Готові списки джерел за темами / Pathophysiology

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Добірка наукової літератури з теми "Pathophysiology"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 30 липня 2024

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Статті в журналах з теми "Pathophysiology"

Evans, Roger. "Campbell’s Pathophysiology NotesCampbell’s Pathophysiology Notes." Nursing Standard 21, no. 30 (April 4, 2007): 31. http://dx.doi.org/10.7748/ns2007.04.21.30.31.b600.

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Huether, Sue E., and Kathryn L. McCance. "Pathophysiology." Dimensions of Critical Care Nursing 13, no. 6 (November 1994): 315. http://dx.doi.org/10.1097/00003465-199411000-00010.

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Werkö, Lars. "PATHOPHYSIOLOGY." Acta Medica Scandinavica 210, S652 (April 24, 2009): 9–11. http://dx.doi.org/10.1111/j.0954-6820.1981.tb06781.x.

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Zreik, Tony G., and David L. Olive. "PATHOPHYSIOLOGY." Obstetrics and Gynecology Clinics of North America 24, no. 2 (June 1997): 259–68. http://dx.doi.org/10.1016/s0889-8545(05)70303-x.

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Rothwell, J. "Pathophysiology." Electroencephalography and Clinical Neurophysiology 103, no. 1 (July 1997): 48. http://dx.doi.org/10.1016/s0013-4694(97)88121-0.

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Komenaka, Ian. "Pathophysiology." Current Surgery 58, no. 2 (March 2001): 186–87. http://dx.doi.org/10.1016/s0149-7944(00)00433-5.

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Woolf, N. "Pathophysiology." Journal of Clinical Pathology 39, no. 8 (August 1, 1986): 931. http://dx.doi.org/10.1136/jcp.39.8.931-a.

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Kersey, Robert D. "Pathophysiology." Athletic Therapy Today 10, no. 2 (March 2005): 60–61. http://dx.doi.org/10.1123/att.10.2.60.

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Dudley, Sharon L. "Pathophysiology." Gastroenterology Nursing 15, no. 5 (April 1993): 212. http://dx.doi.org/10.1097/00001610-199304000-00010.

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Shepeleva, A. D., D. F. Shamardanov, and E. V. Ponomarenko. "PATHOPHYSIOLOGY OF MULTIPLE SCLEROSIS." European Journal of Natural History, no. 4 2022 (2022): 12–16. http://dx.doi.org/10.17513/ejnh.34281.

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Дисертації з теми "Pathophysiology"

Farrán, Díaz-Cano Aina. "Pathophysiology of osteoarthritis." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/456376.

