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Статті в журналах з теми "Lungs Pathophysiology":

1
Reddy, R. Chandramouli, Basavaraj Devaranavadagi, and Kusal K. Das. "Nickel Induced Alteration of Pathophysiology of Lungs in Experimental Rats." Indian Journal of Public Health Research & Development 10, no. 8 (2019): 145. http://dx.doi.org/10.5958/0976-5506.2019.01867.9.
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2
Das, Mita, W. Michael Zawada, James West, and Kurt R. Stenmark. "JNK2 regulates vascular remodeling in pulmonary hypertension." Pulmonary Circulation 8, no. 3 (May 2018): 204589401877815. http://dx.doi.org/10.1177/2045894018778156.
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Pulmonary arterial (PA) wall modifications are key pathological features of pulmonary hypertension (PH). Although such abnormalities correlate with heightened phosphorylation of c-Jun N-terminal kinases 1/2 (JNK1/2) in a rat model of PH, the contribution of specific JNK isoforms to the pathophysiology of PH is unknown. Hence, we hypothesized that activation of either one, or both JNK isoforms regulates PA remodeling in PH. We detected increased JNK1/2 phosphorylation in the thickened vessels of PH patients’ lungs compared to that in lungs of healthy individuals. JNK1/2 phosphorylation paralleled a marked reduction in MAP kinase phosphatase 1 (JNK dephosphorylator) expression in patients’ lungs. Association of JNK1/2 activation with vascular modification was confirmed in the calf model of severe hypoxia-induced PH. To ascertain the role of each JNK isoform in pathophysiology of PH, wild-type (WT), JNK1 null (JNK1-/-), and JNK2 null (JNK2-/-) mice were exposed to chronic hypoxia (10% O2 for six weeks) to develop PH. In hypoxic WT lungs, an increase in JNK1/2 phosphorylation was associated with PH-like pathology. Hallmarks of PH pathophysiology, i.e. excessive accumulation of extracellular matrix and vessel muscularization with medial wall thickening, was also detected in hypoxic JNK1-/- lungs, but not in hypoxia-exposed JNK2-/- lungs. However, hypoxia-induced increases in right ventricular systolic pressure (RVSP) and in right ventricular hypertrophy (RVH) were similar in all three genotypes. Our findings suggest that JNK2 participates in PA remodeling (but likely not in vasoconstriction) in murine hypoxic PH and that modulating JNK2 actions might quell vascular abnormalities and limit the course of PH.
3
Sundar, Isaac K., Hongwei Yao, Michael T. Sellix, and Irfan Rahman. "Circadian molecular clock in lung pathophysiology." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 10 (November 2015): L1056—L1075. http://dx.doi.org/10.1152/ajplung.00152.2015.
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Disrupted daily or circadian rhythms of lung function and inflammatory responses are common features of chronic airway diseases. At the molecular level these circadian rhythms depend on the activity of an autoregulatory feedback loop oscillator of clock gene transcription factors, including the BMAL1:CLOCK activator complex and the repressors PERIOD and CRYPTOCHROME. The key nuclear receptors and transcription factors REV-ERBα and RORα regulate Bmal1 expression and provide stability to the oscillator. Circadian clock dysfunction is implicated in both immune and inflammatory responses to environmental, inflammatory, and infectious agents. Molecular clock function is altered by exposomes, tobacco smoke, lipopolysaccharide, hyperoxia, allergens, bleomycin, as well as bacterial and viral infections. The deacetylase Sirtuin 1 (SIRT1) regulates the timing of the clock through acetylation of BMAL1 and PER2 and controls the clock-dependent functions, which can also be affected by environmental stressors. Environmental agents and redox modulation may alter the levels of REV-ERBα and RORα in lung tissue in association with a heightened DNA damage response, cellular senescence, and inflammation. A reciprocal relationship exists between the molecular clock and immune/inflammatory responses in the lungs. Molecular clock function in lung cells may be used as a biomarker of disease severity and exacerbations or for assessing the efficacy of chronotherapy for disease management. Here, we provide a comprehensive overview of clock-controlled cellular and molecular functions in the lungs and highlight the repercussions of clock disruption on the pathophysiology of chronic airway diseases and their exacerbations. Furthermore, we highlight the potential for the molecular clock as a novel chronopharmacological target for the management of lung pathophysiology.
