Veronica M. Catanese, M.D.

The many missions of medical schools
Smith, Lawrence G; Catanese, Veronica M
2010 Jun 15;152(12):818-819, Annals of internal medicine
— id: 133616, year: 2010, vol: 152, page: 818, stat: Journal Article,

Creating a new structure for research on health care effectiveness
Kupersmith, J; Sung, N; Genel, M; Slavkin, H; Califf, R; Bonow, R; Sherwood, L; Reame, N; Catanese, V; Baase, C; Feussner, J; Dobs, A; Tilson, H; Reece, EA
2005 MAR ;53(2):67-72, Journal of investigative medicine
Effectiveness research (a term we use in preference to the more confining and difficult health services or outcomes research) evaluates the clinical setting and the health care system on which it depends. It uses a variety of health care assessment techniques and the practical clinical trial to inform clinical practice, quality interventions, and health policy decisions. Effectiveness research had not had sufficient public or private funding to produce the information needed to facilitate evidence-based health care improvement. However, recent trends, such as the likelihood for continued substantial increases in health care costs and concern regarding the quality and safety of the US health care system, are among the important arguments for increasing its funding and capacity. We propose a new entity, a public-private consortium to expand and offer new capability and resources in this area. The consortium would consist of all relevant public and private entities. It would be organized into an executive committee, which would identify research priorities and panels to design requests for proposals. Competitive peer-reviewed proposals, transparency and balance of forces in choice of topics, conduct of research, and interpretation of results would be important features. Metrics for success would be use of the data derived from consortium projects in medical decision making and benefit design. The consortium would provide balance and potential mediation of conflicting or competing interests in which all stakeholders will be present to establish the rules. Broad representation of all interests would serve to avoid the economic, policy, and political issues that have bedeviled past efforts. Models for the consortium include the Health Effectiveness Institute, the Centers for Education and Research on Therapeutics, and the Transportation Research Board
— id: 51761, year: 2005, vol: 53, page: 67, stat: Journal Article,

Clinical research in the United States at a crossroads - Proposal for a novel public-private partnership to establish a National Clinical Research Enterprise
Crowley, WF; Sherwood, L; Salber, P; Scheinberg, D; Slavkin, H; Tilson, H; Reece, EA; Catanese, V; Johnson, SB; Dobs, A; Genel, M; Korn, A; Reame, N; Bonow, R; Grebb, J; Rimoin, D
2004 MAR 3 ;291(9):1120-1126, JAMA
The clinical research infrastructure of the United States is currently at a critical crossroads. To leverage the enormous biomedical research gains made in the past century efficiently, a drastic need exists to reengineer this system into a coordinated, safe, and more efficient and effective enterprise. To accomplish this task, clinical research must be transformed from its current state as a cottage industry to an enterprise-wide health care pipeline whose function is to bring the novel research from both government and private entities to the US public. We propose the establishment of a unique public-private partnership termed the National Clinical Research Enterprise (NCRE). Its agenda should consist of informed public participation, supportive information technologies, a skilled workforce, and adequate funding in clinical research. Devoting only 0.25% of the budgets from all health care stakeholders to support the NCRE would permit adequate funding to build the infrastructure required to address these problems in an enterprise fashion. All participants in the US health care delivery system must come together to focus on system-wide improvements that will benefit the public
— id: 42478, year: 2004, vol: 291, page: 1120, stat: Journal Article,

