Relevant bibliographies by topics / Physiopathology

Contents

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

Academic literature on the topic 'Physiopathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 March 2025

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Journal articles on the topic "Physiopathology"

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Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 116 (June 15, 2018): 653–55. http://dx.doi.org/10.4000/annuaire-cdf.13463.

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Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 117 (September 1, 2019): 639–40. http://dx.doi.org/10.4000/annuaire-cdf.14766.

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Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 118 (December 30, 2020): 661–63. http://dx.doi.org/10.4000/annuaire-cdf.16154.

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Rouach, Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France 121 (2024): 695–97. http://dx.doi.org/10.4000/12kvr.

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Rouach, Responsable :. Nathalie. "Interactions neurogliales en physiopathologie cérébrale / Neuroglial interactions in cerebral physiopathology." L’annuaire du Collège de France, no. 120 (February 13, 2023): 544–45. http://dx.doi.org/10.4000/annuaire-cdf.18789.

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Jullien, D. "Psoriasis physiopathology." Journal of the European Academy of Dermatology and Venereology 20, s2 (November 2006): 10–23. http://dx.doi.org/10.1111/j.1468-3083.2006.01768.x.

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Bonanno, FabrizioGiuseppe. "Physiopathology of shock." Journal of Emergencies, Trauma, and Shock 4, no. 2 (2011): 222. http://dx.doi.org/10.4103/0974-2700.82210.

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García Rodríguez, Diego Felipe, and Carlos Abud Mendoza. "Physiopathology of fibromyalgia." Reumatología Clínica (English Edition) 16, no. 3 (May 2020): 191–94. http://dx.doi.org/10.1016/j.reumae.2020.02.004.

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Venance, Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France, no. 116 (June 15, 2018): 657–59. http://dx.doi.org/10.4000/annuaire-cdf.13492.

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Venance, Laurent. "Dynamique et physiopathologie des réseaux neuronaux / Dynamics and physiopathology of neuronal networks." L’annuaire du Collège de France, no. 117 (September 1, 2019): 645. http://dx.doi.org/10.4000/annuaire-cdf.14783.

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Dissertations / Theses on the topic "Physiopathology"

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Zumerle, Sara. "Tissue-specific role of hepcidin in iron homeostasis and innate immunity." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T002.

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Le fer est un élément vital pour l’organisme, mais peut s’avérer toxique si présent en excès. L’hepcidine est le régulateur principal de l’homéostasie du fer dans l’organisme. Un défaut d’expression d’hepcidine est à l’origine de l’hémochromatose, une maladie génétique humaine caractérisée par une surcharge en fer ; inversement, une hypersécrétion d’hepcidine est la cause de différents types d’anémie. L’hepcidine est secrétée principalement par le foie, mais des découvertes récentes ont montré que de nombreux tissus de l’organisme sont capables de produire l’hormone. Au laboratoire nous avons généré un modèle de souris transgénique permettant d’invalider le gène codant pour l’hepcidine dans les tissus d’intérêt. Ce modèle permet d’étudier la contribution de différents tissus dans l’homéostasie du fer. En comparant les souris déficientes pour l’hepcidine spécifiquement dans le foie (HepcΔfoie) avec les souris présentant une délétion de l’hepcidine dans tout l’organisme (HepcΔtot), j’ai pu montrer que les souris HepcΔfoie présentent la même surcharge en fer que les souris HepcΔtot ; dans la circulation sanguine des souris HepcΔfoie, l’hepcidine n’est pas détectable, montrant ainsi que l l’hépatocyte est la source majeure d’hepcidine pour réguler les niveaux de fer dans l’organisme. En conclusion, mes résultats ont permis de montrer que l’hepcidine hépatique est le régulateur principal de l’homéostasie du fer, et que les autres tissus ne sont pas capables de compenser
Iron is fundamental for the organism, but can be toxic if in excess. The major regulator of iron homeostasis is hepcidin, first identified as an antimicrobial peptide. Hepcidin deficiency is associated with hereditary hemochromatosis, a human genetic disease characterized by iron overload. Conversely, abnormal hepcidin induction is the cause of some types of anemia. Hepcidin is produced and secreted mainly by the liver, but many cells and tissues express low levels of the hormone. To investigate the contribution of hepcidin-producing tissues in iron homeostasis, we generated a new mouse model in which the hepcidin gene can be conditionally inactivated: the hepcidin floxed mice. The main aim of my thesis was to evaluate the contribution of different tissues in hepcidin production and iron homeostasis regulation. I generated hepcidin liver-specific knockout mice and compared them to total knockouts: hepatic hepcidin ablation fully recapitulates the severe iron overload phenotype observed in the total knockout. Moreover, hepcidin was undetectable in the plasma of liver-specific knockouts, showing that hepatocytes are the main source of the peptide in the bloodstream. These results demonstrate that hepatic hepcidin is the major regulator of iron homeostasis and that tissues other than the liver are not able to compensate. The hepcidin floxed mice provide a useful tool for the investigation of hepcidin role in extra-hepatic tissues in physiological and pathological conditions
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Gu, Xiaomei Everett Eric T. "Physiopathology of osteoclast in bone." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1870.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Curriculum of Oral Biology." Discipline: Oral Biology; Department/School: Dentistry.
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GAMBASSI, SILVIA. "Novel insights into alkaptonuria physiopathology." Doctoral thesis, Università di Siena, 2016. http://hdl.handle.net/11365/1004463.

