Relevant bibliographies by topics / Heart involvement

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Heart involvement'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Heart involvement"

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Lorenzoni, R. "Cardiac involvement in idiopathic hypereosinophilic syndrome." Heart 87, no. 6 (June 1, 2002): 553. http://dx.doi.org/10.1136/heart.87.6.553.

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NAKAYAMA, Y. "Echocardiographic features of cardiac involvement in Fabry's disease." Heart 83, no. 6 (June 1, 2000): 695. http://dx.doi.org/10.1136/heart.83.6.695.

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Marupakula, Vidyasagargoud, Karyne L. Vinales, Mohammad Q. Najib, Louis A. Lanza, Howard R. Lee, and Hari P. Chaliki. "Occurrence of left-sided heart valve involvement before right-sided heart valve involvement in carcinoid heart disease." European Heart Journal - Cardiovascular Imaging 12, no. 3 (December 17, 2010): E18. http://dx.doi.org/10.1093/ejechocard/jeq171.

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Doehner, Wolfram. "Mental involvement in heart failure." Revista Portuguesa de Cardiologia 40, no. 8 (August 2021): 557–59. http://dx.doi.org/10.1016/j.repc.2021.04.003.

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Doehner, Wolfram. "Mental involvement in heart failure." Revista Portuguesa de Cardiologia (English Edition) 40, no. 8 (August 2021): 557–59. http://dx.doi.org/10.1016/j.repce.2021.07.026.

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Šerpytis, Pranas, Žaneta Petrulionienė, Urtė Gargalskaitė, Aurelija Gedminaitė, and Violeta Panavienė. "Heart Involvement in Kawasaki Disease." Sveikatos mokslai 24, no. 3 (August 14, 2014): 27–32. http://dx.doi.org/10.5200/sm-hs.2014.039.

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Ferri, C., D. Giuggioli, M. Sebastiani, M. Colaci, and M. Emdin. "Heart involvement and systemic sclerosis." Lupus 14, no. 9 (September 2005): 702–7. http://dx.doi.org/10.1191/0961203305lu2204oa.

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Azevedo, E. M., M. Scaff, E. R. Barbosa, A. E. Gouveia Neto, and H. M. Canelas. "Heart involvement in hepatolenticular degeneration." Acta Neurologica Scandinavica 58, no. 5 (January 29, 2009): 296–303. http://dx.doi.org/10.1111/j.1600-0404.1978.tb02890.x.

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Clements, Philip J., and Daniel E. Furst. "Heart involvement in systemic sclerosis." Clinics in Dermatology 12, no. 2 (April 1994): 267–75. http://dx.doi.org/10.1016/s0738-081x(94)90331-x.

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Koju, Rajendra, R. Gurung, P. Pant, B. Pokharel, and TRS Bedi. "Pattern of Heart Valve Involvement in Rheumatic Heart Disease." Nepalese Heart Journal 6, no. 1 (November 24, 2017): 17–22. http://dx.doi.org/10.3126/njh.v6i1.18449.

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Rheumatic heart disease is the most important consequence of acute rheumatic fever. Both are common cardiovascular problems in Nepal. Echocardiographic detection of rheumatic heart disease is important to establish the diagnosis. The involvement of valves and their severity guides the therapeutic options. A total of 133 valvular heart disease cases attended in Dhulikhel Hospital between July 2008 to June 2009 were analyzed. Fifty-one patients, in whom the problems were rheumatic in origin were studied. Among them, 12% (6) had isolated aortic valve involvement, 35%(18) had isolated mitral valve and 53%(27) ahd mixed involvement. Severe mitral stenosis accounts for 24% of all mitral stenosis and severe aortic stenosis is 20% fo all aortic stenosis. The rates for severe mitral regurgitation and severe aortic regurgitaiton are 30% and 28% respectively. Although the study population has a high number of female patients, the differences in the rates of involvement of aortic or mitral valve in both genders are statistically insignificant. The study, although small, confirms that in this population, females are more commonly affected, that the mitral valve is the most commonly damaged valve and that disease affecting multiple valves is marginally more common than isolated valve disease. The detection of valvular involvement at different stages can guide the therapeutic options.
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Dissertations / Theses on the topic "Heart involvement"

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Loonat, Aminah Ahmed. "The involvement of p38 gamma MAPK in pathological cardiac hypertrophy." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-involvement-of-p38gamma-mapk-in-pathological-cardiac-hypertrophy(f00e26a7-dab2-474d-9d3e-a52dfe9e873e).html.

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p38-mitogen activated protein kinases (p38-MAPKs) are stress activated serine/threonine kinases that are activated during several different cardiac pathologies. Classically, studies have focused solely on p38α signaling in the heart. However, there is also high cardiac expression of the p38γ isoform but little is known about its cardiac function. The aim of this study was to elucidate the signaling pathway of p38γ, with a particular focus on its role in the progression of pathological cardiac hypertrophy. Comparisons of cardiac function and structure of wild type (WT) and p38γ knock out (KO) mice, in response to abdominal aortic banding, found that KO mice developed less ventricular hypertrophy than their corresponding WT controls, and have preserved cardiac function. Basal p38γ myocardial staining was primarily localised at the membranes and throughout the cytoplasm. Following aortic constriction, nuclear staining of p38γ increased, but no accumulation of p38α was observed. This suggests that the two isoforms play distinct roles in the heart. To elucidate its signaling pathway, we generated an analogue sensitive p38γ, which is mutated at a gatekeeper residue, to specifically track and identify its endogenous substrates in the myocardium. The mutation allows only the mutant kinase, but not WT kinases, to utilise analogues of ATP that are expanded at the N6 position and contain a detectable tag on the γ-phosphate. Transfer of this tag to substrates allows subsequent isolation and identification. Furthermore, unlike other p38-MAPKs, p38γ contains a C-terminal PDZ domain interacting motif. We have utilised this motif in co pull-down assays to identify interacting proteins of p38γ in the heart. Using these techniques we have identified, amongst other substrates, LDB3 and calpastatin as novel substrates of p38γ and we have determined the residues that are targeted for phosphorylation. Lastly we have shown that phosphorylation of calpastatin reduces its efficiency as a calpain inhibitor in vitro, hence proposing a mechanism by which p38γ may mediate its pro-hypertrophic role.
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Pell, Theresa Jane. "The involvement of ATP-sensitive potassium channels in novel forms of myocardial protection." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314289.

