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Article: White's operation: the history of 19

Nicholson, Tristan M / Best, Sara L / Ricke, Emily A / Timms, Barry G / Ricke, William A

American journal of clinical and experimental urology

2022 Volume 10, Issue 6, Page(s) 462–466

Abstract: To understand the roots of ... ...

Abstract	To understand the roots of 19
Language	English
Publishing date	2022-12-25
Publishing country	United States
Document type	Editorial
ISSN	2330-1910
ISSN	2330-1910
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Article ; Online: Prostate development: a historical perspective.

Timms, Barry G

Differentiation; research in biological diversity

2008 Volume 76, Issue 6, Page(s) 565–577

Abstract: The regional anatomy of the human prostate has been debated periodically over the last century with various levels of controversy and agreement, beginning with the concept of lobes and replaced by the current model of zones. During this period a variety ... ...

Abstract	The regional anatomy of the human prostate has been debated periodically over the last century with various levels of controversy and agreement, beginning with the concept of lobes and replaced by the current model of zones. During this period a variety of classifications have been proposed, based upon the studies of glandular morphogenesis, responses to hormones or histopathology. The current paradigm suggests that the regional differences seen in the prostate of both animal models and the human are a consequence of specific epithelial-mesenchymal interactions along the cranial-caudal axis of the urogenital sinus. The distinctive regional patterns seen in the rodent prostate and the histological heterogeneity of the human adult gland all point to the modification of the distal portion of the ducts, while the proximal segments retain their spatial relationship to the urethra that was formed during fetal development. This suggests that the early epithelial budding that occurs in utero represents a common, fairly symmetrical pattern of growth in many species, while the regional differences in branching morphogenesis and cytodifferentiation are controlled by the instructional influences of mesenchyme and temporal expression of growth factors. Perturbation of the normal processes involved during critical periods of fetal development during reproductive organ development may also play a role in the susceptibility of the prostate to disease in adulthood. Past descriptions of detailed anatomical studies, which span over a century, have provided much insight into the architecture and processes that form a complex tubulo-alveolar gland. New insights into the ductal detail and the advent of sophisticated analyses of cell-cell interactions and molecular mechanisms controlling pathways of cellular growth, differentiation, and apoptosis will likely lead to new approaches for prevention and therapy of prostatic diseases.
MeSH term(s)	Animals ; Humans ; Male ; Models, Animal ; Prostate/anatomy & histology ; Prostate/embryology ; Prostate/growth & development
Language	English
Publishing date	2008-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1111/j.1432-0436.2008.00278.x
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Article ; Online: Prostate development and growth in benign prostatic hyperplasia.

Timms, Barry G / Hofkamp, Luke E

Differentiation; research in biological diversity

2011 Volume 82, Issue 4-5, Page(s) 173–183

Abstract: The etiology of benign prostatic hyperplasia [BPH] in elderly men has intrigued anatomists, pathologists and scientists for centuries. Studies of morbid anatomy, clinical observations and contemporary cellular biology have contributed to an evolving ... ...

Abstract	The etiology of benign prostatic hyperplasia [BPH] in elderly men has intrigued anatomists, pathologists and scientists for centuries. Studies of morbid anatomy, clinical observations and contemporary cellular biology have contributed to an evolving interpretation of the causality of the disease. Insights into the detailed microanatomy and ductal architecture of the prostate during stages of fetal and early postnatal development suggest that mechanisms involved in the early growth period become aberrantly expressed in elderly men. Age, hormones and epithelial-mesenchymal interactions are all contributing factors to the pathogenesis of BPH. Control of the microenvironment in normal and abnormal growth is a multifactorial process. Susceptibility to the disease may include clinical comorbid diseases, region-specific changes in cell-cell interactions and a variety of signaling pathways including a novel hypothesis regarding the role of the primary cilium as a regulator of signal transduction mechanisms. Recent work in animal models has shown that there are region-specific differences within the prostate that may be significant because of the dynamic and intricate interplay between the epithelium and mesenchyme. Because of the focal nature of BPH a closer examination of normal morphogenesis patterns, which defines the gland's architecture, may facilitate a detailed understanding of the atypical growth patterns.
MeSH term(s)	Aged ; Androgens/metabolism ; Cilia/metabolism ; Cilia/pathology ; Disease Susceptibility ; Epithelial Cells/pathology ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Humans ; Insulin/metabolism ; Male ; Mesoderm/growth & development ; Mesoderm/pathology ; Prostate/anatomy & histology ; Prostate/embryology ; Prostate/growth & development ; Prostate/pathology ; Prostatic Hyperplasia/embryology ; Prostatic Hyperplasia/etiology ; Prostatic Hyperplasia/pathology ; Signal Transduction ; Stromal Cells/metabolism ; Tumor Microenvironment
Chemical Substances	Androgens ; Hedgehog Proteins ; Insulin
Language	English
Publishing date	2011-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2011.08.002
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Article ; Online: Development of the human prostate.

