controlling the fetal stress hormones and we lack safe and effective ways of manipulating fetal stress hormone secretion. This proposal is aimed at providing a novel understanding of fetal stress hormones and novel approaches towards manipulating the fetal stress response
Project start date: 2009-01-15
Project end date: 2013-12-31
Budget start date: 1-JAN-2010
Budget end date: 31-DEC-2010
PFA/PA: PA-07-070
5R01HD057561-02 (2010): $270854
3R01HD057561-01A2S1 (2009): $86063
Sponsored Links Excellgen http://Excellgen.com
Estrogen Influences On Fetal Adrenocorticotropin
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 5R01HD042135-05 from National Institute Of Child Health And Human Development IRG: HED
Abstract: The overall goal of the experiments performed in this laboratory are to identify the mechanisms controlling the activity of the hypothalamus-pituitary-adrenal (HPA) axis in fetal sheep. Providing a more complete understanding of the activity of the HPA axis will be key to understanding fetal stress, homeostasis, and (in sheep and perhaps in other species) the control of parturition. In past years, we have investigated several of the physiological and endocrine mechanisms controlling the activity of the ovine fetal HPA axis. Recently, we have reported that estrogen potently stimulates the activity of the fetal HPA axis. The present proposal is to investigate this endocrine interaction more completely to elucidate the role of brain prostanoids as mediators of this interaction. Specifically, we propose two general aims 1) to elucidate the spontaneous (preparturient) effects of development and endogenous estrogens on brain prostanoids; and 2) to elucidate the effects of exogenous estrogen on brain prostanoids to elucidate the influence of estrogen on prostaglandin endoperoxide synthase (PGHS) isoforms in the fetal central nervous system and to demonstrate that estrogen-stimulated prostaglandin synthesis mediates the effect of estrogen on fetal ACTH secretion. To achieve these aims, we will perform experiments using in vivo, biochemical, and molecular techniques designed to study the prostaglandin biosynthesis system at the mRNA, protein, and posttranslational processing levels. All of the experiments will be based on the study of the HPA axis control in chronically-catheterized fetal sheep. Experiments designed for the first aim will include the measurement of brain PGHS-1 and PGHS-2 abundance and brain prostanoid production in response to estrogen treatment of fetal sheep, and other experiments which will test the effect of blockade of endogenous estrogen synthesis on HPA control, expression of PGHS isoforms and generation of prostaglandins within the brain. Experiments designed for the second aim will reveal the number of days required for estrogen stimulation of HPA function. Experiments designed for the second aim will investigate the effect of exogenous (physiological) estrogen administration on PGHS-1 and PGHS-2 expression, posttranslational processing, and colocalization with either known forms of the estrogen receptor.
Keywords: adrenocorticotropic hormone, estrogen, hormone regulation /control mechanism, mammalian embryology, neuroendocrine system, prostaglandin, prostaglandin endoperoxide synthase, developmental neurobiology, estrogen receptor, hypothalamic pituitary adrenal axis, posttranslational modification, sheep
Project start date: 2002-09-27
Project end date: 2008-08-31
5R01HD042135-05 (2006): $284033
5R01HD042135-04 (2005): $291211
5R01HD042135-03 (2004): $291523
5R01HD042135-02 (2003): $290988
1R01HD042135-01A1 (2002): $291079
FETAL RESPONSES TO SULFOCONJUGATED ESTROGENS
Charles E Wood, Professor And Chair
Physiology & Functional Genomicsuniversity Of Florida
219 Grinter Hall
gainesville, Fl 326115500
Grant 5R03HD038733-02 from Eunice Kennedy Shriver National Institute Of Child Health & Human Development IRG: HED
