Thematische Bibliographien / Fibrosis

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Auswahl der wissenschaftlichen Literatur zum Thema „Fibrosis“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 16. November 2024

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Zeitschriftenartikel zum Thema "Fibrosis"

Egea-Zorrilla, Alejandro, Zuri馿 Blasco-Iturri, Borja Saez und Ana Pardo-Saganta. „The Notch3 Pathway in Organ Fibrosis“. Fibrosis 2, Nr. 4 (2024): 10007. http://dx.doi.org/10.70322/fibrosis.2024.10007.

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&NA;. „Cystic fibrosis and fibrosing colonopathy“. Advances in Anatomic Pathology 3, Nr. 2 (März 1996): 112. http://dx.doi.org/10.1097/00125480-199603000-00015.

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Smyth, R. L. „Fibrosing colonopathy in cystic fibrosis.“ Archives of Disease in Childhood 74, Nr. 5 (01.05.1996): 464–68. http://dx.doi.org/10.1136/adc.74.5.464.

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Albera, Carlo, Giulia Verri, Federico Sciarrone, Elena Sitia, Mauro Mangiapia und Paolo Solidoro. „Progressive Fibrosing Interstitial Lung Diseases: A Current Perspective“. Biomedicines 9, Nr. 9 (16.09.2021): 1237. http://dx.doi.org/10.3390/biomedicines9091237.

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Interstitial lung diseases (ILDs) are a large and diverse group of rare and chronic respiratory disorders, with idiopathic pulmonary fibrosis (IPF) being the most common and best-studied member. Increasing interest in fibrosis as a therapeutic target and the appreciation that fibrotic mechanisms may be a treatable target of IPF prompted the development and subsequent approval of the antifibrotics, pirfenidone and nintedanib. The management of ILDs has changed considerably following an understanding that IPF and some ILDs share similar disease behavior of progressive fibrosis, termed “progressive fibrosing phenotype”. Indeed, antifibrotic treatment has shown to be beneficial in ILDs characterized by the progressive fibrosing phenotype. This narrative review summarizes current knowledge in the field of progressive fibrosing ILDs. Here, we discuss the clinical characteristics and pathogenesis of lung fibrosis and highlight relevant literature concerning the mechanisms underlying progressive fibrosing ILDs. We also summarize current diagnostic approaches and the available treatments of progressive fibrosing ILDs and address the optimization of treating progressive fibrosing ILDs with antifibrotics in clinical practice.

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Hernandez-Gonzalez, Fernanda, Rosa Faner, Mauricio Rojas, Alvar Agustí, Manuel Serrano und Jacobo Sellarés. „Cellular Senescence in Lung Fibrosis“. International Journal of Molecular Sciences 22, Nr. 13 (29.06.2021): 7012. http://dx.doi.org/10.3390/ijms22137012.

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Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence.

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Waters, Brenda L. „Cystic Fibrosis with Fibrosing Colonopathy in the Absence of Pancreatic Enzymes“. Pediatric and Developmental Pathology 1, Nr. 1 (Januar 1998): 74–78. http://dx.doi.org/10.1007/s100249900009.

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Fibrosing colonopathy, characterized by dense submucosal fibrosis in the large bowel, is a disorder associated with bowel dysfunction in patients with cystic fibrosis who receive pancreatic enzyme supplementation. Most commonly, patients present with a distended abdomen and abdominal pain. Radiographs frequently demonstrate colonic wall thickening and luminal narrowing. Here I describe a neonate with cystic fibrosis who presented with both clinical and histological features of fibrosing colonopathy who had not received pancreatic enzymes. This report expands our understanding of the pathogenesis of fibrosing colonopathy.

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Gibson, Sarah E., Carol F. Farver und Richard A. Prayson. „Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy: An Autopsy Case and Review of the Literature“. Archives of Pathology & Laboratory Medicine 130, Nr. 2 (01.02.2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.

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Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.

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Carrino, David A., Sam Mesiano, Nichole M. Barker, William W. Hurd und Arnold I. Caplan. „Proteoglycans of uterine fibroids and keloid scars: similarity in their proteoglycan composition“. Biochemical Journal 443, Nr. 2 (27.03.2012): 361–68. http://dx.doi.org/10.1042/bj20111996.

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Fibrosis is the formation of excess and abnormal fibrous connective tissue as a result of either a reparative or reactive process. A defining feature of connective tissue is its extracellular matrix, which provides structural support and also influences cellular activity. Two common human conditions that result from fibrosis are uterine fibroids (leiomyomas) and keloid scars. Because these conditions share a number of similarities and because their growth is due primarily to excessive extracellular matrix deposition, we compared the proteoglycans of uterine fibroids and keloid scars with corresponding normal tissues. Our analysis indicates that uterine fibroids and keloid scars contain higher amounts of glycosaminoglycans relative to normal myometrium and normal adult skin respectively. Proteoglycan composition is also different in the fibrotic tissues. Compared with unaffected tissues, uterine fibroids and keloid scars contain higher relative amounts of versican and lower relative amounts of decorin. There is also evidence for a higher level of versican catabolism in the fibrotic tissues compared with unaffected tissues. These qualitative and quantitative proteoglycan differences may play a role in the expansion of these fibroses and in their excessive matrix deposition and matrix disorganization, due to effects on cell proliferation, TGF (transforming growth factor)-β signalling and/or collagen fibril formation.

