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Article ; Online: TAK1 signaling regulates p53 through a mechanism involving ribosomal stress.

Zonneville, Justin / Wong, Vincent / Limoge, Michelle / Nikiforov, Mikhail / Bakin, Andrei V

2020 Volume 10, Issue 1, Page(s) 2517

Abstract: Triple-negative breast cancer (TNBC) is among the most aggressive forms of breast cancer with limited therapeutic options. TAK1 is implicated in aggressive behavior of TNBC, while means are not fully understood. Here, we report that pharmacological ... ...

Abstract	Triple-negative breast cancer (TNBC) is among the most aggressive forms of breast cancer with limited therapeutic options. TAK1 is implicated in aggressive behavior of TNBC, while means are not fully understood. Here, we report that pharmacological blockade of TAK1 signaling hampered ribosome biogenesis (RBG) by reducing expression of RBG regulators such as RRS1, while not changing expression of ribosomal core proteins. Notably, TAK1 blockade upregulated expression of p53 target genes in cell lines carrying wild type (wt) TP53 but not in p53-mutant cells, suggesting involvement of ribosomal stress in the response. Accordingly, p53 activation by blockade of TAK1 was prevented by depletion of ribosomal protein RPL11. Further, siRNA-mediated depletion of TAK1 or RELA resulted in RPL11-dependent activation of p53 signaling. Knockdown of RRS1 was sufficient to disrupt nucleolar structures and resulted in activation of p53. TCGA data showed that TNBCs express high levels of RBG regulators, and elevated RRS1 levels correlate with unfavorable prognosis. Cytotoxicity data showed that TNBC cell lines are more sensitive to TAK1 inhibitor compared to luminal and HER2
MeSH term(s)	Cell Line, Tumor ; Female ; Humans ; MAP Kinase Kinase Kinases/metabolism ; Ribosomes/metabolism ; Signal Transduction ; Triple Negative Breast Neoplasms/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25)
Language	English
Publishing date	2020-02-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-59340-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Tumor-fibroblast interactions stimulate tumor vascularization by enhancing cytokine-driven production of MMP9 by tumor cells.

Limoge, Michelle / Safina, Alfiya / Beattie, Amy / Kapus, Lauren / Truskinovsky, Alexander M / Bakin, Andrei V

Oncotarget

2017 Volume 8, Issue 22, Page(s) 35592–35608

Abstract: Advance-stage breast carcinomas include significant amounts of fibroblasts and infiltrating immune cells which have been implicated in tumor growth, recurrence, and response to therapy. The present study investigated the contribution of fibroblasts to ... ...

Abstract	Advance-stage breast carcinomas include significant amounts of fibroblasts and infiltrating immune cells which have been implicated in tumor growth, recurrence, and response to therapy. The present study investigated the contribution of fibroblasts to tumor growth using direct tumor-fibroblast co-cultures and tumor xenograft models. Our findings revealed that fibroblasts enhance breast carcinoma growth by promoting the tumor vasculature via the MMP9-dependent mechanism. In tumor-fibroblast co-cultures, fibroblasts increased expression of TGF-β, TNF, and IL-1β cytokines in tumor cells. These cytokines cooperatively induced expression of matrix metalloproteinase MMP9 in tumor cells. Knockdown of MMP9 by shRNA significantly reduced tumor vascularization induced by fibroblasts. Mechanistically, our findings argue that expression of MMP9 in tumor cellsis regulated by crosstalk of TGF-β with TNF and/or IL-1β cytokines. The mechanism of this cooperative response did not involve cross-activation of the canonical signaling pathways as TGF-β did not activate RELA/p65 signaling, while TNF did not affect SMAD signaling. Instead, TGF-β and TNF cytokines co-stimulated MAP kinases and expression of JUN and JUNB, AP1 transcription factor subunits, which together with RELA/p65 were essential for the regulation of MMP9. Depletion of JUN and JUNB or RELA in tumor cells blocked the cooperative induction of MMP9 by the cytokines. Thus, our studies uncovered a previously unappreciated role of tumor-fibroblast interactions in the stimulation of tumor angiogenesis, and an essential role of the MAPK-AP1 axis in the cooperative up-regulation of the angiogenic driver MMP9 by cytokine crosstalk.
Language	English
Publishing date	2017-05-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.16022
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Article ; Online: Tumor p38MAPK signaling enhances breast carcinoma vascularization and growth by promoting expression and deposition of pro-tumorigenic factors.