Abstract: The overall goal of the experiments performed in this laboratory are to identify the mechanisms controlling the activity of the hypothalamus-pituitary-adrenal (HPA) axis in fetal sheep. Providing a more complete understanding of the activity of the HPA axis will be key to understanding fetal stress, homeostasis, and (in sheep and perhaps in other species) the control of parturition. In past years, we have investigated several of the physiological and endocrine mechanisms controlling the activity of the ovine fetal HPA axis. Recently, we have reported that estrogen potently stimulates the activity of the fetal HPA axis. At the end of gestation in sheep and in other species, there is an increase in the plasma concentrations of estrogen. The estrogen in fetal plasma is both unconjugated and sulfoconjugated. The present proposal is assess the efficacy of sulfoconjugated estrogens in the stimulation of the fetal HPA axis. To achieve these aims, we will perform experiments using in vivo, biochemical, and molecular techniques. All of the experiments will be based on the study of the HPA axis control in chronically-catheterized fetal sheep. The proposed experiments will test the hypothesis that estrogen receptors and steroid sulfatase (STS) are co-localized in neurons within brain regions which are important for control of the HPA axis. Additional experiments will quantify the transfer of sulfoconjugated estrogens across the blood-brain barrier, and will test the effect of STS inhibition on the stimulation of fetal HPA function by both sulfoconjugated and unconjugated estrogens. We propose that rising concentrations of estrogens in fetal plasma at the end of gestation, themselves dependent upon increasing fetal HPA axis activity, contribute to the function of an endocrine positive feedback loop which augments both basal and stimulated fetal ACTH secretion and ultimately culminates in the birth of the fetus. The experiments proposed in this grant application will provide evidence that sulfoconjugated estrogens can be biologically active within the fetal brain and that they can be physiologically relevant in terms of fetal HPA axis control. We believe that this is highly logical, given the high activity of STS within the fetal brain and given the incomplete nature of the fetal blood-brain barrier. These experiments will provide important information which will be of critical importance for submission of an R01 application focused on STS within the fetal brain. These experiments will likely reveal an enzymatic step within the HPA-estrogen positive feedback loop which is pharmacologically manipulable. If so, the results are relevant to the control of parturition as well as the control of responses to stress
Keywords: adrenocorticotropic hormone, chemical conjugate, estrogen, hormone regulation /control mechanism, hypothalamic pituitary adrenal axis, prenatal stress, sulfur birth, blood brain barrier, enzyme activity, enzyme feedback, estrogen receptor, gestational age, homeostasis, neuron, pharmacokinetics, protein localization, sulfatase embryo /fetus, sheep
Project start date: 2000-06-01
Project end date: 2002-05-31
5R03HD038733-02 (2001): $72250
1R03HD038733-01 (2000): $72250
CONTROL OF CORTICOTROPIN IN THE FETUS
Charles E Wood, Professor And Chair
Physiology & Functional Genomicsuniversity Of Florida
219 Grinter Hall
gainesville, Fl 326115500
Grant 5R01HD024250-06 from National Institute Of Child Health And Human Development IRG: HED
Abstract: The hypothalamus-pituitary-adrenal axis in fetal sheep plays an important role in fetal maturation, in the timing of parturition, and in homeostatic responses to stress. Elucidation of the physiological mechanisms controlling this axis will improve our understanding of essential processes that direct the transition from fetal to adult fife. A major focus of experiments in this laboratory has been the study of developmental changes in the sensitivity of the ACTH secretory activity of the hypothalamopituitary unit to negative feedback inhibition by cortisol. Previous experiments in this laboratory have demonstrated that the sensitivity of stimulated ACTH secretion to negative feedback inhibition is