Relevant bibliographies by topics / Protein fibrillation

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

Academic literature on the topic 'Protein fibrillation'

Author: Grafiati
Published: 1 April 2023

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Journal articles on the topic "Protein fibrillation"

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Gorensek-Benitez, Annelise H., Bryan Kirk, and Jeffrey K. Myers. "Protein Fibrillation under Crowded Conditions." Biomolecules 12, no. 7 (July 6, 2022): 950. http://dx.doi.org/10.3390/biom12070950.

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Protein amyloid fibrils have widespread implications for human health. Over the last twenty years, fibrillation has been studied using a variety of crowding agents to mimic the packed interior of cells or to probe the mechanisms and pathways of the process. We tabulate and review these results by considering three classes of crowding agent: synthetic polymers, osmolytes and other small molecules, and globular proteins. While some patterns are observable for certain crowding agents, the results are highly variable and often depend on the specific pairing of crowder and fibrillating protein.
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St. Rammos, Kyriakos, George J. Koullias, Moustafa O. Hassan, Nikolaos P. Argyrakis, Christos G. Voucharas, Steven J. Scarupa, and Tomas G. Cowte. "Low Preoperative HSP70 Atrial Myocardial Levels Correlate Significantly with High Incidence of Postoperative Atrial Fibrillation after Cardiac Surgery." Cardiovascular Surgery 10, no. 3 (June 2002): 228–32. http://dx.doi.org/10.1177/096721090201000309.

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Purpose of the study. Atrial fibrillation after cardiac surgery is still a frequent encountered complication and has been associated with increased hospital length of stay and numerous postoperative complications. The pathogenesis of atrial fibrillation involves an overall sequence of perioperative events, collectively termed as ischemia-reperfusion injury. Heat-shock proteins have been found to provide increased protection during ischemia-reperfusion as well as increased postischemic cardiac functional recovery. We sought to determine whether preoperative atrial heat shock levels were correlated with the appearance of postoperative atrial fibrillation Basic methods. Preoperative atrial myocardial samples obtained just before cannulation from 101 patients were used to detect immunohistochemically the expression of heat-shock proteins. The derived results were compared statistically with the incidence of postoperative atrial fibrillation, its time of appearance, duration and resistance to administered antiarrhythmics. Principal findings. The overall incidence of postoperative atrial fibrillation was 22.3%. Of these patients, 58.3% had no detectable heat shock proteins in their cytoplasm, in sharp contrast with 100% of the patients with no atrial fibrillation who were positive for heat shock proteins ( p<0.01). Four percent of our patient group had prolonged atrial fibrillation (defined as duration >48 h). These patients had significantly less ( p<0.01) nuclear heat shock protein expression compared with the non-atrial fibrillation group. However, the difference of the heat shock protein expression between the prolonged atrial fibrillation and the rest of the atrial fibrillation patients was not significant ( p = 0.891). Conclusions. Our results indicate that patients with low preoperative atrial heat shock protein expression have a significantly greater incidence of postoperative atrial fibrillation. Heat shock protein expression did not, however, correlate with the onset of atrial fibrillation and the resistance to administered medications. Heat shock protein preoperative induction as a measure of myocardial preconditioning may potentially decrease the incidence of postoperative atrial fibrillation.
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Ohkubo, Kimie, Ichiro Watanabe, Yasuo Okumura, Keiko Takahashi, Kazuki Iso, Rikitake Kogawa, Kazumasa Sonoda, et al. "High-Sensitivity C-Reactive Protein: A Novel Predictor of Recurrence of Atrial Fibrillation After Initial Catheter Ablation of Paroxysmal Atrial Fibrillation." Journal of Nihon University Medical Association 75, no. 3 (2016): 118–22. http://dx.doi.org/10.4264/numa.75.3_118.

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Tachibana, Hideki, Shunta Kubomura, Kaoru Shinohara, and Ryohei Kono. "3P081 Seeded-Fibrillation of Lysozyme Disulfide-Variant Proteins(Protein: Property,The 48th Annual Meeting of the Biophysical Society of Japan)." Seibutsu Butsuri 50, supplement2 (2010): S159. http://dx.doi.org/10.2142/biophys.50.s159_1.

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Dev, Shubhda. "MOLECULAR DOCKING ANALYSIS OF NATRIURETIC PEPTIDE RECEPTOR-C TOWARDS THE DESIGN OF POTENTIAL ATRIAL FIBRILLATION INHIBITORS." Journal of Medical Pharmaceutical And Allied Sciences 9, no. 5 (October 15, 2020): 2595–600. http://dx.doi.org/10.22270/jmpas.v9i5.974.