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Alkaptonuria (AKU) is an ultra-rare genetic disease resulting from a deficient activity of the enzyme homogentisate 1,2- dioxygenase (HGD), responsible for the catabolism of the aromatic amino acids Phenylalanine and Tyrosine. This condition leads to the accumulation of a toxic metabolite, HGA and of its product of oxidation BQA, whose polymerization generates melanin-like aggregates, with amyloidogenic properties, leading to the phenomenon of “Ochronosis”. The most affected structures by the deposition of these ochronotic aggregates are joints, which undergo severe arthropathy; therefore, articular cartilage is the main investigated tissue for the comprehension of AKU physiopathology. Articular cartilage homeostasis is maintained by articular chondrocytes, which have an important role in the synthesis and release of extracellular matrix (ECM) components, essential to properly respond to mechanical compression processes the tissue is constantly subjected to. This mechanism is mediated by chondrocyte cytoskeleton, including the microtubule-based organelle primary cilium, which exerts its function through the activation of the Hedgehog (Hh) signaling pathway. On the basis of the previous considerations, for the aims of this thesis, the set-up of in vitro AKU cellular and tissue models, was fundamental to counteract problems related to the collection of AKU samples, due to the rarity of the disease. Both experimental models were properly characterized, by highlighting the role of HGA in mediating pigment deposition and cartilage degradation processes, through histological and cytological analyses and immunofluorescence assays. Results showed that the ochronotic pigment deposits following HGA treatment lead to an oxidative stress status and to the accumulation of serum amyloid A (SAA) protein in the cartilaginous tissue. Another in vitro model was used to analyse the ability of AKU chondrocytes to respond to mechanical loading in terms of production of ECM components, by applying a 10% strain on adherent cell cultures. AKU chondrocytes resulted unable to respond properly to mechanical strain and HGA seemed to be involved in this altered responsiveness. Afterwards, a deep investigation of the cytoskeleton characteristics of AKU chondrocytes was performed, mainly by focusing on the interaction of each cytoskeletal marker with the amyloidogenic protein serum amyloid A (SAA). An in situ proximity ligation assay confirmed the co-localization of cytoskeletal marker with SAA, thus explaining the severe alterations observed in AKU cytoskeleton. Furthermore, another cytoskeletal component was characterized, the primary cilium, both investigating on its structural features and on its function in terms of Hedgehog (Hh) signaling activation. Primary cilia of AKU chondrocytes resulted shorter than normal chondrocytes and HGA treatment led to the same ciliary phenotype. In order to investigate the activation of the Hh pathway, the expression of the constitutive activator of the pathway (Gli-1) was evaluated both at the gene and at the protein level. This protein was found overexpressed in AKU/HGA-treated chondrocytes. Finally, given the role of Hh activation in mediating processes of cartilage degradation in osteoarthritis-like diseases, a therapeutic approach based on the inhibition of the Hh signaling was adopted, by using treatment with lithium chloride and with small molecule antagonists of the Hh receptor Smoothened (Smo). All the testing compounds resulted efficient in inhibiting Hh signal and in restoring cilia lengths, suggesting the use of these compounds as a potential therapeutic approach for the treatment of AKU.
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De, Marco Margot. "BAG3 role in cardiomyocytes physiopathology." Doctoral thesis, Universita degli studi di Salerno, 2013. http://hdl.handle.net/10556/896.