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Prosser, Hamish Charles Graydon. "Involvement of Novel Cardiac Peptides in Healthy and Ischemic Hearts." Thesis, University of Canterbury. Biological Sciences, 2009. http://hdl.handle.net/10092/2731.

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The role and functions of Urotensin II (UII), Urotensin II-related peptide (URP) and proangiotensin-12 (PA12) are currently ambiguous, either due their relatively new identification and isolation from their host species, or due to contrasting and conflicting reports observing the physiological and pathophysiological role of these spasmogens within the mammalian cardiovascular system. Accordingly, we sought to determine the true physiological functions of these peptides in both healthy and diseased states. The initial task was to reveal potential reasons for the contrasting responses to UII, and to define the role of UII within the isolated rat heart. UII and URP retain a highly conserved cyclic region, shown to be necessary in receptor binding and activation, with the high inter-species variance within the N-terminus reported to be of little importance. Our research revealed UII to be highly species-specific, stimulating potent, sustained vasodilation of the coronary arteries in response to the native form infused, while non-native UII peptides had either no effect, or caused significant vasoconstriction. UII-induced vasodilative effects were found to be mediated by nitric oxide and prostaglandin activity combined. Reviewing publications to date it was evident that many studies employed UII foreign to the host species, reporting potentially untrue effects, based on our findings. Recent studies have identified UII as a potent agent in developing and promoting atherosclerosis and coronary artery disease through UII-induced mitogenic activity and promoting foam cell formation. Hence, we observed the effect of infusing the native species of UII and URP into a model of cardiac ischemia-reperfusion. Both preconditioning the heart with UII or URP, or infusing UII or URP upon reperfusion caused significant coronary vasodilation following ischemia, and significantly attenuated ischemic-induced myocardial injury. These studies indicated elevating UII and URP provided a level of cardioprotection, not only when administered into healthy hearts prior to an ischemic event, but also in hearts having already undergone ischemia and the resultant endothelial damage. PA12 was the third peptide tested in the current thesis. Being newly identified and suggested to be a new component of the renin-angiotensin system (RAS) it was important to define the physiological role of PA12 upon the cardiovasculature, as the RAS is heavily associated with the development and progression of cardiovascular disease. Utilising the Langendorff isolated rat heart technique, PA12 was found to cause potent vasoconstriction of the coronary arteries, mediated by the angiotensin II type 1 receptor (AT₁R). Furthermore, using subjecting the perfusate samples to radioimmunoassay and RP-HPLC revealed PA12 was converted to AngII. Both PA12-induced vasoconstriction and generation of AngII were found to be dependent upon chymase activity, with inhibition of ACE1 having little effect. Myography was employed to further study the vascular response to PA12 throughout the rat arterial system from the common carotid to the femoral arteries. PA12-induced vasoconstriction displayed a potency gradient, with greatest constriction observed in vessels closest to the heart, with potency reduced and eventually lost further from the heart. PA12-induced vasoactivity was shown to be dependent upon both chymase and ACE1 activity, with ACE1 regulating PA12 activity with greater potency. The intracellular pathways stimulated in response to PA12 were defined using western blotting, with PA12 stimulating phosphorylation of ERK1/2, JNK, p38 and PKCα/β₁₁, but having no influence on PKCδ/θ. Stimulation of these pathways is consistent with the observed PA12-induced vasoconstriction, and also indicates that PA12 activation of AT₁R and the subsequent cytokines, could potentially stimulate hypertrophy, apoptosis, cell growth and differentiation, and inflammation, promoting cadiovascular remodelling and progressing atherosclerosis, hypertension and other vascular diseases if not sufficiently regulated. Taken together, these studies indicate PA12 may have a primary role within the local, tissue-based RAS, providing an alternate substrate to angiotensin I, while ACE1 is the primary regulatory enzyme within the circulation. Our findings also display the chymase-dependent PA12/AT₁R pathway as potential novel targets for pharmacological inhibition of RAS activity to ameliorate hypertension and maladaptive vascular remodelling.
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Bryson, Shona H. "Human anti-(bovine milk fat globule membrane) antibodies : involvement in coronary heart disease." Thesis, University of Bath, 1989. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328539.

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Dean, David C. "Apoptosis in the isolated perfused rat heart, involvement of reperfusion, oxidants and protein synthesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq26315.pdf.

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Knezevic, Tijana. "TRANSLATIONAL APPROACH TO INVESTIGATE INVOLVEMENT OF BAG3 IN PROTEIN QUALITY CONTROL AND HEART FAILURE." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/374885.

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Biology
Ph.D.
Heart failure continues to be a global problem, even with all the drugs currently available, leading to a need of new therapeutics to decrease incidence of heart failure. Heart failure is the inability of the heart muscle to pump sufficient blood and oxygen to the rest of the body. One of the causes of heart failure is cardiomyopathy, where cardiac muscle becomes larger and weaker. Genetic mutations in genes encoding sarcomeric, structural and cytoskeletal proteins were found in families that developed cardiomyopathy. Our laboratory has indentified a family with heart failure in whom a novel mutation in the BCL2-associated athanogene 3 (BAG3) has been characterized. Among other cardiomyopathy-causing BAG3 mutations reported in various laboratories. Several BAG3 mutations in humans are known to cause familial dilated cardiomyopathy, myofibrilar myopathy, and giant axonal neuropathy. BAG3 is a stress induced co-chaperone protein that interacts with several heat shock proteins and acts as an important regulator of protein quality control. Expression of BAG3 is high in cardiac, skeletal and smooth muscle. BAG3 is localized at the z-disk of cardiomyocytes and was shown to be essential in keeping a normal assembly of z-disk proteins during mechanical stretch. Interaction of BAG3 with actin capping protein CapZbeta1 prevents degradation of CapZbeta1 via proteasome system and maintains the integrity of the z-disk. BAG3 was shown to promote clearance of misfolded proteins, such as filamin C, via autophagy. Not only that BAG3 is able to promote clearance of dysfunctional filamin C, but it was found to enhance synthesis of the new filamin. BAG3 deficient mice develop fulminant myopathy and cardiomyopathy with disorganization of z-disk and die after one month of age. Not only that BAG3 is involved in myofibrilar stability in the cardiomyocytes and that patients with BAG3 mutations develop cardiomyopathy, but our lab showed that patients with heart failure have decrease levels of BAG3. Since heart failure patients have decreased levels of BAG3, the therapy where BAG3 levels are restored to normal levels may improve heart function. Here, I show that in mouse model of heart failure after MI left ventricle function is restored after administration of AAV9 BAG3. BAG3 overexpression in mouse heart helped the stability of z-disk proteins after mechanical stress and myocardial infarction. Overexpressed BAG3 localizes to z-disk and is also able to increase autophagy in cardiomyocytes and help with clearance of misfolded proteins. Taken together, this study shows that BAG3 is a valid and promising new therapeutic target for heart failure patients. BAG3 overexpression is able to induce autophagy and help the heart cope better with stress. Also, AAV9 vector is robustly expressed in the heart after systemic administration, and is a promising vector for gene delivery in the patient heart.
Temple University--Theses
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Näsström, Lena. "Participation in heart failure home-care : Patients’ and partners’ perspectives." Doctoral thesis, Linköpings universitet, Avdelningen för omvårdnad, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-117095.

