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Medical HEALTH "> Clinical Respiratory system diseases Summary of idiopathic pulmonary fibrosis diagnosis and treatment of reRecommended online full-text collection of paper hearts Zhang Yang Min Weifang Medical College Yidu Central Hospital, Weifang City, Shandong, breathing Disease Institute, 262500, "New Medicine" Volume 36, 2005 7 Investigation of fast food awards Abstract: Continuing medical professor, idiopathic pulmonary fibrosis is a syndrome? Professor of idiopathic pulmonary fibrosis, also known as implicit induced fibrosing alveolitis, is an unexplained diffuse alveolar inflammation, fibrosis and pulmonary alveolar structural disorder characterized by chronic progressive interstitial lung disease. Severe pulmonary fibrosis as the disease, so the poor prognosis, patients typically survived for 2 to 4 years, 5-year survival of 30% to 50%. In recent years, at home and abroad idiopathic pulmonary fibrosis, a great deal of clinical and basic research experiments, and made some new progress, especially in idiopathic pulmonary fibrosis concept, classification, diagnostic criteria, incidence mechanism and treatment methods, have some new understanding. Number of pages: 2 Page Range :421-422 Key words: idiopathic pulmonary fibrosis, the performance of antioxidants in the immune function of CT immunosuppressive drugs subject classification: R563 [medicine, HEALTH "within SCIENCES" Respiratory and Chest Dise Lung disease] Related Articles: Topics related citations (2)<


br>Affiliated Hospital of Shandong University of TCM, Dr. respiratory Neike Lu Xu Hong
Abstract idiopathic pulmonary fibrosis (idiopathic puhponary fibrosis, IPF) is an unexplained, histology showed usual interstitial pneumonia (usual interstitial pneumonia, UIP) were of diffuse parenchymal lung damage and fibrosis. Recent studies focus on the treatment of IPF began with the traditional anti-inflammatory cytokines and the treatment of fibroblasts as the main therapeutic target of anti-fibrosis treatment changes, and made some basic research results. This paper will present commonly used treatment and modern treatment of an overof the new progress. Affiliated Hospital of Shandong University of Traditional Chinese Medicine Zhang Department of Respiratory Medicine
Key words interstitial lung disease; pulmonary fibrosis; treatment; Summary
Idiopathic pulmonary fibrosis (idiopathic puhponary fibrosis, IPF) is an unexplained, histology showed usual interstitial pneumonia (usual interstitial pneumonia, UIP) of diffuse parenchymal damage and progressive pulmonary fibrosis [ 1]. The etiology is unknown, the pathogenesis is unclear, IPF average survival after diagnosis is 2 to 4 years, 5-year survival of 30% to 50% [2]. Including idiopathic pulmonary fibrosis (IPF) with acute type, and the disease is particularly dangerous situation, and most die within six months, but also several weeks or days to be fatal. Another report is closely related to IPF and lung cancer, chronic lung inflammation and fibrosis in the process of gene expression in cancer, evidence [3]. This shows that the disease dangerous condition, the prognosis is poor, but the current lack of effective treatment, this according to pathological changes of IPF on its targeted therapy process to do a systematic re.
An anti-inflammatory, immunosuppressive therapy
Once lung injury, alveolar epithelium and first capillary endothelial cell damage, various types of stimuli activated macrophages release various factors to promote chemotaxis of inflammatory neutrophils (PMN) and macrophage accumulation to the stimulus, PMN can secretion of oxygen free radicals, tissue specific protease, elastin protease, cathepsin and collagenase, damage lung tissue and to interstitial lung damage. The first anti-inflammatory treatment for this clinical application.