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2010 - 2011
The anti-apoptotic protein BAG3 is expressed at high levels in skeletal and cardiac muscle in vivo. Our group recently focused its interest on BAG3 role in myocardiocyte proliferation, survival and response to stressful stimuli. We found that BAG3 is upregulated during the differentiation of cardiomyoblasts. Our results prompted us to verify whether bag3 silencing could affect the differentiation state of cardiocytes and we found that bag3 silencing resulted in highly reducing the levels of myogenin. Furthermore, we analyzed BAG3 expression and localization following cell exposure to oxidative stress. In particular, we found that epinephrine in vitro increases BAG3 expression in adult human cardiomyocytes. We evaluated whether BAG3 could be involved in the Tako-tsubo cardiomyopathy (or stress cardiomyopathy) pathogenesis that is characterized by left ventricular dysfunction, with symptoms that can mimic an acute coronary syndrome. The absence of significant cardiovascular risk factors in patients affected by stress cardiomyopathy suggested that it might be associated with a possible genetic etiology. Therefore, we sequenced bag3 gene to check for polymorphisms in 29 patients and 1043 healthy donors. Three polymorphism were highly represented among patients (R71Q, C151R, P407L). We also showed for the first time that BAG3 protein is released from stressed cardiomyocytes and is found in chronic heart failure (HF) patients’ sera. Since anti-BAG3 antibodies are also present in patients’ sera, we developed an ELISA test for their specific detection. In serum samples from chronic HF patients, we found significantly higher values of anti-BAG3 antibodies respect to samples from healthy donors. The presence of anti-BAG3 antibodies in chronic HF patients’ sera and the availability of an ELISA test for their detection can contribute a novel tool for diagnostic and prognostic evaluations. [edited by author]
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Pénicaud, Sidonie. "Insights about age of language exposure and brain development : a voxel-based morphometry approach." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111591.

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Early language experience is thought to be essential to develop a high level of linguistic proficiency in adulthood. Impoverished language input during childhood has been found to lead to functional changes in the brain. In this study, we explored if delayed exposure to a first language modulates the neuroanatomical development of the brain. To do so, voxel-based morphometry (VBM) was carried out in a group of congenitally deaf individuals varying in the age of first exposure to American Sign Language (ASL). To explore a secondary question about the effect of auditory deprivation on structural brain development, a second VBM analysis compared deaf individuals to matched hearing controls. The results show that delayed exposure to sign language is associated with a decrease in grey-matter concentration in the visual cortex close to an area found to show functional reorganization related to delayed exposure to language, while auditory deprivation is associated with a decrease in white matter in the right primary auditory cortex. These findings suggest that a lack of early language experience alters the anatomical organization of the brain.
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MURESAN, XIMENA MARIA. "Role of Scavenger receptor B1 in cutaneous physiopathology." Doctoral thesis, Università degli studi di Ferrara, 2017. http://hdl.handle.net/11392/2488039.