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Introduction: Patient participation is important for improving outcomes and respecting selfdetermination and legal aspects in care. Heart failure is a chronic condition that puts high demands on self-care and patient participation. Patients often need advanced care due to deterioration of their heart failure symptoms, and one option is to provide care as home-care. There is limited knowledge of how patients with heart failure and their partners view participation in home-care. Aim: The overall aim of this thesis was to describe different perspectives of participation in structured heart failure home-care among patients with heart failure and their partners. Methods: All patients in this thesis received structured heart failure home-care, according to a model aiming to facilitate care, where safety, participation, and gaining knowledge about the illness and treatment, are in focus. Study I had a prospective pre-post longitudinal design including 100 patients with heart failure receiving home-care. Data was collected by selfadministered questionnaires. Study II had a descriptive design. Nineteen patients receiving home-care were interviewed, and data was analysed using qualitative content analysis. Study III had a descriptive and explorative design. Data was collected by video-recorded observations of 19 home visits and analysed by qualitative content analysis. Study IV had a parallel convergent mixed-method design including 15 partners of patients receiving structured home-care. Data was collected by interviews and self-administered questionnaires. Datasets were first analysed separately and then together. Results: Better self-care behaviour was significantly associated with all measured aspects of participation. Participation by received information increased significantly during the 12-month follow-up (I). Patients’ descriptions of participation included communication between patients and health care professionals, access to care, active involvement in care, a trustful relation with health care professionals, and options for decision-making(II). Observed care encounters revealed that participation was made possible by; (i) interaction, including exchange of care-related information, care-related reasoning, and collaboration, (ii) an enabling approach, including the patient expresses own wishes and shows an active interest, and the nurse is committed and invites to a dialogue (III). Partners scored fairly positive for their participation in care and they performed different levels of caregiving tasks. Descriptions of participation included; adapting to the caring needs and illness trajectory, mastering caregiving demands, interacting with care providers, and gaining knowledge to comprehend the health situation. The mixed-method results showed both convergent results and expanded knowledge (IV). Conclusions: Structured heart failure home-care facilitated participation both for patients and their partners. Patient participation with regard to received information improved significantly after receiving home-care. Aspects of patient participation were consistently associated with better self-care behaviour. Patients’ and partners’ descriptions revealed many aspects of participation, and observed home visits revealed how interaction and an enabling approach underpinned participation.
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Harley, Margaret Pauline. "Touching the heart : an exploration of business involvement with young people in recovery from substance abuse /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19405.pdf.

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Windt, Leon Johannes de. "Ischemia and reperfusion-induced damage of the isolated mouse heart involvement of type IIA secretory phospholipase A2 /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=6892.

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Larsson, Annika. "Medin amyloid - a matter close to the heart : Studies on medin amyloid formation and involvement in aortic pathology." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9275.

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Amyloidoses are a group of protein misfolding diseases characterized by deposits of insoluble fibrillar protein aggregates. Medin amyloid, which is the focus of this thesis, appears in the media of the thoracic aorta in nearly all individuals over 50 years. The fibrils are derived from a 50 amino acid residue fragment of the precursor protein lactadherin. How medin amyloid arises is unknown, but in paper I we demonstrated, with immunohistochemical and in vitro binding experiments, that both lactadherin and medin interact with elastin, implying that the elastic fibre is central in amyloid formation. In paper II, we further showed that the last 18-19 amino acid residues constitute the amyloid-promoting region. In paper III, the consequence of medin deposition was investigated. Aortic specimens from patients with thoracic aorta aneurysm and dissection were examined for medin content. The tissue findings indicated that the two disease groups contained more medin oligomers than normal aortas. Interestingly, recent reports demonstrate that the toxicity of amyloid proteins is attributed to prefibrillar oligomeric aggregates rather than to mature fibrils. In support of this finding, we observed that prefibrillar medin, in contrast to medin fibrils, was toxic in cell culture. Amyloid formation is a nucleation-dependent process. Addition of preformed fibrils to an amyloid protein solution dramatically accelerates fibrillation, a phenomenon called seeding. In paper IV, serum amyloid A-derived (AA) amyloid was found co-localized with medin deposits in the aorta. In vitro, medin fibrils enhanced the formation of AA fibrils, indicative of a seeding mechanism. The data are of great importance as they suggest that one type of amyloid is capable of inducing fibrillation and deposition of another amyloid type. In conclusion, the results of this thesis shed light on how medin is formed, the function of lactadherin and the consequences of medin deposition for aortic pathology.
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Books on the topic "Heart involvement"

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Tagi tote e loto haaku =: My heart is crying a little : Niue Island involvement in the great war, 1914-1918. Alofi, Niue: Government of Niue, 2000.

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Platt, Stephen. Heard or ignored: Tenant involvement in housing associations. London: National Federation of Housing Associations, 1987.

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Cesal, Barbara P. Heart to Heart for Primary Grades: Family Involvement in Primary Reading. Innovative Learning, 1993.

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Popova, Svetlana, and Jürgen Rehm. Substance Involvement and Physical Health. Edited by Kenneth J. Sher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199381708.013.13.

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Substance use, mainly defined as the consumption of alcohol, tobacco, and illegal drugs, is a major risk factor for disease, disability, and mortality. Alcohol consumption can cause a number of chronic diseases, including several types of cancer, diseases of the gastrointestinal tract, various cardiovascular diseases, alcohol use disorders and infectious diseases, such as tuberculosis and pneumonia. Certain patterns of light moderate drinking, without heavy drinking occasions, may incur a protective effect on ischemic disease categories and diabetes. Finally, alcohol has been established as a causal factor for unintentional and intentional injury. Illegal drug use has been mainly linked to four health outcomes: overdose and other injury, noncommunicable diseases, certain mental disorders, and infectious diseases. In the final section, a comprehensive list of diseases attributable to tobacco smoking is provided, and the most important selected medical conditions are described. These include lung cancer, chronic obstructive pulmonary disease, and ischemic heart disease.
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Hagendorff, Andreas. Cardiac involvement in systemic diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0020.