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Atrial fibrillation (AF) stands the most widely recognized kind of clinical arrhythmia. Right now accessible anti-Atrial Fibrillation drugs are restricted by just moderate adequacy and an unfavorable safety profile. There is a perceived requirement for enhanced antiarrhythmic agents including activities that are specific for the fibrillating atrium. Therefore, it is of interest to design an appropriate medication for the disease Atrial Fibrillation using Molecular Docking techniques through protein-ligand interaction analysis. Hence, we document the Molecular docking analysis of natriuretic peptide receptor-C towards the design of potential Atrial Fibrillation inhibitors (Aprindine, Inclacumab, and Budiodarone) with the most favorable binding features for further consideration. This study centers around the process for drug discovery finding appropriate medication for the disease Atrial Fibrillation by Molecular Docking technique through protein-ligand interaction. The examination uncovered that out of a couple of molecules that were chosen as target, three of them were seen as most reasonable having the least energies compared to the other molecules. Aprindine, which is utilized in arrhythmia patients as a cardiac depressant. Inclacumab, which is an investigational sedate utilized in trials to look at the treatment and evasion of Myocardial Infarction, Peripheral Arterial Disease (PAD), and Coronary Heart Disease. Budiodarone, which is an antiarrhythmic drug at present in clinical preliminaries identified with amiodarone.
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Sata, Naoyuki, Naokazu Hamada, Takashi Horinouchi, Shigeru Amitani, Takuya Yamashita, Yukinori Moriyama, and Kenkichi Miyahara. "C-reactive Protein and Atrial Fibrillation." Japanese Heart Journal 45, no. 3 (2004): 441–45. http://dx.doi.org/10.1536/jhj.45.441.

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Huang, Kun, Jian Dong, Nelson B. Phillips, Paul R. Carey, and Michael A. Weiss. "Proinsulin Is Refractory to Protein Fibrillation." Journal of Biological Chemistry 280, no. 51 (October 20, 2005): 42345–55. http://dx.doi.org/10.1074/jbc.m507110200.

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Linse, S., C. Cabaleiro-Lago, W. F. Xue, I. Lynch, S. Lindman, E. Thulin, S. E. Radford, and K. A. Dawson. "Nucleation of protein fibrillation by nanoparticles." Proceedings of the National Academy of Sciences 104, no. 21 (May 7, 2007): 8691–96. http://dx.doi.org/10.1073/pnas.0701250104.

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Hernández Madrid, Antonio, and Concepción Moro. "Atrial Fibrillation and C-Reactive Protein." Journal of the American College of Cardiology 49, no. 15 (April 2007): 1649–50. http://dx.doi.org/10.1016/j.jacc.2007.02.009.

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Wood, Mark A., Kenneth A. Ellenbogen, and Bruce S. Stambler. "Atrial fibrillation from liquid protein diet." American Heart Journal 127, no. 6 (June 1994): 1667–68. http://dx.doi.org/10.1016/0002-8703(94)90422-7.

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Dissertations / Theses on the topic "Protein fibrillation"

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Vannoy, Charles Harvey. "Behavioral Effects of Functionalized CdSe/ZnS Quantum Dots in Self-Organization and Protein Fibrillation." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/431.

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Advances in recent nanoscience technologies have generated a new compilation of biocompatible, fluorescent nanoparticles derived from semiconductor quantum dots (QDs). QDs are extremely small in size and possess very large surface areas, which gives them unique physical properties and applications distinct from those of bulk systems. When exposed to biological fluid, these QDs may become coated with proteins and other biomolecules given their dynamic nature. These protein-QD systems may affect or enhance the changes in protein structure and stability, leading to the destruction of biological function. It is believed that these QDs can act as nucleation centers and subsequently promote protein fibril formation. Protein fibrillation is closely associated with many fatal human diseases, including neurodegenerative diseases and a variety of systemic amyloidoses. This topic of protein-QD interaction brings about many key issues and concerns, especially with respect to the potential risks to human health and the environment. Herein, the behavioral effects of dihydrolipoic acid (DHLA)-capped CdSe/ZnS (core/shell) QDs in hen egg-white lysozyme (HEWL) and human serum albumin (HSA) protein systems were systematically analyzed. This study gives rise to a better understanding of the potentially useful application of these protein-QD systems in nanobiotechnology and nanomedicine as a bioimaging tool and/or as a reference for controlled biological self-assembly processes.
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Höglund, Niklas. "Atrial fibrillation : treatment, associated conditions and quantification of symptoms." Doctoral thesis, Umeå universitet, Kardiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-138378.