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Osteoarthritis (OA) is a multifactorial disease characterized by a progressive degeneration and eventual failure of the synovial joint functionality. Although it has been traditionally considered as an exclusive disease of the articular cartilage, nowadays it is considered as a whole joint disease. Therefore, the progression of the disease involves articular cartilage degeneration, osteochondral bone sclerosis and synovial membrane hypertrophy. Articular cartilage is a connective tissue resistant to tensile and shears strength that is composed of water (>70%) and a dense extracellular matrix (ECM) that encompasses the unique cellular type of the cartilage, the chondrocytes. The major component of the ECM is the collagen network consisting mainly of type II collagen fibers and type IX and XI collagen macromolecules attached to the surface of the fiber. Non-collagenous components such as GAGs, aggregated proteoglycans (mainly aggrecan) and small leucine rich proteoglycans (SLRP’s) are also binding the collagen fiber. Cartilage is a no innervated and also an avascular tissue, thus gets its nutrients by diffusion from the synovial fluid. Due to this condition, chondrocytes live in a hypoxic environment, and intracellular survival factors, such as hypoxia-inducible factor 1α, are required for maintenance of homeostasis and adaptation to the mechanical environment. Under physiological conditions, the collagen network and proteoglycan content is maintained by the chondrocytes. However, local and systemic risk factors could lead chondrocytes to fail to maintain the ECM and thus the cartilage tissue is progressively degraded. To this point, the three general objectives of this thesis are: 1. Collagenase-3 (COL3) also known as MMP13, is a matrix metalloproteinase abnormally over-expressed in pathological processes. Several COL3 transcripts are expressed in human chondrocytes although their role in OA is still unknown. This study aimed to characterize the presence of two non-canonical COL3 isoforms, named COL3-DEL (deleted form) and COL3-9B (exon 9 added form) in human OA cartilage, and to analyse their proteolytic activity. 2. Opticin (OPTC), a SLRP known to play a role in the assembly of the fibrillar collagens and the structural stability of the extracellular matrix, was previously demonstrated to be produced and degraded in osteoarthritic (OA) human cartilage. Here, we further investigated the OPTC role in OA cartilage by the study of the in vivo effect of OPTC deficiency in mouse model 3. Chondroitin sulfate (CS) is a Symptomatic Slow acting Drug against Osteoarthritis (SySADOA) with anti-inflammatory effects. In this study, we tried to unveil the mechanism of action on osteoarthritic synovial membrane. The general discussion of this thesis is: OA is a heterogeneous disease that encloses multiple phenotypes. In order to develop new diagnostic and prognostic tools and eventually advance in the discovery of successful treatments, clearly defining the different phenotypes of OA is of great importance. In this line, the findings comprised in this thesis reveal two different approaches to identify patient’s subgroups. On one hand, and as described in chapter 1, the presence of a new discovered collagenase-3 (COL3) isoform (COL3-DEL) resulting from a mutation of the canonical COL3, could be used as an indicator of differential extracellular matrix degradation in human articular cartilage. On the other hand, results from chapter 2 suggest that the compositions of the members of SLRP super-family in the human extracellular matrix of the articular cartilage could be applied as a new tool for OA prognosis classification. Finally, the controversy regarding the efficacy of systemic treatment with nutraceuticals – including chondroitin sulfate - may arrive to an end if new tools are used to predict which patients are best suited for a given drug. Importantly, further work remains to be done to understand how to integrate these findings into a final and comprehensive concept that could explain the patient’s heterogeneity and the differential prognosis of OA disease.