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Systemic diseases are generally an interdisciplinary challenge in clinical practice. Systemic diseases are able to induce tissue damage in different organs with ongoing duration of the illness. The heart and the circulation are important targets in systemic diseases. The cardiac involvement in systemic diseases normally introduces a chronic process of alterations in cardiac tissue, which causes cardiac failure in the end stage of the diseases or causes dangerous and life-threatening problems by induced acute cardiac events, such as myocardial infarction due to coronary thrombosis. Thus, diagnostic methods—especially imaging techniques—are required, which can be used for screening as well as for the detection of early stages of the diseases. Two-dimensional echocardiography is the predominant diagnostic technique in cardiology for the detection of injuries in cardiac tissue—e.g. the myocardium, endocardium, and the pericardium—due to the overall availability of the non-invasive procedure.The quality of the echocardiography and the success rate of detecting cardiac pathologies in patients with primary non-cardiac problems depend on the competence and expertise of the investigator. Especially in this scenario clinical knowledge about the influence of the systemic disease on cardiac anatomy and physiology is essential for central diagnostic problem. Therefore the primary echocardiography in these patients should be performed by an experienced clinician or investigator. It is possible to detect changes of cardiac morphology and function at different stages of systemic diseases as well as complications of the systemic diseases by echocardiography.The different parts of this chapter will show proposals for qualified transthoracic echocardiography focusing on cardiac structures which are mainly involved in different systemic diseases.
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Ogbunugafor, Fanny. MY HEART BEATS FAST AND MY STOMACH HURTS: A True Story of Parental Involvement in Education. AuthorHouse, 2004.

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Elliott, Perry, and Giuseppe Limongelli. Cardiac Aspects of INHERITED METABOLIC DISEASES. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0070.

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More than 40 inherited metabolic disorders cause heart disease, including fatty acid oxidation defects, glycogen storage disorders, lysosomal storage disorders, peroxisomal diseases, mitochondrial cytopathies, organic acidemias, aminoacidopathies, and congenital disorders of glycosylation. The pattern and severity of cardiac involvement varies between disorders but includes congenital heart diseases, heart muscle diseases, arrhythmias and sudden death, and heart failure. The majority of IMDs are multisystem diseases, but in a few cases cardiac disease is the predominant clinical feature and the main determinant of prognosis. For an increasing number of IEMs there are specific therapies designed to treat or ameliorate the effects of the underlying metabolic defect. In some cases, these therapies have an important effect on the progression of cardiac disease.
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Schmidt, Jens. Extramuscular complications occurring in myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0004.

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Extra-muscular complications affecting patients suffering from the idiopathic inflammatory myopathies (IIM) are common, and appear in recognizable patterns affecting the skin, lungs, joints, oesophagus or heart, although these complications rarely all occur simultaneously. During the initial presentation of symptoms, involvement of organs other than muscle can aid the confirmation of the correct IIM subtype. Extra-muscular manifestations can be severe and life-threatening, e.g. with respiratory or cardiac involvement. Escalations of immunosuppression and other treatment modalities will likely be required in such cases since standard immunosuppression usually is not sufficient for an effective treatment of e.g. interstitial lung disease. IIM patients should therefore be regularly checked for extra-muscular manifestations, and management altered as appropriate.
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Lancellotti, Patrizio, and Bernard Cosyns. Systemic Disease and Other Conditions. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0017.

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This chapter describes the effect of various activities on the heart and associated disorders. It details the echocardiographic findings of athlete’s heart and differential diagnosis. It considers pregnancy which induces several haemodynamic changes: increase in heart rate, stroke volume, cardiac output, and decrease in systemic vascular resistance. Several echocardiographic changes may also present in normal pregnancy and these must be recognized. Echocardiography should be performed in each pregnant woman with cardiac signs or symptoms to search for new cardiac disease occurring during pregnancy and especially peripartum cardiomyopathy. Pregnancy is well tolerated by most woman with cardiac disease. Pregnancy in contraindicated in woman with pulmonary hypertension. Although the heart is not the principal affected organ in systemic disease there is some involvement. This chapter also details the echo findings of a range of systemic diseases including amyloidosis, connective tissue disease, endocrine disease, and HIV.
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Bass, Cristina, Barbara Bauce, and Gaetano Thiene. Arrhythmogenic right ventricular cardiomyopathy: diagnosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0360.

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Arrhythmogenic cardiomyopathy is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias and pathologically by an acquired and progressive dystrophy of the ventricular myocardium with fibrofatty replacement. The clinical manifestations of arrhythmogenic cardiomyopathy vary according to the ‘phenotypic’ stage of the underlying disease process. Since there is no ‘gold standard’ to reach the diagnosis of arrhythmogenic cardiomyopathy, multiple categories of diagnostic information have been combined. Different diagnostic categories include right ventricular morphofunctional abnormalities (by echocardiography and/or angiography and/or cardiovascular magnetic resonance imaging), histopathological features on endomyocardial biopsy, electrocardiogram, arrhythmias, and family history, including genetics. The diagnostic criteria were revised in 2010 to improve diagnostic sensitivity, but with the important prerequisite of maintaining diagnostic specificity. Quantitative parameters have been put forward and abnormalities are defined based on the comparison with normal subject data. A definite diagnosis of arrhythmogenic cardiomyopathy is achieved when two major, or one major and two minor, or four minor criteria from different categories are met. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, sarcoidosis, dilated cardiomyopathy, right ventricular infarction, congenital heart diseases with right ventricular overload, and athlete’s heart. Among diagnostic tools, contrast-enhanced cardiovascular magnetic resonance is playing a major role in detecting subepicardial-midmural left ventricular free wall involvement, even preceding morphofunctional abnormalities. Moreover, electroanatomical mapping is an invasive tool able to detect early right ventricular free wall involvement in terms of low-voltage areas. Both techniques are increasingly used in the diagnostic work-up although are not yet part of diagnostic criteria.
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Book chapters on the topic "Heart involvement"

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Florian, Anca R., and Ali Yilmaz. "Mitochondrial Heart Involvement." In Diagnosis and Management of Mitochondrial Disorders, 257–79. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05517-2_16.