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Background: Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia. There is a need for new pharmacological treatment strategies since the current antiarrhythmic drugs have a modest efficacy and may have severe side effects. Cardioversion (CV) of AF offers an opportunity to study related conditions in sinus rhythm (SR) and during AF. Since catheter ablation of AF is a symptomatic treatment, it is important to have tools for measurement of arrhythmia-related symptoms. Aims: To evaluate the effect of atorvastatin on maintaining SR after CV of persistent AF. To assess if highsensitivity C-reactive protein (hsCRP) predicts the recurrence of AF after CV in a population randomized to treatment with either atorvastatin or placebo. To quantify the symptomatic effect of left atrial catheter ablation of AF. To assess if the restoration of SR by CV, in a population with persistent AF, affects sleep apnea. Methods: Paper I: A total of 234 patients were randomized to treatment with either high dose atorvastatin or placebo prior to CV. Paper II: In a pre-specified substudy which included 128 of the patients in study I, hsCRP was analyzed before and after CV. Paper III: Umea 22 Arrhythmia Questions (U22) is a questionnaire that quantifies paroxysmal tachycardia symptoms. A total of 105 patients underwent first-time pulmonary vein isolation and answered U22 forms at baseline and follow-up 304 (SD 121) days after ablation. Paper IV: Polysomnography was performed before and after CV in 23 patients with persistent AF scheduled for elective CV. Results: Paper I: An intention-to-treat analysis with the available data, by randomization group, showed that 57 (51%) in the atorvastatin group and 47 (42%) in the placebo group were in SR 30 days after CV (OR 1.44, 95%CI 0.85–2.44, P=0.18). Paper II: HsCRP did not significantly predict recurrence of AF at 30 days. However, after adjusting for treatment with atorvastatin, hsCRP predicted the recurrence of AF (OR 1.14, 95% CI 1.01–1.27). Six months after CV, hsCRP at randomization predicted recurrence of AF in both univariate analysis (OR 1.30, 95% CI 1.06–1.60) and in multivariate logistic regression analysis (OR 1.33, 95% CI 1.06– 1.67). Paper III: The U22 scores for well-being, arrhythmia as cause for impaired well-being, derived timeaspect score for arrhythmia, and discomfort during attack detected relevant improvements of symptoms after the ablation. U22 showed larger improvement in patients undergoing only one procedure than in patients who later underwent repeated interventions. Paper IV: Obstructive sleep apnea occurred in 17/23 patients (74%), and central sleep apnea in 6/23 patients (26%). Five patients had both obstructive and central sleep apnea. SR at follow-up was achieved in 16 patients. The obstructive apnea-hypopnea index, central apneahypopnea index, and the number of patients with obstructive or central sleep apnea did not differ before and after restoration of SR. Conclusions: Atorvastatin is not a treatment option with regards to maintaining SR after CV in patients with persistent AF. HsCRP was associated with AF recurrence 1 and 6 months after successful CV of persistent AF. U22 quantifies the symptomatic improvement after AF ablation with adequate internal consistency and construct validity. Both obstructive and central sleep apneas are highly prevalent in patients with persistent AF. Obstructive sleep apneas are unaffected by the CV of AF to SR.
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Opel, A. "The role of regulators of G-protein signalling (RGS) in the predisposition to atrial fibrillation." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1394270/.

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The electrophysiological basis of atrial fibrillation (AF) is unknown. Regulators of G-protein signalling (RGS) act to deactivate G-protein signalling; they interact with the α subunit and accelerate intrinsic GTP-ase activity. RGS 4 negatively regulates inhibitory Gαi/o and Gαq/11 signalling. Absence of RGS 4 may increase G-protein gated inwardly rectifying potassium (GIRK) currents, shorten the atrial effective refractory period and promote atrial arrhythmia. The absence of RGS 4 results in continued Gαq/11 and thus calcium (Ca2+) signalling which may predispose to atrial arrhythmia. Does attenuation of RGS 4 promote AF? What is the mechanism? In vivo studies were performed in global RGS 4 knockout (-/-) and wild type (+/+) mice. Electrophysiological studies (EPS) were performed and ECG and EP parameters recorded. AF induction was attempted. Telemetry probes were inserted and conscious mouse ECGs were studied for AF and atrial ectopics (AE). Heart rate variability (HRV) was measured. Atrial cardiomyocytes were studied with patch-clamping and confocal microscopy. ECG and EP parameters were comparable. RGS 4 (-/-) developed AF. Conscious RGS 4 (-/-) were tachycardic, and had an enhanced bradycardic response to carbachol (CCh). ECG and HRV parameters of RGS 4 (+/+) and RGS 4 (-/-) without and with CCh were comparable. CCh-treated RGS 4 (-/-) had disrupted HRV, pauses and AE compared to RGS 4 (-/-) alone, but no AF. At patching, GIRK was not implicated but single cell restitution curves showed a steeper slope in RGS 4 (-/-). There was an increase in frequency of Ca2+ sparks in RGS 4 (-/-) compared to RGS 4 (+/+) in the absence and presence of endothelin-1 (ET-1). 2-aminoethoxydiphenyl borate (2-APB) abolished sparks. Sparks were reduced in amplitude in RGS 4 (-/-) in the absence of ET-1, but were longer in duration, time to peak and tau. A subset analysis showed that the left atrium had a greater frequency of Ca2+ sparks than the right atrium, and that these were comparatively longer in duration, time to peak and tau. RGS 4 (-/-) mice are predisposed to AF. There is good evidence that this is mediated via Gαq/11-IP3-Ca2+. RGS 4 is a potential therapeutic target in the treatment of AF. More recently RGS 6 has been found to be expressed in the heart and negatively regulates inhibitory Gαi/o signalling. EPS with AF induction were performed in RGS 6 (-/-) and RGS 6 (+/+) mice, with greater inducibility in RGS 6 (-/-) mice. It is possible that RGS 6 mediates its effects via Gαi-GIRK and could be a therapeutic target in the treatment of AF but further mechanistic studies are underway.
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Sievers, Stuart Aaron. "Structural characterization of amyloid-like protein segments ann the rational design of peptide inhibitors of fibrillation." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1581476191&sid=1&Fmt=2&clientId=48051&RQT=309&VName=PQD.