L’artrosi (OA) és la malaltia articular més comuna i es caracteritza, principalment, per la destrucció del cartílag articular. El principal paper del cartílag articular és el de suportar les forces de tensió i compressió a les que es troba sotmès i que recau principalment en els seus components: el col·lagen i els proteoglicans. Durant el metabolisme normal del cartílag hi ha un equilibri entre la síntesi i degradació d’aquest components, però a l’artrosi, aquest equilibri es trenca i el metabolisme catabòlic supera l'anabòlic. Durant el desenvolupament de l'OA, els condròcits expressen la proteasa més involucrada en la degradació del cartílag, la MMP-13, que a diferència d’altres MMPs, en humans presenta 3 transcrits diferents. Malauradament, tot i la seva elevada prevalença, l'OA es troba orfe d’una bona tècnica diagnòstica, ja que actualment es realitza per mitjà de tècniques radiològiques que presenten l'inconvenient de que la malaltia només es reflecteix quan l’articulació es troba molt afectada. Actualment, els tractaments farmacològics més utilitzats són analgèsics, AINEs, i els nutracèutics, anomenats SYSADOA per les seves sigles en anglès (Symptomatic Slow Acting Drugs for Osteoarthritis) d’entre els que destaca el sulfat de glucosamina i el condroitin sulfat. Amb aquests antecedents previs, els objectius de la tesis són: 1. Demostrar la presència de 3 isoformes de MMP-13 en humans • Clonació (sistema Bac-to-bac) i purificació de les 3 isoformes en cèl·lules d’insecte (Sf9). • Producció d’anticossos policlonals específics de cada isoforma al Servei de Producció d’Anticossos de la UAB • Cerca de les isoformes en pacients artròsics per WB. • Comprovació de l’activitat de cada isoforma en front a diferents components matricials. 2. Estudiar l'efecte "in vivo" de la deleció del gen de l'Opticina en un model murí d'artrosi. • Confirmar l'expressió de l' OPTC al cartílag articular dels ratolins. • Induïr OA mitjançant el mètode de destabilització del menisc medial (DMM) a ratolins Optc-/- i Optc +/+ de 10 setmanes d'edat. • Analitzar l'efecte de la deficiència de l'OPTC al desenvolupament de l'OA, evaluant la degradació del cartílag i la hipertròfia de la membrana sinovial, deu setmanes després de l'inducció de l'OA per DMM. • Comparar l'expressió de marcadors pro-inflamatoris, catabòlics i anabòlics entre ratolins Optc-/- i Optc+/+. • Analitzar la producció al cartílag de differents SLRPs. • Analitzar l'organització i l'ultraestructura de les fibres de colàgen. 3. Estudiar l'efecte anti-angiogenic del condroitin sulfat en sinoviòcits sota condicions d'hipòxia i d'hipòxia més inflamació. • Mimetitzar condicions inflamatòries i d'hipòxia "in vitro" en sinoviòcits humans. • Estudiar l'expressió i la producció de mediadors angiogènics per sinoviòcits artròsics sota condicions d'hipòxia i inflamació. • Estudiar l'efecte del pretractament del CS en cultius de sinoviòcits humans artròsics • Estudiar l'interacció entre els sinoviòcits artròsics i les cèl·lules endotelials sota hipòxia i inflamació, amb o sense pretractament de CS. L'artrosi és una malaltia que engloba diferents fenotips, però tots comparteixen una sèrie de característiques com la degeneració del cartílag articular, inflamació de la membrana sinovial i esclerosi de l'ós subcondral. Aquestes característiques resulten en un conjunt de símptomes que impedeixen la correcte mobilitat del pacient i creen dolor que pot arribar a ser crònic. Alhora de desenvolupar noves eines de diagnòstic i prognòstic i eventualment avançar en el descobriment de tractaments exitosos, definir clarament els diferents fenotips de l'artrosi és de gran interès. En aquesta línia, els descobriments compresos en aquesta tesis revelen dues possibles maneres d'identificar subgrups de pacients. Per una part, com es descriu al capítol 1, la presència d'una nova isoforma de la colagenasa-3 podria utilitzar-se com a un indicador de diferencies en la degradació matricial del cartíleg humà articular. Per una altre banda, els resultats del capítol 2 suggereixen que la composició dels membres de la famíla de SLRP a la matriu extracel·lular del cartíleg podria aplicar-se com a una nova eina de classificació del prognòstic de la malaltia artròsic. Finalment, la controversia sobre l'eficàcia del tractament amb nutracèutics com el condroitin sulfat podria arribar a solucionar-se si es descobreixen noves eines per predir quins pacients poden respondre millor a un medicament donat. És important tenir en compte que s'ha de continuar investigant per entendre com integrar aquests resultats en un concepte final que pogués explicar l'heterogeneïtat dels pacients i les diferències en el prognòstic de l'artrosi.