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Cottin, Vincent, Lutz Wollin, Aryeh Fischer, Manuel Quaresma, Susanne Stowasser und Sergio Harari. „Fibrosing interstitial lung diseases: knowns and unknowns“. European Respiratory Review 28, Nr. 151 (27.02.2019): 180100. http://dx.doi.org/10.1183/16000617.0100-2018.

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Patients with certain types of fibrosing interstitial lung disease (ILD) are at risk of developing a progressive phenotype characterised by self-sustaining fibrosis, decline in lung function, worsening quality of life, and early mortality. It has been proposed that such progressive fibrosing ILDs, which show commonalities in clinical behaviour and in the pathogenetic mechanisms that drive progressive fibrosis, may be “lumped” together for the purposes of clinical research and, potentially, for treatment. At present, no drugs are approved for the treatment of ILDs other than nintedanib and pirfenidone for the treatment of idiopathic pulmonary fibrosis. For other progressive fibrosing ILDs, the mainstay of drug therapy is immunosuppression. However, it is postulated that, once the response to lung injury in fibrosing ILDs has reached the stage at which fibrosis has become progressive and self-sustaining, targeted antifibrotic therapy would be required to slow disease progression. Nintedanib, an intracellular inhibitor of tyrosine kinases, has shown antifibrotic, anti-inflammatory and vascular remodelling effects in several non-clinical models of fibrosis, irrespective of the trigger for the injury. Ongoing clinical trials will provide insight into the role of antifibrotic treatment with nintedanib or pirfenidone in the management of fibrosing ILDs with a progressive phenotype.

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Khan, Khaleque N., Akira Fujishita, Akemi Koshiba, Kanae Ogawa, Taisuke Mori, Hiroshi Ogi, Kyoko Itoh, Satoshi Teramukai und Jo Kitawaki. „Expression profiles of E/P receptors and fibrosis in GnRHa-treated and -untreated women with different uterine leiomyomas“. PLOS ONE 15, Nr. 11 (13.11.2020): e0242246. http://dx.doi.org/10.1371/journal.pone.0242246.

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Differential expressions of estrogen/progesterone receptors (ER/PR) and individual component of extracellular matrices derived from fibroid are reported. Information on the pattern of change in ER/PR expression and amount of tissue fibrosis after hormonal treatment is unclear. We investigated pattern of change in ER/PR expression and percentage of tissue fibrosis in different uterine leiomyomas after gonadotropin-releasing hormone agonist (GnRHa) treatment. Biopsy specimens from fibroids and adjacent myometria were collected after surgery from women with submucosal myoma (SMM, n = 18), intramural myoma (IMM, n = 16) and subserosal myoma (SSM, n = 17). A proportion of women in each group of fibroid underwent treatment with GnRHa for a variable period of 3–6 months. Tissue expression of ER and PR was analyzed by immunohistochemistry. In vitro cell proliferation effect of GnRHa on human umbilical vein endothelial cells (HUVECs) was examined. Distribution of tissue fibrosis was examined by Masson’s trichrome staining with computer-captured image analysis of fibrosis derived from different types of fibroid. PR content was significantly higher than ER in tissues derived from GnRHa-untreated women with SMM and SSM (p = 0.04 for both). Comparing to untreated group, GnRHa-treatment significantly decreased either ER or PR expression in different fibroids. Exogenous treatment with GnRHa dose-dependently decreased proliferation of HUVECs. No significant difference was observed in the percentage of fibrosis in tissues collected from GnRHa-treated and -untreated women with fibroids. The distribution of fibrosis in myoma/myometria and occurrence of fibrosis in perivascular area showed an increasing trend with higher age of the women and with larger size of fibroids. Our findings suggest that despite estrogen dependency, higher PR content in GnRHa-untreated group may indicate a potential role of progesterone in leiomyoma growth. Although GnRHa therapy may shrink fibroids and reduce risk of bleeding during surgery, the occurrence of diffuse tissue fibrosis may impair effective reduction of fibroid size after hormonal treatment.

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Dissertationen zum Thema "Fibrosis"

Enes, Giovana da Silva Tavares 1982. „Fibrose cística = estreitando laços maternos = Cystic fibrosis : strengthening maternal ties“. [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308361.