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Schwartzkopff, B., G. Breithardt, M. Borggrefe, B. Lösse, K. V. Toyka, and H. Frenzel. "Cardiac Involvement in Kearns-Sayre Syndrome." In Heart & Brain, Brain & Heart, 293–310. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83456-1_25.

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Parker, Brent M. "Valvular Involvement in Cancer." In Cancer and the Heart, 264–70. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4898-9_24.

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Vintilă, Ana-Maria, Mihaela Horumbă, and Vlad Damian Vintilă. "Right Heart Involvement in Haematologic Disorders." In Right Heart Pathology, 455–73. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73764-5_27.

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Vintilă, Ana-Maria, Monica Dobrovie, and Vlad Damian Vintilă. "Right Heart Involvement in Hepatic Diseases." In Right Heart Pathology, 475–88. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73764-5_28.

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Bilgic, A., and Dedee F. Murrell. "Cardiac Involvement in Epidermolysis Bullosa." In Skin and the Heart, 33–48. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-54779-0_3.

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Varagic, Jasmina, and Carlos M. Ferrario. "Salt and Heart: RAAS Involvement." In The Local Cardiac Renin-Angiotensin Aldosterone System, 165–73. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-0528-4_16.

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Dustan, Harriet P. "The multifaceted aspects of cardiac involvement in hypertension." In The Heart in Hypertension, 5–12. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-0941-0_2.

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Li, Wei, Michael Henein, and Michael A. Gatzoulis. "Other Congenital Heart Diseases with Major Right Ventricular Involvement." In Echocardiography in Adult Congenital Heart Disease, 77–111. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-816-6_7.

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Sadeghian, Hakimeh, and Zahra Savand-Roomi. "Involvement of Coronary Artery Due to Kawasaki Disease." In Echocardiographic Atlas of Adult Congenital Heart Disease, 511. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12934-1_157.

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Conference papers on the topic "Heart involvement"

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Martusewicz-Boros, M., P. Boros, M. Paciorek, and D. Piotrowska-Kownacka. "Heart involvement in patients shortly after COVID-19 infection – easy detectable risk factors." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1270.

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Johnston, M., and J. Boggs. "When Löfgren Breaks the Heart: An Unusual Presentation of Löfgren’s Syndrome with Cardiac Involvement." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1537.

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Vashakmadze, Nato, LS Namazova-Baranova, NV Zhurkova, and GV Revunenkov. "80 Genetics Heart and cardiovascular involvement in Russian patients with mucopolysaccharidosis: effects of enzyme replacement therapy." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.80.

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Stanescu, Monica, and Marius Stoicescu. "USING HEART RATE MONITOR TO IMPROVE THE PERCEIVED EXERTION." In eLSE 2016. Carol I National Defence University Publishing House, 2016. http://dx.doi.org/10.12753/2066-026x-16-237.

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In order to develop the effort capacity, the relationship between the effort rate and the physiological response of the body is a defining aspect of the physical training process. To achieve this objective it is necessary to obtain a constant feedback from the subject. The perception of physical exertion issues from a subjective assessment of physiological answers. The integration of this information provides fine-tuning of the exertional responses. One method to build the individual capacity of self-assessment and self-regulating of involvement in the effort is the rate of perceived exertion (RPE). The RPE scale measures feelings of effort and fatigue experienced during the training process. This method is based on the interaction between physiological and perceptual manifestations of the subject and proved to be effective in guiding different types of activities (physical education, sports and leisure activities). This paper aims to present the role of modern technology in the development of the capacity to perceive the effort intensity, when it is used as a supporting tool for the above mentioned method. The research was conducted on a group of four athletes aged 12 - 14 years, practicing tennis at Steaua Bucharest Club, who participated for 2 months in 16 training lessons. In 8 of such activities it have been used also the heart rate monitor watches in order to compare the RPE scale results with the body's physiological responses expressed in terms of the heart rate. The research results highlight the application of technologies in improving the perception of effort, but also the accuracy of this perception in relation to the objective data.
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Pilav, Aida, and Anes Jogunčić. "DIAGNOSTICS OF PREVENTABLE DISEASES IN CARDIOLOGY." In International Scientific Symposium “Diagnostics in Cardiology and Grown-Up Congenital Heart Disease (GUCH)”. Academy of Sciences and Arts of Bosnia and Herzegovina, 2021. http://dx.doi.org/10.5644/pi2021.199.03.

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Despite many efforts to diagnose and treat preventable cardiovascular diseases (CVD), more specifically to detect known risk factors, these diseases continue to be the leading cause of morbidity and mortality. Bosnia and Herzegovina belongs among the high-risk countries with standardized death rate (SDR) of 385 per 100 000 inhabitants in 2018. Two leading causes of death are acute myocardial infraction, with rate around 90 deaths per 100 000 inhabitants and stroke with the rate around 80 deaths per 100 000 inhabitants in one year. Both incidents are preventable. Digital interventions are necessary for strengthening of the healthcare system. Benefits of eHealth could be seen in transmission of customized health information for different audiences: transmission of health-event alerts to a specified population group; transmission of health information based on health status or demographics; alerts and reminders to clients; transmission of diagnostic results (or of the availability of results) or even notifications and reminders for appointments, medication adherence, or follow-up services. Successful implementation of digital health requires multidisciplinary approaches, from mass dissemination of recommendations through public health education programs directly in the field, to clinical treatments for patients. All this requires the involvement of numerous actors, from the strategic to the operational level of management within the healthcare system in the country.
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Bagge, L., E. Holmer, S. O. Nystroöm, H. Tydeén, and T. Wahlberg. "FRAGMIN VS HEPARIN AT RECYCLING OE HUMAN BLOOD IN HEART-LUNG MACHINE (HLM)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643042.

