Guide Asbestosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

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Anemia A Medical Dictionary Bibliography and Annotated Research Guide to Internet References

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Er is vaak sprake van verlies van baan, medische problemen en familieproblemen. The morphological evidence significant differences between the experimental groups in the proceess of maturation of the newly-formed connective tissue. Do not leave this medicine in the car on hot days. During the procedure, your doctor may put a special type of dye in the catheter. Methotrexate, a slow acting agent that inhibits dihydrofolate reductase, has become the gold standard of RA therapy.

The result of its pharmacologic effects is impairment in the functioning of inflammatory cells that mediate the rheumatoid process.

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In addition to its medical effectiveness, methotrexate is well tolerated and relatively inexpensive. However, its potential toxic effects include bone marrow suppression, hepatotoxicity, interstitial pneumonitis, pulmonary fibrosis, increased susceptibility to infection, and pseudo sun sensitivity. Although the immunosuppressive agent cyclosporine has been used to treat RA in Europe for more than a decade, it is rarely used by American and Canadian rheumatologists. It is typically used in combination with methotrexate in patients who do not respond to methotrexate alone.

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Various cytotoxic drugs have been found to be helpful in the treatment of recalcitrant RA; however, their usefulness is limited by the severity of their toxic side effects. Newly emerging drugs for RA include leflunomide, tumor necrosis factor TNF -alpha inhibitors such as infliximab and etanercept, and interleukin-1 IL-1 inhibitors. Leflunomide, the first antipyrimidine agent to be used to treat RA, inhibits the ability of dihydroorotate dehydrogenase to convert dihydroorotate to orotate.

Efficacy studies have demonstrated the effectiveness of the agent. Infliximab contains monoclonal antibodies that bind circulating TNF-alpha, thereby inhibiting the proinflammatory effects of the circulating lymphokine. Although infliximab awaits final approval by the Food and Drug Administration, for use in RA, patients have shown definite clinical improvement after intravenous administration of the agent.

However, adverse reactions are common. Etanercept is the first effective biologic antirheumatic therapeutic agent to become available for clinical use. This agent has been effective in relieving RA symptoms and improving function, and its reported adverse effects have been modest. However, its use is limited by the need to administer it parenterally and 6 Pulmonary Fibrosis its excessive cost. The most effective IL-1 inhibitor is a human recombinant IL-1 receptor antagonist that is now under investigation. Government supports a variety of research studies relating to pulmonary fibrosis.

You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to pulmonary fibrosis. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore pulmonary fibrosis. OVA-treated mice display a disease strikingly similar to allergen-induced human asthma.

In our mouse model of asthma, we have found that leukotrienes are key mediators of the mucus release and eosinophil infiltration of the airways. These studies will be performed in both our standard protocol and a long-term model of allergen-induced lung fibrosis in mice. Our goal will be to define immune mechanisms by which leukotrienes influences the activation and effector functions of T cells and dendritic cells, key cells in the mediation of allergic airway inflammation.

Our specifi aims are as follows: Specific Aim 1. Specific Aim 2.

To determine the mechanisms by which leukotriene inhibition blocks allergic pulmonary inflammation and AHR in the murine model of asthma. The more specific our knowledge of the biochemical and immunological changes becomes, the more likely it is that specific interventions producing more benefit than harm in reducing leukotriene-reduced inflammation, will be found.

Eric Hoffman and Dietrich Stephan whose primary interests are focused on muscle disease and leukemia are PI and Co-PI on the Program's Expression Array Core and have extensive experience with all aspects of array use and data analysis. They have established collaborations with Dr. Michael Bitmer, Dr. As a post-doctoral fellow in the laboratory of Dr. Stephan developed several alternative approaches to label total RNA for efficient signal detection under varying circumstances which have become the standard protocol used at NHGRI and has become a quite robust and reliable system for detecting signals over several orders of magnitude.

In addition to building and using 7K expression arrays, Dr. Hoffman's laboratory is particularly interested in systematic assessments of the sensitivity and specificity of the Affymetrix vs. Indeed, the proposed systematic comparison of the Affymetrix and cDNA array experimental platforms should be the first of this type of quality control of expression array data, and should prove highly valuable to both Program investigations and the research community at large.