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Orientador: Antonio Fernando Ribeiro
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A Fibrose Cística é uma doença autossômica recessiva, sistêmica, hereditária, crônica e progressiva e pode levar à morte. São características da doença as secreções mucosas espessas e viscosas que obstrui os ductos das glândulas exócrinas e contribuem para o aparecimento de doença pulmonar obstrutiva crônica, insuficiência pancreática com má digestão e má absorção e conseqüente desnutrição secundária, além de níveis elevados de eletrólitos no suor. Por ser uma doença crônica, ela exige cuidados sistemáticos pela vida toda, e na maioria dos casos quem exerce a função de cuidadora é a mãe. Além de viver uma nova experiência de ser mãe, ela terá que conviver com a frustração dele ser doente.Com este estudo foi possível compreender a relação que mãe e filho doente crônico constroem desde o momento do diagnóstico e conhecimento do tratamento, permeados por sentimentos como culpa e solidão. Assim, essas mães renunciam suas próprias vidas em função do cuidado do filho. Cuidados esse compartilhado com uma equipe de saúde multiprofissional ainda deficitária. Apesar de ter sido avaliado por elas como positivo, as sugestões por melhorias também surgiram: como uma melhor articulação entre os serviços de saúde nos diversos níveis, uma maior divulgação da doença e o aumento do número de dias de atendimento. Outro aspecto importante encontrado foi sobre importância do papel do psicólogo não só na atuação com o paciente e a família durante todo o tratamento; mas também na necessidade de oferecer um espaço para que os profissionais de saúde despreparados pudessem compartilhar suas angústias e frustrações o que reflete diretamente na assistência prestada
Abstract: The Cystic Fibrosis is a disease systemic, hereditary, chronic and progressive and it can lead to the death. There are characteristic of the disease the thick and viscous mucous secretions what it obstructs the ducts of the exocrine glands and contribute to the appearance of chronic obstructive pulmonary disease, pancreatic insufficiency with bad digestion and bad absorption and consequent secondary malnutrition, besides elevated levels of electrolytes in the sweat. Because of being a chronic disease, she demands systematic cares for the life completely, and in most of the cases who plays the function of care is the mother. Besides surviving a new experience of being a mother, she will have to coexist in spite of the fact that his frustration to be doente.Com this study there were possible understood the relation what mother and chronic sick son build from the moment of the diagnosis and knowledge of the treatment, permeated by feelings as fault and solitude. So, these mothers renounce his lives themselves in function of the care of the son. Taken care this shared one with a team of still deficient multiprofessional health. In spite of having been valued by them like positive, the suggestions for improvements also appeared: like a better articulation between the health services in several levels, a bigger spread of the disease and the increase of the number of service days. Another considered important aspect was on importance of the paper of the psychologist not alone in the acting with the patient and the family during the whole treatment; but also in the necessity of offering a space so that the unprepared health professionals could share his anguishes and frustrations what thinks straightly about the given presence
Mestrado
Saude da Criança e do Adolescente
Mestre em Ciências

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Yi, Hao. „The Effect of Metformin on Inflammatory and Fibrotic Responses in Renal Fibrosis“. Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21855.

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Chronic kidney disease (CKD) is a worldwide public health problem, with adverse outcomes of kidney failure, cardiovascular disease, and premature death. It is well recognised that renal fibrosis is the unifying pathology in almost all forms of progressive CKD. To date, kidney transplantation and dialysis are the only options for the management of end-stage kidney disease, which results in a significant burden on the health system. Hence innovative strategies are needed to both prevent and treat CKD. It is well recognised that inflammatory pathways play a central role in the progression of CKD and TGFβ-1 is a profibrotic cytokine found in CKD regardless of aetiology, which initiates and modulates a variety of pathophysiological processes. In renal disease, TGFβ-1 is upregulated and induces renal cells to produce extracellular matrix proteins leading to glomerulosclerosis as well as tubulointerstitial fibrosis. Different types of renal cells undergo different pathophysiological changes induced by TGF-β1, leading to apoptosis, hypertrophy and abnormalities of podocyte foot processes, which ultimately result in renal dysfunction. Regardless of the cause of CKD, multiple cytokines, growth factors, pro-inflammatory and fibrotic signalling pathways participate in the development of the pathological process in the kidney. Excessive deposition of extracellular matrix (ECM) is the most striking and common feature of renal fibrosis. Hence, targeting inflammatory and fibrotic responses, and ECM deposition, holds promise to limit fibrosis. Metformin, a biguanide, is a widely used drug in the treatment of type 2 diabetes mellitus (T2DM). It has been well-reviewed that metformin plays an important role in limiting cardiac and vascular fibrosis. Increasing evidence studies indicates metformin may be protective in renal fibrosis. However, the exact mechanisms of protection in renal injury are not fully understood or experimentally investigated. Thus, I initially examined the effect of metformin in TGFβ-1 induced fibrosis in human proximal tubular cells line (HK2 cells). Therefore, I further examined the effect of metformin on renal fibrosis in two mouse models of acute kidney injury (AKI; Folic Acid model (FA)) and chronic kidney injury (CKI, Adenine model). The studies have shown that metformin inhibited monocyte chemoattractant protein-1 (MCP-1) expression and TGFβ-1 signalling pathways in kidney proximal tubular cells exposed to TGFβ-1 by reducing mRNA, protein levels or phosphorylation of signalling molecules of non-Smad and Smad signalling pathways. Metformin also inhibited TGFβ-1 induced extracellular matrix deposition by reducing the expression of fibronectin and collagen IV in kidney proximal tubular cells exposed to TGF-β1. In animal studies, the acute phase of renal fibrosis was successfully established by giving folic acid via intraperitoneal injection, and then the antifibrotic effect of metformin was assessed by administering animals metformin or control for 14 days. The acute renal fibrosis mice model was successfully established by given adenine via gavage, and then treated with or without metformin for 14 days. The in vivo data has shown that folic acid induced impairment of renal function and the overexpression of fibronectin and collagen IV and inflammatory molecular MCP-1, F4/80 and intercellular adhesion molecule-1 (ICAM1) in kidneys compared to control groups; and the impaired renal function and inflammatory and fibrotic response were at least partially attenuated by metformin treatment. The chronic renal fibrosis mice model was successfully established by giving adenine through gavage daily and treatment with or without metformin for 21 days. The data showed that adenine induced renal dysfunction and the overexpression of fibronectin and collagen IV and inflammatory molecular MCP-1, F4/80 and ICAM in kidneys compared to control groups. Renal dysfunction and the inflammatory and fibrotic responses were reversed by metformin treatment. Collectively, these results suggest that metformin may have potential therapeutic value for the treatment of renal fibrosis independent of the cause of CKD.

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Correia, Cyntia Arivabeni de Araujo. „Estudo dos genes TNF alfa, ADIPOQ e STATH entre portadores de fibrose cistica“. [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308583.