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During cardio-pulmonary bypass (CPB), Heparin inhibits EXa (EXal), thrombin and platelet activity and is also reported to induce fibrinolysis. Eragmin (Erag) has 25% thrombin inhibition capacity as related to that of Heparin (Hep). An in_vitro study was performed to compare Frag with Hep by circulating blood in a pure artificial system. In 20 experiments, 400 ml of freshly collected blood with Frag or Hep were recycled for 2 h. HLM was primed with 400 ml of Ringeracetate. Blood sampling: donor, blood pack and every 20 min from the oxygenator. V_a£i£ble£/jassay/:ACT/Hemochron/5 APTT , TT and NT/Nyegaard/;FXaI, FVIII and ATIiT t"ATA)/amydolytic/; AT 111 (ATAg) and vWF/IEP/;Plasminogen (Pig) and albumine/immuno-diffusion/;FDP/Wellcome/;Platelet function/Adeplat S/;Fibrinogen (Fbg)/clottable/;Hemolysis (HL)/photometric/; (β -Thromboglobulin ((βTG)/RTA/;EVF, Hb, platelet count (PC) and Leucocyte count (LC)/ conventional). Corrections for hemo-/plasma dilutions were calculated. Dosages (n): Frag: 750 (1), 1500 (3), 2100 (4), 2500 (4) FXal-U (U); Hep: 1000 (3), 1500 (6) IU clinical level. Clotting only occurred at Frag 750 (1) and 1500 (2) U, when ACT, APTT, FVIII, Fbg and ATA were significantly lowered. Generally, PC fell 75% during the recycling, while PF was constant'∼20% and (βTG increased. Neither presence of FDP nor Pig consumption were detected. FXal, ACT, APTT, TT and NT were dose dependent for both drugs. ATA was directly dose-related to Frag but inversely to Hep. LC decreased with the Frag-dose but inversely to that of Hep. HL increased generally. Several proteins increased (clotting excl): Fbg 30%, ATAg 25%, ATA 45?o and vWF 60%. Conclusions. Prevention of clotting required about the double dosage of Frag. Shortened ACT and APTT predicted clotting while the levels of FXal, TT and NT did not. Thus, an effective thrombin inhibition is needed under this conditions. Consumptions of FVIII, Fbg and ATA but no further drop in PC at clotting, indicate weak platelet aggregation involvement. Absence of fibrinolytic signs supports that the fibrinolysis seen at CPB, is not a genuine effect of Hep (or Frag). Increases in some proteins may be caused by cytolysis. The rise in vWF is probably due to release from platelet surfaces.
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Fonseca, Abner Lourenço da. "Constrictive Pericarditis." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-079.

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Abstract The pericardium is a fibrous membrane that surrounds the heart and is composed of two components: visceral pericardium and parietal pericardium. Under physiological conditions, it performs important functions, such as lubrication, which minimizes friction between the organ and adjacent structures, limits intrathoracic cardiac motion, aids in filling the cardiac chambers, and participates in the balancing between the right and left ventricles during diastole and systole interactions. Constrictive Pericarditis occurs when the pericardium is thickened, fibrotic and often calcified, significantly reducing its compliance and preventing adequate cardiac filling during diastole. This is a relatively rare condition, with varied causes. The main cause is idiopathic, followed by involvement after heart surgery or radiotherapy, and also - especially in developing countries - of infectious and parasitic etiology, especially tuberculosis. The diagnosis is often challenging, since this disease typically presents with insidious and chronic symptoms, predominantly with systemic venous congestion, mimicking other disorders such as restrictive cardiomyopathy. In the last two decades, the evolution of noninvasive imaging examinations have facilitated the early recognition of Constrictive Pericarditis. Echocardiogram (transthoracic and transesophageal), central and transvalvular pressure Doppler measurements, Magnetic Resonance Imaging and Catheterization are the main exams of choice for the diagnosis. Although drug treatment alleviates the symptoms of heart failure, severe cases may require pericardiotomy.
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Boisseau, M. R., J. Bonnet, G. Freyburger, P. Desbordes, L. Brottier, J. M. Orgogozo, and H. Bricaud. "HEMOSTASIS AND HEMORHEOLOGY AFTER ISCHEMIC STROKE IN PATIENTS WITHOUT CARDIOPATHY AND OTHER LOCALISATION OF ATHEROSCLEROSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644210.

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Hemorheological parameters (whole blood filtration, whole blood viscosity, plasma viscosity and erythrocyte deformability by ektacytometry) and fibrinolysis parameters (Euglobulin Lysis Time ELT, t-PA activity, and Plasminogen ActivatorInhibitor -PAI- before and after Venous Occlusion Test -VOT-) were measured in 20 stroke patients. All these patients had a crerebrovascular accident (CVA) localised to the carotid arterial tree. They has no signs of heart disease and were without risk factors for atherosclerosis (high blood pressure, diabetes) ; they were investigated in the week following the CVA. They were divided into 4 groups : 1/ transcient ischemic accident, 2,3,4/ size of infarct classified from results of C. T. Scan carried out 2 or 3 days after the stroke (2/small +, 3/moderate ++, 4/large +++).For the hemorheological parameters we noted only a slight increase in whole blood filtration (27±8“ vs 21±2”, p<0,05).The ELT was however significantly increased in these patients (258 ±57 min. vs 133 ±33,p<0,001)suggesting impairement of fibrinolysis. The following points were noteworthy : the ELT return to normal after to VOT,there was a relationship between stroke severity and the PAI levels and the viscosity at low shear stress. These two parameters were dramatically impaired in the most severely affected patients. Transcient ischemic accidents had comparable features to the CVA of moderate size.The extend of the disorders of the hemorheological disorders and the abnormalities in fibrinolysis seemed to be related to the severity of the involvement in patients with ischemic stroke with no evidence of heart disease or atherosclerosis in other systems.
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Gensini, G. F., C. Rostango, R. Abbate, S. Favilla, P. M. Mannucci, G. G. Neri, and S. Sernery. "INCREASED PROTEIN C AND FIBRINOPEPTIDE A CONCENTRATION IN PATIENTS WITH ANGINA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643779.

