The Experts below are selected from a list of 23355 Experts worldwide ranked by ideXlab platform
David Cruset - One of the best experts on this subject based on the ideXlab platform.
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from hydroplastic to brittle deformation controls on fluid flow in fold and thrust belts insights from the lower pedraforca thrust sheet se pyrenees
Marine and Petroleum Geology, 2020Co-Authors: David Cruset, Irene Cantarero, Antonio Benedicto, Cedric M John, Jaume Verges, Richard Albert, Axel Gerdes, Anna TraveAbstract:Abstract We present a multidisciplinary study to decipher the controls of deformation on fluid flow regime in fold and thrust belts using the Lower Pedraforca thrust sheet in the SE Pyrenees as an example. We integrate field-based and petrographic observations and geochemical and geochronological data to differentiate seven types of fractures, eight types of calcite cement (Cc1 to Cc8) and two sets of stylolites during the deformation stretching the studied thrust sheet. During syn-sedimentary hydroplastic normal faulting affecting poorly consolidated Upper Cretaceous and Eocene syn-orogenic sediments, calcite cement did not precipitate. During burial, bed-parallel stylolites formed and Cc1 and Cc2 precipitated from formation waters in a closed palaeohydrological system. During the layer-parallel shortening, Cc3 precipitated from formation waters (~+5.4‰ VSMOW) with 87Sr/86Sr ratios of 0.707922 and at ~70 °C. Cc4 precipitated from formation waters recording different burial conditions, as the up to 4‰ dispersion in δ18O of this cement suggests. Contrarily, during folding and thrusting, Cc5 to Cc7 precipitated in an open palaeohydrological system. Cc6 precipitated from formation waters (~+5‰ VSMOW), with 87Sr/86Sr ratios of 0.707817 and at ~75 °C. These fluids carried hydrocarbons and probably interacted with Upper Triassic evaporites. An 87Sr/86Sr ratio of 0.708230 for Cc5 indicates that formation waters also interacted with clays within continental deposits. During this period, stylolites formed in relation to faulting, and previous hydroplastic normal faults reactivated as reverse and strike-slip faults allowing fluid flow. Cc7 precipitated after Cc6, also from fluids in isotopic disequilibrium with their adjacent host rock. The fluid system continued open during the Oligocene, when Cc8 precipitated in normal faults affecting syn-orogenic conglomerates deposited during the reactivation of the Lower Pedraforca thrust sheet. The influence of deformation on fluid flow observed in the Lower Pedraforca thrust sheet is similar to that observed in other fractured areas worldwide.
Jean Claude Reubi - One of the best experts on this subject based on the ideXlab platform.
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high gastrin and cholecystokinin cck gene expression in human neuronal renal and myogenic stem cell tumors comparison with cck a and cck b receptor contents
The Journal of Clinical Endocrinology and Metabolism, 1999Co-Authors: Jeanclaude Schaer, Jean Claude ReubiAbstract:Gastrin and cholecystokinin (CCK) are two major regulatory peptides synthesized by human gut and brain tissues as well as by selected tumors, in particular gastrin-producing neuroendocrine tumors. In the present study we have evaluated gastrin and CCK gene expression in a group of primary human tumors, including neuronal, renal, and myogenic stem cell tumors, using in situ hybridization techniques. In addition, CCK-A and CCK-B receptors were evaluated in the same group of tumors with receptor autoradiography. Most tumors had gastrin messenger ribonucleic acid (mRNA): 10 of 11 medulloblastomas, 5 of 5 central primitive neuroectodermal tumors, 11 of 11 Ewing sarcomas, 8 of 10 neuroblastomas, 4 of 4 Wilms’ tumors, 5 of 5 rhabdomyosarcomas, and 10 of 10 leiomyosarcomas. CCK mRNA was restricted predominantly to Ewing sarcomas (9 of 11) and leiomyosarcomas (5 of 10). CCK-A and CCK-B receptors were not frequently found in these tumors, except for leiomyosarcomas. These data suggest that gastrin and CCK may play ...