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Orientador: Carmen Silvia Bertuzzo
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A Fibrose Cística (FC) possui uma grande variabilidade de expressão fenotípica, o que significa que crianças com o mesmo genótipo podem diferir quanto à sua apresentação. A proteína defeituosa formada é chamada CFTR (proteína reguladora da conductância iônica), causa transporte anormal de sódio e cloro através da membrana apical das células epiteliais das vias aéreas, pâncreas, intestino e aparelho reprodutor. Essa proteína é codificada por um único gene que recebe o mesmo nome da proteína, CFTR, e localiza-se no braço longo do cromossomo 7, região 7q3.1. Gêmeos monozigóticos apresentam maior concordância em relação à gravidade da doença pulmonar que os dizigóticos, sugerindo que a FC seja modulada por fatores genéticos secundários - genes modificadores - além do gene CFTR. A característica mais importante na FC é a sobrevida que é influenciada pela doença pulmonar. Portanto, genes que estejam envolvidos na imunidade, inflamação, reparação do epitélio e produção de muco são candidatos a genes modificadores da doença. Os objetivos foram: 1) determinar a prevalência dos polimorfismos -308G/A e -238G/A do gene TNF a entre portadores de FC e verificar existência de associação entre esses polimorfismos e a gravidade do quadro pulmonar, 2) identificar alterações de sequencia nos exons e junções exon/ intron dos genes ADIPOQ e STATH e verificar existência de associação entre possíveis variações nesses genes e a gravidade da FC. Foi realizada PCR seguida por digestão enzimática para o polimorfismo -308G/A do gene TNF a, reação em cadeia da polimerase ARMS para o polimorfismo -238G/A do gene TNF a, e para os genes ADIPOQ e STATH foi feita a triagem de mutações através de cromatografia líquida de alta resolução por desnaturação - DHPLC com posterior sequenciamento da região onde foi encontrada alteração. Foram analisados 49 pacientes com FC em seguimento no Ambulatório de Mucoviscidose do HC/UNICAMP, homozigotos para a mutação F508 ou heterozigotos compostos para mutações de classe I ou II ou homozigotos para mutações de classe II, que são alterações que não levam à formação de proteína funcional. Além disso, foram selecionados indivíduos que apresentem alteração de eletrólitos no suor. Para o polimorfismo -308G/A do gene TNFa os genótipos GG, AA e GA foram encontrados com as seguintes frequencias: 14,28, 67,35 e 18,36% respectivamente. Estes dados se opõem ao relatado na literatura. Tal diferença deve ocorrer pelas características populacionais da população brasileira. Para o polimorfismo -238G/A do gene TNFa, os genótipos GG e AG tiveram as seguintes frequencias: 79,59 e 20,41% respectivamente. O genótipo AA não foi encontrado na amostra analisada. A alta frequencia do genótipo GG comparado com o AA, concorda com a literatura. Não foi encontrada alteração na sequencia dos genes STATH e ADIPOQ. Não foi possível estabelecer uma associação entre a gravidade da FC e os genes TNFa, STATH e ADIPOQ, nas regiões analisadas.
Abstract: Cystic Fibrosis (CF) has a great variety expression, which means that the seriousness of the disease can vary a lot among people who have it. The defective protein, called CFTR (Cystic Fibrosis Transmenbrane Regulator), causes abnormal transportation of chloride and sodium through the apical membrane of the epithelial cells of the airway, liver, intestine and masculine reproductive tract. This protein is encoded by a single gene which has the same name, CFTR, and is located within the long arm of chromosome 7, region 7q3.1. CF is a disease which expressivity is much variable, with different degrees of damage and the age when the symptoms begins is also much variable, even within individuals of the same family, like twins. Because of it, it is been said that others genetic factors besides CFTR, can be modulating the clinical presentation. As the pulmonary state is the great responsible for the mortality of the disease genes that are involved in host defense, inflammation, epithelial repair, mucin production, and airway reponsiveness are of great interest. Base on this the objectives of this work were: determine the prevalence of the polymorphisms -308G/A e -238G/A from the TNF a gene and verify if there is an association between these polymorphisms pulmonary disease severity, and identify alterations on ADIPOQ and STATH genes and verify if there is an association between these polymorphisms and CF severity. PCR followed by restriction enzyme digestion was performed to detect the polymorphism -308G/A from the TNF a gene, ARMS PCR to the polymorphism -238G/A from the TNF a gene the DHPLC method associated to the sequencing to analyze ADIPOQ and STATH genes, were used. We performed analyses of 49 cystic fibrosis patients that are followed in a Cystic Fibrosis center from HC/UNICAMP, that are \F508 homozygous or compound heterozygous to mutations from class I or II, or that are homozygous to class II mutations, which are alterations that do not produce functional protein. Besides this, were selected individuals that have sweat test altered. To the polymorphism 308G/A from TNFa gene the genotypes GG, AA e AG were in the following frequencies: 14,28, 67,35 e 18,36%. This data is contradictory to the literature and may occur because of the racial admixture of the Brazilian population. To the polymorphism -238G/A from TNFa gene, the genotypes GG AG were in the following frequencies 79,59 e 20,41%. The genotype AA was not found in the analyzed group. The high frequency of the genotype GG is in agreement of the data. It was not possible to find any alteration on ADIPOQ and STATH genes. And also it was not possible to make any correlation between the severity of the CF disease and the genes TNFa, STATH and ADIPOQ between the analyzed regions.
Doutorado
Ciencias Biomedicas
Doutor em Ciências Médicas

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Chadwick, Helen Kay. „Cognitive function in cystic fibrosis and cystic fibrosis related diabetes (CFRD)“. Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/16912/.