high in fetal sheep between 117 and 131 days´ gestation, but is very low in fetal sheep at term. The experiments proposed in the continuation of this project will investigate the mechanism of this decreased negative feedback sensitivity. Specifically, these experiments are designed to test a) the possible role of estrogens, androgens, or progesterone in the reduction of sensitivity to negative feedback sensitivity; b) the possibility that increases in fetal brain levels of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) at the end of gestation desensitizes negative feedback; c) whether changes in hypothalamic or hippocampal glucocorticoid receptor number or synthesis (reflected by changes in the level of glucocorticoid receptor mRNA) mediate changes in negative feedback sensitivity; d) whether estrogen, androgen, or progesterone alter cortisol negative feedback sensitivity by altering glucocorticoid receptor number or mRNA concentration or 11beta-HSD activity in the fetal brain; and 5) the possibility that blockade of 11beta-HSD or blockade of estrogen action in the brain prolongs gestation. Chronically catheterized, unanesthetized fetal sheep will be studied. The fetal sheep will be subjected to intracerebroventricular infusions of estrogen, androgen, progesterone, or blockers of 11beta-HSD or of estrogen. In experiments designed to investigate negative feedback sensitivity, nitroprusside-induced hypotension as a stimulus to ACTH secretion. Blood samples will be analyzed for plasma concentrations of ACTH, and cortisol using specific radioimmunoassays. Fetal blood pressure and heart rate will be monitored using a microcomputer on-line. These experiments represent an extension of the work initiated in the first three years of this project. The goal of the experiments is, to investigate the mechanism of the change in feedback sensitivity at term and to investigate the effect of the alterations in feedback sensitivity on the length of gestation
Project start date: 1988-06-01
Project end date: 1996-06-30
5R01HD024250-06 (1994): $154793
FETAL REFLEX RESPONSES TO CEREBRAL HYPOPERFUSION
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 5R01HD033053-02 from National Institute Of Child Health And Human Development IRG: ZRG2
Abstract: Fetal sheep respond to hypotension with reflex hormonal and hemodynamic responses which return blood pressure to normal levels. We have demonstrated that the reflex vasomotor and heart rate responses and the reflex hormonal responses are mediated by both baroreceptor- and chemoreceptor- reflexes. However, a significant portion of the reflex hormonal and hemodynamic responses to hypotension are not mediated by either peripheral baroreceptors or chemoreceptors. We have hypothesized that hypotension reduces fetal cerebral blood flow and that the reduced blood flow is transduced within the brain to stimulate hormonal and hemodynamic responses. Specifically, we have hypothesized that reductions in cerebral blood flow stimulate the local production of prostanoids within the central nervous system which, in turn, stimulate adrenocorticotropin (ACTH) and cardiovascular responses. The proposed experiments will focus on two prostanoids, prostaglandin E2 (PGE2) and thromboxane A2 (TxA2), which we know to potently alter blood pressure, heart rate, and ACTH secretion by an action at the brain. In support of this hypothesis, we have demonstrated that 1) a significant proportion of the reflex hormonal and hemodynamic responses to hypotension in the fetus is not dependent upon arterial or cardiopulmonary baroreceptors or chemoreceptors; 2) both PGE2 and TxA2 act at the brain to alter cardiovascular and endocrine function in both the fetus and the adult animal; and 3) prostanoids can be made within the brain. Results of experiments from other laboratories demonstrate that both PGE2 and TxA2 are produced within the central nervous system in response to a reduction in cerebral blood flow. In all experiments, we will use chronically catheterized and instrumented fetal sheep and