Gotowa bibliografia na temat „Myocardial”
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Artykuły w czasopismach na temat "Myocardial"
A. Meenakshi, Martin, i Erik G. Seth. "Protective role of TAT-HSP70 after myocardial I/R injury". American Journal of BioMedicine 5, nr 3 (22.09.2017): 279–84. http://dx.doi.org/10.18081/2333-5106/015-04/289-294.
Pełny tekst źródłaMicic-Labudovic, Jelena, Tatjana Atanasijevic, Vesna Popovic, Zoran Mihailovic, Slobodan Nikolic i Dragana Puzovic. "Myocardial bridges: A prospective forensic autopsy study". Srpski arhiv za celokupno lekarstvo 143, nr 3-4 (2015): 153–57. http://dx.doi.org/10.2298/sarh1504153m.
Pełny tekst źródłaZhong, Ze, Jia-qing Hu, Xin-dong Wu, Yong Sun i Jun Jiang. "Anti-apoptotic effects of myocardin-related transcription factor-A on rat cardiomyocytes following hypoxia-induced injury". Canadian Journal of Physiology and Pharmacology 94, nr 4 (kwiecień 2016): 379–87. http://dx.doi.org/10.1139/cjpp-2014-0461.
Pełny tekst źródłaBhattacharya, Aniket, Nadia Al-Sammarraie, Mengistu G. Gebere, John Johnson, John F. Eberth i Mohamad Azhar. "Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development". Journal of Cardiovascular Development and Disease 8, nr 3 (2.03.2021): 26. http://dx.doi.org/10.3390/jcdd8030026.
Pełny tekst źródłaBerry, Mark F., Adam J. Engler, Y. Joseph Woo, Timothy J. Pirolli, Lawrence T. Bish, Vasant Jayasankar, Kevin J. Morine, Timothy J. Gardner, Dennis E. Discher i H. Lee Sweeney. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance". American Journal of Physiology-Heart and Circulatory Physiology 290, nr 6 (czerwiec 2006): H2196—H2203. http://dx.doi.org/10.1152/ajpheart.01017.2005.
Pełny tekst źródłaKhubulava, G. G., A. N. Shishkevich, S. S. Mikhailov i E. Yu Bessonov. "Myocardial reperfusion syndrome. Pathogenesis, clinic, diagnosis". Bulletin of the Russian Military Medical Academy 22, nr 1 (15.12.2020): 196–200. http://dx.doi.org/10.17816/brmma25992.
Pełny tekst źródłaHirsch, Alan T., John A. Opsahl, Mary M. Lunzer i Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction". American Journal of Physiology-Heart and Circulatory Physiology 276, nr 6 (1.06.1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.
Pełny tekst źródłaBrown, TA. "Hibernating myocardium". American Journal of Critical Care 10, nr 2 (1.03.2001): 84–91. http://dx.doi.org/10.4037/ajcc2001.10.2.84.
Pełny tekst źródłaXiao, Ying, Tao Wang, Xin Song, Dan Yang, Qing Chu i Y. James Kang. "Copper promotion of myocardial regeneration". Experimental Biology and Medicine 245, nr 10 (8.03.2020): 911–21. http://dx.doi.org/10.1177/1535370220911604.
Pełny tekst źródłaAbdrahmanova, A. I., N. B. Amirov i N. A. Cibulkin. "Application of Perfusion Single Photon Emission Computed Tomography of the Myocardium in Pain-Free Myocardial Ischemia". Russian Archives of Internal Medicine 10, nr 5 (9.10.2020): 340–47. http://dx.doi.org/10.20514/2226-6704-2020-10-5-340-347.
Pełny tekst źródłaRozprawy doktorskie na temat "Myocardial"
Egan, Jonathan Rogers. "The role of myocardial membrane proteins and myocardial oedema in postoperative myocardial dysfunction". Thesis, The University of Sydney, 2009. http://hdl.handle.net/2123/5975.
Pełny tekst źródłaEgan, Jonathan Rogers. "The role of myocardial membrane proteins and myocardial oedema in postoperative myocardial dysfunction". Faculty of Medicine, 2009. http://hdl.handle.net/2123/5975.
