The Experts below are selected from a list of 267 Experts worldwide ranked by ideXlab platform
Rajiv Chopra - One of the best experts on this subject based on the ideXlab platform.
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mr thermometry in the human Prostate Gland at 3 0t for transurethral ultrasound therapy
Journal of Magnetic Resonance Imaging, 2013Co-Authors: Elizabeth Ramsay, Rajiv Chopra, Michael Bronskill, Masoom A Haider, Charles Mougenot, Max O Kohler, Laurence KlotzAbstract:Purpose To investigate the spatial, temporal and temperature resolution of a segmented gradient echo echo-planar imaging (EPI) technique as applied to proton resonance frequency (PRF) shift thermometry at 3 T in the human Prostate Gland, and to determine appropriate sequence parameters for MRI-controlled transurethral ultrasound thermal therapy.
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In vivo MR elastography of the Prostate Gland using a transurethral actuator.
Magnetic resonance in medicine, 2009Co-Authors: Rajiv Chopra, Arvin Arani, Yuexi Huang, Mireia Musquera, Jeff Wachsmuth, Michael Bronskill, Donald B. PlewesAbstract:Conventional approaches for MR elastography (MRE) using surface drivers have difficulty achieving sufficient shear wave propagation in the Prostate Gland due to attenuation. In this study we evaluate the feasibility of generating shear wave propagation in the Prostate Gland using a transurethral device. A novel transurethral actuator design is proposed, and the performance of this device was evaluated in gelatin phantoms and in a canine Prostate Gland. All MRI was performed on a 1.5T MR imager using a conventional gradient-echo MRE sequence. A piezoceramic actuator was used to vibrate the transurethral device along its length. Shear wave propagation was measured transverse and parallel to the rod at frequencies between 100 and 250 Hz in phantoms and in the Prostate Gland. The shear wave propagation was cylindrical, and uniform along the entire length of the rod in the gel experiments. The feasibility of transurethral MRE was demonstrated in vivo in a canine model, and shear wave propagation was observed in the Prostate Gland as well as along the rod. These experiments demonstrate the technical feasibility of transurethral MRE in vivo. Further development of this technique is warranted. Magn Reson Med, 2009. © 2009 Wiley-Liss, Inc.
Gail S. Prins - One of the best experts on this subject based on the ideXlab platform.
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the role of wnt5a in Prostate Gland development
Developmental Biology, 2009Co-Authors: Liwei Huang, Lynn Birch, Douglas Lucciocamelo, Terry Yamaguchi, Gail S. PrinsAbstract:Abstract The Wnt genes encode a large family of secreted glycoproteins that play important roles in controlling tissue patterning, cell fate and proliferation during development. Currently, little is known regarding the role(s) of Wnt genes during Prostate Gland development. The present study examines the role of the noncanonical Wnt 5a during Prostate Gland development in rat and murine models. In the rat Prostate, Wnt 5a mRNA is expressed by distal mesenchyme during the budding stage and localizes to periductal mesenchymal cells with an increasing proximal-to-distal gradient during branching morphogenesis. Wnt 5a protein is secreted and localizes to periductal stroma, extracellular matrix and epithelial cells in the distal ducts. While Wnt 5a expression is high during active morphogenesis in all Prostate lobes, ventral Prostate (VP) expression declines rapidly following morphogenesis while dorsal (DP) and lateral lobe (LP) expression remains high into adulthood. Steroids modulate prostatic Wnt 5a expression during early development with testosterone suppressing Wnt 5a and neonatal estrogen increasing expression. In vivo and ex vivo analyses of developing mouse and rat Prostates were used to assess the functional roles of Wnt 5a. Wnt 5a −/− murine Prostates rescued by organ culture exhibit disturbances in bud position and directed outgrowth leading to large bulbous sacs in place of elongating ducts. In contrast, epithelial cell proliferation, ductal elongation and branchpoint formation are suppressed in newborn rat Prostates cultured with exogenous Wnt 5a protein. While renal grafts of Wnt 5a −/− murine Prostates revealed that Wnt 5a is not essential for cyto- and functional differentiation, a role in luminal cell polarity and lumenization of the ducts was indicated. Wnt 5a suppresses prostatic Shh expression while Shh stimulates Wnt 5a expression in a lobe-specific manner during early development indicating that Wnt 5a participates in cross-talk with other members of the gene regulatory network that control Prostate development. Although Wnt 5a does not influence prostatic expression of other Wnt morphogens, it suppresses Wif -1 expression and can thus indirectly modulate Wnt signaling. In summary, the present finds demonstrate that Wnt 5a is essential for normal Prostate development where it regulates bud outgrowth, ductal elongation, branching, cell polarity and lumenization. These findings contribute to the growing body of knowledge on regulatory mechanisms involved in Prostate Gland development which are key to understanding abnormal growth processes associated with aging.