Limoge, Michelle / Safina, Alfiya / Truskinovsky, Alexander M / Aljahdali, Ieman / Zonneville, Justin / Gruevski, Aleksandar / Arteaga, Carlos L / Bakin, Andrei V

Oncotarget

2017 Volume 8, Issue 37, Page(s) 61969–61981

Abstract: The breast carcinoma microenvironment strikingly influences cancer progression and response to therapy. Various cell types in the carcinoma microenvironment show significant activity of p38 mitogen-activated protein kinase (MAPK), although the role of ... ...

Abstract	The breast carcinoma microenvironment strikingly influences cancer progression and response to therapy. Various cell types in the carcinoma microenvironment show significant activity of p38 mitogen-activated protein kinase (MAPK), although the role of p38MAPK in breast cancer progression is still poorly understood. The present study examined the contribution of tumor p38MAPK to breast carcinoma microenvironment and metastatic capacity. Inactivation of p38MAPK signaling in metastatic breast carcinoma cells was achieved by forced expression of the kinase-inactive mutant of p38/MAPK14 (a dominant-negative p38, dn-p38). Disruption of tumor p38MAPK signaling reduced growth and metastases of breast carcinoma xenografts. Importantly, dn-p38 markedly decreased tumor blood-vessel density and lumen sizes. Mechanistic studies revealed that p38 controls expression of pro-angiogenic extracellular factors such as matrix protein Fibronectin and cytokines VEGFA, IL8, and HBEGF. Tumor-associated fibroblasts enhanced tumor growth and vasculature as well as increased expression of the pro-angiogenic factors. These effects were blunted by dn-p38. Metadata analysis showed elevated expression of p38 target genes in breast cancers and this was an unfavorable marker of disease recurrence and poor-outcome. Thus, our study demonstrates that tumor p38MAPK signaling promotes breast carcinoma growth, invasive and metastatic capacities. Importantly, p38 enhances carcinoma vascularization by facilitating expression and deposition of pro-angiogenic factors. These results argue that p38MAPK is a valuable target for anticancer therapy affecting tumor vasculature. Anti-p38 drugs may provide new therapeutic strategies against breast cancer, including metastatic disease.
Language	English
Publishing date	2017-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.18755
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Article ; Online: Integrin-β5 and zyxin mediate formation of ventral stress fibers in response to transforming growth factor β.

Bianchi-Smiraglia, Anna / Kunnev, Dimiter / Limoge, Michelle / Lee, Amy / Beckerle, Mary C / Bakin, Andrei V

Cell cycle (Georgetown, Tex.)

2013 Volume 12, Issue 21, Page(s) 3377–3389

Abstract: Cell adhesion to the extracellular matrix is an essential element of various biological processes. TGF-β cytokines regulate the matrix components and cell-matrix adhesions. The present study investigates the molecular organization of TGF-β-induced matrix ...

Abstract	Cell adhesion to the extracellular matrix is an essential element of various biological processes. TGF-β cytokines regulate the matrix components and cell-matrix adhesions. The present study investigates the molecular organization of TGF-β-induced matrix adhesions. The study demonstrates that in various mouse and human epithelial cells TGF-β induces cellular structures containing 2 matrix adhesions bridged by a stretch of actin fibers. These structures are similar to ventral stress fibers (VSFs). Suppression of integrin-β5 by RNA interference reduces VSFs in majority of cells (> 75%), while overexpression of integrin-β5 fragments revealed a critical role of a distinct sequence in the cytoplasmic domain of integrin-β5 in the VSF structures. In addition, the integrity of actin fibers and Src kinase activity contribute to integrin-β5-mediated signaling and VSF formation. TGF-β-Smad signaling upregulates actin-regulatory proteins, such as caldesmon, zyxin, and zyxin-binding protein Csrp1 in mouse and human epithelial cells. Suppression of zyxin markedly inhibits formation of VSFs in response to TGF-β and integrin-β5. Zyxin is localized at actin fibers and matrix adhesions of VSFs and might bridge integrin-β5-mediated adhesions to actin fibers. These findings provide a platform for defining the molecular mechanism regulating the organization and activities of VSFs in response to TGF-β.
MeSH term(s)	Amino Acid Sequence ; Animals ; Cell Adhesion ; Cell Line ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/ultrastructure ; Extracellular Matrix/drug effects ; Extracellular Matrix/metabolism ; Extracellular Matrix/ultrastructure ; Female ; Focal Adhesions/drug effects ; Focal Adhesions/metabolism ; Focal Adhesions/ultrastructure ; Gene Expression Regulation ; Humans ; Integrin beta Chains/genetics ; Integrin beta Chains/metabolism ; LIM Domain Proteins/genetics ; LIM Domain Proteins/metabolism ; Mice ; Molecular Sequence Data ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Protein Structure, Tertiary ; Sequence Alignment ; Sequence Homology, Amino Acid ; Signal Transduction ; Smad Proteins/genetics ; Smad Proteins/metabolism ; Stress Fibers/drug effects ; Stress Fibers/metabolism ; Stress Fibers/ultrastructure ; Transforming Growth Factor beta/pharmacology ; Zyxin/genetics ; Zyxin/metabolism
Chemical Substances	CSRP1 protein, human ; Integrin beta Chains ; LIM Domain Proteins ; Nuclear Proteins ; Smad Proteins ; Transforming Growth Factor beta ; Zyxin ; integrin beta5
Language	English
Publishing date	2013-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.26388
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Zs.A 5881: Show issues