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Stoodley, Marcus A. "Pathophysiology of Syringomyelia /." Title page, contents and abstract only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phs882.pdf.

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Robinson, Monique Renee. "Cardiac pathophysiology of obesity." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414224.

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Padera, Timothy P. (Timothy Patrick) 1975. "Lymphatic pathophysiology of tumors." Thesis, Massachusetts Institute of Technology, 2003. http://hdl.handle.net/1721.1/29591.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2003.
Includes bibliographical references (leaves 146-166).
Lymph node metastases have a negative impact on cancer survival, but the mechanisms for lymphatic metastasis are not well understood. The universal finding in solid tumors of an absence of functional lymphatic vessels seems paradoxical, as cancer cells do travel through lymphatics in order to disseminate. In order to address some of these issues, this thesis proposes two etiologies for the absence of functional lymphatic vessels in solid tumors. The first hypothesis addresses whether Vascular Endothelial Growth Factor-C (VEGF-C), a lymphangiogenic factor, was sufficient to induce lymphatic function in tumors. The overexpression of VEGF-C in tumors leads to an increase in lymph node metastasis as well as structures that positively stain for lymphatic markers, but does not induce functional lymphatics within the tumor. Thus VEGF-C is not sufficient to grow functional lymphatic vessels in tumors. The second hypothesis addresses whether mechanical forces generated by the proliferation of cancer cells in a confined space compress lymphatic vessels in tumors. The mechanical forces inside of the tumor were reduced by the selective killing of human cancer cells grown in mice by Diphtheria Toxin. Tumor cell death leads to an increase in the fraction of lymphatics with open lumen. In addition, lymphatic vessels with open lumen are surrounded by a lower cellular density than collapsed vessels. Thus, relieving solid stress allows lymphatic vessels to open. However, function was not restored in these vessels. This is presumably due to the inability of the lymphatic vessels to completely open along its entire length, leaving focal areas of lymphatic collapse. Compressive forces are common to all growing tumors, giving credence to the mechanical etiology of the absence of functional lymphatic vessels in tumors, regardless of tumor type or organ site.
(cont.) These findings lead to an interesting question: Does cancer treatment in humans relieve the mechanical compression allowing lymphatic and blood vessels to open? Furthermore, would the resumption of function of compressed blood and lymphatic vessels lead to a paradoxical increase in metastasis? These questions require further investigation.
by Timothy P. Padera.
Ph.D.

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Fletcher, Jessica Louise. "Pathophysiology of canine fucosidosis." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10420.

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Pathophysiology of Canine Fucosidosis by Jessica L Fletcher Understanding processes involved in the onset and progression of fucosidosis, a childhood neurodegenerative lysosomal storage disease, is critical to the development of effective treatment. Fucosidosis is caused by deficiency of the lysosomal hydrolase α-L-fucosidase due to inherited mutations in the FUCA1 gene. Canine fucosidosis, the only preserved animal model, was used to characterise preclinical pathophysiology, to establish potential markers of disease progression and test their capacity to measure responses to early therapy. Statistical interrogation of clinical data revealed that clinical signs are consistent from 12 months, and that rapid decline is signalled by sensory dysfunction from 18 months of age. Regression analysis against existing neuropathological data identified apoptosis and neuroinflammation as significant contributors to clinical dysfunction. Gene expression profiling of the frontal cortex at 16 weeks identified neuroinflammation to be prominent in fucosidosis pathogenesis (33% of differentially expressed genes) with both neuroinflammatory and mitochondrial-mediated pathways contributing to apoptotic cell death. Myelin genes were significantly downregulated, prompting investigation of oligodendrocyte populations in preclinical disease. Mature oligodendrocytes were reduced by 45-67%. Intracisternal enzyme replacement therapy from 8-16 weeks improved oligodendrocyte survival by 21%, and 29% of Purkinje neurons demonstrated reduced vulnerability to apoptosis. Neuroinflammatory cytokines and chemokines were investigated in cerebrospinal fluid to identify candidate biomarkers. MCP-1/CCL2 and KC/CXCL1 demonstrated potential, with significant increases with disease progression, and reductions with enzyme replacement therapy. Overall, these findings provide tools for disease management and a revised model of pathophysiology which can be used as a framework for future investigations into fucosidosis pathogenesis and therapy.

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Kirk, Calum Norman Robert. "Pathophysiology of anoctaminopathy (LGMD2L)." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3861.

