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John J Morrison - One of the best experts on this subject based on the ideXlab platform.
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17 alpha hydroxyprogesterone caproate vehicle castor oil enhances the contractile effect of oxytocin in human myometrium in pregnancy
American Journal of Obstetrics and Gynecology, 2010Co-Authors: Michael D Osullivan, Mark P Hehir, Yvonne M Obrien, John J MorrisonAbstract:Objective The possibility exists that the vehicle for 17-alpha-hydroxyprogesterone caproate, castor oil, exerts an effect on human uterine Contractility. The aim of this study was to evaluate its effects on Contractility of myometrial preparations that were obtained during pregnancy. Study Design Myometrial strips were suspended under isometric conditions. Contractility was induced with oxytocin. Strips were incubated in castor oil or physiologic salt solution and suspended for a further oxytocin challenge. Contractile integrals were compared between both groups. Results Strips that were exposed to castor oil demonstrated increased contractile activity that was elicited by oxytocin (mean Contractility value, 165.53% ± 17.03%; n=8; P = .004), compared with control strips (mean Contractility value, 72.57% ± 7.48%; n=8; P = .003). There was a significant increase in contractile activity of the castor oil–exposed strips, compared with those that were exposed to physiologic salt solution (n = 8; P Conclusion Exposure of human myometrial preparations to castor oil results in enhanced oxytocin-induced Contractility.
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Modulation of human uterine smooth muscle cell collagen Contractility by thrombin, Y-27632, TNF alpha and indomethacin
Reproductive Biology and Endocrinology, 2009Co-Authors: Joan Fitzgibbon, John J Morrison, Terry J Smith, Margaret O'brienAbstract:Background Preterm labour occurs in approximately 10% of pregnancies and is a major cause of infant morbidity and mortality. However, the pathways involved in regulating Contractility in normal and preterm labour are not fully elucidated. Our aim was to utilise a human myometrial Contractility model to investigate the effect of a number of uterine specific Contractility agents in this system. Therefore, we investigated the contractile response of human primary uterine smooth muscle cells or immortalised myometrial smooth muscle cells cultured within collagen lattices, to known mediators of uterine Contractility, which included thrombin, the ROCK-1 inhibitor Y-27632, tumour necrosis factor alpha (TNF alpha) and the non-steroidal anti-inflammatory indomethacin. Methods Cell Contractility was calculated over time, with the collagen gel contraction assay, utilising human primary uterine smooth muscle cells (hUtSMCs) and immortalised myometrial smooth muscle cells (hTERT-HM): a decrease in collagen gel area equated to an increase in Contractility. RNA was isolated from collagen embedded cells and gene expression changes were analysed by real time fluorescence reverse transcription polymerase chain reaction. Scanning electron and fluorescence microscopy were employed to observe cell morphology and cell collagen gel interactions. Statistical analysis was performed using ANOVA followed by Tukey's post hoc tests. Results TNF alpha increased collagen Contractility in comparison to the un-stimulated collagen embedded hUtSMC cells, which was inhibited by indomethacin, while indomethacin alone significantly inhibited contraction. Thrombin augmented the Contractility of uterine smooth muscle cell and hTERT-HM collagen gels, this effect was inhibited by the thrombin specific inhibitor, hirudin. Y-27632 decreased both basal and thrombin-induced collagen Contractility in the hTERT-HM embedded gels. mRNA expression of the thrombin receptor, F2R was up-regulated in hUtSMCs isolated from collagen gel lattices, following thrombin-stimulated Contractility. Conclusion TNF alpha and thrombin increased uterine smooth muscle cell collagen Contractility while indomethacin had the opposite effect. Thrombin-induced collagen Contractility resulted in F2R activation which may in part be mediated by the ROCK-1 pathway. This study established the in vitro human myometrial model as a viable method to assess the effects of a range of uterotonic or uterorelaxant agents on Contractility, and also permits investigation of the complex regulatory pathways involved in mediating myometrial Contractility at labour.