Cunha, Gerald R / Vezina, Chad M / Isaacson, Dylan / Ricke, William A / Timms, Barry G / Cao, Mei / Franco, Omar / Baskin, Laurence S

Differentiation; research in biological diversity

2018 Volume 103, Page(s) 24–45

Abstract: This paper provides a detailed compilation of human prostatic development that includes human fetal prostatic gross anatomy, histology, and ontogeny of selected epithelial and mesenchymal differentiation markers and signaling molecules throughout the ... ...

Abstract	This paper provides a detailed compilation of human prostatic development that includes human fetal prostatic gross anatomy, histology, and ontogeny of selected epithelial and mesenchymal differentiation markers and signaling molecules throughout the stages of human prostatic development: (a) pre-bud urogenital sinus (UGS), (b) emergence of solid prostatic epithelial buds from urogenital sinus epithelium (UGE), (c) bud elongation and branching, (d) canalization of the solid epithelial cords, (e) differentiation of luminal and basal epithelial cells, and (f) secretory cytodifferentiation. Additionally, we describe the use of xenografts to assess the actions of androgens and estrogens on human fetal prostatic development. In this regard, we report a new model of de novo DHT-induction of prostatic development from xenografts of human fetal female urethras, which emphasizes the utility of the xenograft approach for investigation of initiation of human prostatic development. These studies raise the possibility of molecular mechanistic studies on human prostatic development through the use of tissue recombinants composed of mutant mouse UGM combined with human fetal prostatic epithelium. Our compilation of human prostatic developmental processes is likely to advance our understanding of the pathogenesis of benign prostatic hyperplasia and prostate cancer as the neoformation of ductal-acinar architecture during normal development is shared during the pathogenesis of benign prostatic hyperplasia and prostate cancer.
MeSH term(s)	Androgens/genetics ; Androgens/metabolism ; Cell Differentiation/genetics ; Epithelial Cells/metabolism ; Estrogens/genetics ; Estrogens/metabolism ; Female ; Humans ; Male ; Mesoderm/growth & development ; Prostate/growth & development ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Urethra/growth & development ; Urogenital System/growth & development ; Urogenital System/metabolism
Chemical Substances	Androgens ; Estrogens
Language	English
Publishing date	2018-09-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2018.08.005
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Article: Prostate development and growth in benign prostatic hyperplasia

Timms, Barry G / Hofkamp, Luke E

Differentiation. 2011 , v. 82, no. 4-5

2011

Abstract	The etiology of benign prostatic hyperplasia [BPH] in elderly men has intrigued anatomists, pathologists and scientists for centuries. Studies of morbid anatomy, clinical observations and contemporary cellular biology have contributed to an evolving interpretation of the causality of the disease. Insights into the detailed microanatomy and ductal architecture of the prostate during stages of fetal and early postnatal development suggest that mechanisms involved in the early growth period become aberrantly expressed in elderly men. Age, hormones and epithelial–mesenchymal interactions are all contributing factors to the pathogenesis of BPH. Control of the microenvironment in normal and abnormal growth is a multifactorial process. Susceptibility to the disease may include clinical comorbid diseases, region-specific changes in cell–cell interactions and a variety of signaling pathways including a novel hypothesis regarding the role of the primary cilium as a regulator of signal transduction mechanisms. Recent work in animal models has shown that there are region-specific differences within the prostate that may be significant because of the dynamic and intricate interplay between the epithelium and mesenchyme. Because of the focal nature of BPH a closer examination of normal morphogenesis patterns, which defines the gland's architecture, may facilitate a detailed understanding of the atypical growth patterns.
Keywords	animal models ; disease resistance ; elderly ; epithelium ; etiology ; hormones ; hyperplasia ; men ; morphogenesis ; pathogenesis ; postnatal development ; scientists ; signal transduction
Language	English
Dates of publication	2011-11
Size	p. 173-183.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2011.08.002
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Article ; Online: Fetal bisphenol A and ethinylestradiol exposure alters male rat urogenital tract morphology at birth: Confirmation of prior low-dose findings in CLARITY-BPA.