1.1 glucocorticoids and immunosuppressive / cytotoxic drugs on hormone therapy in IPF remains controversial. 33 ~ 66% of clinical patients receiving glucocorticoid therapy, only 10 to 30% of IPF patients on glucocorticoid treatment has some effect [4], which are mostly effective in the pulmonary manifestations of collagen vascular disease or to pulmonary vasculitis as the main manifestation of vasculitis, and truly meet the diagnostic criteria of IPF in patients with poor response to glucocorticoid treatment. Therefore, some scholars do not recommend corticosteroid therapy alone in patients with IPF. And glucocorticoid side effects, clinical application is limited. Schwarz ATS annual meeting in 2004 pointed out that in the following cases of glucocorticoid IPF patients may benefit from: (1) early in the disease; (2) diagnostic treatment observed in the experiment is unclear; (3) acute exacerbation of the disease when shock therapy; (4) ease cough symptoms. Therefore, we used anti-inflammatory therapy should be weighed against the treatment of IPF. Early application and evaluation to achieve, and develop individualized treatment programs. January 2006 the British scholar Hoyles [5] proposed a new program of two drugs: the first choice of small doses of corticosteroids (prednisolone) combined with azathioprine treatment. In addition, Wang Dafang and Hongyang [6] observed in a clinical trial, budesonide inhalation therapy in patients with IPF, the results obtained with the same therapeutic effects of oral prednisone, and few side effects and better compliance. Therefore, before the advent of new effective drugs, of corticosteroids and immunosuppressive agents in the use of the program and the route of administration to seek a better efficacy and fewer side effects is also essential.
1.2 erythromycin erythromycin has anti-inflammatory and immunomodulatory effects. Tan Wei et al [7] found that erythromycin can inhibit neutrophil (PMN) on the chemokine response, inhibition of PMN adhesion in lung epithelial cells and reduce the alveolar PMN accumulation; Li Yongchun, etc. [8] Inhibition of nuclear factor KB activity, transforming growth factor (TGF- ) mRNA expression, which play the role of anti-inflammatory and anti-fibrosis. Houcheng Yun et al [9] The Ambroxol 15mg, erythromycin 0.25g, TMP 100mg, 40ml saline inhalation of IPF patients observed treatment, Bid, 1 month to 1 course of treatment, rest 1 week, re- aerosol inhalation treatment, a total of 6 to 8 cycles. The control group treated with corticosteroids, treatment for 6 to 12 months. Clinical results show that the observed group of patients with PaO2, VC, difficulty breathing, chest X ray, etc. to improve the role better than the control group (P <0.05).
2 cytokine therapy theory
With the development of molecular biology techniques and perfect, has a variety of cytokines in the disease process the activation of fibroblasts, collagen deposition value added and have a preliminary understanding of the mechanisms for these aspects of drug research in progress .
2.1 Interferon- (IFN- ) T helper type 1 cells (Thl) cytokine response may promote the repair of normal tissue structure, type 2 helper T cells (Th2) cytokine response is helpful for daily life fibroblast growth , extracellular matrix (ECM) protein deposition and fibrosis. IFN- as Th1 factors, and animal and human studies have clearly exist in the pulmonary fibrosis of the relative lack of IFN- . Increased Th1-type cytokine response, especially added IFN- , restore equilibrium Thl/Th2 type cytokine, has become a new strategy against pulmonary fibrosis.
Theoretically, IFN- has anti-fibrosis, but home and abroad reported the efficacy of IFN- treatment of IPF is uncertain. Rughu [10] published in 2004 showed that of 330 cases of multi-center, then double-blind, placebo-controlled study showed that IFN- 1b treatment and control groups were 43.6% and 51.8% of patients had disease progression or death The difference was not statistically significant (P = 0.08), but IFN- lb treatment group the incidence of respiratory problems, oxygen utilization rate than the control group decreased. And found that IFN- lb mild to moderate pulmonary disease had severe damage to lung damage degree preferred. Gudmundsson et al [11] also reported the occurrence of hypersensitivity pneumonitis requires the participation of INF- , INF- which show that under certain conditions, may induce lung inflammation, promotion of pulmonary fibrosis, even in the acute respiratory failure ( ARF). For INF- treatment of IPF patients is still experimental and clinical study in depth how to take advantage of favorable factors, to reduce their side effects, to avoid ARF will be subject of further study.