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The present study has been designed to investigate protein C (as protein C antigen) and fibrinopeptide A (FpA) concentration in plasma from patients suffering from ischemic heart disease in relation to the frequency of ischemic attacks , in order to estabilish if modifications in protein C levels could contribute to blood clotting activation. Protein C and FpA levels in plasma were measured in 30 controls and in two groups of patients with angina. The first group was formed by 27 patients suffering from spontaneous ischemic attacks (active angina). The second one was formed by patients who previuosly suffered from angina, but were free from myocardial ischemic attacks for at least one month (inactive angina). Protein C (measured by electroimmunoassay) was higher in the whole group of patients than in controls (122.1+ 20.2 vs. 96.5+±14 p<0.001)? Moreover significantly higher values were found in patients with active angina in comparison to patients with inactive disease (132.5+±15.7 vs 112.3+±17.6,p<0.001).Similarly patients suffering from active angina had FpA levels higher than patients with inactive angina (8.6+±9.4 vs 5.5+±7.0,p<0.01) or controls (1.6+±1.0,p<0.001). A high concordance (76%) between protein C and FpA levels exceeding normal limits was found in patients with active angina (p < 0.05) but no statistically significant correlation existed between protein C and FpA levels and between protein C or FpA levels and coronary pathoanatomy. These results confirm a significant involvement of blood clotting system in ischemic heart disease and especially in active angina.
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Brown, R. A., C. Blahnik, and J. P. Karger. "CANADIAN INVOLVEMENT IN RBMK SAFETY IMPROVEMENT PROGRAMMES." In Heat and Mass Transfer in Severe Nuclear Reactor Accidents. Proceedings of the International Symposium. Connecticut: Begellhouse, 1995. http://dx.doi.org/10.1615/ichmt.1995.radtransfprocheatmasstransfsevnuclreactacc.60.

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Reports on the topic "Heart involvement"

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Lenhardt, Amanda. Progress Towards Meaningful Women’s Participation in Conflict Prevention and Peacebuilding Decision-makingt prevention and peacebuilding decision-making. Institute of Development Studies, December 2021. http://dx.doi.org/10.19088/k4d.2022.044.

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The Women, Peace and Security or Gender Peace and Security (WPS/GPS) agenda has expanded significantly over the 20+ years of concerted efforts at many levels to expand the role of women in conflict resolution and peacebuilding. Yet many authors note that the expansion of international agreements and national plans to support greater women’s participation in decision-making have yet to translate into concrete changes. This report examines progress in promoting women’s meaningful participation in decision making processes in conflict prevention and peacebuilding, with a focus on changes since 2018. Evidence on women’s meaningful participation in decision-making tends to focus on a small range of measurable outcomes with some studies considering the outcomes of women’s involvement in those processes to determine the extent to which they might be ‘meaningful’. Few studies examine differential outcomes of such initiatives for different groups of women, and most data does not allow for the disaggregation of intersecting identities between gender, ethnicity, race, disability, migration status and other key factors. Evidence collected for this report suggests that policies and programmes seeking to support greater women’s participation in decision-making in conflict prevention and peacebuilding often struggle to address the broader structural factors that inhibit women’s empowerment. Tackling longstanding and often deeply embedded harmful social norms has proven challenging across sectors, and in conflict or post-conflict settings with highly complex social dynamics, this can be especially difficult. Many of the issues highlighted in the literature as hindering progress on the WPS agenda relate to cross-cutting issues at the heart of gender inequality. Multiple authors from within women’s movements in conflict and post-conflict settings emphasise the need for policies and programmes that support women to act as agents of change in their own communities and which amplify their voices rather than speak on their behalf. Recent achievements in South Sudan and the Pacific region are indicative of the potential of women’s movements to affect change in conflict prevention and peacebuilding and suggest progress is being made in some areas, though gender equality in these processes may be a long way off.
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Watkins, Chris B., Susan Lurie, Amnon Lers, and Patricia L. Conklin. Involvement of Antioxidant Enzymes and Genes in the Resistance Mechanism to Postharvest Superficial Scald Development. United States Department of Agriculture, December 2004. http://dx.doi.org/10.32747/2004.7586539.bard.

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The objective of this research project was to evaluate the involvement of antioxidant enzymes and genes in the resistance mechanism to postharvest superficial scald development using two primary systems: 1. Resistant and susceptible progenies of an apple cross between a scald resistant crab apple, ‘White Angel’ and a scald susceptible cultivar, ‘Rome Beauty’; 2. Heat-treatment of ‘Granny Smith’, which is known to reduce scald development in this cultivar. In 2002 we asked for, and received (October 14), permission to revise our initial objectives. The US side decided to expand their results to include further work using commercial cultivars. Also, both sides wanted to include an emphasis on the interaction between these antioxidant enzymes and the á-farnesene pathway, with the cooperation of a third party, Dr. Bruce Whitaker, USDA-ARS, Beltsville. Background: Superficial scald is a physiological storage disorder that causes damage to the skin of apple and pear fruit. It is currently controlled by use of an antioxidant, diphenylamine (DPA), applied postharvest by drenching or dips, but concern exists about such chemical usage especially as it also involves application of fungicides. As a result, there has been increased emphasis on understanding of the underlying mechanisms involved in disorder development. Our approach was to focus on the oxidative processes that occur during scald development, and specifically on using the two model systems described above to determine if the levels of specific antioxidants and/or antioxidant enzyme activities correlated with the presence/absence of scald. It was hoped that information about the role of antioxidant-defense mechanisms would lead to identification of candidate genes for future transgenic manipulation. Major conclusions, solutions, achievements: Collectively, our results highlight the complexity of superficial scald developmental processes. Studies involving comparisons of antioxidant enzyme activities in different crab apple selection, commercial cultivars, and in response to postharvest heat and 1-methylcyclopropene (1-MCP) treatments, show no simple direct relationships with antioxidant contents and susceptibility of fruit to scald development. However, a correlative relationship was found between POX activity or isoenzyme number and scald resistance in most of the studies. This relationship, if confirmed, could be exploited in breeding for scald resistance. In addition, our investigations with key genes in the á-farnesenebiosynthetic pathway, together with antioxidant processes, are being followed up by analysis of exposed and shaded sides of fruit of cultivars that show different degrees of scald control by 1-MCP. These data may further reveal productive areas for future research that will lead to long term control of the disorder. However, given the complexity of scald development, the greatest research need is the production of transgenic fruit with down-regulated genes involved in á- farnesene biosynthesis in order to test the currently popular hypothesis for scald development.
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Wolfenson, David, William Thatcher, Rina Meidan, M. Drost, and Amiel Berman. Utero-Ovarian-Conceptus Response to Heat Stress in the Dairy Cow and its Involvement in Low Summer Fertility. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7603812.bard.

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El Halawani, Mohamed, and Israel Rozenboim. Temperature Stress and Turkey Reproduction. United States Department of Agriculture, May 2002. http://dx.doi.org/10.32747/2002.7570546.bard.