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Cystic fibrosis (CF) is a complex multisystem disease caused by a gene mutation of a protein called the CF Transmembrane Conductance Regulator (CFTR). Glucose tolerance abnormalities are common in CF and the prevalence of CF related diabetes (CFRD), which shares clinical characteristics with type 1 (T1DM) and type 2 diabetes (T2DM), increases with age. Impaired glucose tolerance (IGT), T1DM and T2DM are associated with cognitive impairment relative to healthy controls. The overall aim of this thesis was to examine cognitive function in CF. Study 1 investigated the impact of CF on cognitive function, in people with CFRD (n=49), people with CF who are not diabetic (CFND, n=49) and healthy controls (n=49). Memory, attention and processing speed, and cognitive flexibility was impaired in CFRD, and to a lesser degree in CFND, relative to healthy controls. Study 2 assessed cognitive function over a 1-3 year period in people with CFRD (N=36) and found no evidence of cognitive decline despite a decline in lung function. Study 3 compared cognitive function in people with CFRD who were post transplant (CFRDTx, n=18), people with CFRD (who were not post transplant, n=18), and healthy controls (n=18). CFRD was associated with impairment in attention and processing speed, spatial working memory, cognitive flexibility and to a lesser extent verbal memory. Cognitive function did not improve post transplantation in people with CFRD. Study 4 followed up people with CFRDTx (N=8) over an 18±6 month period and found no decline in cognitive function. Taken together, the evidence presented in this thesis suggests that diabetes in CF is associated with cognitive impairment, and that maintaining glycaemic control protects against cognitive decline. The cognitive impairment observed in people with CF is of clinical significance and has implications for self care and disease management. The recent discovery that CFTR is present in the pancreas and the brain has important implications for the effects of the new CFTR potentiator and corrector therapies on cognitive function in CF.

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Karlas, Thomas, Joachim Berger, Nikita Garnov, Franziska Lindner, Harald Busse, Nicolas Linder, Alexander Schaudinn et al. „Estimating steatosis and fibrosis“. Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-169692.

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Katre, Ashwini A. „Ozone and lung fibrosis“. Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009m/katre.pdf.

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Kahre, Tiina. „Cystic fibrosis in Estonia /“. Online version, 2004. http://dspace.utlib.ee/dspace/bitstream/10062/577/5/KahrePhD.pdf.

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Dwyer, Tiffany Jane. „Exercise in cystic fibrosis“. Thesis, The University of Sydney, 2010. http://hdl.handle.net/2123/6349.

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Exercise and physical activity have many benefits for adults with cystic fibrosis (CF), including the potential to aid mucus clearance, improve lung function, exercise capacity and quality of life. Despite the recommendations from consensus documents for CF adults to engage in regular physical activity, exercise participation amongst this population is often very low. No in-depth study has been undertaken to explore the determinants of exercise participation for this group and no studies have examined the benefits of habitual physical activity on the health status and quality of life of CF adults. As well, the current methods to quantify physical activity are problematic. The series of studies, involving CF adults, in this thesis was therefore undertaken in order to examine the physiological rationale for the use of exercise as an airway clearance technique, to understand the decision making process to engage in exercise, to determine if health status and quality of life were affected by exercise participation, and to establish the accuracy of a recently-developed objective measure of physical activity. The study in Chapter 2 provided some physiological rationale for choosing treadmill exercise to aid airway clearance in CF. The main findings were that a single bout of moderate intensity exercise increased the subjective ease of expectoration, most likely due to the increased ventilation with exercise, and that sputum viscoelasticity was favourably decreased immediately following treadmill exercise compared to cycle exercise and control. The studies in Chapters 3 and 4 identified the main beliefs regarding exercise for CF adults and highlighted that the main predictors of exercise intention and participation for this group were aspects of perceived and actual control to exercise, namely self-efficacy or confidence to exercise, feeling healthy, receiving encouragement to exercise, and rating exercise as a high priority treatment. Positive ratings of these aspects of control either increased exercise participation directly, indirectly by increasing intention, or strengthened the conversion of exercise intention to participation. Strategies aimed at targeting these aspects of control are therefore likely to be effective in increasing exercise participation for CF adults. The study in Chapter 5 demonstrated that CF adults, who reportedly performed at least 90 minutes of moderate to strenuous exercise per week, had significantly higher quality of life and fewer days in hospital over the following year than their peers, who exercised less. The difference in hospitalisation between the CF adults, who reportedly exercised more than 90 minutes per week and those who did not, was independent of baseline lung function, and the females who reportedly performed less than 90 minutes of exercise per week had three times as many days in hospital than their high-activity peers. The study in Chapter 6 showed that the SenseWear Pro3 Armband activity monitor provided a reasonable estimate of energy expenditure and step count. Also, its accuracy was not affected by diagnosis with CF, despite the potential for the high salt content in the sweat to interfere with the device’s physiological sensors placed on the skin. Overall, this series of studies adds to the growing evidence of the physical and psychological benefits from exercise participation for CF adults, as well as providing some empirical evidence upon which to base strategies to improve exercise participation for this group and support for an objective measure of physical activity.

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Dwyer, Tiffany Jane. „Exercise in cystic fibrosis“. Discipline of Physiotherapy, Faculty of Health Sciences, University of Sydney, 2010. http://hdl.handle.net/2123/6349.

