The Experts below are selected from a list of 117 Experts worldwide ranked by ideXlab platform
Richard E. Peterson - One of the best experts on this subject based on the ideXlab platform.
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In Utero and Lactational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin in the C57BL/6J Mouse Prostate: Lobe-Specific Effects on Branching Morphogenesis
Toxicological Sciences, 2002Co-Authors: Kinarm Ko, H. Michael Theobald, Richard E. PetersonAbstract:Branching morphogenesis is an essential component of Prostate development. This study was conducted to test the hypothesis that in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure differentially inhibits branching morphogenesis and ductal canalization in the ventral, dorsal, lateral, and anterior mouse Prostate. Pregnant C57BL/6J mice were given TCDD (5 g/kg, orally) or vehicle on gestation day (GD) 13 and their pups examined at 1, 7, 14, 21, 35, and 90 days of age. Prostate Lobes were microdissected after incubation in 0.5% collagenase and the num- bers of ductal tips, main ducts, and ductal tips per main duct were determined by examining photographs of microdissected, whole- mount specimens. Ductal canalization was determined using his- tological sections of the dorsolateral and anterior Prostate Lobes. TCDD inhibited branching morphogenesis in all Prostate Lobes. The ventral Prostate (VP) was extremely small throughout devel- opment and never developed any ductal structure. TCDD reduced the numbers of ductal tips and main ducts in the dorsal (DP) and lateral Prostate (LP), but reductions in ductal tip numbers ap- peared to result entirely from reductions in the number of main ducts. Dorsolateral Prostate (DLP) weights were slightly reduced by TCDD, but there was no effect on ductal canalization in the dorsal, lateral, or anterior Lobes. TCDD had no effect on main duct number in the anterior Prostate, but weight, ductal tip number, and the number of ductal tips per main duct was substantially reduced. These results demonstrate that the severe inhibition in ventral Prostate development caused by in utero and lactational TCDD exposure is accompanied by a complete absence of branch- ing morphogenesis. The impairment in dorsal, lateral, and ante- rior Prostate (AP) development is associated with a Lobe-specific inhibition of the various processes involved in duct formation.
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in utero and lactational exposure to 2 3 7 8 tetrachlorodibenzo p dioxin in the c57bl 6j mouse Prostate Lobe specific effects on branching morphogenesis
Toxicological Sciences, 2002Co-Authors: Kinarm Ko, Michael H Theobald, Richard E. PetersonAbstract:Branching morphogenesis is an essential component of Prostate development. This study was conducted to test the hypothesis that in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure differentially inhibits branching morphogenesis and ductal canalization in the ventral, dorsal, lateral, and anterior mouse Prostate. Pregnant C57BL/6J mice were given TCDD (5 g/kg, orally) or vehicle on gestation day (GD) 13 and their pups examined at 1, 7, 14, 21, 35, and 90 days of age. Prostate Lobes were microdissected after incubation in 0.5% collagenase and the num- bers of ductal tips, main ducts, and ductal tips per main duct were determined by examining photographs of microdissected, whole- mount specimens. Ductal canalization was determined using his- tological sections of the dorsolateral and anterior Prostate Lobes. TCDD inhibited branching morphogenesis in all Prostate Lobes. The ventral Prostate (VP) was extremely small throughout devel- opment and never developed any ductal structure. TCDD reduced the numbers of ductal tips and main ducts in the dorsal (DP) and lateral Prostate (LP), but reductions in ductal tip numbers ap- peared to result entirely from reductions in the number of main ducts. Dorsolateral Prostate (DLP) weights were slightly reduced by TCDD, but there was no effect on ductal canalization in the dorsal, lateral, or anterior Lobes. TCDD had no effect on main duct number in the anterior Prostate, but weight, ductal tip number, and the number of ductal tips per main duct was substantially reduced. These results demonstrate that the severe inhibition in ventral Prostate development caused by in utero and lactational TCDD exposure is accompanied by a complete absence of branch- ing morphogenesis. The impairment in dorsal, lateral, and ante- rior Prostate (AP) development is associated with a Lobe-specific inhibition of the various processes involved in duct formation.