Uchtmann, Kristen S / Taylor, Julia A / Timms, Barry G / Stahlhut, Richard W / Ricke, Emily A / Ellersieck, Mark R / Vom Saal, Frederick S / Ricke, William A

Reproductive toxicology (Elmsford, N.Y.)

2019 Volume 91, Page(s) 131–141

Abstract: Bisphenol A (BPA) is a contaminant in virtually all Americans. To examine BPA's adverse effects, the FDA-NCTR, NIEHS, and 14 groups of academic scientists formed a consortium: CLARITY-BPA. The purpose of our study was to investigate the effects of a wide ...

Abstract	Bisphenol A (BPA) is a contaminant in virtually all Americans. To examine BPA's adverse effects, the FDA-NCTR, NIEHS, and 14 groups of academic scientists formed a consortium: CLARITY-BPA. The purpose of our study was to investigate the effects of a wide range of doses of BPA on fetal development of the NCTR CD-SD male rat urogenital sinus (UGS). Pregnant rats were administered BPA or positive control ethinylestradiol (EE2) daily, via oral gavage, from gestational day 6 through parturition. Tissues were collected on postnatal day 1 and the UGS was analyzed using computer-assisted 3-D reconstruction. Importantly, only low doses of BPA, as well as EE2, significantly changed birth weight and UGS morphology, including an increased size of the colliculus and decreased size of the urethra, consistent with prior reported BPA and EE2 effects. Our findings provide further evidence that BPA mediates nonmonotonic developmental effects on the fetal urogenital sinus.
MeSH term(s)	Animals ; Benzhydryl Compounds/toxicity ; Endocrine Disruptors/toxicity ; Estrogens/toxicity ; Ethinyl Estradiol/toxicity ; Female ; Fetal Development/drug effects ; Fetus ; Humans ; Male ; Maternal-Fetal Exchange ; Phenols/toxicity ; Pregnancy ; Rats, Sprague-Dawley ; Urogenital Abnormalities/chemically induced
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Estrogens ; Phenols ; Ethinyl Estradiol (423D2T571U) ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2019-11-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639342-1
ISSN	1873-1708 ; 0890-6238
ISSN (online)	1873-1708
ISSN	0890-6238
DOI	10.1016/j.reprotox.2019.11.007
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Article ; Online: Atypical fetal prostate development is associated with ipsilateral hypoplasia of the wolffian ducts in the ACI rat.

Hofkamp, Luke E / Bradley, Sarahann / Geliebter, Jan / Timms, Barry G

Anatomical record (Hoboken, N.J. : 2007)

2010 Volume 293, Issue 5, Page(s) 747–753

Abstract: For over a half century, the ACI (August x Copenhagen) rat has been a primary model for studying renal agenesis and ipsilateral hypoplasia (IHP) of the Wolffian-derived structures (WDS). Because the ACI rat is also used as a model for prostate research, ... ...