Medical humanities at New York University School of Medicine: an array of rich programs in diverse settings
Krackov, Sharon K; Levin, Richard I; Catanese, Veronica; Rey, Mariano; Aull, Felice; Blagev, Denitza; Dreyer, Benard; Grieco, Anthony J; Hebert, Cristy; Kalet, Adina; Lipkin, Mack Jr; Lowenstein, Jerome; Ofri, Danielle; Stevens, David
2003 Oct;78(10):977-982, Academic medicine
The New York University School of Medicine has a rich tradition of cultivating programs in medical humanities and professionalism. They are drawn from the departments, centers, students, and faculty in the School of Medicine, have linkages throughout the university, and are interwoven into the fabric and culture of the institution. Some are centrally based in the School of Medicine's deans' office, and others are located in individual departments and receive support from the dean's office. This article describes representative programs for medical students and faculty. Curricular initiatives, the fundamental components of medical students' learning, include a course entitled 'The Physician, Patient, and Society,' a clerkship essay in the Medicine Clerkship, an opportunity for reflection during the medicine clerkship, and a medical humanities elective. In 2002, the Professionalism Initiative was launched to enhance and reflect the values of the medical profession. Its curriculum consists of a series of events that coordinate, particularly, with existing elements of the first-year curriculum (e.g., orientation week, a session during anatomy, a self-assessment workshop, and a peer-assessment workshop). The Master Scholars Program is a group of five, theme-based master societies consisting of faculty and students who share common interests around the society's themes. Programs developed for the societies include colloquia, faculty-led seminars, a mandatory student-mentoring program, and visiting scholars. Finally, the authors describe three high-quality literary publications created at New York University School of Medicine. Each of the initiatives undergoes regular critical examination and reflection that drive future planning
— id: 39038, year: 2003, vol: 78, page: 977, stat: Journal Article,

Central challenges facing the national clinical research enterprise
Sung, NS; Crowley, WF; Genel, M; Salber, P; Sandy, L; Sherwood, LM; Johnson, SB; Catanese, V; Tilson, H; Getz, K; Larson, EL; Scheinberg, D; Reece, EA; Slavkin, H; Dobs, A; Grebb, J; Martinez, RA; Korn, A; Rimoin, D
2003 MAR 12 ;289(10):1278-1287, JAMA
Medical scientists and public health policy makers are increasingly concerned that the scientific discoveries of the past generation are failing to be translated efficiently into tangible human benefit. This concern has generated several initiatives, including the Clinical Research Roundtable at the Institute of Medicine, which first convened in June 2000. Representatives from a diverse group of stakeholders in the nation's clinical research enterprise have collaborated to address the issues it faces. The context of clinical research is increasingly encumbered by high costs, slow results, lack of funding, regulatory burdens, fragmented infrastructure, incompatible databases, and a shortage of qualified investigators and willing participants. These factors have contributed to 2 major obstacles, or translational blocks: impeding the translation of basic science discoveries into clinical studies and of clinical studies into medical practice and health decision making in systems of care. Considering data from across the entire health care system, it has become clear that these 2 translational blocks can be removed only by the collaborative efforts of multiple system stakeholders. The goal of this article is to articulate the 4 central challenges facing clinical research at present-public participation, information systems, workforce training, and funding; to make recommendations about how they might be addressed by particular stakeholders; and to invite a broader, participatory dialogue with a view to improving the overall performance of the US clinical research enterprise
— id: 34085, year: 2003, vol: 289, page: 1278, stat: Journal Article,

Academic medicine in the 21st century: lessons from the dinosaurs
Catanese VM
1997 Aug;45(6):362-365, Journal of investigative medicine
— id: 12292, year: 1997, vol: 45, page: 362, stat: Journal Article,