will measure ACTH and cardiovascular (blood pressure, heart rate, and distribution of combined ventricular output). There are four studies proposed. In the first study, we will measure responses to reduced cerebral perfusion pressure. From data existing in the literature, we expect that reductions in cerebral perfusion pressure will reduce cerebral blood flow and will stimulate local (prostanoid generation) and reflex (hormonal and hemodynamic) responses. In the second study, we will measure hormonal and hemodynamic responses to administration of U46619, a TxA2 mimetic, or PGE2, into the cerebral ventricles to test the specific effects of these prostanoids on ACTH and cardiovascular responses. In the third study, we will test the role of endogenously generated TxA2 and PGE2 on the reflex responses to reduced fetal cerebral blood flow. In the fourth study, we will use immunocytochemistry to determine the localization of the prostanoid synthetic enzymes, PGHS1, PGHS2 and thromboxane synthetase, in the regions of the brain, hypothalamus and brainstem, responsible for control of ACTH and cardiovascular function. We will also use Western blots to determine if the levels of these enzymes are altered with hypoperfusion. We believe that, because of the potent effects of these prostanoids on the fetal brain, the proposed experiments will identify an important mechanism for the maintenance of blood pressure in the fetus. Ultimately, understanding the mechanisms important for the control of fetal blood pressure is important for the clinical management of women in late gestation and their fetuses. Clinical management of late-gestation fetal human patients has included, recently, fetal surgery for correction of congenital anomalies. Surgery without knowledge of mechani5R01AG011441-02
Keywords: 1994
Project start date: 1996-05-03
Project end date: 2000-04-30
5R01HD033053-02 (1997): $161663
5R01HD033053-04 (1999): $174853
Sponsored Links Excellgen http://Excellgen.com
5R01HD033053-03 (1998): $168129
PROGESTIN ACTIONS IN THE PRIMATE BREAST AND UTERUS
Charles E Wood, Assistant Professor
Wake Forest University Health Sciences, Winston-salem, Nc 27157
Grant 5K01RR021322-05 from National Center For Research Resources
Abstract: Dr. Charles Wood is seeking SERCA support to advance development as an independent investigator in comparative medicine. The career development plan will combine the unique resources of the Wake Forest University School of Medicine with expertise from international leaders in cancer research. The research plan will complement the candidate´s current skills in pathology with a strong focus in molecular analyses of breast tissue. The overall research objective of this proposal is to evaluate the breast cancer risk profile of different postmenopausal hormone therapies and to investigate underlying mechanisms. Over 10 million postmenopausal women in the U.S. currently take hormone therapy (HT). The most common type of HT for women in the U.S. with a uterus is the combination of conjugated equine estrogens (CEE) and medroxyprogesterone acetate (MPA). Recent evidence indicates that the addition of MPA significantly increases the risk of breast cancer, and this has led to considerable uncertainty and concern regarding progestin use. A major question in women´s health at this time is whether these adverse effects are specific to MPA or characteristic of all progestins. Given the diverse and in some cases opposing cellular actions of different progestin types, it is likely that these compounds have distinctive effects in the breast. In Phase 1 of this project we will use a surgically postmenopausal non-human primate model to compare the breast effects of MPA and natural progesterone (P4) when given with estradiol. We hypothesize that these progestins will have type-specific effects on proliferation, apoptosis, and estrogen metabolism in the breast and that P4will have the most favorable profile. The aims of the project are as follows (1) to determine progestin effects on breast proliferation and apoptosis; (2) to evaluate the glucocorticoid activities of MPA and P4 in relation to cell survival; and (3) to determine progestin effects on estrogen metabolism. In the second phase we will contrast the breast cancer risk profile of the optimal estrogen+progestin combination from Phase 1 with that of alternative hormone therapies. This work will have immediate public health relevance to postmenopausal women seeking the safest form of hormone therapy