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Ageing is a natural process, which is characterised by progressive decline in physiological functions and increased susceptibility to disease and death. Brain is particularly susceptible to structural and functional changes, which is more evident in disorders associated with ageing such as Alzheimer disease (AD). Copper is necessary for the protection against oxidative stress, energy production and neurotransmitter processing in the brain. However, higher copper levels can increase oxidative stress, resulting in neuronal damage. In order to avoid copper induced cytotoxicity, cells have to regulate copper levels through distribution into three intracellular pathways. By identifying changes in the copper pathways in the healthy and AD brain and by estimating the effects of copper chelation or supplementation in model cell line a better understanding of copper function in the brain will be obtained. In order to accomplish that copper, activity and protein levels of cytochrome c oxidase (COX) and superoxide dismutase (SOD) were measured in the healthy, AD brain and in HEK293 cell treated with copper chelators or supplemented with copper. Copper concentration was significantly decrease by more than 40% in healthy ageing brain and in the AD brain. Copper loss did not seem to affect the activity or protein level of the COX and SOD, since their levels were significantly increased in the ageing and AD brain. On the other hand, cells treated with copper chelators for three days faced a more than 75% decrease in intracellular copper concentration, which led to a more than 85% inhibition of the COX and SOD activity. Copper levels should be regulated properly in order to meet body’s metabolic demands and avoid cytotoxicity. Brain seems to have a mechanism where its energy demands have to be fulfilled even under low copper concentrations. Whereas, the prolonged and severe copper loss can dramatically affect the energy production and antioxidant defence systems which could be fatal to the cells.

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Cheng, Allen Cheuk-Seng, and allencheng@ozemail com au. "MELIOIDOSIS: EPIDEMIOLOGY, PATHOPHYSIOLOGY AND MANAGEMENT." Flinders University. Medicine, 2005. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20051121.141305.

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In under a century, melioidosis, the infection due to Burkholderia pseudomallei, has emerged from Whitmores series of glanders-like infections amongst the morphia addicts in Burma to a major cause of mortality in northeastern Thailand and northern Australia. Also endemic in other parts of south-east Asia, melioidosis may have varied presentations ranging from severe, overwhelming infection to chronic, low grade disease. Observational evidence had suggested that granulocyte colony stimulating factor (G-CSF), a naturally occurring substance produced by the body in response to infection, may have been useful in reducing the high mortality associated with the more severe forms of this infection. Other observations linked the occurrence of this disease to various environmental factors, such as contamination of drinking water and the annual rainfall. This thesis explores and attempts to quantify these associations. There are three parts to this thesis. In the first part, I reviewed the epidemiology and management of patients with melioidosis. The use of G-CSF and meropenem was associated with a fall in mortality, although other factors may have at least partially contributed to this effect. In the second part, I progressed towards a clinical trial of G-CSF. There was no other evidence supporting the use of G-CSF in severe sepsis and ethical issues precluded a trial in Darwin. There was not evidence from laboratory models of G-CSF action in melioidosis to support the use of G-CSF in patients, although there remained some doubt regarding the applicability of such models to human disease. I examined clinical methods to identify patients at high risk of death from melioidosis. A simple scoring system based on clinical and laboratory parameters was developed and externally validated. However, clinical definitions of severe sepsis appeared to be better predictors of mortality. A clinical trial based on clinical definitions was commenced in Thailand. In the final part, I explored the question of whether different strains or B. pseudomallei or different environmental conditions caused different patterns of infection. There was no evidence that strain types of this bacterium determine the pattern or severity of disease, but weather conditions appeared to influence the distribution of disease in northern Australia.

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Berg, Erika L. "Endocrinology of equine metabolic pathophysiology." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4472.

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Thesis (Ph. D.) University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on July 31, 2007) Includes bibliographical references.

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Sethia, Krishna Kumar. "The pathophysiology of detrusor instability." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235958.

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Steele, Ian Conrad. "Pathophysiology of chronic cardiac failure." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337046.