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Scavenger receptor B1 (SR-B1) è una proteina transmembrana, coinvolta nel trasporto inverso di colesterolo a livello tissutale e definita anche recettore per HDL. Diversi studi hanno dimostrato che SR-B1 è implicato anche in altri processi, come regolazione dei livelli intracellulari di vitamine, riconoscimento di batteri e cellule apoptotiche e internalizzazione di vescicole. Nonostante il recettore sia localizzato principalmente a livello del fegato e dei tessuti steroidogenici, esso è significativamente espresso anche in altri tessuti compresa la cute umana, in special modo nell’epidermide. L’epidermide conferisce alla cute la funzione di barriera, attraverso la presenza dello strato corneo composto da acidi grassi, colesterolo, ceramidi, proteine e corneociti, quest’ultimi racchiusi da un involucro lipidico. La sua localizzazione e composizione fa della pelle un bersaglio per i fattori di stress ambientali. Studi in vitro condotti su cheratinociti in coltura hanno mostrato che stressors ambientali quali il fumo da sigaretta riducono l’espressione del recettore. Lo scopo del presente studio è stato quello di valutare il ruolo fisiologico di SR-B1 nella cute, attraverso l’uso di modelli cutanei 2D e 3D in cui l’espressione di SRB1 è stata geneticamente manipolata. I nostri dati dimostrano che SR-B1 è coinvolto nella proliferazione e nella migrazione cellulare. Infatti, il silenziamento di SR-B1 ha indotto una diminuzione dell’espressione di ciclina D1, così come dei livelli di MMP9 accompagnati da un difetto nella riorganizzazione del citoscheletro, influenzando perciò la capacità dei cheratinociti di riparare la ferita. Inoltre, SR-B1-KO ha un effetto sull’attivazione di NF-kB ed inoltre in modelli tridimensionali di cute ha causato cambiamenti sia a livello dello spessore che nella morfologia degli strati epidermici, insieme ad un aumento dei marcatori di differenziamento cellulare. In aggiunta, il recettore sembra avere un ruolo anche nella distribuzione epidermica dei lipidi e sul tipo di lipidi oltre ad essere implicato anche nel metabolismo lipidico nei sebociti. In fine il nostro studio ha dimostrato che i fattori di stress ambientali portano ad una riduzione di SR-B1 e questo effetto è evitato dall’uso di molecole naturali quali il resveratrolo. Riassumendo, i nostri dati suggeriscono che SR-B1 gioca un ruolo importante nella cicatrizzazione, così come nel differenziamento epidermico e nella composizione lipidica della cute, perciò la sua perdita indotta dall’esposizione ad agenti ossidanti potrebbe influenzare l’omeostasi cutanea.
Scavenger receptor B1 (SR-B1) is a trans-membrane protein, known as HDLs main receptor and involved in tissue reverse cholesterol transport. Several studies have demonstrated that SR-B1 is also implicated in other processes, such as regulation of intracellular vitamins levels, recognition of bacteria and apoptotic cells and vesicles uptake. Although this receptor is mainly localized in the liver and steroidogenic tissues, it is significantly expressed also in human skin, especially in the epidermis. The epidermis provides the barrier function of skin, due to the presence of stratum corneum, composed by proteins and corneocytes, which are distributed in a lipid envelope. Its localization and composition makes the skin a target for environmetantal stressors. In vitro studies on cultured keratinocytes have shown that SR-B1 protein expression is down-regulated by environmental oxidants such as cigarette smoke. Therefore, the purpose of our study was to evaluate the physiological role of SR-B1 in the skin, with more focus on the not vascularized cutaneous epidermal layer, by using 2D and 3D skin models. We demonstrated that SR-B1 is involved in cellular proliferation and migration, since SR-B1 knockdown keratinocytes presented reduced capacity to proliferate and migrate. In fact, SR-B1 knockdown induced a decrease of Cyclin D1 expression, as well as MMP9 levels accompanied by a defect in cytoskeleton rearrangement, affecting keratinocytes ability to recover from wound scratch. Furthermore, SR-B1 appeared to affect NF-kB activation. SR-B1 knockdown in tridimensional organotypic skin equivalents induced changes in epidermis thickness and deeper layers morphology, together with increased markers of terminal differentiation. Not only, but the scavenger receptor resulted to be essential for lipids expression and epidermal distribution, and it is implicated also in sebocytes lipids metabolism. Moreover, our study demonstrated that environmental stressors down-regulate SR-B1 also in three-dimensional reconstructed epidermis and human skin and, by the use of a natural polyphenol, we showed that such down-regulation was mediated by oxidative damage. Altogether, our findings suggest that SR-B1 plays an important role in keratinocytes recovery from injuries, as well as in epidermal differentiation and lipid composition, therefore its loss induced by oxidants exposure could affect cutaneous homeostasis.
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Calara, Federico Ben. "The vascular response to oxidative and mechanical stress /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980924cala.

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Bileviciute-Ljungar, Indre. "Bilateral neurogenic mechanisms following acute unilateral inflammation /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3168-2/.