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effects of aryl hydrocarbon receptor null mutation and in utero and lactational 2 3 7 8 tetrachlorodibenzo p dioxin exposure on Prostate and seminal vesicle development in c57bl 6 mice
Toxicological Sciences, 2002Co-Authors: Kinarm Ko, Ulla Simanainen, Robert W Moore, Terry D Oberley, Richard E. PetersonAbstract:Experiments were conducted to determine the effects of aryl hydrocarbon receptor (AhR) null mutation and in utero and lac- tational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure, alone and in combination, on Prostate and seminal vesicle devel- opment in C57BL/6 mice. AhR heterozygous (Ahr /- ) mice were mated, and pregnant females were dosed orally on gestation day 13 with TCDD (5 g/kg) or vehicle. Pups underwent necropsy on postnatal days (PNDs) 35 and 90. Comparison of vehicle-exposed AhR knockout (AhRKO; Ahr -/- ) with wild-type (Ahr / ) pups revealed that the AhR is necessary for normal dorsolateral pros- tate, anterior Prostate, and seminal vesicle development but ap- parently not for ventral Prostate development. In wild-type mice, in utero and lactational TCDD exposure reduced ventral Prostate weight by 79 - 87% and mRNA expression for its major androgen- dependent secretory protein (MP25) by 99%. Yet high levels of mRNA for a secretory protein normally produced primarily by the lateral Prostate (PSP94) were expressed. These effects were pre- dominantly AhR dependent because TCDD had little if any effect in AhRKO mice. TCDD reduced dorsolateral Prostate weight in wild-type but not AhRKO mice and had no significant effect on expression of mRNA for PSP94 or for probasin, a major androgen- dependent secretory protein. The PSP94 results suggest that TCDD may have caused a respecification of prostatic gene expres- sion. TCDD reduced anterior Prostate weight by more than half, and expression of mRNA for its major androgen-dependent secre- tory protein (renin-1) was greatly reduced. These effects were AhR dependent. Seminal vesicle weight was reduced by TCDD in wild-type mice but was increased in AhRKO mice on PND 35 and decreased on PND 90 (relative weight only). Androgen receptor mRNA levels were not significantly altered in any Prostate Lobe, and all organs appeared histologically normal in all groups. Serum testosterone concentrations were unchanged, and modest reduc- tions in serum 5-androstane-3,17-diol concentrations could not account for the effects on sex organs. Collectively, these results indicate that the AhR signaling pathway plays a role in normal accessory sex organ development and that in utero and lactational TCDD exposure disrupts development of these organs via spa-
Hans-jürgen Wester - One of the best experts on this subject based on the ideXlab platform.
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^68Ga-PSMA PET/CT Imaging Predicting Intraprostatic Tumor Extent, Extracapsular Extension and Seminal Vesicle Invasion Prior to Radical Prostatectomy in Patients with Prostate Cancer
Nuclear Medicine and Molecular Imaging, 2017Co-Authors: Christoph-alexander J. Klot, Axel S. Merseburger, Alena Böker, Sebastian Schmuck, Tobias L. Ross, Frank M. Bengel, Markus A. Kuczyk, Christoph Henkenberens, Hans Christiansen, Hans-jürgen WesterAbstract:Purpose ^68Ga-labeled Prostate-specific membrane antigen (PSMA) ligand positron emission tomography/computed tomography (PET/CT) has shown promising results in patients with biochemical recurrence after primary therapy for Prostate cancer. In this study, we evaluated the usefulness of PSMA I&T (imaging and therapy) PET/CT prior to radical Prostatectomy. Methods The study population consisted of 21 patients with Prostate cancer who underwent ^68Ga-PSMA I&T PET/CT before either open or laparoscopic radical Prostatectomy. Intraprostatic tumor extent, extracapsular extension (ECE) and seminal vesicle invasion (SVI) were assessed on the PET/CT scans. Tracer uptake was quantified in terms of standardized uptake values (SUVs). Imaging findings were correlated with final whole-gland histopathology. Results Of the 21 patients, two had T stage 2b disease, nine stage 2c, six stage 3a and four stage 3b. The median Gleason score was 7. The SUV_mean of the primary tumors was 9.5 ± 8.8. SUV_mean was higher in tumors with ECE than in organ-confined tumors (13.8 ± 11.0 vs. 5.6 ± 3.2, p = 0.029). Peak tracer uptake was significantly positively correlated with Gleason score ( r _s = 0.49, p = 0.025). Sensitivity, specificity, positive predictive value and negative predictive value were, respectively, 94.7%, 75.0%, 97.3% and 60.0% for tumor infiltration of an individual Prostate Lobe, 75.0%, 100.0%, 100.0% and 97.4% for SVI, and 90.0%, 90.9%, 90.0% and 90.9% for ECE, using an angulated contour of the Prostate as the criterion. Tumor volume derived from ^68Ga-PSMA I&T PET/CT was significantly correlated with preoperative Prostate-specific antigen value ( r _p = 0.75, p
Kinarm Ko - One of the best experts on this subject based on the ideXlab platform.