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Книги з теми "Pathophysiology"

L, Banasik Jacquelyn, ed. Pathophysiology. 4th ed. St. Louis, Mo: Saunders Elsevier, 2010.

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Sandra, Kim, and Flomin Olga E, eds. Pathophysiology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.

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Lippincott Williams & Wilkins., ed. Pathophysiology. Ambler: Lippincott Williams & Wilkins, 2007.

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1943-, Brozenec Sally A., ed. Pathophysiology. Springhouse, Pa: Springhouse Corp., 1999.

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Sandra, Kim, and Flomin Olga E, eds. Pathophysiology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006.

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M, Crutchlow Eileen, ed. Pathophysiology. Thorofare, NJ: Slack, 2002.

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Copstead, Lee Ellen. Pathophysiology. 3rd ed. St. Louis, Mo: Elsevier Saunders, 1994.

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Madara, Bernadette. Pathophysiology. 2nd ed. Sudbury, Mass: Jones and Bartlett, 2008.

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Kathleen, Gutierrez, and Peterson Phyllis Gayden, eds. Pathophysiology. Philadelphia: W.B. Saunders, 2002.

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Ellen, Copstead Lee, and Banasik Jacquelyn L, eds. Pathophysiology. 3rd ed. St. Louis, MO: Elsevier Saunders, 2005.

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Частини книг з теми "Pathophysiology"

Louie, A. H. "Pathophysiology." In IFSR International Series on Systems Science and Engineering, 195–210. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6928-5_12.

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Stokes, K. B. "Pathophysiology." In Oesophageal Atresia, 59–73. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-3079-8_5.

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Leppäniemi, Ari. "Pathophysiology." In Emergency Surgery Course (ESC®) Manual, 31–35. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-21338-5_4.

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Witthöft, Michael. "Pathophysiology." In Encyclopedia of Behavioral Medicine, 1634–36. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_43.

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De Paris, Valerio, Federico Biondi, Davide Stolfo, Marco Merlo, and Gianfranco Sinagra. "Pathophysiology." In Dilated Cardiomyopathy, 17–25. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-13864-6_3.

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Witthöft, Michael. "Pathophysiology." In Encyclopedia of Behavioral Medicine, 1443–45. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_43.

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George, Bernard, and Claude Laurian. "Pathophysiology." In The Vertebral Artery, 102–13. Vienna: Springer Vienna, 1987. http://dx.doi.org/10.1007/978-3-7091-6967-4_10.

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Kaul, Sunny. "Pathophysiology." In Managing Chronic Obstructive Pulmonary Disease, 1–12. West Sussex, England: John Wiley & Sons Ltd, 2008. http://dx.doi.org/10.1002/9780470697603.ch1.

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Böhm, Michael, and Erland Erdmann. "Pathophysiology." In Chronic Heart Failure, 17–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-85913-7_4.

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Boudes, Mathieu, and Dirk De Ridder. "Pathophysiology." In Overactive Bladder, 7–21. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118640562.ch2.

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Тези доповідей конференцій з теми "Pathophysiology"

Widyasari, Rastita, Iswan Abbas Nusi, Poernomo Boedi Setiawan, Herry Purbayu, Titong Sugihartono, Ummi Maimunah, Ulfa Kholili, et al. "Pathophysiology of Irritable Bowel Syndrome." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007340704700476.

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"Pathophysiology of Acute Cerebral Hemorrhage Injury." In 2020 International Conference on Educational Science. Scholar Publishing Group, 2020. http://dx.doi.org/10.38007/proceedings.0000445.

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Lauwerys, B. "SP0148 Pathophysiology of established ra synovitis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7282.

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Liu, Yixuan. "The Pathophysiology of Phantom Limb Pain." In 2020 3rd International Conference on Humanities Education and Social Sciences (ICHESS 2020). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/assehr.k.201214.521.