2.2 Transforming growth factor (TGF- ) in mammals have 4 TGF- , TGF- 1 which is most closely with pulmonary fibrosis. TGF- 1 is a powerful regulator of cell proliferation by platelet-derived growth factor can promote the proliferation of lung fibroblasts. TGF- 1 for the structure of cells such as fibroblasts have a very important direct effect is the most important stimulator of ECM proteins, TGF- 1 was activated fibroblasts can promote abnormal deposition of PGs in the lung [12]. By blocking the role of TGF- into the treatment of IPF has recently been a research hotspot. Rube et al [13] observed in an animal experiment by blocking TGF- TGF- monoclonal antibody to treat fibrotic diseases, can significantly reduce the deposition of collagen. In addition to blocking extracellular TGF- effects, regulation of intracellular TGF- signaling pathway is also desirable. Nakao, have aly confirmed in the mouse model of bleomycin intracellular signaling molecules Smad 7 overexpression can antagonize TGF- signaling, so that fibrosis can be improved, so the Smad 7 is an antagonist of TGF- signaling [14]. However, the biological role of TGF- is very broad, blocking its activity, the other result is that the class may lead to fatal autoimmune diseases. Therefore, the use of genetic engineering, protein engineering transformation TGF- , in order to obtain more effective and more specifically the role of the new molecule TGF- is another research focus in the future.
Nepal coffee topiramate ketone (pirfenidone) pyrazole in vivo studies have confirmed that coffee is a new Nepal ketone orally active anti-fibrosis drugs. Can reduce the in vitro expression and fibrosis related media, such as transforming growth factor- (TGF- ) and platelet-derived factor (PDGF) gene expression, thus inhibiting fibrosis. Found in vivo can inhibit TGF- induced collagen synthesis, reducing ECM production, blocking the mitogenic PDGF effect, inhibition of fibroblast proliferation. A recent multicenter, randomized, double-blind controlled clinical trials have shown that pirfenidone significantly improved the parameters of pulmonary function, and on the progress of IPF is also true of [15]. Although most coffee on topiramate treatment of Nigerian ketone results in patients with IPF exciting, but still a large number of prospective randomized treatment study to further affirmed the efficacy of topiramate brown Nepal ketone.
2.3 Connective tissue growth factor (CTGF) CTGF blocking therapy is the downstream mediator of TGF- 1 mediates some of its biological functions such as promoting the proliferation of fibroblasts and extracellular matrix. In the normal state, CTGF expression is very low, and mainly expressed in stromal cells, therefore, blocking CTGF expression or inhibit its biological activity may be more specific, more effective means of treatment of fibrosis. Jin Zhe et al [16] confirmed by animal experiments, CTGF antisense oligonucleotide expression of CTGF gene can be closed, reducing the expression of CTGF protein, thereby reducing its biological effects. Currently, further research CTGF and fibrosis in normal cell , expression regulation will help to explore a new therapeutic strategy against fibrosis.
2.4 TNF-a antagonist released after lung injury in a large number of TNF-a and macrophage release of fibronectin (FN) interact to form the initial acute lung inflammation, a large release of TNF-a on the one hand increase the inflammatory response, and the other On the one hand can promote the proliferation of fibroblasts and secrete large amounts of collagen. Therefore, the application of TNF-a inhibitors have a certain effect of anti-fibrosis treatment. Liu et al [17] reported that TNF-a receptor knockout mice with bleomycin, asbestos and other fibrosing decreased sensitivity of material, type alveolar epithelial proliferative activity decreased. Of course, TNF-a inhibitors IPF clinical efficacy needs further verification.
2.5 endothelin (ET) receptor antagonist Endothelin is a potent vasoconstrictor, is also a proinflammatory cytokine and mediator induced fibrosis, which can stimulate TNF-a, TGF- release of such , but also stimulate fibroblast proliferation and collagen production. Bosentan (bosentan) is a non-selective endothelin receptor inhibitors. Some scholars have confirmed through animal experiments bosentan can reduce the bleomycin model of pulmonary fibrosis rats induced lung collagen deposition.
3 for the treatment of collagen metabolism
There are 18 different types of collagen in lung type and collagen is more. After the formation of collagen, only human matrix metalloproteinases (MMPs) and collagenase to dissolve. Many organizations metalloproteinase inhibitors (TIMPs) inhibit the MMPs activity courses; and a variety of inflammatory cytokines and growth factors and the role of fibroblasts in vitro transformation of collagen, the collagen synthesis and degradation of the lungs is a complex dynamic equilibrium process; lung collagen increased, depending on the increase in procollagen synthesis, collagenase production decline or increase in tissue inhibitor of metalloproteinase combination of factors.