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Löfgren, Olle. "Contribution of the sensory nervous system in thermally induced inflammation : an experimental study in the rat /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3288-3/.

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Oldner, Anders. "Splanchnic organ homeostasis in experimental endotoxin shock : with special reference to the endothelin and renin-angiotensin systems /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3574-2/.

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Books on the topic "Physiopathology"

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Bkaily, Ghassan, ed. Membrane Physiopathology. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2.

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Ghassan, Bkaily, ed. Membrane physiopathology. Boston: Kluwer Academic Publishers, 1994.

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Bastard, Jean-Philippe, and Bruno Fève, eds. Physiology and Physiopathology of Adipose Tissue. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0343-2.

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European, Congress on Magnesium (1st 1983 Lisbon Portugal). Magnesium deficiency: Physiopathology and treatment implications. Basel: Karger, 1985.

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Michel, Revel, ed. IL-6: Physiopathology and clinical potentials. New York: Raven Press, 1992.

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L, Catapano Alberico, Bernini Franco, and Corsini Alberto, eds. High density lipoproteins: Physiopathology and clinical relevance. New York: Raven Press, 1993.

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Paolo, Pancheri, and Zichella L, eds. Biorhythms and stress in the physiopathology of reproduction. New York: Hemisphere Pub. Corp., 1988.

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Gérard, Marguerie, Zwaal R. F. A, European Thrombosis Research Organisation, and Institut national de la santé et de la recherche médicale (France), eds. Biochemistry and physiopathology of platelet membrane =: Biochimie et physiopathologie de la membrane plaquettaire : proceedings of the Working Party on Platelet Membrane : Biochemistry and Physiopathology, held in Villard-de-Lans (France), 29-31 Januagy 1987. London: Libbey, 1988.

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Working Party on Platelet Membrane: Biochemistry and Physicology (1987 Villard de Lans, France). Biochemistry and physiopathology of platelet membrane: Proceedings of the Working Party on Platelet Membrane, Biochemistry, and Physiopathology, held in Villard-de-Lans (France) 29-31 January 1987 = Biochimie et physiopathologie de la membrane plaquettaire. Paris: Editions INSERM, 1988.

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Peter, Schauder, ed. Branched-chain amino acids: Biochemistry, physiopathology, and clinical science. New York: Raven Press, 1992.

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Book chapters on the topic "Physiopathology"

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Bricout, Nathalie. "Physiopathology." In Breast surgery, 171. Paris: Springer Paris, 1996. http://dx.doi.org/10.1007/978-2-8178-0926-7_13.

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Tonni, Gabriele, Edward Araujo Júnior, and Maria Paola Bonasoni. "Physiopathology." In Fetal Growth Restriction, 41–64. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00051-6_4.

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Jasmin, Gaétan, and Libuse Proschek. "Hamster Cardiomyopathy: New Insights in the Pathogenesis of this Hereditary Disease." In Membrane Physiopathology, 1–11. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_1.

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Sperelakis, Nicholas, Zhiling Xiong, and John Lorenz. "Regulation of Ca2+ Channels in Vascular Smooth Muscle Cells by Cyclic Nucleotides and by G-Protein Gating." In Membrane Physiopathology, 155–72. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_10.

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Bkaily, Ghassan, Pedro d’Orléans-Juste, Radha Naik, Demetri Economos, Shimin Wang, Elias Abdulnour, and Jean-Luc Ardilouze. "Role of the R-Type Ca2+ Channel in Cardiovascular Physiopathology." In Membrane Physiopathology, 173–83. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_11.

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Plante, Gérard E., and Mouna Chakir. "Passive Endothelial Transport: Studies in Experimental Arterial Hypertension, Diabetes Mellitus and Chronic Renal Failure." In Membrane Physiopathology, 185–206. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_12.

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D’Orléans-Juste, Pedro, and Sabine Télémaque. "Pharmacology of the Human Precursors of Endothelin: Role of Functional Receptors and Endothelin-Converting Enzyme." In Membrane Physiopathology, 207–26. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_13.