Antihypertensive agents that limit ventricular hypertrophy inhibit cardiac expression of insulin-like growth factor-I
Donohue TJ; Dworkin LD; Ma J; Lango MN; Catanese VM
1997 Dec;45(9):584-591, Journal of investigative medicine
BACKGROUND: Left ventricular hypertrophy (LVH) is a generalized adaptation to altered myocardial load. Hypertension induces significant increases in ventricular IGF-I gene expression that occur coordinately with development of LVH. To test whether IGF-I promotes initiation of LVH, we examined ventricular IGF-I mRNA content in spontaneously hypertensive rats (SHRs) treated with antihypertensive drugs that limit or permit LVH. METHODS: Prehypertensive SHRs were left untreated or treated with enalapril, nifedipine, or hydralazine. Systolic blood pressure (SBP), hypertrophy index (ventricular weight/body weight), and ventricular IGF-I mRNA levels were examined 2, 4, and 6 weeks after beginning therapy in the experimental groups. RESULTS: Systolic blood pressure reached hypertensive levels after 2 weeks in untreated animals, and was controlled in the treated animals. The hypertrophy index in untreated animals was significantly elevated at 4 weeks. By 6 weeks, the hypertrophy indices of both the enalapril- and nifedipine-treated groups were significantly lower than that of the untreated group. In contrast, the hypertrophy index of the hydralazine-treated animals remained comparable to that of the untreated animals. By 4 weeks, IGF-I mRNA levels in the enalapril- and nifedipine-treated groups were significantly lower than those in the untreated and hydralazine-treated groups. CONCLUSIONS: We conclude that: (1) antihypertensive drugs that reduce LVH blunt ventricular IGF-I mRNA content; and (2) the hemodynamic effects of antihypertensives may be dissociated from their ability to promote or limit a hypertrophic response. The clear association of LVH with ventricular IGF-I mRNA content suggests that IGF-I is an important determinant of ventricular growth. Our data also suggest that angiotensin-converting enzyme inhibitors and calcium channel blockers may reduce LVH by inhibiting cardiac IGF-I gene expression
— id: 57375, year: 1997, vol: 45, page: 584, stat: Journal Article,

Correlation of glioma cell regression with inhibition of insulin-like growth factor 1 and insulin-like growth factor-binding protein-2 expression
Wang ZH; Ma J; Zeng BJ; Catanese VM; Samuels S; Gama Sosa MA; Kolodny EH
1997 Sep;66(3):203-211, Neuroendocrinology
To explore the antitumor effect of insulin-like growth factor 1 (IGF-I) antisense RNA and the interaction of IGF-I with insulin-like growth factor-binding proteins (IGFBPs) in glioma cells, a recombinant retrovirus expressing IGF-I antisense RNA was constructed and introduced into C6 glioma cells. IGF-I antisense RNA reverses the transformed phenotype in glioma cells and inhibits glioma cell growth by blocking overexpression of endogenous IGF-I. Expression of IGFBP-2 is increased in glioma cells as compared with normal adult glial cells. IGF-I antisense RNA also inhibits expression of IGFBP-2 in glioma cells, but does not influence expression of the other IGFBPs. Although IGFBP-2 in conditioned medium from wild-type C6 cell cultures itself does not directly influence glioma cell growth, it synergistically enhances exogenous IGF-I-mediated DNA synthesis in IGF-I-negative C6 cells. These findings indicate the inhibitory effect of IGF-I antisense RNA on growth and development of glioma cells. IGF-I-dependent glioma cell growth may, in some circumstances, require IGFBP-2 as a cofactor. The antitumor effect of IGF-I antisense RNA is also associated with inhibition of IGFBP-2 expression
— id: 9851, year: 1997, vol: 66, page: 203, stat: Journal Article,

Transforming growth factor-beta (TGF-beta) and insulin-like growth factor-I (IGF-I) regulate IGF binding protein expression in human mesangial cells by distinct pre- and post-translational mechanisms
Ma, JX; Catanese, VM
1996 MAR ;44(3):A307-A307, Journal of investigative medicine
— id: 52965, year: 1996, vol: 44, page: A307, stat: Journal Article,

Insulin-like growth factor-I (IGF-I) stimulates transforming growth factor-beta (TGF-beta) production by mesangial cells: A molecular mechanism for coupling cellular proliferation and matrix expansion
Ma, JX; Munger, J; Catanese, VM
1996 MAR ;44(3):A231-A231, Journal of investigative medicine
— id: 52944, year: 1996, vol: 44, page: A231, stat: Journal Article,

Secondary diabetes
Catanese VM; Kahn CR
Principles and practice of endocrinology and metabolism Philadelphia : J.B. Lippincott Co., 1995,
— id: 3523, year: 1995, vol: , page: 1220, stat: Chapter,