3.1 colchicine: in vivo experiments showed that colchicine can inhibit fibroblast proliferation, inhibition of collagen (I, type) mRNA expression and protein synthesis and secretion, and promote collagenase activity, and promote matrix metalloproteinase (MMP) -1 , MMP-9 activity increased, thereby reducing the production and deposition of collagen, promote collagen breakdown, played the role of anti-fibrosis [18-20]. Another study suggests that colchicine can inhibit the release of alveolar macrophage fibronectin and alveolar macrophage derived growth factor. Anti-inflammatory effect of colchicine also help inhibit the metabolism of polynuclear leukocytes, chemotaxis and cytokine release. Douglas et al [21] conducted a prospective treatment study, 26 patients with IPF patients were divided into two groups, one group with prednisone (60mg / d) with another group of colchicine (0.6 ~ 12mg / d), the results found that colchicine is safe and effective than prednisone. Oral colchicine 0.6mg, 1 or 2 times a day, alone or in combination with immunosuppressive agents, IPF has been recommended as first-line hormonal therapy or treatment resisters. When Douglas and other retrospective study analyzed 487 cases from 1994 to 1996 of usual interstitial pneumonia (UIP) patient outcomes: treatment with colchicine in 167 patients, 54 patients treated with prednisone, prednisone colchicine 71 cases, 38 cases of other treatments, no treatment of 157 patients showed that survival rates among the groups was no clear difference. The study confirmed that colchicine has the potential anti-fibrosis, can be used for the treatment of IPF, but the effectiveness of their treatment can not be sure, still a large number of clinical studies.
3.2 metalloproteinase inhibitors and antibody in lung fibrosis, the excessive extracellular matrix degradation, deposition of extracellular matrix may homeostasis, protease / antiprotease imbalance in a relationship system. Present study shows that, MMPs / TIMPs balance changes may lead to the collapse of the lung tissue, ECM accumulation and the resulting repair has not been enough to cause lung injury. Research shows that factors such as promoting fibrosis IGFs, TGF- , TNF- by matrix metalloproteinase-mediated release of the activation and that these factors are starting and the progress of pulmonary fibrosis important regulatory factor. Therefore, in the treatment of pulmonary fibrosis, MMPs inhibitor of the above three factors and their synergistic effect of antibodies will be important to our future direction.
4 apoptotic resistance
Pulmonary fibrosis, abnormal cell proliferation is not only a disease, abnormal cell death is a disease [22]. Many experimental results show that apoptosis in pulmonary fibrosis plays an important role. Fas, cascade enzymes, TNF- , reactive oxygen species, nitric oxide, angiotensin converting enzyme, TGF, P53 and P21, IL-6 can contribute to Fas-mediated apoptosis, this resistance or interference by Fas -FasL interactions or cascade down to control the progress of inflammation and fibrosis.
4.1 antioxidants anatomy of the lung, location and physiological function, are extremely sensitive to oxygen damage is oxygen free radicals (OFR) to attack the target organs. Under normal physiological conditions, the protection of the human body have a beneficial effect, can help maintain the vitality of the energy transfer, promote cell kill germs, eliminate inflammation, break down toxic substances and so on. Once the imbalance in the body rise and fall OFR, IPF, the alveolar epithelial cells, endothelial cells, inflammatory cells and other cell membrane by lipid peroxidation, causing increased membrane permeability, fluidity decreased allosteric membrane receptor proteins, enzymes protein inactivation, ion channel dysfunction, so that cell dysfunction, cell rupture, plasmin release or accelerated apoptosis, which damage lung tissue.
N-acetyl cysteine (NAC) glutathione (GSH) is an important intracellular antioxidant, in lung epithelial cells in fluid concentrati00 times higher than plasma, but has now confirmed that the lung epithelium in IPF patients fluid within the cortex and alveolar epithelial cells there is a serious shortage of GSH. NAC into the body to become de-acyl cysteine, as a precursor of GSH is an ideal antioxidant. Shen Ning et al [23] IPF patients given daily 1800mg NAC, glutathione was found to increase the level of the lung and improve lung function. An international multi-center, double-blind, randomized, placebo-controlled, parallel testing, observation combined with high dose prednisone and azathioprine treatment of 1 year NAC is able to mitigate the decline in lung function in patients with IPF, results show that the treatment with simple application of prednisone and azathioprine compared to the standard program, tidal volume and can slow the decline in diffusing capacity [24]. Overall, the current treatment of IPF that the NAC can be used as auxiliary treatment, of course, need more to support clinical practice.