Pełny tekst źródłaThe vast majority of children undergoing surgical repair of cardiac lesions do spectacularly well. However a significant proportion, ~ 25%, struggle to progress in the early postoperative period and require additional pharmacological and occasionally mechanical circulatory support. All children typically have some degree of postoperative myocardial dysfunction, with the severe spectrum termed the low cardiac output state (LCOS). LCOS is clinically defined as the requirement for new or escalated inotrope therapy, a widened arteriovenous oxygen difference, cardiac arrest or the need for reinstitution of mechanical circulatory support. LCOS is largely responsible for the morbidity and mortality involved in paediatric cardiac surgery. Despite the predictability of LCOS in the initial postoperative hours, the underlying pathophysiology remains unclear. The period of decline in cardiac function that typifies LCOS is temporally associated with the development of oedema in the tissues of the body, including the heart. This relationship between oedema and dysfunction has increasingly become blurred, with a tendency to elevate the temporal association to a causal link. We sought to explore the causes and contributions to myocardial dysfunction in this setting, including the roles of oedema and ischaemia within the heart. In focusing on oedema and ischaemia we also examined the effects of these insults on relevant myocardial membrane proteins, including those that permit rapid water transport – aquaporins (AQPs), and those involved in membrane mechanics – dystrophin, and membrane repair – dysferlin. Experimental settings which enabled the in vitro dissection of these insults and proteins of interest were combined with a clinically accurate in vivo model. This thesis describes a series of thematically linked experiments that examined LCOS, myocardial oedema and the role of various membrane proteins. We performed isolated cardiomyocyte studies, isolated heart studies as well as a clinically relevant large animal (lamb) cardiopulmonary bypass (CPB) model. Across these models we also explored the role of therapeutically protecting myocardial membranes with Poloxamer 188 (P188) and assessed any influence on myocardial function, oedema and membrane proteins. vi The results from these three models suggest that the clinically accepted dogma of a causative link between myocardial oedema and dysfunction overstates the contribution of myocardial oedema to LCOS. We found that ischaemia/reperfusion was of primary importance in causing myocardial dysfunction. Myocardial oedema without ischaemia had a mild and reversible contribution to myocardial dysfunction, but this was minor in comparison to the gross dysfunction attributable to ischaemia. Isolated cardiomyocytes, with induced oedema, functioned well. Whilst ischaemic cardiomyocytes, with less swelling still had severe contractile dysfunction. Isolated hearts, perfused with an oedema inducing crystalloid perfusate developed myocardial oedema and had minimal reversible systolic and diastolic dysfunction. Isolated hearts which experienced global ischaemia had comparable degrees of myocardial oedema, and significantly greater degrees of myocardial dysfunction that increased in severity with increasing duration of ischaemia. In the lamb CPB model, only those lambs which underwent aortic cross clamping and had a period of ischaemia had poor myocardial function. These lambs also had swollen hearts, raised myocardial AQP1 mRNA and reduced membrane dysferlin protein expression. Membrane dystrophin protein expression was not altered, somewhat unexpectedly with CPB with or without ischaemia. Lambs placed on CPB without ischaemia had good myocardial function, minimal oedema and unchanged membrane protein expression during the survival period. In a blinded lamb CPB trial of P188 there were improved haemodynamics and indicies of myocardial function associated with its use. This was also associated with preservation of dysferlin expression and reduced membrane injury. In parallel isolated heart trials of this therapy, there was a reduction in myocardial oedema associated with its use in non-ischaemic experiments. There was also a suggestion of improved diastolic function in ischaemic experiments, but no change in myocardial water content. In conclusion, we have highlighted the primacy of ischaemia/reperfusion over oedema in contributing to LCOS. We have refuted the accepted dogma that myocardial oedema causes significant dysfunction in itself, with important oedema likely to result from ischaemia. We have shown that AQP1 may be involved in the pathogenesis of the capillary leak syndrome. Finally we have hinted at a role for prophylactic P188 in the vii setting of LCOS, possibly highlighting the role of membrane repair in recovery after surgery. Isolated heart trials of P188 further support a non-rheological mechanism of action and also lend support to the causal separation of myocardial oedema and dysfunction. The integral membrane protein dysferlin, rather than dystrophin, is relevant in the setting of LCOS in the current era.