Pre- and post-translational regulation of renal insulin-like growth factor binding protein-1 in insulin-deficient diabetes
Kaufman CR; Catanese VM
1995 Apr;43(2):178-186, Journal of investigative medicine
BACKGROUND: Renal size and production of insulin-like growth factor-I (IGF-I) increase rapidly after the onset of insulin-deficient diabetes, despite decreases in serum and hepatic levels of IGF-I and linear growth retardation in affected animals and humans. This increase in kidney IGF-I gene expression is mediated both by pre- and post-translational mechanisms, with the relative contributions of each locus of control varying with the severity and/or duration of diabetes. Since the actions of IGF-I are modified by specific circulating as well as locally produced IGF binding proteins (IGF BPs), and since kidney IGF BP1 content is increased in diabetes, we asked whether: 1) the time course of induction of increased BP1 expression paralleled that for induction of IGF-I; 2) severity and/or duration of diabetes affected pre- and post-translational renal expression of this protein as it does expression of IGF-I itself; and 3) insulin deficiency or hyperglycemia was responsible for this increase in kidney IGF BP1 content. METHODS: Adult rats were made diabetic by injection of streptozotocin (STZ), and kidney BP1 mRNA and protein were assessed by Northern and Western ligand blotting, respectively, in comparison with nondiabetic, insulin-treated diabetic, and phlorizin-treated diabetic animals. RESULTS: Rapid time- and STZ dose-dependent increases in both pre- and post-translational renal IGF BP1 expression were noted in the untreated diabetic animals. Comparison of the relative changes in kidney BP1 mRNA and protein contents suggested that with increasing severity of diabetes, at least 20% of this effect was mediated pre-translationally and, therefore, did not merely reflect trapping of circulating BP1. Treatment with insulin completely inhibited the pre-translational and potently inhibited the post-translational component of the response, while correction of hyperglycemia with phlorizin did not. These observations were specific for BP1, with renal IGF BP3 mRNA and protein contents noted to be low basally and unaffected by diabetes. CONCLUSIONS: These data suggest that insulin strongly regulates pre- and post-translational renal IGF BP1 gene expression and implicate BP1 as an important determinant of IGF-I activity in diabetic kidney. The similarity of the time course of BP1 induction to that of IGF-I in animals of the same age and severity of diabetes suggests that local IGF-I/BP1 interactions may potentiate kidney IGF-I activity and promote initiation of the early stages of diabetic renal hypertrophy
— id: 56665, year: 1995, vol: 43, page: 178, stat: Journal Article,

Transforming growth factor-beta inhibits synthesis and secretion of insulin-like growth factor binding proteins by emsangial cells
Ma JX; Catanese VM
1995 ;43(Suppll 2):264A-264A, Journal of investigative medicine
— id: 55829, year: 1995, vol: 43, page: 264A, stat: Journal Article,

Estradiol enhances the stimulatory effect of insulin-like growth factor-I (IGF-I) on mammary development and growth hormone-induced IGF-I messenger ribonucleic acid
Ruan, W; Catanese, V; Wieczorek, R; Feldman, M; Kleinberg, D L
1995 Mar;136(3):1296-1302, Endocrinology
Pubertal mammary development in the rat is largely dependent upon GH and estrogen. We recently showed that insulin-like growth factor-I (IGF-I) can substitute for GH in inducing mammary development in male rats, suggesting that IGF-I mediates GH action. The present study investigated whether IGF-I, like GH, required estradiol (E2) to act or whether IGF-I could substitute for both GH and E2. The effects of IGF-I were tested in the presence and absence of E2. Elvax pellets containing IGF-I or des(1-3) IGF-I were implanted into right lumbar mammary glands of sexually immature, hypophysectomized, oophorectomized female rats, with control BSA-containing pellets in the contralateral glands. After 5 days, both lumbar mammary glands were removed and examined in whole mounts for mammary development by counting terminal end buds and alveolar structures. E2, administered in SILASTIC brand capsules, had no independent effect on mammary development. In the absence of E2, des(1-3) IGF-I had a small, but significant, independent effect on mammary development; native IGF-I was ineffective. The addition of E2 significantly enhanced the effects of IGF-I and des(1-3) IGF-I on mammary development, similar to that noted when E2 was given along with GH. We also studied the effects of E2 and/or hGH on mammary gland IGF-I messenger RNA (mRNA) in hypophysectomized castrated male animals. E2 alone did not increase mammary gland IGF-I mRNA concentrations, but E2 enhanced the effect of hGH on IGF-I mRNA by 4- to 6-fold. These studies indicate that IGF-I can have a small independent effect on mammary development, but like GH, E2 is required for a full effect. They also indicate that E2 is capable of synergizing with GH in the production or expression of IGF-I mRNA, and that the action of E2 on mammary development may take place at multiple sites. If locally produced IGF-I does indeed mediate the action of GH in mammary development, then although E2 is capable of enhancing the effect of GH on IGF-I mRNA, its major effect in mammary development occurs after IGF-I is produced
— id: 138562, year: 1995, vol: 136, page: 1296, stat: Journal Article,