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modulation of human uterine smooth muscle cell collagen Contractility by thrombin y 27632 tnf alpha and indomethacin
Reproductive Biology and Endocrinology, 2009Co-Authors: Joan Fitzgibbon, John J Morrison, Terry J Smith, Margaret ObrienAbstract:Preterm labour occurs in approximately 10% of pregnancies and is a major cause of infant morbidity and mortality. However, the pathways involved in regulating Contractility in normal and preterm labour are not fully elucidated. Our aim was to utilise a human myometrial Contractility model to investigate the effect of a number of uterine specific Contractility agents in this system. Therefore, we investigated the contractile response of human primary uterine smooth muscle cells or immortalised myometrial smooth muscle cells cultured within collagen lattices, to known mediators of uterine Contractility, which included thrombin, the ROCK-1 inhibitor Y-27632, tumour necrosis factor alpha (TNF alpha) and the non-steroidal anti-inflammatory indomethacin. Cell Contractility was calculated over time, with the collagen gel contraction assay, utilising human primary uterine smooth muscle cells (hUtSMCs) and immortalised myometrial smooth muscle cells (hTERT-HM): a decrease in collagen gel area equated to an increase in Contractility. RNA was isolated from collagen embedded cells and gene expression changes were analysed by real time fluorescence reverse transcription polymerase chain reaction. Scanning electron and fluorescence microscopy were employed to observe cell morphology and cell collagen gel interactions. Statistical analysis was performed using ANOVA followed by Tukey's post hoc tests. TNF alpha increased collagen Contractility in comparison to the un-stimulated collagen embedded hUtSMC cells, which was inhibited by indomethacin, while indomethacin alone significantly inhibited contraction. Thrombin augmented the Contractility of uterine smooth muscle cell and hTERT-HM collagen gels, this effect was inhibited by the thrombin specific inhibitor, hirudin. Y-27632 decreased both basal and thrombin-induced collagen Contractility in the hTERT-HM embedded gels. mRNA expression of the thrombin receptor, F2R was up-regulated in hUtSMCs isolated from collagen gel lattices, following thrombin-stimulated Contractility. TNF alpha and thrombin increased uterine smooth muscle cell collagen Contractility while indomethacin had the opposite effect. Thrombin-induced collagen Contractility resulted in F2R activation which may in part be mediated by the ROCK-1 pathway. This study established the in vitro human myometrial model as a viable method to assess the effects of a range of uterotonic or uterorelaxant agents on Contractility, and also permits investigation of the complex regulatory pathways involved in mediating myometrial Contractility at labour.
Karin Furer - One of the best experts on this subject based on the ideXlab platform.
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inhibition of porcine detrusor Contractility by the flavonoid fraction of bryophyllum pinnatum a potential phytotherapeutic drug for the treatment of the overactive bladder syndrome
Phytomedicine, 2015Co-Authors: Mennetvon M Eiff, Maria De Mieri, Karin Furer, Rudolf Brenneisen, Olivier Potterat, Daniel Eberli, Cornelia Betschart, Matthias Hamburger, Martin SchnelleAbstract:Aims: To determine if the phytotherapeutic agent, Bryophyllum pinnatum, could serve as an alternative drug for the overactive bladder syndrome, and to characterise the fraction responsible for the inhibition of detrusor Contractility. Methods: Fractions were prepared from the MeOH extract of B. pinnatum and further analysed by HPLCPDA-MS. Detrusor muscle strips were prepared from porcine bladders and the electrically induced muscle Contractility measured by organ bath. The effect of B. pinnatum leaf press juice (2.5–10%), a flavonoid fraction (0.1–1 mg/ml), and a bufadienolide fraction (0.1–40 μg/ml) on detrusor Contractility was assessed and compared with controls (polar fraction (0.5–5 mg/ml) and oxybutynin (10−8–10−6 M)). Results: The press juice, at a concentration of 10% led to a reduction of detrusor Contractility. Bladder strips treated with the flavonoid fraction showed a significant reduction of the Contractility to 21.3 ± 5.2% (1 mg/ml) while the bufadienolide fraction had no inhibitory effect in the investigated concentrations. The polar fraction showed a reduction of the Contractility in a pH-dependent fashion. At 10 −6 M concentration oxybutynin reduced the detrusor Contractility to 21.9 ± 4.7%. Conclusions: The flavonoid fraction of Bryophyllum pinnatum reduces the porcine detrusor Contractility in a dose- and time-dependent manner. Fractions from B. pinnatum may be a new pharmacological approach for the treatment of OAB. © 2015 Published by Elsevier GmbH.
Joan Fitzgibbon - One of the best experts on this subject based on the ideXlab platform.