Abstract	For over a half century, the ACI (August x Copenhagen) rat has been a primary model for studying renal agenesis and ipsilateral hypoplasia (IHP) of the Wolffian-derived structures (WDS). Because the ACI rat is also used as a model for prostate research, it is important to examine the relationship of IHP and urogenital sinus (UGS) development. The prostate is dependent on androgens for proper growth and differentiation. Alteration in androgen production and/or delivery to the UGS has the potential to perturbate normal development. In this study, we investigate whether the ipsilateral loss of the WDS is associated with altered prostate development. Digital images of serial-sectioned fetal ACI rat UGS were used to create three-dimensional (3-D) surface-rendered models of the developing prostate, seminal vesicle, vas deferens, and utricle on gestational day 21. The number and volume of prostate ducts developing from the UGS were calculated from the 3-D model data. Animals exhibiting IHP had a significant decrease in total fetal prostate volume (40%; P < 0.005) with significant regional specific differences when compared with normal male ACI rats. Anatomical and histological differences in the utricle, abnormal histology of the ipsilateral testes, and a truncation of the ipsilateral Wolffian ductal mesenchyme were also seen in the animals with IHP. Additional research is needed to further understand the mechanisms and consequences of IHP on prostate growth and development. Alterations to normal prenatal development of the male accessory sex organs can have important consequences for the growth and morphology of the adult gland.
MeSH term(s)	Androgens/deficiency ; Androgens/metabolism ; Animals ; Disease Models, Animal ; Imaging, Three-Dimensional/methods ; Male ; Mesoderm/abnormalities ; Mesoderm/metabolism ; Mesoderm/physiopathology ; Models, Anatomic ; Organogenesis/physiology ; Prostate/abnormalities ; Prostate/metabolism ; Prostate/physiopathology ; Rats ; Rats, Inbred ACI ; Sex Differentiation/physiology ; Testis/abnormalities ; Testis/metabolism ; Testis/physiopathology ; Urogenital Abnormalities/etiology ; Urogenital Abnormalities/metabolism ; Urogenital Abnormalities/physiopathology ; Wolffian Ducts/abnormalities ; Wolffian Ducts/metabolism ; Wolffian Ducts/physiopathology
Chemical Substances	Androgens
Language	English
Publishing date	2010-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2269667-2
ISSN	1932-8494 ; 1932-8486
ISSN (online)	1932-8494
ISSN	1932-8486
DOI	10.1002/ar.21073
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Article: 2,3,7,8-tetrachlorodibenzo-p-dioxin interacts with endogenous estradiol to disrupt prostate gland morphogenesis in male rat fetuses.

Timms, Barry G / Peterson, Richard E / vom Saal, Frederick S

Toxicological sciences : an official journal of the Society of Toxicology

2002 Volume 67, Issue 2, Page(s) 264–274

Abstract: Fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interferes with normal development of the male reproductive system in rats and mice. We examined the effects of TCDD on the initial development of the urogenital system (urethra, prostate, and ... ...

Abstract	Fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interferes with normal development of the male reproductive system in rats and mice. We examined the effects of TCDD on the initial development of the urogenital system (urethra, prostate, and seminal vesicles) in male rat fetuses on gestation day (GD) 20. The number of prostatic buds and size of prostate glands as well as seminal vesicle size was determined by computer-assisted 3D reconstruction. Pregnant Holtzman rats received a single oral dose of TCDD (1 microg/kg) on GD 15. The intrauterine position (IUP) of male fetuses was identified based on the sex of adjacent fetuses: 2F males were located between 2 females and 2M males were located between 2 males. Control 2F males had elevated serum estradiol and larger prostates than control 2M males, which had elevated serum testosterone and larger seminal vesicles, confirming prior findings. There was no effect of TCDD on serum testosterone. TCDD significantly decreased the number of buds in the dorsocranial and dorsolateral regions of the urogenital sinus and overall prostate size, and was associated with a significant decrease in serum estradiol only in 2F males. In contrast, in 2M males both serum estradiol and the number and size of prostatic buds in these same regions of the prostate were unaffected by TCDD, although seminal vesicle size was reduced. These findings show that individual differences in gonadal steroid levels influence the response of the developing prostate to TCDD in male fetuses. In addition, these TCDD effects may be mediated in part by a decrease in serum estradiol levels.
MeSH term(s)	Abnormalities, Drug-Induced ; Animals ; Embryonic and Fetal Development/drug effects ; Environment ; Estradiol/blood ; Estradiol/physiology ; Female ; Fetus/drug effects ; Fetus/physiology ; Male ; Polychlorinated Dibenzodioxins/toxicity ; Pregnancy ; Prostate/abnormalities ; Prostate/drug effects ; Rats ; Rats, Sprague-Dawley ; Teratogens/toxicity ; Testosterone/blood ; Uterus/physiology
Chemical Substances	Polychlorinated Dibenzodioxins ; Teratogens ; Testosterone (3XMK78S47O) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2002-06
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/67.2.264
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Article: Implications for human health of the extensive bisphenol A literature showing adverse effects at low doses: a response to attempts to mislead the public.