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Bernardo, Juliana Matos Ferreira, Artur Bruno Silva Gomes, Felipe Jatobá Leite Nonato de Sá, Júlia Gonçalves Ferreira, and Maria Rosa da Silva. "Phantom pain: pathophysiology and therapeutic approaches." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.496.

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Background: Phantom pain is a mentally debilitating neuropathy that affects post-amputees. It interferes with the independence and performance of activities, therefore affecting the quality of life. Its pathophysiology ranges from lesions in peripheral innervations, to spinal functional changes, modulation of cortical circuits and psychological factors Objectives : Demonstrate new therapeutic approaches and establish a relation with the pathophysiological mechanisms. Methods: Integrative review applying the descriptors: “phantom pain”, “physiopathology”, “post amputation pain”, “treatment”, and the Boolean operator AND. The searches were carried out at PUBMED with 142 results, at BVS with 113, and at Scielo ,showing no results. At the end, 9 papers were selected. No linguistic filters were used and articles published between 2016 and May 2020 were incorporated. Results: (1) Motor images, mental and visual representation of the limb and its function; (2) peripheral interfaces enables prosthetic control; both techniques active cortical reorganization by promoting sensory feedback to motor stimuli. (3) repetitive transcranial magnetic stimulation and (4) direct current, a non-invasive approach, for maladaptive cortical neuromodulation, in addition to stimulate peripheral innervation. In surgical interventions, (5) targeted muscle reinnervation is used in the residual nerves on amputation process to reinnervate the motor terminal of the remaining muscles, promoting nerve growth and organization. Conclusions Physiological investigation applied to treatments enables effective therapeutics, anticipating rehabilitation. The representation of images, peripheral interfaces, brain stimulation and less invasive surgical techniques.

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Rizzi, Liara, and Marcio Balthazar. "THE SUSPECTED NON-ALZHEIMER’S DISEASE PATHOPHYSIOLOGY." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda070.

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Background: Individuals that are negative for amyloid biomarkers and positive for p-Tau and/or neurodegeneration ones are known as with the suspected non-Alzheimer’s disease pathophysiology (SNAP). It is a biomarker-based concept that underlying etiology has not been completely understood. Objective: To report the main characteristics of the SNAP group. Methods: PubMed was searched to identify articles about the SNAP for inclusion. Results: The prevalence of SNAP varies from 18% to 35% among cognitively normal individuals, from 16,6% to 35% among mild cognitive impairment (MCI), and from 7% to 39% among clinical probable Alzheimer’s Disease (AD). SNAP subjects have a lower risk of clinical progression to MCI or AD dementia than those with positive amyloid biomarkers, but higher than those whose biomarkers for amyloid and neurodegeneration are negative. SNAP predominate in older men and have a lower incidence of the APOE ε4 allele than in individuals with AD. Cognitive decline in SNAP subjects is related to neuronal damage. They present greater hippocampal atrophy than AD, but a similar pattern of hypometabolism. Hippocampus-specific pathologies and cerebrovascular diseases may underlie neurodegeneration and cognitive impairments. Conclusion: The construct of SNAP has been challenging, therefore, a deeper understanding of the main pathways that underlie SNAP can allow substrates for disease prevention and/or remission in the future.

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Friedrich, I., L. Paschos, T. J. Donovan, and A. Paraforos. "Digital Learning: Cardiac Physiology and Pathophysiology." In 51st Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1742908.

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Rueda, Alice, J. C. Vásquez-Correa, Cristian David Rios-Urrego, Juan Rafael Orozco-Arroyave, Sridhar Krishnan, and Elmar Nöth. "Feature Representation of Pathophysiology of Parkinsonian Dysarthria." In Interspeech 2019. ISCA: ISCA, 2019. http://dx.doi.org/10.21437/interspeech.2019-2490.

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Wang, Yu, and Jack M. Winters. "Modeling the adaptive pathophysiology of essential hypertension." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090239.