Zhou, Xiaopeng. "Myocardial T1 Mapping Techniques for Quantification of Myocardial Fibrosis". Cleveland State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=csu1355418392.
Pełny tekst źródłaLöwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.
Pełny tekst źródłaPark, Jade. "Myocardial fibrosis and effect of AZT in myocardium of Y995CB mouse". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12581.
Pełny tekst źródłaPyrimidine nucleoside reverse transcriptase inhibitors (NRTIs), one of the primary classes of HIV/AIDS antiretroviral drugs, are known to cause mitochondrial toxicity by inhibiting polymerase gamma during extending mitochondrial DNA replication. Extensive, prolonged use of NRTIs, such as zidovudine (3'-azido-2',3'-deoxythymidine; AZT), is associated with cardiovascular complications, such as dilated cardiomyopathy, the most common form of heart failure in which cardiac fibrosis is seen. Moreover, cardiac fibrosis is part of the pathological response of the heart during the progression of heart failure. Thus, we hypothesized that AZT treatment will contribute to the progression of cardiac fibrosis indirectly. Our study specifically focused on the effects of AZT and the development of cardiac fibrosis in the myocardium of wildtype (WT) and Y955CB transgenic mice (TG). Y955CB TG expresses a dominant negative cardiac specific mutant mitochondrial DNA polymerase gamma and were used to enhance the mtDNA toxic effect of AZT. To estimate fibrosis, myocardial collagen levels in each treatment group were assessed using both the hydroxyproline assay and histological image analysis. WT mice treated with AZT 0.22 mg/day for 35 days revealed no change in the level of hydroxyproline. However, a significant increase in hydroxyproline abundance correlated with histologically detectable fibrosis in vehicle-treated Y955CB TG mice. Interestingly, there was no additional increase in the abundance of collagen in AZT-treated Y955CB mice. Taken together, these data demonstrate that Y955CB TG displays an increase in the collagen level of the heart, concomitant with its documented cardiomyopathy. However AZT treatment was insufficient to increase the abundance of collagen in the heart.
Dwivedi, Girish. "A Comparison between Myocardial Contrast Echocardiography and Radionuclide Myocardial perfusion Imaging in Patients with Acute Myocardial Infarction". Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521583.
Pełny tekst źródłaTreibel, Thomas Alexander. "Aortic stenosis : a myocardial disease : insights from myocardial tissue characterisation". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1574742/.
Pełny tekst źródłaWhite, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium". Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.
Pełny tekst źródłaSingh, Hardial. "Quantitative assessment of myocardial ischaemia with thallium-201 myocardial perfusion imaging". Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/19297.
Pełny tekst źródłaFrostfeldt, Gunnar. "Coagulation Inhibition and Development of Myocardial Damage in ST-Elevation Myocardial Infarction". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5322-8/.
Pełny tekst źródłaKsiążki na temat "Myocardial"
Salerno, Tomas A., i Marco Ricci, red. Myocardial Protection. Elmsford, New York, USA: Blackwell Publishing, 2003. http://dx.doi.org/10.1002/9780470987452.
Pełny tekst źródłaIskandrian, Ami E., i Ernst E. Van Der Wall, red. Myocardial Viability. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5.
Pełny tekst źródłaKaski, Juan Carlos, i David W. Holt, red. Myocardial Damage. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2380-0.
Pełny tekst źródłaCokkinos, Dennis V., red. Myocardial Preservation. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4.
Pełny tekst źródłaIskandrian, Abdulmassih S., i Ernst E. Van Der Wall, red. Myocardial viability. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1170-6.
Pełny tekst źródłaDhalla, Naranjan S., Ian R. Innes i Robert E. Beamish, red. Myocardial Ischemia. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5.
Pełny tekst źródłaWainwright, Cherry L., i James R. Parratt. Myocardial Preconditioning. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22206-5.
Pełny tekst źródłaCokkinos, Dennis V., Constantinos Pantos, Gerd Heusch i Heinrich Taegtmeyer, red. Myocardial Ischemia. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6.