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Zhang, Yanhui, and 张雁惠. "Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47161644.

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My PhD project investigated the regulation of human cardiac transient outward potassium current (Ito) by protein tyrosine kinases (PTKs) and the functional expression of transient receptor potential (TRP) channels in human atrial myocytes to make an advanced understanding of human cardiac electrophysiology and pathophysiology. The modulation of human cardiac Itoby PTKs was studied in human atrial myocytes and HEK 293 cells expressing hKv4.3 (coding human cardiac Ito). We found that the broad-spectrum PTK inhibitor genistein, the selective EGFR kinase inhibitor AG556, and the Src-family kinases inhibitor PP2 inhibited human atrial Itoand the inhibitory effect was countered by the protein tyrosine phosphatase (PTP) inhibitor orthovanadate. Similar results were observed in hKv4.3-HEK cells. Interestingly, tyrosine phosphorylation of hKv4.3channels was reduced by genistein, AG556, and PP2,and the reduction was antagonized by orthovanadate. The mutant Y136F of hKv4.3 lost the inhibitory response to AG556, whileY108F lost the response to PP2.The double mutant Y108F-Y136F hKv4.3 failed to respond to both AG556 and PP2, and exhibited a dramatic reduction of tyrosine phosphorylation. These results indicate that native cardiac Itois regulated by both EGFR and Src family kinases. In the second part, we studied whether TRPC channels would mediate the nonselective cation current described previously in human atrial myocytes. It was found that TRPC1 channel activator thapsigargin activated the current, and the effect was suppressed by La3+or prevented by intracellular anti-TRPC1 antibody. Endothelin-1 and angiotensin II stimulated the current, andthe effect was inhibited by La3+and/or 2-APB. RT-PCR and Western blot analysis revealed that in addition to the TRPC1 channels mediating the nonselective cation current, the components of store-operated Ca2+channels (SOCs), STIM1 and Orai1 were abundantly expressed in human atria. The interaction of TRPC1, STIM1, and Orai1 was confirmed by co-immunoprecipitation. Interestingly, we found that protein expression of TRPC1 and STIM1, but not Orai1, was up-regulated in human atria with atrial fibrillation. The third part of the project determined whether TRPM7 channels were expressed in human atrial myocytes, since this channel was reported in human atrial fibroblasts, conferring atrial fibrosis in human atria with atrial fibrillation. We found a TRPM7 -like current which was potentiated by acidic pH, and inhibited by La3+and 2-APB, and a Ca2+-activated TRPM4 current. RT-PCR and Western blot analysis confirmed the expression of TRPM7 and TRPM4 channels in human atria. Moreover, we found TRPM7 protein, but not TRPM4 protein was significantly up-regulated in human atria with atrial fibrillation, suggesting the potential participation of TRPM7 channels in atrial remodeling of human atria with atrial fibrillation. Collectively, this PhD thesis project has demonstrated for the first time that human cardiac Itois modulated by EGFR kinase and Src kinases via phosphorylating Y136and Y108, respectively. TRPC1 channels mediate the nonselective cation current and SOCs.TRPM7 channels are expressed in human atrial myocytes. The up-regulation of TRPC1, STIM1, and TRPM7 channels in human atria with atrial fibrillation suggest that they are likely involved in atrial electrical and/or structure remodeling in patients with atrial fibrillation.
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Schirmer, Claire. "Chaperons moléculaires et tauopathies : effets de Hsp90 sur la fibrillation in vitro du peptide VQIVYK issu de la protéine tau." Thesis, Rennes 1, 2014. http://www.theses.fr/2014REN1S162/document.

