The primary purpose ofthe Biostatistics Core (Core D) is to continue to provide biostatistical expertise for the design and analysis of all the protocols contained in the Program Project Grant.
The Specific Aims of Core D are:
Aim I. Assist in the design of experimental protocols and insure the proper sample size is selected to provide reasonable power Aim II. Facilitate data transfer and data quality assurance for all projects Aim III. Analyze and interpret the results from data gathered from the experiments Aim IV. Assist in the preparation of statistical components of presentations, reports and manuscripts Aim V. Develop and disseminate new biostatistical approaches for the analysis of the data;
and Aim V I. Participate in discussions and present statistical seminars As we have done in the past, every new experimental protocol will be written in conjunction with a biostatistician from Core D who will provide design expertise and sample size justification for the animal care protocol. Members of the Core will attend the weekly Department of Hypertension and Vascular Research staff meetings. This will facilitate introductions to new PPG staff and also enable the scheduling of biostatistical seminars to cover topics of interest. We anticipate that the efforts of the Biostatistics Core staff (50%) will be divided equally with all four projects contained in this application. We reiterate that the presence of a Core provides availability of a set of biostatisticians with dedicated time and multiple years of experience with the Program Project. This availability is essential to the continuing success of the grant. Although located in a separate building the Biostatistics Core staff are a short walk from the Hypertension and Vascular Research Division, always available by e-mail, and always available for face-to-face meetings to discuss project design and contribute to the preparation of both manuscripts and grants.
|Kumar, Nitin; Liao, Tang-Dong; Romero, Cesar A et al. (2018) Thymosin ?4 Deficiency Exacerbates Renal and Cardiac Injury in Angiotensin-II-Induced Hypertension. Hypertension 71:1133-1142|
|Bryson, Timothy D; Gu, Xiaosong; Khalil, Remonda M et al. (2018) Overexpression of prostaglandin E2 EP4 receptor improves cardiac function after myocardial infarction. J Mol Cell Cardiol 118:1-12|
|Cerniello, Flavia M; Carretero, Oscar A; Longo Carbajosa, Nadia A et al. (2017) MAS1 Receptor Trafficking Involves ERK1/2 Activation Through a ?-Arrestin2-Dependent Pathway. Hypertension 70:982-989|
|Ramseyer, Vanesa D; Ortiz, Pablo A; Carretero, Oscar A et al. (2016) Angiotensin II-mediated hypertension impairs nitric oxide-induced NKCC2 inhibition in thick ascending limbs. Am J Physiol Renal Physiol 310:F748-F754|
|González, Germán E; Rhaleb, N-E; D'Ambrosio, Martin A et al. (2016) Cardiac-deleterious role of galectin-3 in chronic angiotensin II-induced hypertension. Am J Physiol Heart Circ Physiol 311:H1287-H1296|
|Gu, Xiaosong; Xu, Jiang; Zhu, Liping et al. (2016) Prostaglandin E2 Reduces Cardiac Contractility via EP3 Receptor. Circ Heart Fail 9:|
|Kumar, Nitin; Nakagawa, Pablo; Janic, Branislava et al. (2016) The anti-inflammatory peptide Ac-SDKP is released from thymosin-?4 by renal meprin-? and prolyl oligopeptidase. Am J Physiol Renal Physiol 310:F1026-34|
|Zhu, Liping; Yang, Xiao-Ping; Janic, Branislava et al. (2016) Ac-SDKP suppresses TNF-?-induced ICAM-1 expression in endothelial cells via inhibition of I?B kinase and NF-?B activation. Am J Physiol Heart Circ Physiol 310:H1176-83|
|Saez, Fara; Hong, Nancy J; Garvin, Jeffrey L (2016) Luminal flow induces NADPH oxidase 4 translocation to the nuclei of thick ascending limbs. Physiol Rep 4:|
|Cerrato, Bruno D; Carretero, Oscar A; Janic, Brana et al. (2016) Heteromerization Between the Bradykinin B2 Receptor and the Angiotensin-(1-7) Mas Receptor: Functional Consequences. Hypertension 68:1039-48|
Showing the most recent 10 out of 381 publications