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high gastrin and cholecystokinin cck gene expression in human neuronal renal and myogenic stem cell tumors comparison with cck a and cck b receptor contents
The Journal of Clinical Endocrinology and Metabolism, 1999Co-Authors: Jeanclaude Schaer, Jean Claude ReubiAbstract:Gastrin and cholecystokinin (CCK) are two major regulatory peptides synthesized by human gut and brain tissues as well as by selected tumors, in particular gastrin-producing neuroendocrine tumors. In the present study we have evaluated gastrin and CCK gene expression in a group of primary human tumors, including neuronal, renal, and myogenic stem cell tumors, using in situ hybridization techniques. In addition, CCK-A and CCK-B receptors were evaluated in the same group of tumors with receptor autoradiography. Most tumors had gastrin messenger ribonucleic acid (mRNA): 10 of 11 medulloblastomas, 5 of 5 central primitive neuroectodermal tumors, 11 of 11 Ewing sarcomas, 8 of 10 neuroblastomas, 4 of 4 Wilms' tumors, 5 of 5 rhabdomyosarcomas, and 10 of 10 leiomyosarcomas. CCK mRNA was restricted predominantly to Ewing sarcomas (9 of 11) and leiomyosarcomas (5 of 10). CCK-A and CCK-B receptors were not frequently found in these tumors, except for leiomyosarcomas. These data suggest that gastrin and CCK may play a previously unrecognized role in this group of human stem cell tumors. If the increased gastrin mRNA indeed translates into increased gastrin production, measurement of gastrinemia may have a diagnostic significance in the early detection of these tumors. As these two hormones have been reported to act as potent growth factors, they may be of pathophysiological relevance for patients with such stem cell tumors.
Anna Trave - One of the best experts on this subject based on the ideXlab platform.
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from hydroplastic to brittle deformation controls on fluid flow in fold and thrust belts insights from the lower pedraforca thrust sheet se pyrenees
Marine and Petroleum Geology, 2020Co-Authors: David Cruset, Irene Cantarero, Antonio Benedicto, Cedric M John, Jaume Verges, Richard Albert, Axel Gerdes, Anna TraveAbstract:Abstract We present a multidisciplinary study to decipher the controls of deformation on fluid flow regime in fold and thrust belts using the Lower Pedraforca thrust sheet in the SE Pyrenees as an example. We integrate field-based and petrographic observations and geochemical and geochronological data to differentiate seven types of fractures, eight types of calcite cement (Cc1 to Cc8) and two sets of stylolites during the deformation stretching the studied thrust sheet. During syn-sedimentary hydroplastic normal faulting affecting poorly consolidated Upper Cretaceous and Eocene syn-orogenic sediments, calcite cement did not precipitate. During burial, bed-parallel stylolites formed and Cc1 and Cc2 precipitated from formation waters in a closed palaeohydrological system. During the layer-parallel shortening, Cc3 precipitated from formation waters (~+5.4‰ VSMOW) with 87Sr/86Sr ratios of 0.707922 and at ~70 °C. Cc4 precipitated from formation waters recording different burial conditions, as the up to 4‰ dispersion in δ18O of this cement suggests. Contrarily, during folding and thrusting, Cc5 to Cc7 precipitated in an open palaeohydrological system. Cc6 precipitated from formation waters (~+5‰ VSMOW), with 87Sr/86Sr ratios of 0.707817 and at ~75 °C. These fluids carried hydrocarbons and probably interacted with Upper Triassic evaporites. An 87Sr/86Sr ratio of 0.708230 for Cc5 indicates that formation waters also interacted with clays within continental deposits. During this period, stylolites formed in relation to faulting, and previous hydroplastic normal faults reactivated as reverse and strike-slip faults allowing fluid flow. Cc7 precipitated after Cc6, also from fluids in isotopic disequilibrium with their adjacent host rock. The fluid system continued open during the Oligocene, when Cc8 precipitated in normal faults affecting syn-orogenic conglomerates deposited during the reactivation of the Lower Pedraforca thrust sheet. The influence of deformation on fluid flow observed in the Lower Pedraforca thrust sheet is similar to that observed in other fractured areas worldwide.
Daniela Eser - One of the best experts on this subject based on the ideXlab platform.