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In Utero and Lactational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin in the C57BL/6J Mouse Prostate: Lobe-Specific Effects on Branching Morphogenesis
Toxicological Sciences, 2002Co-Authors: Kinarm Ko, H. Michael Theobald, Richard E. PetersonAbstract:Branching morphogenesis is an essential component of Prostate development. This study was conducted to test the hypothesis that in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure differentially inhibits branching morphogenesis and ductal canalization in the ventral, dorsal, lateral, and anterior mouse Prostate. Pregnant C57BL/6J mice were given TCDD (5 g/kg, orally) or vehicle on gestation day (GD) 13 and their pups examined at 1, 7, 14, 21, 35, and 90 days of age. Prostate Lobes were microdissected after incubation in 0.5% collagenase and the num- bers of ductal tips, main ducts, and ductal tips per main duct were determined by examining photographs of microdissected, whole- mount specimens. Ductal canalization was determined using his- tological sections of the dorsolateral and anterior Prostate Lobes. TCDD inhibited branching morphogenesis in all Prostate Lobes. The ventral Prostate (VP) was extremely small throughout devel- opment and never developed any ductal structure. TCDD reduced the numbers of ductal tips and main ducts in the dorsal (DP) and lateral Prostate (LP), but reductions in ductal tip numbers ap- peared to result entirely from reductions in the number of main ducts. Dorsolateral Prostate (DLP) weights were slightly reduced by TCDD, but there was no effect on ductal canalization in the dorsal, lateral, or anterior Lobes. TCDD had no effect on main duct number in the anterior Prostate, but weight, ductal tip number, and the number of ductal tips per main duct was substantially reduced. These results demonstrate that the severe inhibition in ventral Prostate development caused by in utero and lactational TCDD exposure is accompanied by a complete absence of branch- ing morphogenesis. The impairment in dorsal, lateral, and ante- rior Prostate (AP) development is associated with a Lobe-specific inhibition of the various processes involved in duct formation.
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in utero and lactational exposure to 2 3 7 8 tetrachlorodibenzo p dioxin in the c57bl 6j mouse Prostate Lobe specific effects on branching morphogenesis
Toxicological Sciences, 2002Co-Authors: Kinarm Ko, Michael H Theobald, Richard E. PetersonAbstract:Branching morphogenesis is an essential component of Prostate development. This study was conducted to test the hypothesis that in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure differentially inhibits branching morphogenesis and ductal canalization in the ventral, dorsal, lateral, and anterior mouse Prostate. Pregnant C57BL/6J mice were given TCDD (5 g/kg, orally) or vehicle on gestation day (GD) 13 and their pups examined at 1, 7, 14, 21, 35, and 90 days of age. Prostate Lobes were microdissected after incubation in 0.5% collagenase and the num- bers of ductal tips, main ducts, and ductal tips per main duct were determined by examining photographs of microdissected, whole- mount specimens. Ductal canalization was determined using his- tological sections of the dorsolateral and anterior Prostate Lobes. TCDD inhibited branching morphogenesis in all Prostate Lobes. The ventral Prostate (VP) was extremely small throughout devel- opment and never developed any ductal structure. TCDD reduced the numbers of ductal tips and main ducts in the dorsal (DP) and lateral Prostate (LP), but reductions in ductal tip numbers ap- peared to result entirely from reductions in the number of main ducts. Dorsolateral Prostate (DLP) weights were slightly reduced by TCDD, but there was no effect on ductal canalization in the dorsal, lateral, or anterior Lobes. TCDD had no effect on main duct number in the anterior Prostate, but weight, ductal tip number, and the number of ductal tips per main duct was substantially reduced. These results demonstrate that the severe inhibition in ventral Prostate development caused by in utero and lactational TCDD exposure is accompanied by a complete absence of branch- ing morphogenesis. The impairment in dorsal, lateral, and ante- rior Prostate (AP) development is associated with a Lobe-specific inhibition of the various processes involved in duct formation.