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Doctor of Philosophy (PhD)
Exercise and physical activity have many benefits for adults with cystic fibrosis (CF), including the potential to aid mucus clearance, improve lung function, exercise capacity and quality of life. Despite the recommendations from consensus documents for CF adults to engage in regular physical activity, exercise participation amongst this population is often very low. No in-depth study has been undertaken to explore the determinants of exercise participation for this group and no studies have examined the benefits of habitual physical activity on the health status and quality of life of CF adults. As well, the current methods to quantify physical activity are problematic. The series of studies, involving CF adults, in this thesis was therefore undertaken in order to examine the physiological rationale for the use of exercise as an airway clearance technique, to understand the decision making process to engage in exercise, to determine if health status and quality of life were affected by exercise participation, and to establish the accuracy of a recently-developed objective measure of physical activity. The study in Chapter 2 provided some physiological rationale for choosing treadmill exercise to aid airway clearance in CF. The main findings were that a single bout of moderate intensity exercise increased the subjective ease of expectoration, most likely due to the increased ventilation with exercise, and that sputum viscoelasticity was favourably decreased immediately following treadmill exercise compared to cycle exercise and control. The studies in Chapters 3 and 4 identified the main beliefs regarding exercise for CF adults and highlighted that the main predictors of exercise intention and participation for this group were aspects of perceived and actual control to exercise, namely self-efficacy or confidence to exercise, feeling healthy, receiving encouragement to exercise, and rating exercise as a high priority treatment. Positive ratings of these aspects of control either increased exercise participation directly, indirectly by increasing intention, or strengthened the conversion of exercise intention to participation. Strategies aimed at targeting these aspects of control are therefore likely to be effective in increasing exercise participation for CF adults. The study in Chapter 5 demonstrated that CF adults, who reportedly performed at least 90 minutes of moderate to strenuous exercise per week, had significantly higher quality of life and fewer days in hospital over the following year than their peers, who exercised less. The difference in hospitalisation between the CF adults, who reportedly exercised more than 90 minutes per week and those who did not, was independent of baseline lung function, and the females who reportedly performed less than 90 minutes of exercise per week had three times as many days in hospital than their high-activity peers. The study in Chapter 6 showed that the SenseWear Pro3 Armband activity monitor provided a reasonable estimate of energy expenditure and step count. Also, its accuracy was not affected by diagnosis with CF, despite the potential for the high salt content in the sweat to interfere with the device’s physiological sensors placed on the skin. Overall, this series of studies adds to the growing evidence of the physical and psychological benefits from exercise participation for CF adults, as well as providing some empirical evidence upon which to base strategies to improve exercise participation for this group and support for an objective measure of physical activity.

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Utley, Courtney, und Kristen L. McHenry. „Advances in Cystic Fibrosis“. Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/2546.

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The purpose of this review was to identify the history of and advances in cystic fibrosis (CF). New treatment plans, medication developments, and a historical perspective of airway clearance therapy (ACT) will be presented. The importance of treatment compliance and time management in the care of cystic fibrosis patients will also be discussed. Furthermore, the development of cystic fibrosis clinics and the pivotal role they play in the treatment of the disease will be addressed. Lastly, a brief discussion concerning the need for and process of lung transplantation will be reported.

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Bücher zum Thema "Fibrosis"

Rittié, Laure, Hrsg. Fibrosis. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8.

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David, Evered, Whelan Julie, Ciba Foundation und Symposium on Fibrosis (1984 : Ciba Foundation), Hrsg. Fibrosis. London: Pitman, 1985.

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Symposium on Fibrosis (1984 : London), Hrsg. Fibrosis. London: Pitman, 1985.

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Symposium, Ciba Foundation. Fibrosis. London: Pitman, 1985.

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Varga, John, David A. Brenner und Sem H. Phan, Hrsg. Fibrosis Research. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1592599400.

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Silverstein, Alvin. Cystic fibrosis. New York: F. Watts, 1994.

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Davis, Stephanie Duggins, Margaret Rosenfeld und James Chmiel, Hrsg. Cystic Fibrosis. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42382-7.

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Moss, Richard B., Hrsg. Cystic Fibrosis. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-0475-6.

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Amaral, Margarida D., und Karl Kunzelmann, Hrsg. Cystic Fibrosis. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-117-8.

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Amaral, Margarida D., und Karl Kunzelmann, Hrsg. Cystic Fibrosis. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-120-8.

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Buchteile zum Thema "Fibrosis"

Bährle-Rapp, Marina. „Fibrose, auch: Fibrosis“. In Springer Lexikon Kosmetik und Körperpflege, 206. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_3985.

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Rosenbloom, Joel, Edward Macarak, Sonsoles Piera-Velazquez und Sergio A. Jimenez. „Human Fibrotic Diseases: Current Challenges in Fibrosis Research“. In Fibrosis, 1–23. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_1.

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Li, Ian M. H., Amy L. Horwell, Grace Chu, Benoit de Crombrugghe und George Bou-Gharios. „Characterization of Mesenchymal-Fibroblast Cells Using the Col1a2 Promoter/Enhancer“. In Fibrosis, 139–61. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_10.

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Weiskirchen, Sabine, Carmen G. Tag, Sibille Sauer-Lehnen, Frank Tacke und Ralf Weiskirchen. „Isolation and Culture of Primary Murine Hepatic Stellate Cells“. In Fibrosis, 165–91. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_11.