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Article ; Online: TAK1-TAB2 signaling contributes to bone destruction by breast carcinoma cells.

Safina, Alfiya / Sotomayor, Paula / Limoge, Michelle / Morrison, Carl / Bakin, Andrei V

Molecular cancer research : MCR

2011 Volume 9, Issue 8, Page(s) 1042–1053

Abstract: Advanced-stage breast cancers frequently metastasize to the bones and cause bone destruction, but the underlying mechanism is not fully understood. This study presents evidence that TGF-β-activated protein kinase 1 (TAK1) signaling in tumor cells ... ...

Abstract	Advanced-stage breast cancers frequently metastasize to the bones and cause bone destruction, but the underlying mechanism is not fully understood. This study presents evidence that TGF-β-activated protein kinase 1 (TAK1) signaling in tumor cells promotes bone destruction by metastatic breast carcinoma cells, controlling expression of prometastatic factors including matrix metalloproteinase (MMP) 9 and COX2. Suppression of TAK1 signaling by dominant-negative TAK1 (dn-TAK1) in breast carcinoma MDA-MB-231 cells impairs bone colonization by carcinoma cells and bone osteolysis in the intracardiac injection model. Mechanistic studies showed that inhibition of TAK1 by dn-TAK1 or siRNA blocked expression of factors implicated in bone metastasis, such as MMP-9, COX2/PTGS2, parathyroid hormone-related protein (PTHrP) and interleukin 8 (IL-8), but did not affect activation of p38MAPK by TGF-β. TAK1 signaling is mediated by TAK1-binding partners TAB1, TAB2, and TAB3. Carcinoma cells express elevated mRNA levels of TAB2 and TAB3, whereas the TAB1 expression is noticeably low. Accordingly, depletion of TAB2 by siRNA reduced expression of MMP-9 and COX2. Together, these studies show that the TAK1-TAB2-TAB3 signaling axis is critical for carcinoma-induced bone lesions, mediating expression of proinvasive and osteolytic factors. These findings identify the TAK1-TAB2 axis as a potential therapeutic target in bone metastasis.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Bone Neoplasms/secondary ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Carcinoma/metabolism ; Carcinoma/pathology ; Cell Line, Tumor ; Cyclooxygenase 2/metabolism ; Female ; Humans ; Interleukin-8/metabolism ; MAP Kinase Kinase Kinases/metabolism ; Male ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mice, SCID ; Prostatic Neoplasms/metabolism ; RNA, Small Interfering/genetics ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/pharmacology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Interleukin-8 ; RNA, Small Interfering ; TAB2 protein, human ; Transforming Growth Factor beta ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2011-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-10-0196
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Zs.A 5744: Show issues

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Article ; Online: A bioinspired route to indanes and cyclopentannulated hetarenes via (3+2)-cyclodimerization of donor-acceptor cyclopropanes.

Ivanova, Olga A / Budynina, Ekaterina M / Skvortsov, Dmitriy A / Limoge, Michelle / Bakin, Andrei V / Chagarovskiy, Alexey O / Trushkov, Igor V / Melnikov, Mikhail Ya

Chemical communications (Cambridge, England)

2013 Volume 49, Issue 98, Page(s) 11482–11484

Abstract: A novel Lewis acid-catalyzed domino (3+2)-cyclodimerization of 2-arylcyclopropane-1,1-diesters and related stepwise cross-reaction of two different cyclopropanes were developed. These processes provide efficient and highly stereoselective access to ... ...