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BLASI, GIUSEPPE, and ALESSANDRO BERTOLINO. "Pathophysiology of Schizophrenia: fMRI and Working Memory." In Modelling Biomedical Signals. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812778055_0011.

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Звіти організацій з теми "Pathophysiology"

Harden, R. N. Pathophysiology of Post Amputation Pain. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568349.

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Harden, R. N. Pathophysiology of Post Amputation Pain. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada601811.

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Nelson, Julie. Feline chronic kidney disease: Pathophysiology and diagnosis. Ames (Iowa): Iowa State University, January 2021. http://dx.doi.org/10.31274/cc-20240624-721.

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Zampell, Jamie, Babak Mehrara, Evan Weitman, Sonia Elhadad, and Alan Yan. Adaptive Immune Responses Regulate the Pathophysiology of Lymphedema. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567843.

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Passariello, Fausto. Pathophysiology and ultrasound assessment of the calf muscle pump. Fondazione Vasculab, 2017. http://dx.doi.org/10.24019/2017.cmp-us.

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Bercovier, Herve, and Paul Frelier. Pathogenic Streptococcus in Tilapia: Rapid Diagnosis, Epidemiology and Pathophysiology. United States Department of Agriculture, October 1994. http://dx.doi.org/10.32747/1994.7568776.bard.

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Within the project "Pathogenic Streptococcus in Tilapia", gram positive cocci pathogens of fish in Israel and in the United States were characterized. We showed that Streptococcus shiloi, the name for an agent causing septicemic infection in fish, is a junior synonym of Streptococcus iniae and that Enterococcus seriolicida is a junior synonym of Lactococcus garvieae, a causative agent of septicemia and meningo-encephalitis in fish. Molecular epidemiology studies on these two pathogens, based on 16S rDNA sequences and ribotyping showed that although each country had specific clones, S. iniae originated probably from the U.S. and L. garvieae from Japan. PCR assays were developed for both pathogens and applied to clinical samples. S. agalactiael S. difficile was also recognized for the first time in the U.S. in tilapia. Our histopathological studies explained the noted paradox (abundant in vitro growth often accompanied by scant to small numbers of organisms within the meninges in histologic sections of brain) in diagnostic of fish streptococcus. The greatest concentration of cocci were consistently observed within macrophages infiltrating the extrameningeal fibroadipose tissue surrounding the brain within the calvarium. These results also suggests that the primary route of meningeal infection may be extension from the extrameningeal connective tissue rather than meningeal vascular emigration of cocci-containing macrophages. Our work has resulted in a cognizance of streptococcus as fish pathogen which goes beyond the pathology observed in tilapia and is already extended to many aquaculture fish species in Israel and in the United States. Finally, our data suggest that vaccines (bivalent or trivalent) could be developed to prevent most of the damages caused by streptococcus in aquaculture.

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Zhang, Jiwang. The Role of Necroptosis in the Pathophysiology of Bone Marrow Failure. Fort Belvoir, VA: Defense Technical Information Center, March 2014. http://dx.doi.org/10.21236/ada604192.

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Daneff, Miriam, and Nafisa Jadavji. The Role of Synaptic Plasticity in the Pathophysiology of Cocaine Addiction. Journal of Young Investigators, October 2019. http://dx.doi.org/10.22186/jyi.37.4.33-38.

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McGovern, Ruth, Vincent McGovern, and Martina Healy. Congenital Diaphragmatic Hernias – Part 1. World Federation of Societies of Anaesthesiologists, February 2024. http://dx.doi.org/10.28923/atotw.526.

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A focused tutorial centred around the management of congenital diaphragmatic hernia in paediatric critical care. We outline the aetiology, pathophysiology and management of congenital diaphragmatic hernia immediately following birth, and in the time leading to definitive surgery.

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Fair, Patricia A., and Gregory D. Bossart. Pathophysiology of Stress in Wild and Managed-Care Bottlenose Dolphins (Tursiops truncatus). Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada578414.

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