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Liew, Lawrence J., Huan Ting Ong und Rodney J. Dilley. „Isolation and Culture of Adipose-Derived Stromal Cells from Subcutaneous Fat“. In Fibrosis, 193–203. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_12.

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Leavitt, Tripp, Michael S. Hu und Michael T. Longaker. „Isolation of Live Fibroblasts by Fluorescence-Activated Cell Sorting“. In Fibrosis, 205–12. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_13.

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Puebla-Osorio, Nahum, Seri N. E. Sarchio, Stephen E. Ullrich und Scott N. Byrne. „Detection of Infiltrating Mast Cells Using a Modified Toluidine Blue Staining“. In Fibrosis, 213–22. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_14.

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Eckes, Beate, Fang Wang, Laure Rittié, Gabriele Scherr und Paola Zigrino. „Cell-Populated Collagen Lattice Models“. In Fibrosis, 223–33. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_15.

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Xie, Tianfa, Jamar Hawkins und Yubing Sun. „Traction Force Measurement Using Deformable Microposts“. In Fibrosis, 235–44. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_16.

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Worthen, Christal A., Laure Rittié und Gary J. Fisher. „Mechanical Deformation of Cultured Cells with Hydrogels“. In Fibrosis, 245–51. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_17.

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Konferenzberichte zum Thema "Fibrosis"

Holmes, Hal, Eli Vlaisavljevich, Ee Lim Tan, Keat G. Ong und Rupak M. Rajachar. „Magnetoelastic Materials as Novel Bioactive Coatings to Improve Integration of Percutaneous Implants“. In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53308.

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Fibroblastic activity is an innate function of the host response. In the presence of many percutaneous biomedical implants, this activity becomes uncontrollable, resulting in significant fibrous overgrowth at the soft tissue-implant interface [1]. The aberrant cell growth associated with pathological fibrosis can lead to extensive remodeling and excessive synthesis of extracellular matrix (ECM) components, preventing proper integration [2]. Furthermore, these areas of irregular fibrotic activity can also serve as sites for opportunistic infection [3]. In brief, interfacial fibrosis is often responsible for the ultimate failure and increased risk of infection of percutaneous biomedical implants.

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Torres Rojas, Aimee M., und Sylvie Lorente. „Vascular Model of Liver Fibrosis“. In ASME 2023 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2023. http://dx.doi.org/10.1115/imece2023-112123.

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Abstract The liver has a very peculiar blood circulatory system composed of two blood supply vascular trees (the hepatic artery and portal venous networks), microcirculation through small functional units called lobules, and a blood drainage vascular tree (the hepatic vein network). In the healthy liver, flow resistance at the microcirculation level is very low and the portal pressure is almost the same as the lobules pressure. On the other hand, vasculature changes due to fibrosis — located predominantly at the lobules level — lead to a marked increase in resistance to flow causing an increase in portal pressure (portal hypertension). Here, a rigid model of the entire liver vasculature is built, where hepatic networks are considered as tree-like fluidic networks and lobules as a porous medium. The model can provide the blood flow and pressure within their healthy physiological ranges at all points of the vasculature. To simulate liver fibrosis, the portal hypertension it causes is reproduced. The high portal pressure values reported for fibrotic patients are used to calculate the necessary lobules permeability resulting in these pressure values at the inlet of the lobules. The decrease in the permeability of the fibrotic lobules causes a redistribution of flow between the two blood supply networks. The alterations of microcirculation due to fibrosis are also analyzed: increases in blood flow through the non-fibrotic lobules and decreases in blood flow through the fibrotic ones are observed, relative to blood flow through the lobules in a healthy liver.

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Sewell-Loftin, M. K., und W. David Merryman. „The Role of SRC in Strain- and Ligand- Dependent Phenotypic Modulation of Mouse Embryonic Fibroblasts“. In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53604.

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Connective tissue fibrosis represents a significant portion of mortality and morbidity in our society. These diseases include many illnesses such as heart valve disease, atherosclerosis, macular degeneration, and cirrhosis, meaning that millions of lives are affected by these conditions each year. Fibrotic tissues form when quiescent fibroblasts activate becoming myofibroblasts, the phenotype of active tissue construction and fibrosis. During this process, the cells produce smooth muscle α-actin (αSMA), a contractile element considered to be the hallmark of cellular activation [1]. Following the production of αSMA, there is an increase in the synthesis of extracellular matrix (ECM) proteins, most notably type I collagen; this increase in ECM proteins causes the stiffening of the tissue characteristic of fibrotic disease. In non-disease states (such as wound healing or tissue development), the myofibroblasts will either deactivate, becoming fibroblasts again, or apoptose before tissue fibrosis occurs. However, when myofibroblasts persist, increased ECM protein deposition causes increased tissue stiffness and activates neighboring cells, causing the fibrosis to propagate. Currently there are no therapies to prevent or reverse fibrosis. Therefore a more thorough understanding of the dynamic mechanical environment and signaling pathways involved in the activation of fibroblasts is required to develop potential treatments.

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Škrbic, Dusan, Mirna Djuric, Jelena Papovic und Branislav Tusek. „COVID-19 vaccine and morbidity in the Adult Cystic Fibrosis Centre in Institute for Pulmonary Diseases of Vojvodina Sremska Kamenica, Serbia“. In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.47.

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Petrova, Guergana, Mila Baycheva, Dimitrinka Miteva, Vera Papochieva, Margarita Nikolova, Miglena Georgieva, Nadezhda Yaneva und Savov Alexey. „Late diagnosed homozygous delF508 patients - is it really rare?“ In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.2.