Pełny tekst źródłaA, Salerno Tomas, i Ricci Marco, red. Myocardial protection. Elmsford, N.Y: Blackwell Pub., 2004.
Znajdź pełny tekst źródłaH, Marwick Thomas, Yu Cheuk-Man i Sun Jingping, red. Myocardial imaging. Malden, Mass: Blackwell Pub., 2007.
Znajdź pełny tekst źródłaCzęści książek na temat "Myocardial"
Cokkinos, Dennis V. "Myocardial Hibernation". W Myocardial Preservation, 185–202. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_10.
Pełny tekst źródłaCokkinos, Dennis V. "Myocardial Stunning". W Myocardial Preservation, 171–84. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_9.
Pełny tekst źródłaPantos, Constantinos, Iordanis Mourouzis i Dennis V. Cokkinos. "Myocardial Ischemia". W Myocardial Ischemia, 11–76. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-28658-6_2.
Pełny tekst źródłaSchwaiger, Markus, i Ulrich Schricke. "Hibernating and stunned myocardium: Pathophysiological considerations". W Myocardial Viability, 1–20. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_1.
Pełny tekst źródłaVan Der Wall, Ernst E., Jeroen J. Bax, Hubert W. Vliegen, Albert V. G. Bruschke i Albert De Roos. "Role of magnetic resonance techniques in viability assessment". W Myocardial Viability, 177–97. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_10.
Pełny tekst źródłaIskandrian, Ami E. "Viability assessment: clinical applications". W Myocardial Viability, 199–227. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_11.
Pełny tekst źródłaIskandrian, Ami S., i Ernst E. Van Der Wall. "Summary". W Myocardial Viability, 229–31. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_12.
Pełny tekst źródłaBaliga, Ragavendra R., Jutta Schaper i Jagat Narula. "Role of apoptosis in myocardial hibernation and myocardial stunning". W Myocardial Viability, 21–45. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_2.
Pełny tekst źródłaSchelbert, Heinrich R. "Assessment of myocardial viability with positron emission tomography". W Myocardial Viability, 47–72. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_3.
Pełny tekst źródłaBax, Jeroen J., Jean-Louis J. Vanoverschelde i Ernst E. Van Der Wall. "Assessment of myocardial viability by thallium-201". W Myocardial Viability, 73–89. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4080-5_4.
Pełny tekst źródłaStreszczenia konferencji na temat "Myocardial"
Discher, Dennis, i Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.
Pełny tekst źródłaTracy Ling, Yik Tung, Vincent Sayseng i Elisa Konofagou. "Myocardial Elastography for Evaluating the Evolution of Strains and Strain Rates in Canine Myocardium After Myocardial Infarction". W 2022 IEEE International Ultrasonics Symposium (IUS). IEEE, 2022. http://dx.doi.org/10.1109/ius54386.2022.9957783.
Pełny tekst źródłaVeress, A. I., A. Giannakidis i G. T. Gullberg. "Mechanical Effects of Myofibril Disarray on Cardiac Function". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14696.
Pełny tekst źródłaZhang, Song, John A. Crow, Robert C. Cooper, Ronald M. McLaughlin, Shane Burgess, Ali Borazjani i Jun Liao. "Detection of Myocardial Fiber Disruption in Artificial Lesions With 3D DT-MRI Tract Models". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193121.
Pełny tekst źródłaHu, Zhenhua, Dimitris Metaxas i Leon Axel. "Heart Composite Material Model for Stress-Strain Analysis". W ASME 2003 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/detc2003/vib-48334.
Pełny tekst źródłaMehri, Sounira, Wided Khamlaoui i Mohamed Hammami. "Acute myocardial infarction". W the Fourth International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3234698.3234741.
Pełny tekst źródłaSingelyn, J. M., J. A. DeQuach i K. L. Christman. "Injectable myocardial matrix as a scaffold for myocardial tissue engineering". W 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334839.