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Molecular signaling pathways that regulate Prostate Gland development
Differentiation; research in biological diversity, 2008Co-Authors: Gail S. Prins, Oliver PutzAbstract:Prostate Gland development is a complex process that involves coordination of multiple signaling pathways including endocrine, paracrine, autocrine, juxtacrine and transcription factors. To put this into proper context, the present manuscript will begin with a brief overview of the stages of Prostate development and a summary of androgenic signaling in the developing Prostate, which is essential for Prostate formation. This will be followed by a detailed description of other transcription factors and secreted morphogens directly involved in Prostate formation and branching morphogenesis. Except where otherwise indicated, results from rodent models will be presented since studies that examine molecular signaling in the developing human Prostate Gland are sparse at the present time.
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Prostate Gland Development and Estrogenic Imprinting
Steroid Hormones and Cell Cycle Regulation, 2002Co-Authors: Oliver Putz, Gail S. PrinsAbstract:The Prostate Gland receives a great deal of research interest not because of its physiologic role as a secretory Gland for seminal plasma components but rather due to the high incidence of abnormal growth and tumor formation with aging in humans. Currently, Prostate cancer is the most common cancer in males and is the second leading cause of cancer deaths in American men. Additionally, benign prostatic hyperplasia (BPH) is the most common benign neoplasia, occurring in ≈50% of men by the age of 60. Despite extensive research, the basis for these high rates of abnormal growth is not understood. It is recognized, however, that steroid hormones play a role in the initiation and progression of Prostate cancer and BPH which is the basis for hormonal treatment strategies (Huggins and Hodges, 1941). It is also speculated that early developmental events which are regulated by steroids in the Prostate Gland may be linked to its predisposition to high rates of disease in adult men (Price, 1963). This review will focus on the potential role of estrogens in imprinting or programming of Prostate Gland development.
Ralph Buttyan - One of the best experts on this subject based on the ideXlab platform.
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Regulation of Apoptosis in the Prostate Gland by Androgenic Steroids
Trends in endocrinology and metabolism: TEM, 1999Co-Authors: Ralph Buttyan, Ahmad Shabsigh, Harris Perlman, Marc ColombelAbstract:The Prostate Gland requires androgenic steroids for its appropriate embryological formation and postpubertal growth and, once at adult size, remains dependent on a continuous supply of androgens for its vitality and function. A reduction of the levels of circulating androgens will rapidly induce apoptosis of the cells of the Prostate, leading to extensive Glandular regression. Studies of rodent models of Prostate response to castration have shown that there are some remarkable changes in the gene activity of Prostate epithelial cells leading up to apoptosis. There is now evidence for a critical cell signaling pathway, regulated by c-fos expression, necessary for castration-induced apoptosis, as well as evidence that this signaling initiates an abrupt and transient alteration in the synthesis of fas antigen, p53, bax and bcl-2 proteins in the androgen receptor-expressing Prostate epithelial cells, the cellular compartment that appears to be the most affected by castration. However, more recent studies suggest that these castration-induced effects on the Prostate epithelial cells might be, at least in part, an indirect response to a critical reduction in blood flow to the Prostate Gland that precedes the onset of epithelial cell apoptosis. The castration effects on blood flow to the Prostate Gland seem to be related to vascular degeneration associated with apoptosis of a subset of Prostate endothelial cells.