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Les maladies dites ''conformationnelles'' sont caractérisées par un mauvais repliement des protéines qui, de ce fait, ne peuvent plus assurer leur fonction biologique. C'est le cas des amyloses, ces pathologies impliquent des protéines ayant la capacité de s'agréger pour former des structures spécifiques appelées « fibres amyloïdes ». Aujourd'hui, une trentaine de protéines humaines sont connues pour former ce type de fibres et notamment la protéine tau. Celle-ci est associée à plusieurs maladies neurodégénératives, regroupées sous le terme de « tauopathies », incluant la maladie d'Alzheimer. En conditions physiologiques, tau est associée aux microtubules et régule leur polymérisation. Dans les tauopathies, elle devient hyperphosphorylée et s'agrège dans les neurones sous forme de neurodégénérescences fibrillaires (NFTs) toxiques. Les protéines chaperons et particulièrement la protéine de choc thermique de 90 kDa, Hsp90, régule l'homéostasie de la protéine tau. L'interaction entre tau et Hsp90 implique différentes régions de la protéine tau dont celle contenant un hexapeptide de séquence VQIVYK. Ce court fragment est nécessaire et suffisant pour induire la fibrillation de la protéine tau entière in vivo. Cet hexapeptide est également capable, à lui seul, de former des fibres amyloïdes, in vitro, comparables à celles retrouvées in vivo. Nous avons donc choisi d'utiliser l'hexapeptide VQIVYK comme modèle d'étude de la fibrillation, in vitro, et testé l'effet de Hsp90 sur les processus agrégatifs du peptide. Nous avons démontré que Hsp90 interagit spécifiquement avec les structures amyloïdes formées par le peptide et qu'elle est capable d'inhiber à la fois la polymérisation et la dépolymérisation des fibres. Ce rôle antagoniste joué par Hsp90 permet la stabilisation d'espèces amyloïdes intermédiaires supposées moins neurotoxiques. Ces résultats confirment l'implication de Hsp90 dans les processus agrégatifs de la protéine tau et ouvrent de nouvelles perspectives thérapeutiques contre les pathologies neurodégénératives. De plus, cette étude apporte des éléments de réponse sur le fonctionnement des chaperons moléculaires vis-à-vis de leur protéine cliente
Conformational diseases are characterized by protein misfolding which causes a loss of biological activity. Amyloidosis is one of these diseases, and it involves the ability of proteins to self-aggregate into specific structures called “amyloid fibers”. At least thirty human proteins, including tau, are known to form amyloid fibers. The tau protein is linked to several neurodegenerative diseases called tauopathies, including Alzheimer’s disease. Tau is in physiological conditions associated with microtubules and regulates their polymerization. In tauopathies, tau becomes hyper-phosphorylated and aggregates into neurotoxic neurofibrillary tangles (NFTs). Molecular chaperones, and particularly the 90-kDa heat shock protein (Hsp90), regulate tau homeostasis. The interaction between tau and Hsp90 involves several tau regions including the sequence VQIVYK. This short fragment is necessary and sufficient on its own to induce aggregation of the full tau protein in vivo. In vitro this hexapeptide is also able to form amyloid fibers similar to those found in vivo. We therefore used this hexapeptide as an in vitro model to study the process of amyloid fibrillation and to test Hsp90’s effects on it. We demonstrated that Hsp90 interacts specifically with peptide fibrillar structures and that Hsp90 is able to inhibit both the polymerization and depolymerization processes. This antagonistic role for Hsp90 allows the stabilization of intermediate amyloid species that may display a lower neurotoxicity. These results confirm that Hsp90 is involved in tau’s aggregation process and paves the way for new therapeutic perspectives in neurodegenerative diseases. Our study also provides clues to the understanding of how molecular chaperones assist in the folding of their client proteins
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Lahtinen, J. (Jarmo). "Predictors of immediate outcome after coronary artery bypass surgery." Doctoral thesis, University of Oulu, 2007. http://urn.fi/urn:isbn:9789514286339.

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Abstract The identification of risk factors for major adverse events after coronary artery bypass surgery is of main importance as it allows outcome prediction, facilitates preoperative patient selection and improves the quality of care. In the present clinical studies we have evaluated the impact of preoperative angiographic severity of a coronary artery disease and preoperative C-reactive protein (CRP) on the immediate outcome after coronary artery bypass surgery. We have reviewed the results of off-pump (OPCAB) versus conventional on-pump coronary artery bypass surgery (CCAB) in high risk patients. We have evaluated the impact of postoperative pulmonary artery blood temperature on the immediate outcome as well. In addition, we have investigated the incidence, timing and outcome of an atrial fibrillation (AF) related stroke after surgery. The multivariate analysis showed that among 2233 patients, the overall coronary angiographic score was predictive of postoperative death (p = 0.03; OR 1.027, 95% CI: 1.003–1.052) and of a low cardiac output syndrome (p = 0.04; OR 1.172, 95% CI: 1.010–1.218). The poor status of the proximal segment of the left circumflex coronary artery, the diagonal branches and the left obtuse marginal artery were most closely associated with adverse postoperative outcome. Patients (114/764) with a preoperative serum concentration of CRP ≥ 1.0 mg/dL had a higher risk of overall postoperative death (5.3% vs. 1.1%, p = 0.001), cardiac death (4.4% vs. 0.8%, p = 0.002), a low cardiac output syndrome (8.8% vs. 3.7%, p = 0.01). Among 179 high risk patients with an additive EuroSCORE6, the 30-day postoperative death and stroke rates were 7.5% and 6.0% in the OPCAB group, and 5.4% (p = 0.75) and 8.0% (p = 0.77) in the CCAB group, respectively. No significant differences were observed in other major outcome end-points between these non-randomised groups either. High pulmonary artery blood temperature on admission to the ICU among 1639 patients was significantly associated with an increased risk of overall postoperative death (p = 0.002), cardiac death (p = 0.03), and a low cardiac output syndrome (p < 0.0001), and was significantly correlated with prolonged length of the ICU stay (r = 0.095; p < 0.0001), and postoperative bleeding (ρ = –0.091; p = 0.001). Among 2,630 patients who underwent coronary artery bypass grafting (CABG), 52 (2.0%) experienced a postoperative stroke. Twelve out of these 52 patients (23.1%) died postoperatively. The ischemic cerebral event occurred after a mean of 3.7 days (0–33). In 19 patients (36.5%), atrial fibrillation preceded the occurrence of neurological complication. The angiographic severity of the coronary artery disease and the preoperative serum concentration of CRP predict postoperative outcome after a CABG operation. OPCAB can be performed safely in high-risk patients with results as satisfactory as those achieved with CCAB. CABG patients with a high pulmonary artery blood temperature on admission to the ICU seem to have a higher risk of postoperative adverse events. Atrial fibrillation occurring after coronary artery bypass grafting is a major determinant of a postoperative stroke.
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LIMA, Sandro Vagner de. "Investigação de sistemas e processos biológicos pela técnica de espectroscopia de impedância elétrica." Universidade Federal de Pernambuco, 2015. https://repositorio.ufpe.br/handle/123456789/17146.