Pełny tekst źródłaBradley, Joshua, J. Bradley, EB Schelbert, LJ Bonnett, GA Lewis, J. Lagan, C. Orsborne i in. "31 Remote myocardial fibrosis predicts adverse outcome following myocardial infarction". W British Society of Cardiovascular Magnetic Resonance (BSCMR) Annual Congress 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2023. http://dx.doi.org/10.1136/heartjnl-2022-bscmr.30.
Pełny tekst źródłaBaron, N., N. Kachenoura, F. Beygui, P. Cluze, P. Grenier, A. Herment i F. Frouin. "Quantification of myocardial edema and necrosis during acute myocardial infarction". W 2008 35th Annual Computers in Cardiology Conference. IEEE, 2008. http://dx.doi.org/10.1109/cic.2008.4749158.
Pełny tekst źródłaVasilchenko, S. Yu, A. A. Stratonnikov, A. I. Volkova, V. B. Loschenov, E. A. Sheptak i S. S. Kharnas. "Investigation of myocardial photodynamic revascularization method on ischemic rat myocardium model". W SPIE Proceedings, redaktor Valery V. Tuchin. SPIE, 2006. http://dx.doi.org/10.1117/12.697420.
Pełny tekst źródłaRaporty organizacyjne na temat "Myocardial"
Moridi, Mina, Parinaz Onikzeh, Aida Kazemi i Hadi Zamanian. CABG versus myotomy in symptomatic myocardial bridge patients : A systematic Review and Meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, listopad 2021. http://dx.doi.org/10.37766/inplasy2021.11.0088.
Pełny tekst źródłaVoynalovich-Khanova, Y. A. SYNDROME OF MYOCARDIAL REMODELING (CLINICAL OBSERVATION). "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-46-49.
Pełny tekst źródłaLi, Xiao, Fayang Ling, Wenchuan Qi, Sanmei Xu, Bingzun Yin, Zihan Yin, Qianhua Zheng, Xiang Li i Fanrong Liang. Preclinical Evidence of Acupuncture on infarction size of Myocardial ischemia: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2022. http://dx.doi.org/10.37766/inplasy2022.6.0044.
Pełny tekst źródłaMcDonough, Kathleen H., i Harvey I. Miller. Myocardial Dysfunction Contributes to Irreversible Hemorrhagic Shock. Fort Belvoir, VA: Defense Technical Information Center, luty 2001. http://dx.doi.org/10.21236/ada389358.
Pełny tekst źródłaPickard, Jeb S., i Joe E. Burton. Flying Waivers for History of Angioplasty and Myocardial Infraction. Fort Belvoir, VA: Defense Technical Information Center, listopad 1994. http://dx.doi.org/10.21236/ada292505.
Pełny tekst źródłaHassanzadeh, Sara, Sina Neshat, Afshin Heidari i Masoud Moslehi. Myocardial Perfusion Imaging in the Era of COVID-19. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2022. http://dx.doi.org/10.37766/inplasy2022.4.0063.
Pełny tekst źródłaDejong, Marla J., Kyungeh An, Candace C. Cherrington i Debra K. Moser. Predictors of Symptom Appraisal for Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, listopad 2004. http://dx.doi.org/10.21236/ada427523.
Pełny tekst źródłaCrowley, James P., C. R. Valeri i Joseph Chazan. Myocardial Infarction and Transfusion Requirements in Transfusion Dependent Anemic Patients. Fort Belvoir, VA: Defense Technical Information Center, maj 1990. http://dx.doi.org/10.21236/ada360239.
Pełny tekst źródłaQIN, Xiaoyu, Chunai WANG, Jie ZHANG, Shuwei WANG i Weiqi ZHANG. Effectiveness and safety of electroacupuncture for myocardial protection in cardiopulmonary bypass patients with myocardial ischemia-reperfusion injury:a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2021. http://dx.doi.org/10.37766/inplasy2021.4.0045.
Pełny tekst źródłaNaydenov, Stefan, Nikolay Runev, Emil Manov, Nadya Naydenova, Mikhail Matveev i Plamen Krastev. Diagnostic Potential of Signal-Averaged Orthogonal Electrocardiography in Acute Myocardial Infarction. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, luty 2021. http://dx.doi.org/10.7546/crabs.2021.02.16.
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