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benzodiazepines counteract rostral anterior cingulate cortex activation induced by cholecystokinin tetrapeptide in humans
Biological Psychiatry, 2013Co-Authors: Daniela Eser, Gregor Leicht, Christoph Mulert, Philipp G Samann, Matthias Ertl, Anna Laenger, S KarchAbstract:Background Benzodiazepines modulate γ-aminobutyric acid type A (GABA A ) receptors throughout the brain. However, it is not fully understood which brain regions within anxiety-related brain circuits are really responsible for their anxiolytic effects and how these regions interact. Methods We investigated whether the benzodiazepine alprazolam affects activity in distinct brain regions within anxiety-related circuits during an experimental anxiety paradigm by means of functional magnetic resonance imaging (fMRI). Panic symptoms were elicited by a bolus injection of the neuropeptide cholecystokinin-tetrapeptide (CCK-4) in 16 healthy male subjects in a double-blind, placebo-controlled design. Functional brain activation patterns were determined before and during the CCK-4-challenge without pretreatment and after treatment with either placebo or 1 mg alprazolam. Results The CCK-4 induced anxiety and elicited widely distributed activation patterns in anxiety-related brain circuits, especially in the rostral anterior cingulate cortex (rACC), which was attenuated after alprazolam treatment. In contrast to placebo, alprazolam abolished the activation of the rACC after challenge with CCK-4 ( p r p = .52; p = .04). Conclusions These findings put forward the rACC as a target for benzodiazepines and suggest that the CCK-4/fMRI paradigm might represent a human translational model for the investigation of anxiolytic drugs.
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panic induction with cholecystokinin tetrapeptide cck 4 increases plasma concentrations of the neuroactive steroid 3 alpha 5 alpha tetrahydrodeoxycorticosterone 3 alpha 5 alpha thdoc in healthy volunteers
Neuropsychopharmacology, 2005Co-Authors: Daniela Eser, P Zwanzger, T C Baghai, Flavia Di Michele, Augusto Pasini, Cornelius Schule, Rainer Rupprecht, Elena RomeoAbstract:3α-reduced neuroactive steroids such as 3α, 5α-tetrahydroprogesterone (3α, 5α-THP) and 3α, 5α-tetrahydrodeoxycorticosterone (3α, 5α-THDOC) are potent positive allosteric modulators of γ-aminobutyric acid type A (GABAA) receptors and display pronounced anxiolytic activity in animal models. Experimental panic induction with cholecystokinin-tetrapeptide (CCK-4) and sodium lactate is accompanied by a decrease in 3α, 5α-THP concentrations in patients with panic disorder, but not in healthy controls. However, no data are available on 3α, 5α-THDOC concentrations during experimental panic induction. Therefore, we quantified 3α, 5α-THDOC concentrations in 10 healthy volunteers (nine men, one woman) before and after panic induction with CCK-4 by means of a highly sensitive and specific gas chromatography/mass spectrometry analysis. CCK-4 elicited a strong panic response as assessed by the Acute Panic Inventory. This was accompanied by an increase in 3α, 5α-THDOC, ACTH and cortisol concentrations. This increase in 3α, 5α-THDOC might be a consequence of hypothalamic–pituitary–adrenal (HPA) axis activation following CCK-4-induced panic, and might contribute to the termination of the anxiety/stress response following challenge with CCK-4 through enhancement of GABAA receptor function.
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effects of alprazolam on cholecystokinin tetrapeptide induced panic and hypothalamic pituitary adrenal axis activity a placebo controlled study
Neuropsychopharmacology, 2003Co-Authors: P Zwanzger, T C Baghai, Cornelius Schule, Daniela Eser, S Aicher, Frank Padberg, R Ella, H J Moller, Rainer RupprechtAbstract:Cholecystokinin-tetrapeptide (CCK-4) induces panic attacks both in patients with panic disorder (PD) and healthy volunteers. It has been shown that panic elicited by CCK-4 is improved after treatment with antidepressants. Moreover, a reduction of CCK-4-induced panic has also been demonstrated after treatment with lorazepam in single subjects and after selective GABAergic treatment with vigabatrin. Although benzodiazepines are widely used as anxiolytics, no controlled study on the effects of benzodiazepines on CCK-4-induced panic symptoms is available so far. Therefore, we investigated the effects of alprazolam and placebo on CCK-4-induced panic symptoms in a double-blind, placebo-controlled study. A total of 30 healthy subjects were challenged with 50 microg CCK-4. Out of these 30 subjects, 26 showed a marked panic response to CCK-4. Subjects were rechallenged after a 7-day interval and treated with 1 mg alprazolam or placebo 1 h prior to the second CCK-4 challenge. Panic was assessed using the acute panic inventory (API) and a DSM-IV-derived panic symptom scale (PSS). Moreover, the number of reported symptoms and self-rated anxiety and arousal were recorded. We found a significant reduction of the API and PSS scores and of the number of reported symptoms compared to placebo. Moreover, compared to placebo the CCK-4-induced ACTH and cortisol release were significantly attenuated during the CCK-4 challenge after alprazolam treatment. However, also placebo treatment reduced CCK-4-induced anxiety and HPA-axis activation to a certain extent. In conclusion, our data show that alprazolam reduces CCK-4-induced panic, which supports the hypothesis of a possible interaction between the GABA and the CCK system.