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rapid reduction in blood flow to the rat ventral Prostate Gland after castration preliminary evidence that androgens influence Prostate size by regulating blood flow to the Prostate Gland and prostatic endothelial cell survival
The Prostate, 1998Co-Authors: Ahmad Shabsigh, David T Chang, Daniel F Heitjan, Alex Kiss, Carl A Olsson, Peter J Puchner, Ralph ButtyanAbstract:BACKGROUND Androgenic steroids regulate the development and size of the mammalian Prostate Gland. The mechanism(s) for this growth control might involve a direct effect on Prostate cell proliferation and survival as well as more complex effects on the tissue environment supporting nourishment and oxygenation. In this study, we evaluated an animal model of androgen action on the Prostate, the rat ventral Prostate Gland, to determine whether acute androgen withdrawal, by means of castration, might alter the primary blood flow to the Prostate Gland and for the effects of castration on prostatic endothelial cell viability. METHODS Groups of rats studied included intact control males, males that had been surgically castrated, or males that received a sham-surgical castration. Relative blood flow (RBF) to the rat ventral Prostate Glands and rat bladders were measured at 18 and 24 hr after castration or sham castration using a fluorescent microsphere infusion technique. Thin sections from fixed and embedded rat ventral Prostate Glands obtained from unoperated or 12-hr castrated rats were analyzed by the TUNEL immunostaining technique to microscopically identify and quantify apoptotic epithelial, stromal, and endothelial cells. RESULTS RBF to the rat ventral Prostate was reduced by 38% at 18 hr after castration when compared with intact or sham-operated rats and by 45% at 24 hr after castration (P = 0.038 unoperated/0.025 sham operated). In contrast, RBF to the bladder was not significantly different between any of the groups in the 24-hr castrate experiment. TUNEL staining analysis of ventral Prostate tissues obtained from 12-hr castrated rats showed only rare TUNEL-positive epithelial cells similar to the control tissue but significantly increased TUNEL labeling for endothelial and other ventral Prostate stromal cells. CONCLUSIONS Castration resulted in a rapid and significant reduction of blood flow to the mature rat ventral Prostate Gland that was not seen in the bladder. This reduction precedes the appearance of apoptosis in the epithelial cells of the tissue but more coincided with the appearance of TUNEL-positive Prostate vascular endothelial and stromal cells, suggesting that androgens support the survival of cells in the vascular and stromal compartment of the rat Prostate as well as in the prostatic epithelium. These preliminary data support the concept that androgen action on the Prostate might involve primary regulation of Prostate blood flow and Prostate vascular cell vitality. Prostate 36:201–206, 1998. © 1998 Wiley-Liss, Inc.
Stuart H. Orkin - One of the best experts on this subject based on the ideXlab platform.
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Restriction of neuroblastoma to the Prostate Gland in transgenic mice.
Molecular and cellular biology, 1991Co-Authors: D. G. Skalnik, David M. Dorfman, David A. Williams, Stuart H. OrkinAbstract:Abstract Male transgenic mice that carry a construct containing 5'-flanking sequences of the gp91-phox gene linked to the early region of the simian virus 40 (SV40) genome reproducibly develop tumors arising from the Prostate Gland. As gp91-phox is expressed exclusively in terminally differentiating hematopoietic cells of the myelomonocytic lineage, the induction of tumors arising from the Prostate Gland was unexpected. These lesions appear to be due to a novel transcription signal that was generated during the construction of the transgene. Surprisingly, the histopathological and biochemical properties of the tumor are diagnostic of neuroblastoma rather than of adenocarcinoma of the Prostate Gland. Tumors produce SV40 T antigen and isoforms of neural cell adhesion molecule characteristic of neuronal cells, and they occur in a testosterone-independent manner. Microscopic examination of Prostate Glands from young transgenic mice reveals the presence of small lesions arising outside of the Prostate Gland epithelium, which is consistent with the diagnosis of neuroblastoma and further distinguishes this tumor from prostatic adenocarcinoma. Prostate Gland tumors occur in all male animals of susceptible lines carrying the gp91-phox promoter/SV40 early-region transgene. However, variability in the time at which gross tumors appear and the presence of cells expressing T antigen prior to tumorigenesis suggest that somatic events in addition to T-antigen production are required for the development of a malignancy. The extraordinary restriction of the site of tumorigenesis in these animals indicates the presence in the Prostate Gland of a novel, tissue-specific neuroectodermal cell of origin. These transgenic animals provide a model system for the study of neuroectodermal malignancies.