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Submitted by Fabio Sobreira Campos da Costa (fabio.sobreira@ufpe.br) on 2016-06-27T12:24:48Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Tese _Sandro Vagner de Lima.pdf: 6041788 bytes, checksum: 30432ac952cb4559dfe9e27b22cd9bf5 (MD5)
Made available in DSpace on 2016-06-27T12:24:49Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Tese _Sandro Vagner de Lima.pdf: 6041788 bytes, checksum: 30432ac952cb4559dfe9e27b22cd9bf5 (MD5) Previous issue date: 2015-10-08
Esta tese de doutorado foi dedicada à investigação do modo como a técnica de espectroscopia de impedância elétrica (EIE) poderia ser usada para acompanhar os processos de mudanças conformacionais de macromoléculas biológicas, como proteínas e DNA. Para isso, usamos como sistemas modelos a proteína albumina do soro bovino (BSA), e a formação do complexo polianilina/DNA (PANI/DNA). Com a caracterização de soluções de DNA e BSA por EIE e sua modelagem elétrica convenientemente descrita pelo circuito de Randles (e sua variante), foram determinados os parâmetros relevantes para descrição dos fenômenos de desnaturação e de agregação da proteína e da precipitação do complexo PANI/DNA. As informações obtidas sobre a solubilidade desses últimos complexos são de grande utilidade para o entendimento dos mecanismos de interação entre cadeias de DNA e de polímeros condutores. Do mesmo ponto de vista da EIE, as sucessivas mudanças da conformação da proteína e os detalhes da cinética de sua agregação na interação com surfactantes foram adequadamente correlacionados com a característica elétrica do circuito de Randles das soluções correspondentes. Finalmente, estudos iniciais foram estendidos para a análise dos processos de fibrilação de proteínas. Para todos os problemas abordados, o uso da resistência de transferência de carga elétrica (RCT) (um parâmetro do circuito de Randles) nos permite sugerir ser a técnica de EIE apropriada para caracterizar as diferentes mudanças conformacionais envolvidas em fenômenos que resultam da interação de biomoléculas com moléculas de prova. Assim, ela se confirma como um método competitivo quando comparado ao uso da fluorescência e da absorção UV-Vis (técnicas rotineiramente adotadas para a análise desses problemas).
This doctoral thesis was devoted to the investigation of the technique of electrical impedance spectroscopy as an alternative method to assess conformational changes of biological macromolecules, such as proteins and DNA. For this, we used protein bovine serum albumin (BSA), and the formation of polyaniline (PANI)/DNA complexes as model systems. With the characterization of DNA and BSA solutions by Electrical Impedance Spectroscopy (EIS) and their electrical modeling conveniently described by the Randles circuit (and its variant), we determined the relevant characteristics of phenomena such as the denaturation and aggregation of proteins (BSA), and polymer/DNA complex formation (PANI/DNA). As a result of this approach we identified the existence of different interaction regimes between the chains of polyaniline and DNA molecules that are dependent on the concentration of PANI/DNA and the existence of equilibrium conditions which separate regions of precipitation/stability the PANI/DNA complex. Also from this point of view, the modes of interaction BSA / surfactants involved in the conformation changes well as typical stages associated with fibrillation kinetics were adequately correlated with the electric characteristic of the Randles circuit. In all studies carry out in this thesis, the analysis of the electric charge transfer resistance behavior (RCT) (a parameter of the Randles circuit) when confronted with the results obtained by standard techniques showed that the EIS presents reliable and some comparative advantages. These results allow us to provide an adequate and competitive alternative to conventional methods such as UV-Visible absorption, fluorescence and the use of probe molecules
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Lindberg, Max. "Fluorescent fusion proteins as probes to characterize tau fibril polymorphism." Thesis, Linköpings universitet, Kemi, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-158263.