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effects of aryl hydrocarbon receptor null mutation and in utero and lactational 2 3 7 8 tetrachlorodibenzo p dioxin exposure on Prostate and seminal vesicle development in c57bl 6 mice
Toxicological Sciences, 2002Co-Authors: Kinarm Ko, Ulla Simanainen, Robert W Moore, Terry D Oberley, Richard E. PetersonAbstract:Experiments were conducted to determine the effects of aryl hydrocarbon receptor (AhR) null mutation and in utero and lac- tational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure, alone and in combination, on Prostate and seminal vesicle devel- opment in C57BL/6 mice. AhR heterozygous (Ahr /- ) mice were mated, and pregnant females were dosed orally on gestation day 13 with TCDD (5 g/kg) or vehicle. Pups underwent necropsy on postnatal days (PNDs) 35 and 90. Comparison of vehicle-exposed AhR knockout (AhRKO; Ahr -/- ) with wild-type (Ahr / ) pups revealed that the AhR is necessary for normal dorsolateral pros- tate, anterior Prostate, and seminal vesicle development but ap- parently not for ventral Prostate development. In wild-type mice, in utero and lactational TCDD exposure reduced ventral Prostate weight by 79 - 87% and mRNA expression for its major androgen- dependent secretory protein (MP25) by 99%. Yet high levels of mRNA for a secretory protein normally produced primarily by the lateral Prostate (PSP94) were expressed. These effects were pre- dominantly AhR dependent because TCDD had little if any effect in AhRKO mice. TCDD reduced dorsolateral Prostate weight in wild-type but not AhRKO mice and had no significant effect on expression of mRNA for PSP94 or for probasin, a major androgen- dependent secretory protein. The PSP94 results suggest that TCDD may have caused a respecification of prostatic gene expres- sion. TCDD reduced anterior Prostate weight by more than half, and expression of mRNA for its major androgen-dependent secre- tory protein (renin-1) was greatly reduced. These effects were AhR dependent. Seminal vesicle weight was reduced by TCDD in wild-type mice but was increased in AhRKO mice on PND 35 and decreased on PND 90 (relative weight only). Androgen receptor mRNA levels were not significantly altered in any Prostate Lobe, and all organs appeared histologically normal in all groups. Serum testosterone concentrations were unchanged, and modest reduc- tions in serum 5-androstane-3,17-diol concentrations could not account for the effects on sex organs. Collectively, these results indicate that the AhR signaling pathway plays a role in normal accessory sex organ development and that in utero and lactational TCDD exposure disrupts development of these organs via spa-
Christoph-alexander J. Klot - One of the best experts on this subject based on the ideXlab platform.