Abstract	A novel Lewis acid-catalyzed domino (3+2)-cyclodimerization of 2-arylcyclopropane-1,1-diesters and related stepwise cross-reaction of two different cyclopropanes were developed. These processes provide efficient and highly stereoselective access to polyoxygenated indanes and cyclopentannulated heteroarene derivatives, which display significant cytotoxicity against several lines of cancer cells (IC50 of 10(-6)-10(-5) M) while being non-toxic for normal cells.
MeSH term(s)	Cell Line, Tumor ; Cell Survival/drug effects ; Dimerization ; Humans ; Hydrocarbons/chemistry ; Hydrocarbons/pharmacology ; Lewis Acids/chemistry ; Stereoisomerism
Chemical Substances	Hydrocarbons ; Lewis Acids
Language	English
Publishing date	2013-04-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1472881-3
ISSN	1364-548X ; 1359-7345 ; 0009-241X
ISSN (online)	1364-548X
ISSN	1359-7345 ; 0009-241X
DOI	10.1039/c3cc44475a
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Article: A bioinspired route to indanes and cyclopentannulated hetarenes via (3+2)-cyclodimerization of donor–acceptor cyclopropanes

Ivanova, Olga A / Bakin, Andrei V / Budynina, Ekaterina M / Chagarovskiy, Alexey O / Limoge, Michelle / Melnikov, Mikhail Ya / Skvortsov, Dmitriy A / Trushkov, Igor V

Chemical communications. 2013 Nov. 14, v. 49, no. 98

2013

Abstract	A novel Lewis acid-catalyzed domino (3+2)-cyclodimerization of 2-arylcyclopropane-1,1-diesters and related stepwise cross-reaction of two different cyclopropanes were developed. These processes provide efficient and highly stereoselective access to polyoxygenated indanes and cyclopentannulated heteroarene derivatives, which display significant cytotoxicity against several lines of cancer cells (IC50 of 10−6–10−5 M) while being non-toxic for normal cells.
Keywords	catalytic activity ; chemical compounds ; chemical reactions ; cross reaction ; cytotoxicity ; inhibitory concentration 50 ; neoplasm cells ; neoplasms ; stereoselectivity
Language	English
Dates of publication	2013-1114
Size	p. 11482-11484.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	1472881-3
ISSN	1364-548X ; 1359-7345 ; 0009-241X
ISSN (online)	1364-548X
ISSN	1359-7345 ; 0009-241X
DOI	10.1039/c3cc44475a
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Insulin response dysregulation explains abnormal fat storage and increased risk of diabetes mellitus type 2 in Cohen Syndrome.

Limoge, Floriane / Faivre, Laurence / Gautier, Thomas / Petit, Jean-Michel / Gautier, Elodie / Masson, David / Jego, Gaëtan / El Chehadeh-Djebbar, Salima / Marle, Nathalie / Carmignac, Virginie / Deckert, Valérie / Brindisi, Marie-Claude / Edery, Patrick / Ghoumid, Jamal / Blair, Edward / Lagrost, Laurent / Thauvin-Robinet, Christel / Duplomb, Laurence

Human molecular genetics

2015 Volume 24, Issue 23, Page(s) 6603–6613

Abstract: Cohen Syndrome (CS) is a rare autosomal recessive disorder, with defective glycosylation secondary to mutations in the VPS13B gene, which encodes a protein of the Golgi apparatus. Besides congenital neutropenia, retinopathy and intellectual deficiency, ... ...