PRESSURE AND VOLUME OVERLOAD ACTIVATE DISCORDANT PROGRAMS OF GENE-EXPRESSION IN THE HYPERTROPHIC VENTRICLE
BERNSTEIN, NE; MINADEO, J; LANGO, RP; LANGO, MN; DONOHUE, TJ; DWORKIN, LD; CATANESE, VM
1994 APR ;42(2):A169-A169, Clinical research
— id: 52489, year: 1994, vol: 42, page: A169, stat: Journal Article,

Induction of myocardial insulin-like growth factor-I gene expression in left ventricular hypertrophy
Donohue TJ; Dworkin LD; Lango MN; Fliegner K; Lango RP; Benstein JA; Slater WR; Catanese VM
1994 Feb;89(2):799-809, Circulation
BACKGROUND: Left ventricular hypertrophy is a generalized adaptation to increased afterload, but the growth factors mediating this response have not been identified. To explore whether the hypertrophic response was associated with changes in local insulin-like growth factor-I (IGF-I) gene regulation, we examined the induction of the cardiac IGF-I gene in three models of systolic hypertension and resultant hypertrophy. METHODS AND RESULTS: The model systems were suprarenal aortic constriction, uninephrectomized spontaneously hypertensive rats (SHR), and uninephrectomized, deoxycorticosterone-treated, saline-fed rats (DOCA salt). Systolic blood pressure reached hypertensive levels at 3 to 4 weeks in all three systems. A differential increase in ventricular weight to body weight (hypertrophy) occurred at 3 weeks in the SHR and aortic constriction models and at 4 weeks in the DOCA salt model. Ventricular IGF-I mRNA was detected by solution hybridization/RNase protection assay. IGF-I mRNA levels increased in all three systems coincident with the onset of hypertension and the development of ventricular hypertrophy. Maximum induction was 10-fold over control at 5 weeks in the aortic constriction model, 8-fold at 3 weeks in the SHR, and 6-fold at 6 weeks in the DOCA salt model. IGF-I mRNA levels returned to control values by the end of the experimental period despite continued hypertension and hypertrophy in all three systems. In contrast, ventricular c-myc mRNA content increased twofold to threefold at 1 week and returned to control levels by 2 weeks. Ventricular IGF-I receptor mRNA levels were unchanged over the time course studied. The increased ventricular IGF-I mRNA content was reflected in an increased ventricular IGF-I protein content, as determined both by radioimmunoassay and immunofluorescence histochemistry. CONCLUSIONS: We conclude that (1) hypertension induces significant increases in cardiac IGF-I mRNA and protein that occur coordinately with its onset and early in the development of hypertrophy, (2) IGF-I mRNA levels normalize as the hypertrophic response is established, (3) in comparison to IGF-I, both c-myc and IGF-I receptor genes are differentially controlled in experimental hypertension. These findings suggest that IGF-I may participate in initiating ventricular hypertrophy in response to altered loading conditions. The consistency of these findings in models of high-, moderate-, and low-renin hypertension suggests that they occur independently of the systemic renin-angiotensin endocrine axis
— id: 56521, year: 1994, vol: 89, page: 799, stat: Journal Article,