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Alzheimer's disease (AD) is a large and growing problem and while we today lack a full understanding of this disease, we know that the protein tau and the amyloid fibrils it forms play a central role in its development. We also know that these fibrils can have different morphologies in different diseases and that fibrils produced in vitro not necessarily adopt any of the morphologies found in patients. This means there is a need for more pathologically relevant fibrils in vitro to be able to understand this disease better. One approach to satisfy this need is to use fibrils found in patients as seeds and thus transfer their morphology to recombinantly purified protein. To facilitate this process this study has attempted to develop a way to differentiate between different fibril morphologies using a FRET based system. This involves fluorescent fusion proteins (tau-EXFPs) and fluorescent amyloid probes as well as seeding experiments with pseudo wild type tau (PWT) and tau with the P301L mutation. Greater differences in terms of fibrillation rates and ThT fluorescence between PWT and P301L was shown than previously reported between WT and P301L. They were also shown to differ in fibril morphology in TEM. The ThT fluorescence intensity was to a certain degree transferable from PWT to P301L by seeding. Furthermore, this study confirms that the tau-EXFP fusion protein can be incorporated into amyloid fibrils and strongly suggests that a FRET effect between EXFP and BTD14 (as well as X34 and ThT) can be achieved. It also demonstrates differences in FRET efficiency between PWT and P301L fibrils using FLIM. These results indicate that a FRET based approach could be a useful method to discern different fibril morphologies from each other, but further measurements and optimization are needed before this method could be reliably applied. The fusion proteins could also be used to investigate tau spreading in vivo, e.g. in D. melanogaster. To find suitable FRET partners to the fusion proteins, a ligand screen was conducted. This could be used as an alternative to the FRET method. With the right selection of fluorescent amyloid probes, a unique fingerprint for each fibril morphology could maybe be generated and fulfill the same intended function as the FRET method.
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Andersson, Jonas. "Inflammation and lifestyle in cardiovascular medicine." Doctoral thesis, Umeå universitet, Medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36221.

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Despite major advances in the treatment and prevention of atherosclerosis the last several decades, cardiovascular disease still accounts for the majority of deaths in Sweden. With the population getting older, more obese and with rising numbers of diabetics, the cardiovascular disease burden may increase further in the future. The focus in cardiovascular disease has shifted with time from calcification and narrowing of arteries to the biological processes within the atherosclerotic plaque. C-reactive protein (CRP) has emerged as one of many proteins that reflect a low grade systemic inflammation and is suitable for analysis as it is more stable and easily measured than most other inflammatory markers. Several large prospective studies have shown that CRP is not only an inflammatory marker, but even a predictive marker for cardiovascular disease. C-reactive protein is associated with several other risk factors for cardiovascular disease including obesity and the metabolic syndrome. Our study of twenty healthy men during a two week endurance cross country skiing tour demonstrated a decline in already low baseline CRP levels immediately after the tour and six weeks later. In a study of 200 obese individuals with impaired glucose tolerance randomised to a counselling session at their health care centre or a one month stay at a wellness centre, we found decreased levels of CRP in subjects admitted to the wellness centre. The effect remained at one, but not after three years of follow-up. In a prospective, nested, case-referent study with 308 ischemic strokes, 61 intracerebral haemorrhages and 735 matched referents, CRP was associated with ischemic stroke in both uni- and multivariate analyses. No association was found with intracerebral haemorrhages. When classifying ischemic stroke according to TOAST criteria, CRP was associated with small vessel disease. The CRP 1444 (CC/CT vs. TT) polymorphism was associated with plasma levels of CRP, but neither with ischemic stroke nor with intracerebral haemorrhage. A study on 129 patients with atrial fibrillation was used to evaluate whether inflammation sensitive fibrinolytic variables adjusted for CRP could predict recurrence of atrial fibrillation after electrical cardioversion. In multivariate iv models, lower PAI-1 mass was associated with sinus rhythm even after adjusting for CRP and markers of the metabolic syndrome. In conclusion, lifestyle intervention can be used to reduce CRP levels, but it remains a challenge to maintain this effect. CRP is a marker of ischemic stroke, but there are no significant associations between the CRP1444 polymorphism and any stroke subtype, suggesting that the CRP relationship with ischemic stroke is not causal. The fibrinolytic variable, PAI-1, is associated with the risk of recurrence of atrial fibrillation after electrical cardioversion after adjustment for CRP. Our findings suggest a pathophysiological link between atrial fibrillation and PAI-1, but the relation to inflammation remains unclear.
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Books on the topic "Protein fibrillation"

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Cardim, Nuno, Denis Pellerin, and Filipa Xavier Valente. Hypertrophic cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0042.

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Hypertrophic cardiomyopathy is a common inherited heart disease caused by genetic mutations in cardiac sarcomeric proteins. Although most patients are asymptomatic and many remain undiagnosed, the clinical presentation and natural history include sudden cardiac death, heart failure, and atrial fibrillation. Echocardiography plays an essential role in the diagnosis, serial monitoring, prognostic stratification, and family screening. Advances in Doppler myocardial imaging and deformation analysis have improved preclinical diagnosis as well as the differential diagnosis of left ventricular hypertrophy. Finally, echocardiography is closely involved in patient selection and in intraoperative guidance and monitoring of septal reduction procedures. This chapter describes the pathophysiology, clinical presentation, role of echocardiography, morphological features, differential diagnosis, diagnostic criteria in first-degree relatives, echo guidance for the treatment of symptomatic left ventricular outflow tract obstruction, and follow-up and monitoring of patients with hypertrophic cardiomyopathy.
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Book chapters on the topic "Protein fibrillation"

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Marasini, Carlotta, and Bente Vestergaard. "SAS-Based Studies of Protein Fibrillation." In Biological Small Angle Scattering: Techniques, Strategies and Tips, 149–65. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6038-0_9.