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Modulation of human uterine smooth muscle cell collagen Contractility by thrombin, Y-27632, TNF alpha and indomethacin
Reproductive Biology and Endocrinology, 2009Co-Authors: Joan Fitzgibbon, John J Morrison, Terry J Smith, Margaret O'brienAbstract:Background Preterm labour occurs in approximately 10% of pregnancies and is a major cause of infant morbidity and mortality. However, the pathways involved in regulating Contractility in normal and preterm labour are not fully elucidated. Our aim was to utilise a human myometrial Contractility model to investigate the effect of a number of uterine specific Contractility agents in this system. Therefore, we investigated the contractile response of human primary uterine smooth muscle cells or immortalised myometrial smooth muscle cells cultured within collagen lattices, to known mediators of uterine Contractility, which included thrombin, the ROCK-1 inhibitor Y-27632, tumour necrosis factor alpha (TNF alpha) and the non-steroidal anti-inflammatory indomethacin. Methods Cell Contractility was calculated over time, with the collagen gel contraction assay, utilising human primary uterine smooth muscle cells (hUtSMCs) and immortalised myometrial smooth muscle cells (hTERT-HM): a decrease in collagen gel area equated to an increase in Contractility. RNA was isolated from collagen embedded cells and gene expression changes were analysed by real time fluorescence reverse transcription polymerase chain reaction. Scanning electron and fluorescence microscopy were employed to observe cell morphology and cell collagen gel interactions. Statistical analysis was performed using ANOVA followed by Tukey's post hoc tests. Results TNF alpha increased collagen Contractility in comparison to the un-stimulated collagen embedded hUtSMC cells, which was inhibited by indomethacin, while indomethacin alone significantly inhibited contraction. Thrombin augmented the Contractility of uterine smooth muscle cell and hTERT-HM collagen gels, this effect was inhibited by the thrombin specific inhibitor, hirudin. Y-27632 decreased both basal and thrombin-induced collagen Contractility in the hTERT-HM embedded gels. mRNA expression of the thrombin receptor, F2R was up-regulated in hUtSMCs isolated from collagen gel lattices, following thrombin-stimulated Contractility. Conclusion TNF alpha and thrombin increased uterine smooth muscle cell collagen Contractility while indomethacin had the opposite effect. Thrombin-induced collagen Contractility resulted in F2R activation which may in part be mediated by the ROCK-1 pathway. This study established the in vitro human myometrial model as a viable method to assess the effects of a range of uterotonic or uterorelaxant agents on Contractility, and also permits investigation of the complex regulatory pathways involved in mediating myometrial Contractility at labour.
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modulation of human uterine smooth muscle cell collagen Contractility by thrombin y 27632 tnf alpha and indomethacin
Reproductive Biology and Endocrinology, 2009Co-Authors: Joan Fitzgibbon, John J Morrison, Terry J Smith, Margaret ObrienAbstract:Preterm labour occurs in approximately 10% of pregnancies and is a major cause of infant morbidity and mortality. However, the pathways involved in regulating Contractility in normal and preterm labour are not fully elucidated. Our aim was to utilise a human myometrial Contractility model to investigate the effect of a number of uterine specific Contractility agents in this system. Therefore, we investigated the contractile response of human primary uterine smooth muscle cells or immortalised myometrial smooth muscle cells cultured within collagen lattices, to known mediators of uterine Contractility, which included thrombin, the ROCK-1 inhibitor Y-27632, tumour necrosis factor alpha (TNF alpha) and the non-steroidal anti-inflammatory indomethacin. Cell Contractility was calculated over time, with the collagen gel contraction assay, utilising human primary uterine smooth muscle cells (hUtSMCs) and immortalised myometrial smooth muscle cells (hTERT-HM): a decrease in collagen gel area equated to an increase in Contractility. RNA was isolated from collagen embedded cells and gene expression changes were analysed by real time fluorescence reverse transcription polymerase chain reaction. Scanning electron and fluorescence microscopy were employed to observe cell morphology and cell collagen gel interactions. Statistical analysis was performed using ANOVA followed by Tukey's post hoc tests. TNF alpha increased collagen Contractility in comparison to the un-stimulated collagen embedded hUtSMC cells, which was inhibited by indomethacin, while indomethacin alone significantly inhibited contraction. Thrombin augmented the Contractility of uterine smooth muscle cell and hTERT-HM collagen gels, this effect was inhibited by the thrombin specific inhibitor, hirudin. Y-27632 decreased both basal and thrombin-induced collagen Contractility in the hTERT-HM embedded gels. mRNA expression of the thrombin receptor, F2R was up-regulated in hUtSMCs isolated from collagen gel lattices, following thrombin-stimulated Contractility. TNF alpha and thrombin increased uterine smooth muscle cell collagen Contractility while indomethacin had the opposite effect. Thrombin-induced collagen Contractility resulted in F2R activation which may in part be mediated by the ROCK-1 pathway. This study established the in vitro human myometrial model as a viable method to assess the effects of a range of uterotonic or uterorelaxant agents on Contractility, and also permits investigation of the complex regulatory pathways involved in mediating myometrial Contractility at labour.
Martin Schnelle - One of the best experts on this subject based on the ideXlab platform.