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Remus, Natascha, Gaetan Leignadier, Elisa Thomas, Celine Delestrain, Michael Shum, Bernard Maitre, Ralph Epaud und Benoit Douvry. „The A-Step - a new incremental exercise test defying space and infection control measures“. In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.17.

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Duplacie, Nele, Trudy Havermans, Janne Houben, Marianne Schulte, Linda Boulanger, Laura Moyens, Cindy Ruelens und Lieven Dupont. „Side-effects and ETI-treatment: a multidisciplinary challenge“. In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.37.

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Daniels, Tanne, Kristel Van Calsteren und Lieven Dupont. „Maternal and obstetric outcomes in women with cystic fibrosis: a retrospective case series of patients in UZ Leuven“. In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.31.

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Skogeland, Ulrika, Anna Hedborg, Cecilia Rodriguez, Adrienn Bánki und Tove Godskesen. „Adherence to medical regimens after lung transplantation among adults with Cystic Fibrosis increased during COVID-19 pandemic“. In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.4.

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Asir, Nadine, Noor Al-Sulaiti, Abdusamea Shabani und Atqah Abdul Wahab. „First case of pott's disease in a cystic fibrosis adolescent with a homozygous CFTR mutation c.3700 A > G (p. Ile1234Val)“. In Adult Cystic Fibrosis Conference abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.acf-2023.29.

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Berichte der Organisationen zum Thema "Fibrosis"

Liu, Xiaopei, Dan Liu und Cong’e Tan. Gut microbiome-based machine learning for diagnostic prediction of liver fibrosis and cirrhosis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, Mai 2022. http://dx.doi.org/10.37766/inplasy2022.5.0133.

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Review question / Objective: The invasive liver biopsy is the gold standard for the diagnosis of liver cirrhosis. Other non-invasive diagnostic approaches, have been used as alternatives to liver biopsy, however, these methods cannot identify the pathological grade of the lesion. Recently, studies have shown that gut microbiome-based machine learning can be used as a non-invasive diagnostic approach for liver cirrhosis or fibrosis, while it lacks evidence-based support. Therefore, we performed this systematic review and meta-analysis to evaluate its predictive diagnostic value in liver cirrhosis or fibrosis. Condition being studied: Liver fibrosis and cirrhosis. Liver fibrosis refers to excessive deposition of liver fibrous tissue caused by various pathogenic factors, such as hepatitis virus, alcohol, and drug-induced chemical injury. Continuous progression of liver fibrosis can lead to liver cirrhosis.

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Hadsall, Katie. Genetic aspects of Pulmonary Fibrosis. Ames (Iowa): Iowa State University, Januar 2020. http://dx.doi.org/10.31274/cc-20240624-784.

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Hua, Zi Bo, und Lv Yuan Chen. Human UCB MSC versus placebo for effect on kidney fibrosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, Oktober 2022. http://dx.doi.org/10.37766/inplasy2022.10.0104.

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Review question / Objective: Human UCB MSC versus placebo for effect on kidney fibrosis Condition being studied: Renal fibrosis is the final outcome of long-term chronic kidney disease, and the kidney will lose its basic function. This experiment will explore the effect of Human UCB MSC for effect on kidney fibrosis. Main outcome(s): Correlation analysis of Human UCB MSC treatment on renalfibrosis.

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Agarwal, Sandeep K. Cadherin-11 Regulation of Fibrosis through Modulation of Epithelial-to-Mesenchymal Transition: Implications for Pulmonary Fibrosis in Scleroderma. Fort Belvoir, VA: Defense Technical Information Center, Oktober 2013. http://dx.doi.org/10.21236/ada591380.

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Barros-Poblete, Marisol, Rodrigo Torres-Castro, Mauricio Henríquez, Anita Guequen, Isabel Blanco und Carlos Flores. Dysbiosis as a prognostic factor for clinical worsening in chronic respiratory disease: A systematic review and metanalysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0089.

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Review question / Objective: Is dysbiosis a prognostic factor for clinical worsening in patients with chronic respiratory diseases?. Condition being studied: Dysbiosis, defined as changes in the quantitative and qualitative composition of the microbiota. Eligibility criteria: Over 18 years old adult patients with chronic respiratory diseases clinical diagnosis (cystic fibrosis, chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, interstitial lung disease, sarcoidosis, bronchiectasis, non-CF bronchiectasis, pulmonary hypertension) according to the International Statistical Classification of Diseases and Related Health Problems (ICD) from OMS) and international guidelines of each disease.

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Artlett, Carol M. The Modulation of Fibrosis in Scleroderma by 3-Deoxyglucosone. Fort Belvoir, VA: Defense Technical Information Center, Juni 2008. http://dx.doi.org/10.21236/ada485008.

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Artlett, Carol M. The Modulation of Fibrosis in Scleroderma by 3-Deoxyglucosone. Fort Belvoir, VA: Defense Technical Information Center, Juni 2010. http://dx.doi.org/10.21236/ada541210.

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Artlett, Carol M. The Modulation of Fibrosis in Scleroderma by 3-deoxyglucosone. Fort Belvoir, VA: Defense Technical Information Center, Juni 2009. http://dx.doi.org/10.21236/ada510087.

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Garber, Alan, und Joseph Fenerty. Costs and Benefits of Prenatal Screening For Cystic Fibrosis. Cambridge, MA: National Bureau of Economic Research, Oktober 1988. http://dx.doi.org/10.3386/w2749.

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