Ahmad Shabsigh - One of the best experts on this subject based on the ideXlab platform.
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Regulation of Apoptosis in the Prostate Gland by Androgenic Steroids
Trends in endocrinology and metabolism: TEM, 1999Co-Authors: Ralph Buttyan, Ahmad Shabsigh, Harris Perlman, Marc ColombelAbstract:The Prostate Gland requires androgenic steroids for its appropriate embryological formation and postpubertal growth and, once at adult size, remains dependent on a continuous supply of androgens for its vitality and function. A reduction of the levels of circulating androgens will rapidly induce apoptosis of the cells of the Prostate, leading to extensive Glandular regression. Studies of rodent models of Prostate response to castration have shown that there are some remarkable changes in the gene activity of Prostate epithelial cells leading up to apoptosis. There is now evidence for a critical cell signaling pathway, regulated by c-fos expression, necessary for castration-induced apoptosis, as well as evidence that this signaling initiates an abrupt and transient alteration in the synthesis of fas antigen, p53, bax and bcl-2 proteins in the androgen receptor-expressing Prostate epithelial cells, the cellular compartment that appears to be the most affected by castration. However, more recent studies suggest that these castration-induced effects on the Prostate epithelial cells might be, at least in part, an indirect response to a critical reduction in blood flow to the Prostate Gland that precedes the onset of epithelial cell apoptosis. The castration effects on blood flow to the Prostate Gland seem to be related to vascular degeneration associated with apoptosis of a subset of Prostate endothelial cells.
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rapid reduction in blood flow to the rat ventral Prostate Gland after castration preliminary evidence that androgens influence Prostate size by regulating blood flow to the Prostate Gland and prostatic endothelial cell survival
The Prostate, 1998Co-Authors: Ahmad Shabsigh, David T Chang, Daniel F Heitjan, Alex Kiss, Carl A Olsson, Peter J Puchner, Ralph ButtyanAbstract:BACKGROUND Androgenic steroids regulate the development and size of the mammalian Prostate Gland. The mechanism(s) for this growth control might involve a direct effect on Prostate cell proliferation and survival as well as more complex effects on the tissue environment supporting nourishment and oxygenation. In this study, we evaluated an animal model of androgen action on the Prostate, the rat ventral Prostate Gland, to determine whether acute androgen withdrawal, by means of castration, might alter the primary blood flow to the Prostate Gland and for the effects of castration on prostatic endothelial cell viability. METHODS Groups of rats studied included intact control males, males that had been surgically castrated, or males that received a sham-surgical castration. Relative blood flow (RBF) to the rat ventral Prostate Glands and rat bladders were measured at 18 and 24 hr after castration or sham castration using a fluorescent microsphere infusion technique. Thin sections from fixed and embedded rat ventral Prostate Glands obtained from unoperated or 12-hr castrated rats were analyzed by the TUNEL immunostaining technique to microscopically identify and quantify apoptotic epithelial, stromal, and endothelial cells. RESULTS RBF to the rat ventral Prostate was reduced by 38% at 18 hr after castration when compared with intact or sham-operated rats and by 45% at 24 hr after castration (P = 0.038 unoperated/0.025 sham operated). In contrast, RBF to the bladder was not significantly different between any of the groups in the 24-hr castrate experiment. TUNEL staining analysis of ventral Prostate tissues obtained from 12-hr castrated rats showed only rare TUNEL-positive epithelial cells similar to the control tissue but significantly increased TUNEL labeling for endothelial and other ventral Prostate stromal cells. CONCLUSIONS Castration resulted in a rapid and significant reduction of blood flow to the mature rat ventral Prostate Gland that was not seen in the bladder. This reduction precedes the appearance of apoptosis in the epithelial cells of the tissue but more coincided with the appearance of TUNEL-positive Prostate vascular endothelial and stromal cells, suggesting that androgens support the survival of cells in the vascular and stromal compartment of the rat Prostate as well as in the prostatic epithelium. These preliminary data support the concept that androgen action on the Prostate might involve primary regulation of Prostate blood flow and Prostate vascular cell vitality. Prostate 36:201–206, 1998. © 1998 Wiley-Liss, Inc.