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Boivin, Dominique, Denis Gingras, and Richard Béliveau. "Carboxyl Methylation of Proteins in Kidney Membranes: Implications in the Repair of Damaged Proteins and in Signal Transduction." In Membrane Physiopathology, 227–48. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_14.

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Sahai, Animesh, and Pallab K. Ganguly. "Transport Systems in Kidney Basolateral Membrane: Pathophysiologic Implications." In Membrane Physiopathology, 249–70. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_15.

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Bikhazi, Anwar B., George E. Haddad, Habib M. Alloush, Fadia H. Uthman, Najla A. Fakruddin, and Muna El-Kasti. "Effect of Insulin and Glucagon on Hepatocellular Alanine Uptake in Normal and Streptozocin-Induced Diabetic Rats." In Membrane Physiopathology, 271–89. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_16.

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Conference papers on the topic "Physiopathology"

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Palmieri, Beniamino, Stefania Capone, and Leonardo Longo. "Biosensors Related LLT: Physiopathology, Background and Rationale." In ADVANCES IN LASEROLOGY - SELECTED PAPERS OF LASER FLORENCE 2010: The 50th Birthday of Laser Medicine World. AIP, 2011. http://dx.doi.org/10.1063/1.3626925.

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Muñoz-Picos, Mercedes, Cristina Contreras, Marina Hernández-Martín, Claudia Rodriguez-Prados, Ana Sanchez, Ángel Agis-Torres, Belén Climent, et al. "DESIGNING PRACTICAL PBL LESSONS FOR FEMALE REPRODUCTIVE SYSTEM PHYSIOPATHOLOGY TEACHING." In 12th annual International Conference of Education, Research and Innovation. IATED, 2019. http://dx.doi.org/10.21125/iceri.2019.1194.

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Kolani, Sylvie Sougoulouman, Meryem Haloua, Youssef Alaoui Lamrani, Meryem Boubbou, and Mustapha Maaroufi. "Hemoptysis on Tuberculosis Sequelae: From the Physiopathology to the Endovascular Treatment." In PAIRS Annual Meeting. Thieme Medical and Scientific Publishers Pvt. Ltd., 2020. http://dx.doi.org/10.1055/s-0041-1729111.

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Pinilla, Lucia, Krish Dodani, Iván Benítez, Neda Esmaeli, Esther Gracia-Lavedán, Gerard Torres, Olga Minguez, et al. "Molecular insights into hypoxic burden physiopathology in OSA: a proteomic perspective." In ERS Congress 2024 abstracts, PA2693. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa2693.

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Stork, Larissa Rosa, Lucca Stephani Ribeiro, Izabella Savergnini Deprá, Luísa D’Ávila Camargo, and Maria Angélica Santos Novaes. "Tau protein and its role in Alzheimer’s disease physiopathology: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.132.

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Background: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a double proteinopathy: deposition of amyloid-β into plaques and hyperphosphorylation of Tau protein. Objectives: To understand the genetic and molecular aspects of Tau protein and its relationship with Alzheimer’s disease. Methods: We conducted a systematic literature search using Pubmed/ MEDLINE and ClinicalKey databases, applying the descriptors: “Alzheimer Disease” AND “Tau proteins’’ AND Tauopathies, during July and August of 2020. The inclusion criteria were English and Portuguese articles published between 2015 and 2020, with human limited study and free full text, excluding images, books, clinical tests, and narrative reviews. After analyzing titles and abstracts, we selected 12 articles and included 7 additional studies. Results: Mapt, the encoder gene of Tau, is located in the 17q21.3 locus and presents 16 exons that, when transcripted, originates 12 copies of mRNA by alternative splicing and 6 Tau’s isoforms. Tau is a microtubule-associated protein (MAP) responsible for cellular cytoskeleton stabilization and maintenance, promoting neuronal axonal transport. A kinase-phosphatase imbalance turns Tau hyperphosphorylated, disassociating it from tubulin and grouping it into insoluble paired helical filaments, which originates neurofibrillary tangles. The tauopathy’s progress causes neurotransmitter destabilization and neuronal death, inducing AD symptomatic manifestations. Conclusions: Due to the gradual worsening of the disease to more debilitating stages, studies focused on deepening the knowledge of genetic and molecular aspects of Tau protein are viable and promising alternatives to improve the quality of patient’s lives.
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Le Ribeuz, Hélène, Mary Dutheil, Veronique Capuano, Olaf Mercier, Marc Humbert, David Montani, and Fabrice Antigny. "Late Breaking Abstract - Implication of the KATP Sur2b/Kir6.1 in the physiopathology of pulmonary arterial hypertension." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa600.