Keywords: (17Beta)-17-hydroxyandrost-4-en-3-one; (6 alpha)-17-(Acetoxy)-6-methylpregn-4-ene-3, 20-dione; 17-beta-Hydroxy-4-Androsten-3-one; 17Alpha-acetoxy-6alpha-methylprogesterone; 6-Alpha-methyl-17alpha-acetoxyprogesterone; 6-alpha-Methyl-17alpha-hydroxyprogesterone Acetate; API4; ARO; ARO1; Advanced Development; Adverse effects; Androgenic Agents; Androgenic Compounds; Androgens; Androst-4-en-17beta-ol-3-one; Apopain; Apoptosis; Apoptosis Inhibitor 4; Apoptosis Inhibitor Survivin; Apoptosis Pathway; Aquadiol; BCEI; BIRC5; Baculoviral IAP Repeat-Containing 5 (Survivin); Baculoviral IAP Repeat-Containing Protein 5; Breast; Breast Tissue; CASP-3; CASP3; CC3; CPP-32; CPP32; CPP32 protein; CPP32B; CPP32beta; CPV1; CYAR; CYP19; CYP19A1; CYP19A1 gene; Cancer of Breast; Caspase 3, Apoptosis-Related Cysteine Protease; Cell Death, Programmed; Cell Survival; Cell Viability; Characteristics; Cleaved cell; Clinical Research; Clinical Study; Complement; Complement Proteins; Conjugated Equine Estrogens; Corlutina; Corluvite; Corpus Luteum Hormone; Cyclogest; Cysteine Protease CPP32; D21S21; DNA Molecular Biology; Delta4-androsten-17beta-ol-3-one; Delta4-pregnene-3, 20-dione; Depo-Medroxyprogesterone Acetate; Development Plans; Dimenformon; Diogyn; Diogynets; EPR-1; ESTs; Endocrine Therapy; Enzymes; Equine Estrogens, Conjugated; Estra-1, 3, 5(10)-triene-3, 17-diol (17beta)-; Estrace; Estradiol; Estradiol-17 beta; Estradiol-17beta; Estraldine; Estrogen Metabolism; Estrogenic Agents; Estrogenic Compounds; Estrogens; Exhibits; Expressed Sequence Tags; Female Health; Genital System, Female, Uterus; Gestagenic Agents; Gestagens; Gestiron; Gestone; Glucocorticoids; HPS2; HTATIP2; HTATIP2 gene; Hormonal; Hormonal Therapy; IAP4; Institution; International; Investigators; Keoxifene; Lipo-Lutin; Luteohormone; Lutocyclin; Lutocylin M; Lutogyl; Lutromone; MPA; Malignant Tumor of the Breast; Malignant neoplasm of breast; Mammals, Primates; Mammary Gland Parenchyma; Mammary Gland Tissue; Medicine; Medroxyprogesterone 17-Acetate; Medroxyprogesterone Acetate; Medroxyprogesteroni Acetas; Methylacetoxyprogesterone; Metipreg; Modeling; Molecular; Molecular Biology; Oral; Ovocyclin; Ovocylin; P-450AROM; PARP Cleavage Protease; Pathology; Phase; Plans, Development; Post-Menopause; Post-menopausal Period; Postmenopausal Period; Postmenopause; Pregn-4-ene-3, 20-dione; Pregn-4-ene-3, 20-dione, 17-(acetyloxy)-6-methyl-, (6alpha)-; Pregnenedione; Primates; Progestagenic Agents; Progestasert; Progestational Agents; Progestational Compounds; Progestational Hormones; Progesterone; Progesterone Agents; Progestins; Progestogel; Progestogens; Progestol; Progeston; Progynon; Prolidon; Proliferation Marker; Proluton; Raloxifene; Reproductive Endocrinology; Research; Research Personnel; Research Resources; Research Training; Researchers; Resources; Risk; Risk Marker; SCA-1; SERMs; SREBP Cleavage Activity 1; Schools, Medical; Science of Medicine; Selective Estrogen Receptor Modulators; Syngesterone; TFF1; TFF1 gene; TIP30; Testosterone; Therapeutic Androgen; Therapeutic Estradiol; Therapeutic Estrogen; Therapeutic Glucocorticoid; Therapeutic Progesterone; Therapeutic Progestin; Therapeutic Testosterone; Time; Training; Trans-Testosterone; Treatment Side Effects; Uncertainty; Universities; Uterus; Utrogestan; Woman; Women`s Health; Wood; Wood material; Work; Yama; Yama protein; [6-Hydroxy-2-(4-hydroxyphenyl)-benzo[b]thien-3-yl][4-[2-(1-piperidinyl)ethoxy]phenyl]metha; anticancer research; cancer research; cancer risk; career development; caspase-3; cleaved; comparative; cysteine protease P32; doubt; experience; forest; hormone therapy; interdisciplinary approach; malignant breast neoplasm; medical schools; new approaches; non-human primate; nonhuman primate; novel approaches; novel strategies; novel strategy; pNR-2; pS2; post-menopausal; postmenopausal; public health relevance; side effect; skills; survivin; therapy adverse effect; treatment adverse effect; womb