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^68Ga-PSMA PET/CT Imaging Predicting Intraprostatic Tumor Extent, Extracapsular Extension and Seminal Vesicle Invasion Prior to Radical Prostatectomy in Patients with Prostate Cancer
Nuclear Medicine and Molecular Imaging, 2017Co-Authors: Christoph-alexander J. Klot, Axel S. Merseburger, Alena Böker, Sebastian Schmuck, Tobias L. Ross, Frank M. Bengel, Markus A. Kuczyk, Christoph Henkenberens, Hans Christiansen, Hans-jürgen WesterAbstract:Purpose ^68Ga-labeled Prostate-specific membrane antigen (PSMA) ligand positron emission tomography/computed tomography (PET/CT) has shown promising results in patients with biochemical recurrence after primary therapy for Prostate cancer. In this study, we evaluated the usefulness of PSMA I&T (imaging and therapy) PET/CT prior to radical Prostatectomy. Methods The study population consisted of 21 patients with Prostate cancer who underwent ^68Ga-PSMA I&T PET/CT before either open or laparoscopic radical Prostatectomy. Intraprostatic tumor extent, extracapsular extension (ECE) and seminal vesicle invasion (SVI) were assessed on the PET/CT scans. Tracer uptake was quantified in terms of standardized uptake values (SUVs). Imaging findings were correlated with final whole-gland histopathology. Results Of the 21 patients, two had T stage 2b disease, nine stage 2c, six stage 3a and four stage 3b. The median Gleason score was 7. The SUV_mean of the primary tumors was 9.5 ± 8.8. SUV_mean was higher in tumors with ECE than in organ-confined tumors (13.8 ± 11.0 vs. 5.6 ± 3.2, p = 0.029). Peak tracer uptake was significantly positively correlated with Gleason score ( r _s = 0.49, p = 0.025). Sensitivity, specificity, positive predictive value and negative predictive value were, respectively, 94.7%, 75.0%, 97.3% and 60.0% for tumor infiltration of an individual Prostate Lobe, 75.0%, 100.0%, 100.0% and 97.4% for SVI, and 90.0%, 90.9%, 90.0% and 90.9% for ECE, using an angulated contour of the Prostate as the criterion. Tumor volume derived from ^68Ga-PSMA I&T PET/CT was significantly correlated with preoperative Prostate-specific antigen value ( r _p = 0.75, p
Christoph Henkenberens - One of the best experts on this subject based on the ideXlab platform.
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^68Ga-PSMA PET/CT Imaging Predicting Intraprostatic Tumor Extent, Extracapsular Extension and Seminal Vesicle Invasion Prior to Radical Prostatectomy in Patients with Prostate Cancer
Nuclear Medicine and Molecular Imaging, 2017Co-Authors: Christoph-alexander J. Klot, Axel S. Merseburger, Alena Böker, Sebastian Schmuck, Tobias L. Ross, Frank M. Bengel, Markus A. Kuczyk, Christoph Henkenberens, Hans Christiansen, Hans-jürgen WesterAbstract:Purpose ^68Ga-labeled Prostate-specific membrane antigen (PSMA) ligand positron emission tomography/computed tomography (PET/CT) has shown promising results in patients with biochemical recurrence after primary therapy for Prostate cancer. In this study, we evaluated the usefulness of PSMA I&T (imaging and therapy) PET/CT prior to radical Prostatectomy. Methods The study population consisted of 21 patients with Prostate cancer who underwent ^68Ga-PSMA I&T PET/CT before either open or laparoscopic radical Prostatectomy. Intraprostatic tumor extent, extracapsular extension (ECE) and seminal vesicle invasion (SVI) were assessed on the PET/CT scans. Tracer uptake was quantified in terms of standardized uptake values (SUVs). Imaging findings were correlated with final whole-gland histopathology. Results Of the 21 patients, two had T stage 2b disease, nine stage 2c, six stage 3a and four stage 3b. The median Gleason score was 7. The SUV_mean of the primary tumors was 9.5 ± 8.8. SUV_mean was higher in tumors with ECE than in organ-confined tumors (13.8 ± 11.0 vs. 5.6 ± 3.2, p = 0.029). Peak tracer uptake was significantly positively correlated with Gleason score ( r _s = 0.49, p = 0.025). Sensitivity, specificity, positive predictive value and negative predictive value were, respectively, 94.7%, 75.0%, 97.3% and 60.0% for tumor infiltration of an individual Prostate Lobe, 75.0%, 100.0%, 100.0% and 97.4% for SVI, and 90.0%, 90.9%, 90.0% and 90.9% for ECE, using an angulated contour of the Prostate as the criterion. Tumor volume derived from ^68Ga-PSMA I&T PET/CT was significantly correlated with preoperative Prostate-specific antigen value ( r _p = 0.75, p
