Anthony L Sica - US grants
Affiliations: | SUNY Downstate, Brooklyn, NY, United States |
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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, Anthony L Sica is the likely recipient of the following grants.Years | Recipients | Code | Title / Keywords | Matching score |
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2001 — 2002 | Sica, Anthony Louis | 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. |
Monitoring a Sids Model in Neonatal Swine @ Suny Downstate Medical Center The long-term objective of the proposed research is to evaluate the role of cardiac mechanisms in the etiology of sudden death in the Sudden Infant Death Syndrome (SIDS). Thus this project is directly related to a problem in infant survival and health. The specific aims of the proposed research are designed to test the hypothesis that a developmental anomaly in cardiac innervation could reduce ventricular electrical stability and favor the onset of sudden cardiac death. The research design and surgical methods have been worked out in the previous grant period; newborn swine with surgically induced imbalance in cardiac autonomic innervation will be continuously monitored (24 hrs.) throughout eight postnatal weeks. Those surviving and similarly surgically prepared littermates will be tested (at ages 2,4,6,8 wks) for cardiovascular responses to: (i) hypoxia, (ii) hypercapnia, (iii) stimulation of cardiopulmonary receptors, and (iv) alterations in baroreceptor afferent inputs. Results obtained from study of these possible precipitating factors should reveal the increased susceptibility of the neonate at risk for sudden death. Sleep is the predominant behavioral state of the neonate and ontogeny of EEG sleep in neonates can be monitored by serial EEG recordings. We plan to examine ECG recordings as a function of state determined by VCR tapes of behavior, diaphragmatic EMG and EEG, and correlate these variables against both age and type of denervation. Nonlinear analysis of heart rate variability in infants has revealed an increase in complexity with maturation and our own results included similar findings in piglets. This grant proposal would pursue these findings and the effects of selected cardiac denervation on this complexity, correlating results with sudden death in denervated piglets. Such studies should confirm our working hypothesis regarding the importance of cardiac innervation in the etiology of sudden death in infants. We are, therefore, postulating an abnormality at the effector level, i.e., at the cardiac level, specifically: maturation of the normal innervation of the heart and its reflex control. |
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2001 — 2004 | Sica, Anthony Louis | 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. |
Postnatal Maturation of Cardiovascular Regulatory System @ Suny Downstate Medical Center DESCRIPTION (Verbatim from the application): The overall goal of this proposal is to provide physiological and anatomical indices of maturation within neural networks involved in cardiorespiratory (CV-RESP) regulation. We shall focus on brainstem circuit neurons that mediate the CV-RESP responses to hypercapnic stress because: (a) this circuit plays an essential role in the maintenance of blood/gas homeostasis and (b) evidence suggesting that maladaptive responses to hypercapnic stimulation may be involved in the pathogenesis of Sudden Infant Death Syndrome (SIDS).The swine model of early development will be used to test the hypothesis that CV-RESP responses to prolonged hypercapnia are: (a) age-related, (b) modulated by peripheral afferent inputs, and (c) mediated by central a2-adrenoceptors. We also hypothesize that the network response to hypercapnia involves area postrema, nucleus tractus solitarii, and their synaptic targets within sympathetic (SYMP) control regions of the lateral medullary reticular formation. We shall test our hypothesis that catecholaminergic cell areas of the piglet medulla, previously shown to be activated by (a) CO2 and (b) hypotension, play crucial roles in the coordinated response. Of special significance are a subset of epinephrinergic neurons located in the SYMP premotor region of the rostral ventrolateral medulla. The effects of prolonged hypercapnia on SYMP outflow from at least two different segmental levels will be recorded, simultaneously with phrenic (PHR) activity. lEG expression will be quantitated with respect to age and brain stem sites. Age-related alterations in physiologic and neqronal responses to hypercapnia will be assessed following blockade of central alpha-2 receptors. Peripheral denervation will determine the importance of peripheral afferent inputs versus central effects ofhypercapnia at different ages. The correlation between lEG expression and SYMP-PHR outflows should reveal whether age-related changes in CV-RESP brain circuits (suggesting periods of vulnerability), are also observed in SYMP-PHR outflows; thus explaining the absence of a linear pattern of maturation of CV responses with stress. These studies should identify apparent dissociation between level of lEG expression (neuronal activation), SYMP coherence (regulatory outflow) and CV-RESP responses to stress (critical developmental period). The results should help in our understanding of the most vulnerable period in the life of the child and the pathogenesis ('window of opportunity') of SIDS. |
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