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High temperature stress is of major concern to turkey producers in Israel and the United States. The decline in the rate of egg production at high environmental temperature is well recognized, but the neuroendocrinological basis is not understood. Our objectives were: 1) to characterize the hypothalamo-hypophyseal axis involvement in the mechanism(s) underlying the detrimental effect of heat stress on reproduction, and 2) to establish procedures that alleviate the damaging effect of heat stress on reproduction. Heat stress (40oC, Israel; 32oC, U.S.) caused significant reduction in egg production, which was restored by VIP immunoneutralization. The decline in egg production did not appear to be entirely related to the expression of incubation behavior due to the rise in circulating PRL in stressed birds. Heat stress was found to increase circulating PRL in ovariectomized turkeys independent of the reproductive stage. Active immunization against VIP was shown for the first time to up-regulate LHb and FSHb subunit mRNA contents. These findings taken together with the results that the heat stress-induced decline in egg production may not be dependent upon the reproductive stage, lead to the suggestion that the detrimental effect of heat stress on reproductive performance may be in part mediated by VIP acting directly on the GnRH/gonadotropin system. Inhibin (INH) immunoneutralization has been shown to enhance FSH secretion and induces ovulation in mammals. It is hypothesized that immunization of heat-stressed turkeys against INH will increase levels of circulating FSH and the number of preovulating follicles which leads to improved reproductive performance. We have cloned and expressed turkey INH-a and INH-bA. Active immunization of turkey hens with rtINH-a increased pituitary FSH-b subunit mRNA and the number of non-graded preovulatory yellow follicles, but no significant increase in egg production was observed.
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Lurie, Susan, David R. Dilley, Joshua D. Klein, and Ian D. Wilson. Prestorage Heat Treatment to Inhibit Chilling Injury and Delay Ripening in Tomato Fruits. United States Department of Agriculture, June 1993. http://dx.doi.org/10.32747/1993.7568108.bard.

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The research had two specific goals; (1) to develop and optimize a postharvest heat treatment and characterize the response of tomato to the heat and subsequent cold storage, and (2) to investigate the involvement of heat shock proteins (HSP) in resistance to chilling injury. For the first goal we have investigated many time-temperature treatments using dry heat and found that 48 h at 38oC is optimum for Israeli cultivars, while 48 h at 42oC worked better for American cultivars in preventing chilling injury. We have also compared hot water to hot air and found hot water to be effective, but less so than hot air. Membrane lipid composition in relation to chilling injury was investigated after hot water and hot air treatments. Investigation of fruit ripening found that mRNAs of ripening-related genes were inhibited by high temperature, but recovered during the subsequent storage period and allowed normal ripening to proceed. Sensory studies showed no difference in the taste of heated or nonheated fruit. Following the production of HSP in heated and stored fruit allowed us to determine that during low temperature storage the HSP remained present in the fruit tissue, and their presence was correlated with resistance to chilling injury. HSP clones have been isolated by both differential screening of a cDNA library of heated and chilled tomatoes (Israel) and by mRNA differential display (United States). These clones are being characterized.
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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.

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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.
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Chen, Junping, Zach Adam, and Arie Admon. The Role of FtsH11 Protease in Chloroplast Biogenesis and Maintenance at Elevated Temperatures in Model and Crop Plants. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7699845.bard.

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specific objectives of this proposal were to: 1) determine the location, topology, and oligomerization of FtsH11 protease; 2) identify the substrate/s of FtsH11 and the downstream components involved in maintaining thermostability of chloroplasts; 3) identify new elements involved in FtsH11 protease regulatory network related to HT adaptation processes in chloroplast; 4) Study the role of FtsH11 homologs from crop species in HT tolerance. Background to the topic: HT-tolerant varieties that maintain high photosynthetic efficiency at HT, and cope better with daily and seasonal temperature fluctuations are in great need to alleviate the effect of global warming on food production. Photosynthesis is a very complex process requiring accurate coordination of many complex systems and constant adjustments to the changing environments. Proteolytic activities mediated by various proteases in chloroplast are essential part of this process and critical for maintaining normal chloroplast functions under HT. However, little is known about mechanisms that contribute to adaptation of photosynthetic processes to HT. Our study has shown that a chloroplast-targeted Arabidopsis FtsH11 protease plays an essential and specific role in maintaining thermostability of thylakoids and normal photosynthesis at moderate HT. We hypothesized that FtsH11 homologs recently identified in other plant species might have roles similarly to that of AtFtsH1. Thus, dissecting the underlying mechanisms of FtsH11 in the adaptation mechanisms in chloroplasts to HT stress and other elements involved will aid our effort to produce more agricultural products in less favorable environments. Major conclusions, solutions, achievements - Identified the chloroplast inner envelope membrane localization of FtsH11. - Revealed a specific association of FtsH11 with the a and b subunits of CPN60. - Identified the involvement of ARC6, a protein coordinates chloroplast division machineries in plants, in FtsH11 mediated HT adaptation process in chloroplast. -Reveal possible association of a polyribonucleotide nucleotidyltransferase (cpPNPase), coded by At3G03710, with FtsH11 mediated HT adaptation process in chloroplast. - Mapped 4 additional loci in FtsH11 mediated HT adaptation network in chloroplast. - Demonstrated importance of the proteolytic activity of FtsH11 for thermotolerance, in addition to the ATPase activity. - Demonstrated a conserved role of plant FtsH11 proteases in chloroplast biogenesis and in maintaining structural and functional thermostability of chloroplast at elevated temperatures. Implications, both scientific and agricultural:Three different components interacting with FtsH11 were identified during the course of this study. At present, it is not known whether these proteins are directly involved in FtsH11mediated thermotolerance network in chloroplast and/or how these elements are interrelated. Studies aiming to connect the dot among biological functions of these networks are underway in both labs. Nevertheless, in bacteria where it was first studied, FtsH functions in heat shock response by regulating transcription level of σ32, a heat chock factor regulates HSPsexpression. FtsH also involves in control of biosynthesis of membrane components and quality control of membrane proteins etc. In plants, both Arc 6 and CPN60 identified in this study are essential in chloroplast division and developments as mutation of either one impairs chloroplast division in Arabidopsis. The facts that we have found the specific association of both α and β CPN60 with FtsH11 protein biochemically, the suppression/ enhancement of ftsh11 thermosensitive phenotype by arc6 /pnp allele genetically, implicate inter-connection of these networks via FtsH11 mediated network(s) in regulating the dynamic adaptation processes of chloroplast to temperature increases at transcriptional, translational and post-translational levels. The conserved role of FtsH11 proteases in maintaining thermostability of chloroplast at HT demonstrated here provides a foundation for improving crop photosynthetic performance at high temperatures.
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