AN EXPLORATION OF THE MOLECULAR-BASIS FOR DIMINISHED GLUCOSE-TRANSPORT IN ALZHEIMERS-DISEASE
MCRAE, T; CATANESE, VM
1994 APR ;42(2):A217-A217, Clinical research
— id: 52495, year: 1994, vol: 42, page: A217, stat: Journal Article,

INSULIN-LIKE GROWTH-FACTOR-I (IGF-I) RECEPTORS ON NORMAL, REMNANT, AND DIABETIC RAT GLOMERULI - EVIDENCE FOR A GLOMERULAR RESPONSE TO INCREASED RENAL IGF-I CONTENT
THOMPSON, N; DWORKIN, LD; TOLBERT, E; CATANESE, VM
1994 APR ;42(2):A143-A143, Clinical research
— id: 98444, year: 1994, vol: 42, page: A143, stat: Journal Article,

Discordant, organ-specific regulation of insulin-like growth factor-I messenger ribonucleic acid in insulin-deficient diabetes in rats
Catanese VM; Sciavolino PJ; Lango MN
1993 Feb;132(2):496-503, Endocrinology
Linear growth retardation is common in uncontrolled insulin-deficient diabetes, but individual organs such as kidney may hypertrophy. To explore whether this heterogeneity of response might be mediated by differential local insulin-like growth factor-I (IGF-I) gene regulation, we injected rats with ip saline, 65, 120, or 175 mg/kg streptozotocin (STZ). Diabetics were untreated or received daily insulin. Animals were killed 24, 48, or 72 h after documentation of diabetes, and liver, kidney, and lung messenger RNA (mRNA) content analyzed by solution hybridization/RNase protection assay. Untreated diabetics had 10- to 100-fold reductions in hepatic IGF-I mRNA apparent as early as 24 h, and the magnitude of these changes varied directly with the severity of diabetes. In contrast, kidney IGF-I mRNA content increased by 400-500% at 24 h in untreated diabetics given 175 mg/kg STZ, and by 100-200% at 48 h in those given 120 mg/kg STZ, with return to control levels by 72 h. Renal IGF-I mRNA levels actually decreased by 250-350% at 24 h in rats injected with 65 mg/kg STZ, returning to supranormal values by 72 h. These results suggest that severity and/or duration of the metabolic abnormality qualitatively and quantitatively affect this response in the kidney. Liver and kidney IGF-I mRNA levels approached normal with insulin therapy and were similar to controls in rats which received STZ but did not develop diabetes. Lung IGF-I mRNA levels were minimally altered in all experimental groups. At the time point and STZ dosage at which liver IGF-I mRNA changes were most dramatic, little change in liver alpha-tubulin mRNA was noted. At the time point and STZ dosages at which kidney IGF-I mRNA induction was most dramatic, renal IGF-I receptor mRNA was only minimally changed, and renal alpha-tubulin mRNA was modestly reduced. In summary: 1) hepatic IGF-I mRNAs are dramatically reduced, and renal IGF-I mRNAs are significantly increased soon after the onset of insulin-deficient diabetes in STZ-treated rats; 2) insulin therapy restores IGF-I mRNA levels toward normal; and 3) these changes in IGF-I mRNA content are specific and are not the result of hepatic or renal STZ toxicity. These data suggest that IGF-I gene expression is regulated in a discordant, organ-specific manner in diabetes, and that metabolic factors in addition to GH may differentially modulate the endocrine and paracrine effects of IGF-I on growth
— id: 8455, year: 1993, vol: 132, page: 496, stat: Journal Article,

INSULIN-LIKE GROWTH FACTOR-I (IGF-I) RECEPTORS ON NORMAL AND REMNANT RAT GLOMERULI - EVIDENCE FOR A GLOMERULAR RESPONSE TO INCREASED RENAL IGF-I CONTENT
THOMPSON, N; CATANESE, VM; TOLBERT, E; DWORKIN, LD
1993 OCT ;41(3):A619-A619, Clinical research
— id: 52229, year: 1993, vol: 41, page: A619, stat: Journal Article,