Project start date: 2005-09-19
Project end date: 2010-08-31
Budget start date: 1-SEP-2009
Budget end date: 31-AUG-2010
5K01RR021322-05 (2009): $121927
5K01RR021322-04 (2008): $121927
1K01RR021322-01A1 (2005): $121927
FETAL CARDIOVASCULAR AND ENDOCRINE REFLEX RESPONSES
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 5R01HD033053-09 from National Institute Of Child Health And Human Development IRG: HED
Abstract: Baroreceptor and chemoreceptor reflexes are actively involved in the control of fetal blood pressure and in the maintenance of blood flow to the placenta and to the metabolizing tissues. The present project is an investigation into the mechanism of the baro- and chemoreflexes. In the first funding period of this project, we discovered an important interaction between endogenously generated prostanoids and reflex activity. During the initial funding period, we made the following conclusions 1) Endogenous generation of prostanoids augment the reflex mechanisms controlling cardiovascular and endocrine responses to hypotension. 2) Neurons, as well as vasculature, contain the enzymes (PGHS-1, PGHS-2, and thromboxane synthase) needed for synthesis of prostanoids. These enzymes are found in neurons important for reflex control of the cardiovascular system (in nucleus of the tractus solitarius, rostral and ventrolateral medulla, intermediolateral column of the spinal cord, paraventricular nucleus). There are ontogenetic changes in the concentrations of these enzymes. 3) PGE2 is released into the interstitial fluid of the brain and thromboxane A2 in released into the bloodstream during hypotension. 4) The so-call inducible form of cyclooxygenase, PGHS-2, is upregulated at both the protein and mRNA level in fetal brain after hypotension. The upregulation of the protein for PGHS-2 is both in neurons and vasculature in the cardiovascular reflex-controlling regions of the fetal brain. 5) Injections of PGE2 or U46619 (thromboxane mimetic) into the cerebrospinal fluid of fetal sheep stimulates responses which are similar to the efferent responses to hypotension (vasoconstriction, secretion of adrenocorticotropin and vasopressin). These discoveries suggest that the production of prostanoids within afferent neural pathways stimulate or modulate reflex responses to cerebral hypoperfusion in the fetus. These findings have led us to propose the following specific aims, to propose to answer the following questions 1) what are the relative contributions of PGHS-1 and PGHS-2 to the control of fetal reflex responses to hypotension? We will answer this question using both in vivo (chronically-catheterized fetal sheep), and in vitro (enzymology) techniques. 2) Does sinoaortic denervation alter the expression and distribution of PGHS-1 and PGHS-2 in fetal brain and does sinoaortic denervation block the PGHS-2 response to hypotension? We will answer this question using immunohistochemistry and RT-PCR. 3) Does hypotension cause the phosphorylation of PGHS-2, rapidly increasing its activity? We will answer this question using immunoprecipitation and immunoblot techniques. 4) Do prostanoids inhibit chloride uptake by GABAA receptors? We will answer this question using synaptoneurosomes (chloride uptake), in situ quantitative autoradiography, and immunohistochemical co-localization studies. In the proposed 5-year continuation of this project, the answers to these questions will significantly enhance our understanding of the mechanism by which prostanoids act within the brain to alter cardiovascular function.
