Buserelin Acetate

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Akira Ueno - One of the best experts on this subject based on the ideXlab platform.

  • potentiating effect of Buserelin Acetate an lhrh agonist on the proliferation of ventral prostatic epithelial cells in testosterone treated castrated rats
    International Journal of Urology, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

  • Potentiating Effect of Buserelin Acetate, an LHRH Agonist, on the Proliferation of Ventral Prostatic Epithelial Cells in Testosterone‐Treated Castrated Rats
    International journal of urology : official journal of the Japanese Urological Association, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

Hiroaki Maezawa - One of the best experts on this subject based on the ideXlab platform.

  • potentiating effect of Buserelin Acetate an lhrh agonist on the proliferation of ventral prostatic epithelial cells in testosterone treated castrated rats
    International Journal of Urology, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

  • Potentiating Effect of Buserelin Acetate, an LHRH Agonist, on the Proliferation of Ventral Prostatic Epithelial Cells in Testosterone‐Treated Castrated Rats
    International journal of urology : official journal of the Japanese Urological Association, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

Hideki Komatsu - One of the best experts on this subject based on the ideXlab platform.

  • potentiating effect of Buserelin Acetate an lhrh agonist on the proliferation of ventral prostatic epithelial cells in testosterone treated castrated rats
    International Journal of Urology, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

  • Potentiating Effect of Buserelin Acetate, an LHRH Agonist, on the Proliferation of Ventral Prostatic Epithelial Cells in Testosterone‐Treated Castrated Rats
    International journal of urology : official journal of the Japanese Urological Association, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

Akira Kawaoi - One of the best experts on this subject based on the ideXlab platform.

  • potentiating effect of Buserelin Acetate an lhrh agonist on the proliferation of ventral prostatic epithelial cells in testosterone treated castrated rats
    International Journal of Urology, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

  • Potentiating Effect of Buserelin Acetate, an LHRH Agonist, on the Proliferation of Ventral Prostatic Epithelial Cells in Testosterone‐Treated Castrated Rats
    International journal of urology : official journal of the Japanese Urological Association, 1997
    Co-Authors: Hiroaki Maezawa, Hideki Komatsu, Akira Kawaoi, Akira Ueno
    Abstract:

    Background: We used Buserelin Acetate ([D-Ser(But)6] LHRH), an LHRH agonist and strong blocker of LH secretion, as a treatment for prostatic cancer. It is possible that this LHRH agonist has a proliferative effect on the prostate in addition to suppressing LH secretion. The purpose of this study was to examine the proliferative effect of LHRH agonist on rat prostatic epithelial cells. Methods: We determined the optimal dose of testosterone necessary to maintain a positive level of proliferating cell nuclear antigen (PCNA) in the ventral prostatic epithelial cells of castrated Wistar rats. Testosterone-treated rats then received various doses of Buserelin Acetate. Castrated rats without exogenous testosterone also received Buserelin Acetate. The PCNA positivity was determined by immunohistochemistry with anti-PCNA monoclonal antibody. Results: The optimal dose of testosterone enanthate was 4mg at 0 and 28 days after castration. Administration of Buserelin Acetate on day 0 and 28 in doses of 0.1 6mg to 1.28mg significantly increased PCNA positivity in a dose-dependent manner. Administration of Buserelin Acetate to castrated rats without testosterone also increased PCNA positivity but there was no statistical significance. Conclusions: Buserelin Acetate has a potentiating effect on the proliferation of ventral prostatic epithelial cells of castrated rat in the presence of a physiological level of exogenous testosterone. This effect may slightly influence the result of hormonal therapy by LHRH agonist.

W. F. Huanca - One of the best experts on this subject based on the ideXlab platform.

  • 165 EFFECT OF INJECTION OF SEMINAL PLASMA ON OVULATION RATE, CORPUS LUTEUM DEVELOPMENT, AND SENSITIVITY TO PROSTAGLANDIN IN ALPACAS (VICUGNA PACOS)
    Reproduction Fertility and Development, 2015
    Co-Authors: C. Mamani, W. F. Huanca
    Abstract:

    The seminal plasma (SP) of camelids contains a protein identified as β Nerve Growth Factor with capacity of induced ovulation and develop a corpus luteum. A study was designed to evaluate the effect of application of SP on the interval of time from injection of stimulus to the ovulation and corpus luteum (CL) size (Experiment 1, n = 24) and on the sensitivity of CL to the injection of prostaglandin (196 µg of tiaprost) (PG) at different periods from ovulation (Experiment 2, n = 86). Exp. 1: Adult female alpacas with presence of a follicle ≥7 mm were assigned to the application of 1 mL of SP via IM (T: n = 12) or application of 50 µg of Acetate of Busereline IM (T2: n = 12). Exp. 2: Alpacas with presence of a follicle ≥7 mm were induced to ovulation with 50 µg of Acetate of Busereline or 1 mL IM of SP. Animals were evaluated by ultrasound to confirm the ovulation and were assigned to the following treatment: T1 (n = 8): SP + PG Day 4; T2 (n = 8): Buserelin Acetate + PG Day 4; T3 (n = 8): SP + PG Day 5; T4 (n = 8): Buserelin Acetate + PG Day 5; T5 (n = 8): SP + PG Day 6; T6 (n = 8): Buserelin Acetate + PG Day 6; T7 (n = 8): SP + PG Day 7; T8 (n = 8): Buserelin Acetate + PG Day 7; T9 (n = 8): SP + PG Day 8; T10 (n = 8): Buserelin Acetate + PG Day 8 and T11 (n = 6) (Control): Application of 1 mL of saline solution. The animals were evaluated by ultrasound with an Aloka SSD500 (Aloka, Tokyo, Japan) and 7.5-MHz linear transducer each 2 h (Exp. 1) and each 12 h (Exp. 2) after of application of PG. In Exp. 1, the ovulation rate was 95.7% to T1 and T2 and an interval of time between injection of stimulus and ovulation was 27.4 ± 2.5 h and 26.8 ± 1.8 to T1 and T2, respectively. In Exp. 2, luteolysis was 0.0%, 0.0%, 25.0%, 0.0%, 100.0%, 100.0%, 100.0%, 100.0%, 100.0%, 100.0%, and 0.0% for the treatments T1, T2, T3, T4, T5, T6, T7, T8, T9, T10, and T11 respectively. The results suggest that no differences exist between in the ovulation rate and interval to the ovulation between the application of Buserelin Acetate or SP and that the CL was sensible at Day 5 to the prostaglandin respect SP and with similar response to the sensibility of CL from Day 6 to Day 8.