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inhibition of porcine detrusor Contractility by the flavonoid fraction of bryophyllum pinnatum a potential phytotherapeutic drug for the treatment of the overactive bladder syndrome
Phytomedicine, 2015Co-Authors: Mennetvon M Eiff, Maria De Mieri, Karin Furer, Rudolf Brenneisen, Olivier Potterat, Daniel Eberli, Cornelia Betschart, Matthias Hamburger, Martin SchnelleAbstract:Aims: To determine if the phytotherapeutic agent, Bryophyllum pinnatum, could serve as an alternative drug for the overactive bladder syndrome, and to characterise the fraction responsible for the inhibition of detrusor Contractility. Methods: Fractions were prepared from the MeOH extract of B. pinnatum and further analysed by HPLCPDA-MS. Detrusor muscle strips were prepared from porcine bladders and the electrically induced muscle Contractility measured by organ bath. The effect of B. pinnatum leaf press juice (2.5–10%), a flavonoid fraction (0.1–1 mg/ml), and a bufadienolide fraction (0.1–40 μg/ml) on detrusor Contractility was assessed and compared with controls (polar fraction (0.5–5 mg/ml) and oxybutynin (10−8–10−6 M)). Results: The press juice, at a concentration of 10% led to a reduction of detrusor Contractility. Bladder strips treated with the flavonoid fraction showed a significant reduction of the Contractility to 21.3 ± 5.2% (1 mg/ml) while the bufadienolide fraction had no inhibitory effect in the investigated concentrations. The polar fraction showed a reduction of the Contractility in a pH-dependent fashion. At 10 −6 M concentration oxybutynin reduced the detrusor Contractility to 21.9 ± 4.7%. Conclusions: The flavonoid fraction of Bryophyllum pinnatum reduces the porcine detrusor Contractility in a dose- and time-dependent manner. Fractions from B. pinnatum may be a new pharmacological approach for the treatment of OAB. © 2015 Published by Elsevier GmbH.
Margaret Obrien - One of the best experts on this subject based on the ideXlab platform.
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modulation of human uterine smooth muscle cell collagen Contractility by thrombin y 27632 tnf alpha and indomethacin
Reproductive Biology and Endocrinology, 2009Co-Authors: Joan Fitzgibbon, John J Morrison, Terry J Smith, Margaret ObrienAbstract:Preterm labour occurs in approximately 10% of pregnancies and is a major cause of infant morbidity and mortality. However, the pathways involved in regulating Contractility in normal and preterm labour are not fully elucidated. Our aim was to utilise a human myometrial Contractility model to investigate the effect of a number of uterine specific Contractility agents in this system. Therefore, we investigated the contractile response of human primary uterine smooth muscle cells or immortalised myometrial smooth muscle cells cultured within collagen lattices, to known mediators of uterine Contractility, which included thrombin, the ROCK-1 inhibitor Y-27632, tumour necrosis factor alpha (TNF alpha) and the non-steroidal anti-inflammatory indomethacin. Cell Contractility was calculated over time, with the collagen gel contraction assay, utilising human primary uterine smooth muscle cells (hUtSMCs) and immortalised myometrial smooth muscle cells (hTERT-HM): a decrease in collagen gel area equated to an increase in Contractility. RNA was isolated from collagen embedded cells and gene expression changes were analysed by real time fluorescence reverse transcription polymerase chain reaction. Scanning electron and fluorescence microscopy were employed to observe cell morphology and cell collagen gel interactions. Statistical analysis was performed using ANOVA followed by Tukey's post hoc tests. TNF alpha increased collagen Contractility in comparison to the un-stimulated collagen embedded hUtSMC cells, which was inhibited by indomethacin, while indomethacin alone significantly inhibited contraction. Thrombin augmented the Contractility of uterine smooth muscle cell and hTERT-HM collagen gels, this effect was inhibited by the thrombin specific inhibitor, hirudin. Y-27632 decreased both basal and thrombin-induced collagen Contractility in the hTERT-HM embedded gels. mRNA expression of the thrombin receptor, F2R was up-regulated in hUtSMCs isolated from collagen gel lattices, following thrombin-stimulated Contractility. TNF alpha and thrombin increased uterine smooth muscle cell collagen Contractility while indomethacin had the opposite effect. Thrombin-induced collagen Contractility resulted in F2R activation which may in part be mediated by the ROCK-1 pathway. This study established the in vitro human myometrial model as a viable method to assess the effects of a range of uterotonic or uterorelaxant agents on Contractility, and also permits investigation of the complex regulatory pathways involved in mediating myometrial Contractility at labour.