Keywords: cardiovascular function, embryo /fetus, endocrine gland /system, enzyme induction /repression, hormone regulation /control mechanism, hypotension, pregnancy circulation, prostaglandin endoperoxide synthase, GABA receptor, adrenocorticotropic hormone, baroreflex, chemoreceptor, chloride ion, gene expression, hemodynamics, phosphorylation, prostaglandin E, protein localization, thromboxane, autoradiography, denervation, embryo /fetus monitoring, immunocytochemistry, polymerase chain reaction, sheep, western blotting
Project start date: 1996-05-03
Project end date: 2006-11-30
5R01HD033053-09 (2005): $256835
5R01HD033053-08 (2004): $257131
5R01HD033053-07 (2003): $257402
5R01HD033053-06 (2002): $257647
Charles E Wood
University Of Florida
Project start date: 2009-01-15
Project end date: 2013-12-31
FETAL CARDIOVASCULAR AND ENDOCRINE REFLEX RESPONSES
Charles E Wood
Department/ Educational Institution Type:
Grant 5R01HD033053-14 from Eunice Kennedy Shriver National Institute Of Child Health & Human Development
Keywords: (5Z, 8Z, 11Z, 14Z)-Icosa-5, 8, 11, 14-tetraenoate, hydrogen-donor[{..}]oxygen oxidoreductase; 1-(4-chlorobenzoyl)-5-methoxy- 2-methyl-1-H-indole-3-acetic acid; 1H-Indole-3-acetic acid, 1-(4-chlorobenzoyl)-5-methoxy-2-methyl-; 2-(2-Chlorophenyl)-2-(methylamino)cyclohexa; ACTH; ACTH (1-39); Acute; Adrenocorticotropic Hormone; Adrenocorticotropin; Aeroseb-HC; Anabolism; Anoxia, Cellular; Anti-Hypertensive Agents; Anti-Hypertensive Drugs; Anti-Hypertensives; Antidiuretic Hormone; Antidiuretic Hormones; Antihypertensive Agents; Antihypertensive Drugs; Antihypertensives; Arachidonic Acid Cyclooxygenase; Area; Autoregulation; Baroreceptors; base; Behavior; beta-Hypophamine; Biochemistry; biological adaptation to stress; Biological Models; biological signal transduction; biosynthesis; Bleeding; Blood flow; Blood gas; blood loss; Blood Pressure; Blood Pressure, Low; Body Tissues; Brain; Brain region; Cardiopulmonary; Cardiovascular; Cardiovascular Body System; cardiovascular function; Cardiovascular Physiology; Cardiovascular system; Cardiovascular system (all sites); Cell Anoxia; Cell Communication and Signaling; Cell Culture Techniques; Cell Hypoxia; Cell Signaling; Cells; Central Nervous System; cerebral hypoperfusion; Cerebral perfusion pressure; Cetacort; Chemistry, Biological; Chemoreceptors; circulatory system; clinical relevance; clinically relevant; Common Rat Strains; Cort-Dome; Cortef; Cortenema; Corticotropin; Corticotropin (1-39); Cortisol; Cortispray; Cortril; COX; COX-1; COX-1 protein; COX-2; COX-2 protein; COX1; COX2; COX2 enzyme; COX3; Cyclo-Oxygenase; cyclo-oxygenase I; cyclo-oxygenase II; Cyclo-Oxygenase-1; Cyclo-Oxygenase-2; Cyclooxygenase; cyclooxygenase 1; cyclooxygenase 2; Cyclooxygenase 3; D-Glucose; Denervation; deprivation; Dermacort; design; designing; Dextrose; Dinoprostone; Dissociative Anesthetics; Eldecort; Embryonic Tissue, Placenta; Encephalon; Encephalons; Endocrine; endoperoxide isomerase; Enzymes; experiment; experimental research; experimental study; Fatty Acid Cyclo-Oxygenase; Fatty Acid Cyclooxygenase; fetal; fetal blood; fetal stress; Fetus; Funding; Gene Action Regulation; Gene Expression; Gene Expression Regulation; Gene Proteins; Gene Regulation; Gene Regulation Process; Generations; Glucose; Goals; hatching; hCOX-2; hemodynamics; Hemorrhage; Homeostasis; Hormonal; Human; Human, General; Hydrocortisone; Hydrocortone; Hydroperoxide Cyclase; Hyporeflexia; Hypotension; Hypotensive Agent; Hypotensive Drugs; Hypotensives; Hypovolemia; Hypoxia; Hypoxia, Cellular; Hypoxic; Hytone; improved; in vivo; in vivo Model; Indocin; Indometacin; Indomethacin; inhibitor; inhibitor/antagonist; Intercellular Fluid; interest; Interruption; Interstitial Fluids; Intracellular Communication and Signaling; Investigation; Investigators; Ischemia; Ketamine; Left; Literature; Maintenance; Maintenances; Mammals, Rats; Man (Taxonomy); Man, Modern; Mediating; Mediation; Mediator; Mediator of Activation; Mediator of activation protein; Messenger RNA; Methods and Techniques; Methods, Other; Minor; Model System; Modeling; Models, Biologic; Molecular; mRNA; N methyl D aspartate; N Methyl D aspartic