4
Bland, Richard D. "Pathophysiology of Neonatal Lung Injury." International Journal of Technology Assessment in Health Care 7, S1 (January 1991): 56–60. http://dx.doi.org/10.1017/s0266462300012514.
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Respiratory distress in newborn and young infants often develops as a result of acute lung injury, in which disruption of the normal barrier function of the pulmonary endothelium and epithelium causes protein-rich interstitial and alveolar edema. Several conditions may initiate acute lung injury, including aspiration of meconium or gastric contents, bacterial or viral infection, overzealous resuscitation, and birth associated with incomplete lung development that requires ventilatory support with positivepressure mechanical ventilation and high concentrations of inspired oxygen. The latter condition usually occurs after premature birth, but it also may occur as a consequence of impaired fetal lung growth secondary to diaphragmatic hernia or chest compression from lack of liquid in the amniotic cavity. Acute lung injury sometimes progresses to a chronic form of lung disease, which is characterized by edema, fibrosis, airway distortion, and nonuniform inflation of the lungs.
5
Arrigo, Mattia, Lars Christian Huber, Stephan Winnik, Fran Mikulicic, Federica Guidetti, Michelle Frank, Andreas J. Flammer, and Frank Ruschitzka. "Right Ventricular Failure: Pathophysiology, Diagnosis and Treatment." Cardiac Failure Review 5, no. 3 (November 2019): 140–46. http://dx.doi.org/10.15420/cfr.2019.15.2.
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The prognostic significance of the right ventricle (RV) has recently been recognised in several conditions, primarily those involving the left ventricle, the lungs and their vascular bed, or the right-sided chambers. Recent advances in imaging techniques have created new opportunities to study RV anatomy, physiology and pathophysiology, and contemporary research efforts have opened the doors to new treatment possibilities. Nevertheless, the treatment of RV failure remains challenging. Optimal management should consider the anatomical and physiological particularities of the RV and include appropriate imaging techniques to understand the underlying pathophysiological mechanisms. Treatment should include rapid optimisation of volume status, restoration of perfusion pressure and improvement of myocardial contractility and rhythm, and, in case of refractory RV failure, mechanical circulatory support.
6
Lindholm, Peter, and Claes EG Lundgren. "The physiology and pathophysiology of human breath-hold diving." Journal of Applied Physiology 106, no. 1 (January 2009): 284–92. http://dx.doi.org/10.1152/japplphysiol.90991.2008.
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This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hemorrhage postdive. However, a remarkable, and so far poorly understood, variation in individual disposition for such problems exists. Mortality connected with breath-hold diving is primarily concentrated to less well-trained recreational divers and competitive spearfishermen who fall victim to hypoxia. Particularly vulnerable are probably also individuals with preexisting cardiac problems and possibly, essentially healthy divers who may have suffered severe alternobaric vertigo as a complication to inadequate pressure equilibration of the middle ears. The specific topics discussed include the diving response and its expression by the cardiovascular system, which exhibits hypertension, bradycardia, oxygen conservation, arrhythmias, and contraction of the spleen. The respiratory system is challenged by compression of the lungs with barotrauma of descent, intrapulmonary hemorrhage, edema, and the effects of glossopharyngeal insufflation and exsufflation. Various mechanisms associated with hypoxia and loss of consciousness are discussed, including hyperventilation, ascent blackout, fasting, and excessive postexercise O2 consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N2 narcosis is also illuminated.
7
Naramala, Srikanth, Sharmi Biswas, Sreedhar Adapa, Vijay Gayam, Romeo C. Castillo, Srinadh Annangi, and Venu Madhav Konala. "Pleomorphic Pulmonary Manifestations of IgG4-Related Disease." Case Reports in Rheumatology 2019 (August 2019): 1–4. http://dx.doi.org/10.1155/2019/7572869.