In addition, there are other antioxidants such as TMP, vitamin E, curcumin, Ambroxol, SOD products, and other research has also made some theoretical results, but there is no precise clinical information. In vitro studies show that TMP system of water-soluble HO-generated O2-and clearance rates were 100% and 44%; curcumin is a fat-soluble antioxidant phenolic compounds, their molecular structure containing phenol and - dione two groups in inactivated OFR has better anti-oxidation [25]. Yuan Sheng et al [26] obtained in animal experiments ambroxol can increase superoxide dismutase (SOD) activity, increased glutathione (GSH) content and enhanced antioxidant capacity of local lung, reducing lung inflammation, thus preventing pulmonary fibrosis.
4.2 Uhal such as angiotensin converting enzyme inhibitors [27] studies have shown that AT II can induce programmed cell death in alveolar epithelial cells; and Marshall RP et al [28 found that the fibroblasts can promote mitosis. ACEI than by blocking the route of experiments in animal models with anti-fibrosis. Wang et al [29] confirmed by animal experiments captopril can reduce pulmonary interstitial collagen deposition, inhibition of alveolar epithelial cells. However, Hassan F. Nadrous, MD and other large clinical studies have shown that, ACEI on the extension of survival in IPF patients and improve the prognosis did not value the role of [30]. Therefore, whether the ACEI in the clinical role of anti fibrosis need more a more comprehensive exploration and research.
5 Other
5.1 Anticoagulation Kubo et al [31] found that, IPF acute exacerbation, patients significantly increased plasma D-dimer, acute exacerbation of IPF patients is an important cause of death. Because D-dimer is a sign of intravascular coagulation, which is to provide a theoretical basis for anticoagulant treatment. Hanwen Yang et al [32] pointed out that Lazar and other preparations of blood plasminogen by uPA and PAI-1 to change the ratio between the completion of the regulation of pulmonary fibrosis. Kubo et al [31] and 5 hospitals, 56 patients were prospectively followed up for 399 days of anticoagulant therapy (median), the display can be extended anticoagulant therapy in patients with a median survival of IPF days, anticoagulants combined cortical hormone therapy in patients with IPF, 3-year survival rate was 63%, compared with corticosteroid therapy alone was significantly increased 35%. Liushao Xia et al [33] treatment of IPF patients in the control group only received oxygen, antibiotics, symptomatic and glucocorticoid and other conventional treatment group on this basis, given the small dose of low molecular weight heparin 50IU.kg, plus saline 20ml , Qd, course of 2 months. The results show that the treatment group, PaO2, and VC, MVV, DLCO, DL / VA all indicators were statistically significant compared with the control group. The conclusion: anticoagulation therapy to reduce mortality in patients with acute exacerbation of IPF can be used as an adjunct to treatment of IPF.
5.2 Gene therapy Gene therapy is a recently developed new technology, with the IPF pathogenesis of a wide range of related molecular mechanisms of deep research, has found some valuable and IPF-related genes, such as maternal and child Tong pulmonary surfactant protein C gene mutations, distribute discover that they IL- receptor gene and susceptibility to TNF- gene and other genes. However, disease-related genes may be involved in IPF to the oxidant / antioxidant and protease / protease inhibitor, Thl/Th2 cytokine gene balance between, IPF in the complexity of gene expression to the challenges of gene therapy.
5.3 lung transplantation for end-stage lung transplantation is the primary means of IPF can significantly improve the quality of life and survival rate of patients, but high costs and s of donor organs limits its application of the difficulties, the reported number of cases is extremely limited.
6 Conclusion
In general, are yet to have any kind of drug or combination with other drugs to achieve effective treatment and prevent the IPF development. Pathogenesis of many recent studies focus on a certain part of the process, and the discovery of many new drugs, most studies of these drugs is only one aspect of basic research confirmed that treatment of fibrosis, the overall effect is still a lack of large-scale clinical studies to be confirmed. In the future, drugs will continue to be the main measure pulmonary fibrosis, which is a cytokine in the field of targeted drug research focus increasing attention anticoagulant adjuvant therapy. In addition, more and more Chinese medicine treatment of IPF medical attention at home and abroad, and many reports of Chinese medicine therapy still remain at the level of personal experience, the lack of evidence-based medicine with a large sample of the Multi center randomized double-blind controlled study, which is the direction of our future efforts.
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