The overall hypothesis of this investigation is that inherited genetic factors predispose individuals to develop pulmonary fibrosis. The goal of this investigation is to identify a group of genetic loci that play a role in the development of familial 8 Pulmonary Fibrosis pulmonary fibrosis. The overall hypothesis is supported by the following observations: familial pulmonary fibrosis is indistinguishable pathologically from idiopathic pulmonary fibrosis and appears to be inherited as an autosomal dominant trait with variable penetrance; pulmonary fibrosis is associated with pleiotropic genetic disorders, such as Hermansky-Pudlak syndrome, neuofibromatosis, tuberous sclerosis, NeimannPick disease, Gaucher's disease, and familial hypocalciuric hypercalcemia; pulmonary fibrosis is frequently observed in autoimmune disease, including rheumatoid arthritis and systemic sclerosis; variable susceptibility is evident among workers who are reported to be exposed occupationally to similar concentrations of fibrogenic dusts; and inbred strains of mice differ in their susceptibility to fibrogenic dust.

In conjunction with the exponential growth of human molecular genetics, the investigators state that these clinical observations suggest that a well organized approach to define the genetic determinants of pulmonary fibrosis is scientifically feasible and justified. This project proposes to use standard genetic methodology linkage analysis to investigate the distribution of polymorphisms for anonymous genetic markers in families with familial pulmonary fibrosis.

The investigators state that their comprehensive genome-wide study, using standard genetic markers, will allow them to identify loci which subsequently may prove to contain novel genes that play a role in the pathogenesis of pulmonary fibrosis. Once genetic loci are defined in familial pulmonary fibrosis, candidate genes can be identified on the basis of both positional and functional criteria.

Moreover, they note that this approach will provide basic information on high priority loci that will be applicable to the rapidly evolving dense human transcript map for pulmonary fibrosis in families with two or more cases of pulmonary fibrosis. Type A NPD is a severe neuro-degenerative disorder, which leads to death in early childhood, while patients with Type B NPD have little or no neurological abnormalities and often survive into adulthood. TGFbeta1 is anti- inflammatory, pro-fibrotic, and casually linked to fibrotic diseases, e.

We found that LAP is a ligand for the epitheliumspecific integrin alphavbeta6, and that cells expressing alphavbeta6 bind and activate latent TGFbeta1. This mechanism can explain the heretofore puzzling phenotype of beta6 integrin knock-out mice: inflammation in lung and skin, and protection from bleomycin-induced pulmonary fibrosis. Our results provide the first evidence that dysregulated TGFbeta1 activation causes fibrosis. Our goals are to understand quantitatively the interactions between LTGFbeta and alphavbeta6 that lead to activation, and to develop an animal model an animal model and knowledge to explore fully the biological role of a of avbeta6-mediated LTGFbeta1 activation.

In Aim 1 we will analyze the activation mechanism by focusing on alphavbeta6- LTGFbeta1 interactions. We will make TGFbeta1-mull alphavbeta6- expressing cells to which specifically engineered forms of LTGFbeta1 will be added either by transfection or as recombinant protein. In this system we will then determine the relative activatability of two major forms of LTGFbeta1 the so-called small and large latent complexes , the relative effects of LTGFbeta1 concentration and alphavbeta6 expression levels of activation, the activatability of soluble and matrix-bound latent TGFbeta1, and the integrin: LTGFbeta1 stoichiometry required for activation.

The results will be incorporated into an activation model and related to activation in vivo. The phenotypes of these mice and beta6 integrin null mice will be compared to confirm that the beta6 null phenotype is due specifically to loss of TGFbeta1 activation. The results of these aims will lead to better understanding of alphavbeta6-mediated TGFbeta1 activation in disease.

Although there has been numerous studies on the mesenchymal epithelial interactions in the developing lung, there have been relatively few studies in the adult lung. The purpose of this project is to define the epithelial mesenchymal interactions in the adult lung especially as they relate to pulmonary fibrosis. KGF is an important growth Studies 11 factor for type H cells and induces differentiation in vitro, whereas TGF-b inhibits proliferation and antagonizes the effects of KGF on differentiation.

Another major question that remains are differences between normal cells and hyperplastic type II cells and if hyperplastic type H cells produced by KGF are different from hyperplastic type H cells seen in fibrotic lung disease. In co-culture normal type II cells inhibit fibroblast growth, but the effect of hyperplastic type II cells from fibrotic lung on fibroblast proliferation is not known.

The in vitro studies in this proposal rely on two new culture systems for rat type II cells to maintain differentiated function of type H cells. One has apical access and the other basolateral access.