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Bhat, Mohd Younus, Laishram Rajendrakumar Singh, and Tanveer A. Dar. "Modulation of Protein Aggregation/Fibrillation by Osmolytes." In Cellular Osmolytes, 121–42. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3707-8_6.

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Ravens, U., E. Wettwer, T. Christ, and D. Dobrev. "G-Protein β3-Subunit Polymorphism and Atrial Fibrillation." In Cardiovascular Genomics: New Pathophysiological Concepts, 213–22. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1005-5_18.

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Sandberg, Alexander, and Sofie Nyström. "Purification and Fibrillation of Recombinant Human Amyloid-β, Prion Protein, and Tau Under Native Conditions." In Methods in Molecular Biology, 147–66. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7816-8_10.

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So, Masatomo, Yuichi Yoshimura, and Yuji Goto. "Ultrasonication-Forced Amyloid Fibrillation of Proteins." In Advances in Organic Crystal Chemistry, 15–29. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55555-1_2.

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Zussa, C., and E. Polesel. "Atrial Fibrillation After Heart Surgery: How to Identify and Protect Predisposed Patients?" In Cardiac Arrhythmias 1999 - Vol.1, 156–64. Milano: Springer Milan, 2000. http://dx.doi.org/10.1007/978-88-470-2139-6_21.

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Hong, Liu, Chiu Fan Lee, and Ya Jing Huang. "Statistical Mechanics and Kinetics of Amyloid Fibrillation." In Biophysics and Biochemistry of Protein Aggregation, 113–86. World Scientific, 2017. http://dx.doi.org/10.1142/9789813202382_0004.

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F. Rosario-Alomar, Manuel, Tatiana Quiñones-Ruiz, Dmitry Kurouski, Valentin Sereda, Eduardo DeBarros-Ferreira, Lorraine De Jesús-Kim, Samuel Hernández-Rivera, et al. "Inhibition of Protein Fibrillation by Hydrogen Sulfide1." In Amyloid Diseases. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.86221.

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Herrera, Maria Georgina, Marco Giampà, Nicolo Tonali, and Veronica Isabel Dodero. "Multimodal methods to study protein aggregation and fibrillation." In Advances in Protein Molecular and Structural Biology Methods, 77–102. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-90264-9.00006-4.

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Shivani, Kummari, Amrita Arpita Padhy, Subhashree Sahoo, Varsha Kumari, and Parul Mishra. "Spectroscopic methods to detect and analyze protein oligomerization, aggregation, and fibrillation." In Advanced Spectroscopic Methods to Study Biomolecular Structure and Dynamics, 415–58. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-323-99127-8.00016-7.

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Conference papers on the topic "Protein fibrillation"

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Abakumets, V. Y., and K. Ya Bulanava. "THE INFLUENCE OF INSULIN FIBRILLATION." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-7-10.

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Violation of protein folding leads to the development of a number of systemic and neurodegenerative diseases-proteinopathy. In these pathologies, proteins acquire an incorrect conformation that differs from the native one, become functionally inactive, toxic, and prone to aggregation and deposition in various organs and tissues. There is a widespread hypothesis that the primary cytotoxic agents in the development of proteinopathies are protein oligomers that are prone to aggregation. These diseases include Parkinson’s disease, Creutzfeldt-Jakob disease, type 2 diabetes, and many others.
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Tonry, C., A. Russell-Hallinan, P. Collier, K. McDonald, M. Ledwidge, B. Collins, and CJ Watson. "48 Identification of novel protein biomarkers for atrial fibrillation." In Irish Cardiac Society Annual Scientific Meeting & AGM (Virtual), October 7th – 9th 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-ics.48.

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Tonry, C., A. Russell-Hallinan, N. Glezeva, P. Collier, K. McDonald, M. Ledwidge, BC Collins, and C. Watson. "19 Identification and evaluation of novel protein biomarkers for atrial fibrillation." In Irish Cardiac Society Annual Scientific Meeting & AGM, October 6th – 8th 2022, Radisson Hotel, Little Island, Cork Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-ics.19.

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Torkko, J., P. Toledo, A. Müller, C. Wegbrod, A. Sönmez, M. Solimena, and M. Ermácora. "ICA512 RESP18 homology domain is protein condensing factor and insulin fibrillation inhibitor." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688114.

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Pyne, Partha, Nirnay Samanta, Himanshu Gohil, S. S. Prabhu, and Rajib Kumar Mitra. "Water: a major requisite for the protein fibrillation as revealed by THz spectroscopy measurements." In 2021 46th International Conference on Infrared, Millimeter and Terahertz Waves (IRMMW-THz). IEEE, 2021. http://dx.doi.org/10.1109/irmmw-thz50926.2021.9567303.

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Deryusheva, E. I., A. V. Machulin, O. M. Selivanova, S. Yu Grishin, A. V. Glyakina, A. K. Surin, and O. V. Galzitskaya. "Investigation of Fibrillation by Amyloidogenic Regions of the Ribosomal S1 Proteins." In Mathematical Biology and Bioinformatics. Pushchino: IMPB RAS - Branch of KIAM RAS, 2020. http://dx.doi.org/10.17537/icmbb20.19.

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