EFFECT OF DIABETES ON RENAL EXPRESSION OF INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEINS
KAUFMAN, CR; CATANESE, VM
1992 APR ;40(2):A221-A221, Clinical research
— id: 51981, year: 1992, vol: 40, page: A221, stat: Journal Article,

INSULIN NEGATIVELY REGULATES PRETRANSLATIONAL AND POSTTRANSLATIONAL RENAL EXPRESSION OF INSULIN-LIKE GROWTH-FACTOR BINDING PROTEIN-1
KAUFMAN, CR; CATANESE, VM
1992 OCT ;40(3):A657-A657, Clinical research
— id: 51877, year: 1992, vol: 40, page: A657, stat: Journal Article,

HEMODYNAMIC MODULATION OF VENTRICULAR INSULIN-LIKE GROWTH FACTOR-I GENE-EXPRESSION
DONOHUE, TJ; LANGO, M; BENSTEIN, JA; DWORKIN, LD; CATANESE, VM
1991 APR ;39(2):A152-A152, Clinical research
— id: 51602, year: 1991, vol: 39, page: A152, stat: Journal Article,

RENAL INSULIN-LIKE GROWTH FACTOR-I GENE-EXPRESSION IS INCREASED AFTER UNILATERAL NEPHRECTOMY - RELATIONSHIP TO GLOMERULAR INJURY
Benstein, JA; Koretz, K; Dworkin, LD; Catanese, VM
1990 Apr;38(2):A327-A327, Clinical research
— id: 31960, year: 1990, vol: 38, page: A327, stat: Journal Article,

INDUCTION OF CARDIAC INSULIN-LIKE GROWTH FACTOR-I MESSENGER-RNA PRECEDES VENTRICULAR HYPERTROPHY IN RESPONSE TO PRESSURE OVERLOAD
Donohue, TJ; Benstein, JA; Dworkin, LD; Slater, WR; Catanese, VM
1990 Oct;82(4):761-761, Circulation
— id: 31914, year: 1990, vol: 82, page: 761, stat: Journal Article,

SEQUENTIAL INDUCTION OF CARDIAC C-MYC AND INSULIN-LIKE GROWTH FACTOR-I GENES PRECEDES VENTRICULAR HYPERTROPHY IN RESPONSE TO PRESSURE OVERLOAD
Donohue, TJ; Benstein, JA; Dworkin, LD; Slater, WR; Catanese, VM
1990 Oct;38(3):A766-A766, Clinical research
— id: 31920, year: 1990, vol: 38, page: A766, stat: Journal Article,

SEQUENTIAL INDUCTION OF CARDIAC C-MYC AND INSULIN-LIKE GROWTH FACTOR-I GENE-EXPRESSION IN RESPONSE TO ELEVATED LEFT- VENTRICULAR AFTERLOAD
Donohue, TJ; Dworkin, LD; Slater, W; Catanese, VM
1990 Apr;38(2):A240-A240, Clinical research
— id: 31952, year: 1990, vol: 38, page: A240, stat: Journal Article,

Non-lactogenic effects of growth hormone on growth and insulin-like growth factor-I messenger ribonucleic acid of rat mammary gland
Kleinberg DL; Ruan W; Catanese V; Newman CB; Feldman M
1990 Jun;126(6):3274-3276, Endocrinology
In contrast to established dogma that PRL is central in mammary development, and GH mimics PRL in affecting growth because of structural similarities, we found that both hGH, which is lactogenic, and rGH, which is non-lactogenic, were significantly more potent than hPRL and rPRL in stimulating mammary growth in rats. Additionally, hGH was more potent than hPRL in increasing mammary IGF-I mRNA content. These data indicate that GH has separate effects on parameters of mammary gland growth, suggesting an independent role for GH in mammary growth
— id: 18392, year: 1990, vol: 126, page: 3274, stat: Journal Article,

REGULATION OF INSULIN-LIKE GROWTH FACTOR-I GENE-EXPRESSION IN INSULIN-DEFICIENT DIABETES
Catanese, VM
1989 Apr;37(2):A447-A447, Clinical research
— id: 31701, year: 1989, vol: 37, page: A447, stat: Journal Article,