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Coşkun, Necmiye Funda, Fadıl Özyener, Aslı Görek Dilektaşlı, and Dane Ediger. "Investigation of Respiratory Physiopathology by Determination of Pulmonary Gas Exchange and Ventilation Dynamics in Chronic Lung Diseases." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa4515.

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Olloquequi, Jordi, Raquel Martin-Venegas, Trinitat Cambras, Maria Del Carmen Moran, Maria Pilar Vinardell, Ruth Ferrer, Jaume Del Valle, et al. "STUDENT PREFERENCES IN LABORATORY LEARNING MODALITIES: FACE-TO-FACE VS. REMOTE INSTRUCTION IN PHYSIOLOGY AND PHYSIOPATHOLOGY EDUCATION." In 18th International Technology, Education and Development Conference. IATED, 2024. http://dx.doi.org/10.21125/inted.2024.0528.

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Reina, MA, OC Nin, A. Oviedo-Baena, LT Le-Wendling, Y. Zasimovich, A. Server, and A. Boezaart. "ESRA19-0616 New concepts in physiopathology of the nerve lesions: intraneural injection microanatomy in humans and animal models." In Abstracts of the European Society of Regional Anesthesia, September 11–14, 2019. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/rapm-2019-esraabs2019.15.

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Julian, D. G. "UNSTABLE ANGINA : DEFINITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643709.

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A satisfactory definition of unstable angina continues to be elusive.Like stable angina, it is a clinicalsyndrome, and mustbe defined in those terms. In both cases, it is understood that myocardial ischaemiabut not infarction is responsible for the symptoms. For angina to earn the “unstable” label, theremust have been the recent development or deterioration of symptoms. Traditionally, “recent” has meant within the last month, but it has become increasingly clear thatthe time frame is of critical importance - the patient with a sudden irruption of severe chest pain in the last two days is likely to have a different pathology and prognosis from the individual who first developed exercise-induced pain two weeks ago, which has not worsened during this period. Likewise, the patient who hadhis last attack of pain one week agois very different from one who had his last attack one hour ago; indeed in the HINT study, there was a high incidence of myocardial infarction undetected on admission in the lattergroup (Br Heart J 1986;56:400-13).A problem that has hardly been addressed is “When does unstable angina stop being unstable?”. The answer must be when it either becomes stable (i.e. stops getting worse),or proceeds to myocardial infarctionor death.Most studies have shown that the vast majority of patients stablise quickly, often losing their symptoms completely. There is, however, a group of patients who fail to respond promptly to medical treatment, and it isthese patients who are most likely to go on to angiography, angioscopy, angioplasty, surgery, myocardial infarction or death. Thus, the enormously valuable information we have obtained from, for example, angiography and necropsy studies applies essentially only to this subset of unstableangina patients, albeit they are themost severe. Unfortunately, such studies tell us relatively little aboutthe more dynamic aspects of the disorder, such as the role of coronary vasomotion.It is only relatively recently that clinicians have appreciated that they have quite simple means of suspecting the mechanisms involved. Thus, the history of progressive exercise-induced angina on the one hand or angina only at rest on theother must tell us something of the underlying physiopathology. Likewise,the fact that the symptoms respond to rest, or beta-blockers, or calcium antagonists also provides evidenceas to causation.Thus, while all would agree that angina is “unstable” whenit has recently developed or worsened, it must bediscussed in subsetsdefined by their history and response to treatment.In this way, we may be able to assign a patient to a particular clinicalgroup, which will indicate that it is likely that he has a particular physiopathology, which inturn will suggest the most appropriate management.
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Reports on the topic "Physiopathology"

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Olszewski, Waldemar, and Fausto Passariello. Physiopathology of Lymphedema. Fondazione Vasculab, March 2016. http://dx.doi.org/10.24019/2016.l-phys.

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