Acid; N-Methyl-D-aspartate; N-Methyl-D-Aspartate Receptors; N-Methylaspartate; Negotiating; Negotiation; Nerve Cells; Nerve Impulse Transmission; Nerve Transmission; Nerve Unit; Nervous System, Brain; Nervous System, CNS; Neural Cell; Neuraxis; Neuroblastoma; Neuroblastoma (Schwannian Stroma-Poor); Neurocyte; Neuroendocrine; Neuroendocrine System; neuronal; Neuronal Transmission; Neurons; Neurosecretory Systems; neurotransmission; NMDA; NMDA Receptor-Ionophore Complex; NMDA Receptors; Nutracort; O element; O2 element; Organ System, Cardiovascular; Ovis; Oxygen; Oxygen Deficiency; pathway; Pathway interactions; Pattern; PGE2; PGE2 alpha; PGE2 isomerase; PGE2alpha; PGG/HS; PGH Synthase; PGH Synthase 1; PGH Synthase 2; PGH2 Synthetase; PGHS-1; PGHS-2; PGHS2; PGR2 E-isomerase; Phosphate Buffer; PHS II; PHS-2; PHS1; Physiological Homeostasis; Placenta; Placenta-Tissue, Cells; Placentoma, Normal; Placentome; Pregn-4-ene-3, 20-dione, 11, 17, 21-trihydroxy-, (11beta)-; prenatal stress; Pressoreceptors; Process; Proctocort; Production; programs; Programs (PT); Programs [Publication Type]; Progress Reports; Prosta-5, 13-dien-1-oic acid, 11, 15-dihydroxy-9-oxo-, (5Z, 11alpha, 13E, 15S)-; Prostaglandin Cyclo-Oxygenase; Prostaglandin Cyclooxygenase; prostaglandin E isomerase; prostaglandin E synthase; Prostaglandin E2; Prostaglandin E2 alpha; prostaglandin E2 isomerase; Prostaglandin E2alpha; prostaglandin endoperoxide E isomerase; Prostaglandin Endoperoxide Synthetase; Prostaglandin G-H Synthase; Prostaglandin G/H Synthase 1; Prostaglandin G/H Synthase 2; Prostaglandin G/H Synthase and Cyclooxygenase; Prostaglandin H Synthase; prostaglandin H synthase-1; prostaglandin H synthase-2; prostaglandin H2 E-isomerase; Prostaglandin H2 Synthase; Prostaglandin H2 Synthase 1; Prostaglandin H2 Synthase 2; Prostaglandin H2 Synthetase; prostaglandin H2-prostaglandin E2 isomerase; Prostaglandin Inhibition; prostaglandin R2 E-isomerase; Prostaglandin Synthase; Prostaglandin Synthetase; Prostaglandin-Endoperoxide Synthase; Prostaglandin-Endoperoxide Synthase 1; Prostaglandin-Endoperoxide Synthase 2; Prostaglandins; Prostanoids; protein expression; Protein Gene Products; PTGS1; PTGS2; PTGS2 gene; Rat; Rattus; reaction; crisis; receptor; Receptor Protein; Receptors, N-Methylaspartate; Reflex; Reflex action; Reflex control; Reflex, Decreased; Reporting; Research Personnel; research study; Researchers; response; RNA, Messenger; Role; Sheep; Signal Transduction; Signal Transduction Systems; Signaling; social role; Solid; Stress; stress response; stress; reaction; Stretch Receptors, Arterial; Stretch Receptors, Vascular; System; System, LOINC Axis 4; Techniques; Testing; Therapeutic Hydrocortisone; Time; Tissues; Up-Regulation; Up-Regulation (Physiology); Upregulation; Vascular Hypotensive Disorder; Vascular, Heart; Vasopressins; Wood; Wood material
Project start date: 1996-05-03
Project end date: 2011-11-30
Budget start date: 1-DEC-2010
Budget end date: 30-NOV-2011
5R01HD033053-14 (2011): $232467
Sponsored Links Excellgen http://Excellgen.com
5R01HD033053-13 (2010): $258810
Progestin Actions In The Primate Breast And Uterus
Charles E Wood
Pathologywake Forest University Health Sciences
medical Center Blvd
winston-salem, Nc 27157
Grant 5K01RR021322-03 from National Center For Research Resources IRG: RIRG
Project start date: 2005-09-19
Project end date: 2010-08-31
5K01RR021322-03 (2007): $121927
5K01RR021322-02 (2006): $121927
SHORT-TERM RESEARCH TRAINING FOR MINORITY STUDENTS
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 5T35HL007930-05 from National Heart, Lung, And Blood Institute IRG: ZHL1
Project start date: 1999-05-01
Project end date: 2004-04-30
5T35HL007930-05 (2003): $58470
FETAL REFLEX RESPONSES TO CEREBRAL HYPOPERFUSION
Charles E Wood, Professor And Chair
University Of Florida 219 Grinter Hall Gainesville, Fl 326115500
Grant 1R01HD033053-01A1 from National Institute Of Child Health And Human Development IRG: ZRG2
Project start date: 1996-05-03
Project end date: 2000-04-30
1R01HD033053-01A1 (1996): $155267