Abstract	Cohen Syndrome (CS) is a rare autosomal recessive disorder, with defective glycosylation secondary to mutations in the VPS13B gene, which encodes a protein of the Golgi apparatus. Besides congenital neutropenia, retinopathy and intellectual deficiency, CS patients are faced with truncal obesity. Metabolism investigations showed abnormal glucose tolerance tests and low HDL values in some patients, and these could be risk factors for the development of diabetes mellitus and/or cardiovascular complications. To understand the mechanisms involved in CS fat storage, we used two models of adipogenesis differentiation: (i) SGBS pre-adipocytes with VPS13B invalidation thanks to siRNA delivery and (ii) CS primary fibroblasts. In both models, VPS13B invalidation led to accelerated differentiation into fat cells, which was confirmed by the earlier and increased expression of specific adipogenic genes, consequent to the increased response of cells to insulin stimulation. At the end of the differentiation protocol, these fat cells exhibited decreased AKT2 phosphorylation after insulin stimulation, which suggests insulin resistance. This study, in association with the in-depth analysis of the metabolic status of the patients, thus allowed us to recommend appropriate nutritional education to prevent the occurrence of diabetes mellitus and to put forward recommendations for the follow-up of CS patients, in particular with regard to the development of metabolic syndrome. We also suggest replacing the term obesity by abnormal fat distribution in CS, which should reduce the number of inappropriate diagnoses in patients who are referred only on the basis of intellectual deficiency associated with obesity.
MeSH term(s)	Adipogenesis ; Adolescent ; Adult ; Body Fat Distribution ; Child ; Child, Preschool ; Developmental Disabilities/complications ; Developmental Disabilities/physiopathology ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/physiopathology ; Female ; Fingers/abnormalities ; Fingers/physiopathology ; Humans ; Insulin/physiology ; Intellectual Disability/complications ; Intellectual Disability/physiopathology ; Male ; Microcephaly/complications ; Microcephaly/physiopathology ; Middle Aged ; Models, Biological ; Muscle Hypotonia/complications ; Muscle Hypotonia/physiopathology ; Mutation ; Myopia/complications ; Myopia/physiopathology ; Obesity/complications ; Obesity/physiopathology ; Risk ; Signal Transduction ; Vesicular Transport Proteins/genetics ; Young Adult
Chemical Substances	Insulin ; VPS13B protein, human ; Vesicular Transport Proteins
Language	English
Publishing date	2015-12-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddv366
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Zs.A 3469: Show issues

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Article: Transcranial electrical stimulation with high frequency intermittent current (Limoge's) potentiates opiate-induced analgesia: blind studies.

Stinus, Louis / Auriacombe, Marc / Tignol, Jean / Limoge, Aimé / Le Moal, Michel

Pain

1990 Volume 42, Issue 3, Page(s) 351–363

Abstract: ... current (100 Hz: Limoge current) has been used for several years in cardiac, thoracic, abdominal ...

Abstract	Transcutaneous cranial electrical stimulation (TCES) with high frequency (166 kHz) intermittent current (100 Hz: Limoge current) has been used for several years in cardiac, thoracic, abdominal, urological and micro-surgery. The main benefits are a reduced requirement for analgesic drugs, especially opiates, and a long-lasting postoperative analgesia. We have confirmed these clinical observations in rats using the tail-flick latency (TFL) test to measure pain threshold. TCES was not found to modify the pain threshold in drug-free rats, but it potentiated morphine-induced analgesia (systemic injection). To obtain a maximal effect, the stimulation must be initiated 3 h before the drug injection and be maintained throughout the duration of its pharmacological action. TCES potentitation was found to depend on the dose of the drug, the intensity of the current and the polarity of electrodes. These findings were confirmed by blind tests of the efficiency of TCES on several opiate analgesic drugs currently used in human surgery (morphine, fentanyl, alfentanil and dextromoramide). The analgesic effect of these 4 opiates (TFL as % of baseline without or with TCES) were respectively: 174%, 306%; 176%, 336%; 160%, 215%; and 267%, 392%. The results were obtained not only after systemic opiate treatment, but also after intracerebroventricular injection of morphine (10 micrograms; analgesic effect 152%, 207% with TCES) suggesting that TCES potentiation of opiate-induced analgesia is centrally mediated.
MeSH term(s)	Alfentanil/pharmacology ; Analgesia ; Animals ; Dextromoramide/pharmacology ; Dose-Response Relationship, Drug ; Double-Blind Method ; Electric Stimulation Therapy/methods ; Electricity ; Electrodes ; Injections, Intraventricular ; Male ; Morphine/pharmacology ; Morphine/therapeutic use ; Narcotics/pharmacology ; Narcotics/therapeutic use ; Pain/drug therapy ; Pain Management ; Rats ; Rats, Inbred Strains ; Time Factors
Chemical Substances	Narcotics ; Alfentanil (1N74HM2BS7) ; Morphine (76I7G6D29C) ; Dextromoramide (9S4S6CIY83)
Language	English
Publishing date	1990-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	193153-2
ISSN	1872-6623 ; 0304-3959
ISSN (online)	1872-6623
ISSN	0304-3959
DOI	10.1016/0304-3959(90)91148-C
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Zs.A 1158: Show issues

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