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Immunoglobulin G4-related disease (IgG4-RD) is a fibroinflammatory disorder which has been first reported in 2001 by Hamano and colleagues in a patient with autoimmune sclerosing pancreatitis. Almost every organ in the human body can be affected by IgG4-RD from infiltration with IgG4-positive plasma cells. Involvement of lungs with IgG4 is reported previously, but still, there is no clear picture of the pathophysiology behind lung involvement. Here, we are presenting a patient who has IgG4-RD presenting as pseudotumor of the lungs.
8
Hirleman, E., and DF Larson. "Cardiopulmonary bypass and edema: physiology and pathophysiology." Perfusion 23, no. 6 (November 2008): 311–22. http://dx.doi.org/10.1177/0267659109105079.
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Edema is a common morbidity following cardiopulmonary bypass (CPB) and can result in injury to many organs, including the heart, lungs, and brain. Generalized edema is also common and can lead to increased post-operative hospital stay and other morbidities. Pediatric patients are more susceptible to post-CPB edema and the consequences are more severe for this population. Hemodilution and systemic inflammatory responses are two suspected causes of CPB-related edema; however, the mechanisms involved are far from understood. Also, the common strategies to improve edema have not been completely successful and there is a need for new strategies at maintaining a fluid balance of patients as close to physiological as possible, especially for pediatric patients. An integrative approach to understanding edema is necessary as the forces involved in fluid homeostasis are dynamic and interdependent. Therefore, this review will focus on the physiology of fluid homeostasis and the pathologies of fluid shifts during CPB which lead to general edema as well as tissue-specific edema.
9
Nielsen, O. S., A. J. Munro, and I. F. Tannock. "Bone metastases: pathophysiology and management policy." Journal of Clinical Oncology 9, no. 3 (March 1991): 509–24. http://dx.doi.org/10.1200/jco.1991.9.3.509.
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The pathophysiology and options for management of bone metastases as well as criteria for determining response to therapy are reviewed. Bone metastases are frequently one of the first signs of disseminated disease in cancer patients. In the majority of patients, the primary tumor is in the breast, prostate, or lungs. Although almost all patients will die of their disease, a proportion of the patients will survive for several years. Treatment is primarily palliative: the intention is to relieve pain, prevent fractures, maintain activity and mobility, and, if possible, to prolong survival. Therapeutic options include local treatment with radiotherapy and/or surgery, and systemic treatment using chemotherapy, endocrine therapy, radioisotopes, agents such as diphosphonates, which inhibit resorption of bone, as well as analgesic and antiinflammatory drugs. The mechanisms by which pain is relieved by several of these therapies remain unclear but actions beyond a simple tumoricidal effect appear to be important. There have been few randomized trials comparing the therapeutic options, and the criteria for assessing response to therapy have, in general, been poorly defined. There is a need for rigorous clinical investigations that assess the efficacy of the various therapeutic possibilities by using well-defined and validated criteria of response.
10
Levvey, Bronwyn, Kovi Levin, Miranda Paraskeva, Glen Westall, and Gregory Snell. "Donation after Brain Death versus Donation after Circulatory Death: Lung Donor Management Issues." Seminars in Respiratory and Critical Care Medicine 39, no. 02 (March 2018): 138–47. http://dx.doi.org/10.1055/s-0037-1615820.
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AbstractLung transplantation (LTx) has traditionally been limited by a lack of suitable donor lungs. With the recognition that lungs are more robust than initially thought, the size of the donor pool of available lungs has increased dramatically in the past decade. Donation after brain death (DBD) and donation after circulatory death (DCD) lungs, both ideal and extended are now routinely utilized. DBD lungs can be damaged. There are important differences in the public's understanding, legal and consent processes, intensive care unit strategies, lung pathophysiology, logistics, and potential-to-actual donor conversion rates between DBD and DCD. Notwithstanding, the short- and long-term outcomes of LTx from any of these DBD versus DCD donor scenarios are now similar, robust, and continue to improve. Large audits suggest there remains a large untapped pool of DCD (but not DBD) lungs that may yet further dramatically increase lung transplant numbers. Donor scoring systems that might predict the donor conversion rates and lung quality, the role of ex vivo lung perfusion as an assessment and lung resuscitation tool, as well as the potential of donor lung quality biomarkers all have immense promise for the clinical field.