Rainer Rupprecht - One of the best experts on this subject based on the ideXlab platform.
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panic induction with cholecystokinin tetrapeptide cck 4 increases plasma concentrations of the neuroactive steroid 3 alpha 5 alpha tetrahydrodeoxycorticosterone 3 alpha 5 alpha thdoc in healthy volunteers
Neuropsychopharmacology, 2005Co-Authors: Daniela Eser, P Zwanzger, T C Baghai, Flavia Di Michele, Augusto Pasini, Cornelius Schule, Rainer Rupprecht, Elena RomeoAbstract:3α-reduced neuroactive steroids such as 3α, 5α-tetrahydroprogesterone (3α, 5α-THP) and 3α, 5α-tetrahydrodeoxycorticosterone (3α, 5α-THDOC) are potent positive allosteric modulators of γ-aminobutyric acid type A (GABAA) receptors and display pronounced anxiolytic activity in animal models. Experimental panic induction with cholecystokinin-tetrapeptide (CCK-4) and sodium lactate is accompanied by a decrease in 3α, 5α-THP concentrations in patients with panic disorder, but not in healthy controls. However, no data are available on 3α, 5α-THDOC concentrations during experimental panic induction. Therefore, we quantified 3α, 5α-THDOC concentrations in 10 healthy volunteers (nine men, one woman) before and after panic induction with CCK-4 by means of a highly sensitive and specific gas chromatography/mass spectrometry analysis. CCK-4 elicited a strong panic response as assessed by the Acute Panic Inventory. This was accompanied by an increase in 3α, 5α-THDOC, ACTH and cortisol concentrations. This increase in 3α, 5α-THDOC might be a consequence of hypothalamic–pituitary–adrenal (HPA) axis activation following CCK-4-induced panic, and might contribute to the termination of the anxiety/stress response following challenge with CCK-4 through enhancement of GABAA receptor function.
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effects of alprazolam on cholecystokinin tetrapeptide induced panic and hypothalamic pituitary adrenal axis activity a placebo controlled study
Neuropsychopharmacology, 2003Co-Authors: P Zwanzger, T C Baghai, Cornelius Schule, Daniela Eser, S Aicher, Frank Padberg, R Ella, H J Moller, Rainer RupprechtAbstract:Cholecystokinin-tetrapeptide (CCK-4) induces panic attacks both in patients with panic disorder (PD) and healthy volunteers. It has been shown that panic elicited by CCK-4 is improved after treatment with antidepressants. Moreover, a reduction of CCK-4-induced panic has also been demonstrated after treatment with lorazepam in single subjects and after selective GABAergic treatment with vigabatrin. Although benzodiazepines are widely used as anxiolytics, no controlled study on the effects of benzodiazepines on CCK-4-induced panic symptoms is available so far. Therefore, we investigated the effects of alprazolam and placebo on CCK-4-induced panic symptoms in a double-blind, placebo-controlled study. A total of 30 healthy subjects were challenged with 50 microg CCK-4. Out of these 30 subjects, 26 showed a marked panic response to CCK-4. Subjects were rechallenged after a 7-day interval and treated with 1 mg alprazolam or placebo 1 h prior to the second CCK-4 challenge. Panic was assessed using the acute panic inventory (API) and a DSM-IV-derived panic symptom scale (PSS). Moreover, the number of reported symptoms and self-rated anxiety and arousal were recorded. We found a significant reduction of the API and PSS scores and of the number of reported symptoms compared to placebo. Moreover, compared to placebo the CCK-4-induced ACTH and cortisol release were significantly attenuated during the CCK-4 challenge after alprazolam treatment. However, also placebo treatment reduced CCK-4-induced anxiety and HPA-axis activation to a certain extent. In conclusion, our data show that alprazolam reduces CCK-4-induced panic, which supports the hypothesis of a possible interaction between the GABA and the CCK system.