vom Saal, Frederick S / Nagel, Susan C / Timms, Barry G / Welshons, Wade V

Toxicology

2005 Volume 212, Issue 2-3, Page(s) 244–52, author reply 253–4

MeSH term(s)	Animals ; Benzhydryl Compounds ; Estrogens, Non-Steroidal/toxicity ; Fraud ; Humans ; Phenols/toxicity ; Public Health ; Reproducibility of Results ; Risk Assessment ; Scientific Misconduct
Chemical Substances	Benzhydryl Compounds ; Estrogens, Non-Steroidal ; Phenols ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2005-09-01
Publishing country	Ireland
Document type	Comment ; Letter
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2005.05.006
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Article ; Online: Testosterone and 17β-estradiol induce glandular prostatic growth, bladder outlet obstruction, and voiding dysfunction in male mice.

Nicholson, Tristan M / Ricke, Emily A / Marker, Paul C / Miano, Joseph M / Mayer, Robert D / Timms, Barry G / vom Saal, Frederick S / Wood, Ronald W / Ricke, William A

Endocrinology

2012 Volume 153, Issue 11, Page(s) 5556–5565

Abstract: Benign prostatic hyperplasia (BPH) and bladder outlet obstruction (BOO) are common in older men and can contribute to lower urinary tract symptoms that significantly impact quality of life. Few existing models of BOO and BPH use physiological levels of ... ...

Abstract	Benign prostatic hyperplasia (BPH) and bladder outlet obstruction (BOO) are common in older men and can contribute to lower urinary tract symptoms that significantly impact quality of life. Few existing models of BOO and BPH use physiological levels of hormones associated with disease progression in humans in a genetically manipulable organism. We present a model of BPH and BOO induced in mice with testosterone (T) and 17β-estradiol (E(2)). Male mice were surgically implanted with slow-releasing sc pellets containing 25 mg T and 2.5 mg E(2) (T+E(2)). After 2 and 4 months of hormone treatment, we evaluated voiding patterns and examined the gross morphology and histology of the bladder, urethra, and prostate. Mice treated with T+E(2) developed significantly larger bladders than untreated mice, consistent with BOO. Some mice treated with T+E(2) had complications in the form of bladder hypertrophy, diverticula, calculi, and eventual decompensation with hydronephrosis. Hormone treatment caused a significant decrease in the size of the urethral lumen, increased prostate mass, and increased number of prostatic ducts associated with the prostatic urethra, compared with untreated mice. Voiding dysfunction was observed in mice treated with T+E(2), who exhibited droplet voiding pattern with significantly decreased void mass, shorter void duration, and fewer sustained voids. The constellation of lower urinary tract abnormalities, including BOO, enlarged prostates, and voiding dysfunction seen in male mice treated with T+E(2) is consistent with BPH in men. This model is suitable for better understanding molecular mechanisms and for developing novel strategies to address BPH and BOO.
MeSH term(s)	Animals ; Estradiol/pharmacology ; Male ; Mice ; Prostate/drug effects ; Prostate/physiopathology ; Prostatic Hyperplasia/chemically induced ; Prostatic Hyperplasia/complications ; Prostatic Hyperplasia/physiopathology ; Testosterone/pharmacology ; Urethra/drug effects ; Urethra/physiopathology ; Urinary Bladder/drug effects ; Urinary Bladder/physiopathology ; Urinary Bladder Neck Obstruction/chemically induced ; Urinary Bladder Neck Obstruction/complications ; Urinary Bladder Neck Obstruction/physiopathology ; Urodynamics/drug effects ; Urodynamics/physiology
Chemical Substances	Testosterone (3XMK78S47O) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2012-09-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2012-1522
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