Дисертації з теми "Lungs Pathophysiology":

1
Chan, Ching Eunice, and 陳清. "Pathogenetic role of aberrant promoter methylation in lung cancer." PG_Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557819.
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2
Smedley, Jeremy Vance. "A Combined In Vivo and In Vitro Approach to the Study of Endotoxemia in Swine." Thesis, Virginia Tech, 2003. http://hdl.handle.net/10919/33947.
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The cardiopulmonary effects of endotoxin administration (1 microgram/kg) were evaluated in 8-10 week old SPF-derived Yorkshire pigs, both because endotoxemia is a common and important swine problem, and because the pig is a good model for human adult respiratory distress syndrome. Physiological changes included sustained increases in mean pulmonary artery pressure, pulmonary vascular resistance, pulmonary arterial wedge pressure, heart rate, hematocrit, and the arterial partial pressure of carbon dioxide. Transient increases were also observed in central venous pressure and airway pressure. Transient increases, followed by decreases, were observed in mean systemic arterial pressures and systemic vascular resistance. Decreases were seen in cardiac output, cardiac index, arterial partial pressure of oxygen and oxygen saturation. The number of circulating leukocytes, lymphocytes and segmented neutrophils decreased with endotoxin infusion. To investigate the role of airway smooth muscle, bronchial rings were isolated and exposed to contractile agents in tissue baths. A hyperresponsiveness of the third generation bronchi to substance P, carbachol, bradykinin and electric field stimulation was observed. However the increase in response to bradykinin and electric field stimulation were not statistically significant. Histopathology of the lungs demonstrated congestion, hemorrhage and neutrophilic infiltration.
Master of Science
3
Farrán, Díaz-Cano Aina. "Pathophysiology of osteoarthritis." DoctoralThesis, Universitat de Barcelona, 2009. 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.
4
Merriman, Carolyn. "Thorax and Lungs." Text, Digital Commons @ East Tennessee State University, 2001. https://dc.etsu.edu/etsu-works/8532.
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5
Robinson, Monique Renee. "Cardiac pathophysiology of obesity." Electronic Thesis or Dissertation, 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.
7
Kirk, Calum Norman Robert. "Pathophysiology of anoctaminopathy (LGMD2L)." Electronic Thesis or Dissertation, 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.
8
De, Lara Raul H. "Lotion in your lungs." Text, VCU Scholars Compass, 2001. https://scholarscompass.vcu.edu/etd/5902.
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Анотація:
This is a document explaining in detail my artistic practice from childhood to the day I graduated VCU. It will perhaps only be understood by those who have themselves already felt such ways, or similar ways – words and ghosts are mostly invisible.
9
Steele, Ian Conrad. "Pathophysiology of chronic cardiac failure." Electronic Thesis or Dissertation, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337046.
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Ong, Patricia Mei Lin. "Pathophysiology of acute intermittent porphyria." Electronic Thesis or Dissertation, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318116.
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Книги з теми "Lungs Pathophysiology":

1
Ali, Juzar, Michael G. Levitzky, and Warren R. Summer. Pulmonary pathophysiology: A clinical approach. 3rd ed. New York: McGraw-Hill Medical, 2010.
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2
Grippi, Michael A. Pulmonary pathophysiology. Philadelphia: Lippincott, 1995.
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3
West, John B. Pulmonary pathophysiology: The essentials. 8th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2012.
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4
West, John B. Pulmonary pathophysiology: The essentials. 7th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.
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5
West, John B. Pulmonary pathophysiology: The essentials. 3rd ed. Baltimore: Williams & Wilkins, 1987.
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6
West, John B. Pulmonary pathophysiology--the essentials. 4th ed. Baltimore: Williams & Wilkins, 1992.
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7
West, John B. Pulmonary pathophysiology--the essentials. 5th ed. Baltimore, Md: Williams & Wilkins, 1998.
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8
Cagle, Philip T. Advances in surgical pathology: Lung cancer. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2011.
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9
Kayser, Klaus. Analytical lung pathology. Berlin: Springer-Verlag, 1992.
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10
Paleček, František. Patofyziologie dýchání. 2nd ed. Praha: Academia, 1999.
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Частини книг з теми "Lungs Pathophysiology":

1
Goltra, Peter S. "Lungs." In Medcin, 95–96. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-2286-6_35.
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2
Hughes, Graham, and Shirish Sangle. "Lungs." In Hughes Syndrome: The Antiphospholipid Syndrome, 57–59. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-739-6_15.
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3
Hruban, Ralph H., William H. Westra, Timothy H. Phelps, and Christina Isacson. "Lungs." In Surgical Pathology Dissection, 82–87. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4757-2548-3_17.
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4
Oates, M. Elizabeth, and Vincent L. Sorrell. "Lungs." In Myocardial Perfusion Imaging - Beyond the Left Ventricle, 71–83. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25436-4_10.
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5
Hughes, Graham, and Munther A. Khamashta. "Lungs." In Hughes Syndrome: Highways and Byways, 39–40. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-5161-6_8.
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6
Westra, William H., Timothy H. Phelps, Ralph H. Hruban, and Christina Isacson. "Lungs." In Surgical Pathology Dissection, 102–9. New York, NY: Springer New York, 2003. http://dx.doi.org/10.1007/0-387-21747-9_20.
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7
Treves, S. T., and A. B. Packard. "Lungs." In Pediatric Nuclear Medicine, 159–97. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4757-4205-3_11.
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Hughes, Graham, Shirish Sangle, and Simon Bowman. "Lungs." In Sjögren’s Syndrome in Clinical Practice, 15–16. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06059-0_4.
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9
Thorek, Philip. "Lungs (Pulmones)." In Anatomy in Surgery, 300–313. New York, NY: Springer New York, 1985. http://dx.doi.org/10.1007/978-1-4613-8286-7_14.
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10
Rabin, Joseph. "The Lungs." In The Shock Trauma Manual of Operative Techniques, 157–72. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2371-7_9.
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Тези доповідей конференцій з теми "Lungs Pathophysiology":

1
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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2
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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3
"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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4
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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5
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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6
Gualillo, O. "SP0162 Adipokines in the pathophysiology of cartilage." 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.7199.
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7
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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8
Kanna, Rishi. "Spinal Tuberculosis - Epidemiology, Pathophysiology and Clinical Features." In eccElearning Postgraduate Diploma in Spine Surgery. eccElearning, 2017. http://dx.doi.org/10.28962/01.3.144.
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9
Zhao, Y. C., S. E. Rees, S. Andreassen, and S. Kjaergaard. "Simulation of Pulmonary Pathophysiology During Spontaneous Breathing." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615892.
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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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Звіти організацій з теми "Lungs Pathophysiology":

1
Fine, Alan. Acute Lung Injury: Making Injured Lungs Perform Better and Rebuilding Healthy Lungs. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada538317.
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2
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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3
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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4
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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5
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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6
Rogers, Peter H., Gary W. Caille, and Thomas N. Lewis. Response of the Lungs to Low Frequency Underwater Sound. Fort Belvoir, VA: Defense Technical Information Center, June 1994. http://dx.doi.org/10.21236/ada299456.
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7
Robbins, E. S. Cellular morphometry of the bronchi of human and dog lungs. Office of Scientific and Technical Information (OSTI), September 1992. http://dx.doi.org/10.2172/6707808.
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8
Robbins, E. S. Cellular morphometry of the bronchi of human and dog lungs. Office of Scientific and Technical Information (OSTI), September 1991. http://dx.doi.org/10.2172/6262282.
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9
Traub, Richard J. Influence of Manufacturing Processes on the Performance of Phantom Lungs. Office of Scientific and Technical Information (OSTI), October 2008. http://dx.doi.org/10.2172/949146.
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10
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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