Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term oxygen therapy improves the life expectancy of hypoxaemic patients with chronic obstructive pulmonary disease (COPD), provided the hypoxaemia is sufficiently pronounced under stable conditions (PaO2 less than 55 mmHg) and oxygen is given for more than 16 out of 24 hours. By extension, the same indications are applicable to hypoxaemia due to other causes (diffuse fibrosis, pneumoconiosis, cystic fibrosis, etc.). Long-term oxygen therapy improves the patients' quality of life and also has favourable effects on oxygen transport, neuropsychological status, polycythaemia and pulmonary hypertension. It is usually delivered by means of O2 extractors, to which may be added small flasks of O2 gas for walking and moving about. Liquid O2 is a good solution for subjects who are motivated and are obliged to do a great deal of walking. The O2 flow rate administered must be such that it rises the PaO2 level above 60 mmHg. Oxygen therapy is only a symptomatic treatment and cannot replace other types of therapy, such as bronchodilators, physiotherapy, etc. It gives satisfactory results but it has not transformed the prognosis of severe hypoxaemic COPD.
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PMID:[Long-term oxygen therapy in chronic respiratory insufficiency. Usefulness, indications, modes of administration]. 153 36

Mycobacterial lung disease is caused by nontuberculous mycobacteria (NTM), also known as atypical mycobacteria. NTM are widely distributed in the environment, particularly in soil and water. Although generally of low pathogenicity to humans, NTM can affect patients with underlying chronic lung diseases, such as cystic fibrosis, bronchiectasis, pneumoconiosis, or healed tuberculosis. Some patients with cystic fibrosis (CF) have disease progression due to NTM, others can have NTM cultured intermittently from respiratory specimens without a significant decline in lung function. Identifying which patients will worsen from NTM and therefore need treatment remains difficult because of the similarity of symptoms in CF and NTM lung disease. The most common species of NTM isolated in CF patients are Mycobacterium avium complex (MAC) and Mycobacterium abscessus. In this paper, we present three different cases of mycobacterial lung disease in patients with cystic fibrosis.
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PMID:[Mycobacterial lung disease in patients with cystic fibrosis--report of three cases]. 2533 67

This review presents and discusses a new frontier for fast, risk-free and potentially inexpensive diagnostics of respiratory diseases by detecting volatile organic compounds (VOCs) present in exhaled breath. One part of the review is a didactic presentation of the overlaying concept and the chemistry of exhaled breath. The other part discusses diverse sensors that have been developed and used for the detection of respiratory diseases (e.g. chronic obstructive pulmonary disease, asthma, lung cancer, pulmonary arterial hypertension, tuberculosis, cystic fibrosis, obstructive sleep apnoea syndrome and pneumoconiosis) by analysis of VOCs in exhaled breath. The strengths and pitfalls are discussed and criticised, particularly in the perspective in disseminating information regarding these advances. Ideas regarding the improvement of sensors, sensor arrays, sensing devices and the further planning of workflow are also discussed.
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PMID:Sensors for detecting pulmonary diseases from exhaled breath. 3124 97

As an evolutionarily conserved intracellular degradation pathway, autophagy is essential to cellular homeostasis. Several studies have demonstrated that autophagy showed an important effect on some pulmonary fibrosis diseases, including idiopathic pulmonary fibrosis (IPF), cystic fibrosis lung disease, silicosis and smoking-induced pulmonary fibrosis. For example, autophagy mitigates the pathological progression of IPF by regulating the apoptosis of fibroblasts and the senescence of alveolar epithelial cells. In addition, autophagy ameliorates cystic fibrosis lung disease via rescuing transmembrane conductance regulators (CFTRs) to the plasma membrane. Furthermore, autophagy alleviates the silica-induced pulmonary fibrosis by decreasing apoptosis of alveolar epithelial cells in silicosis. However, excessive macrophage autophagy aggravates the pathogenesis of silicosis fibrosis by promoting the proliferation and migration of lung fibroblasts in silicosis. Autophagy is also involved in smoking-induced pulmonary fibrosis, coal workers' pneumoconiosis, ionizing radiation-mediated pulmonary fibrosis and heavy metal nanoparticle-mediated pulmonary fibrosis. In this review, the role and signalling mechanisms of autophagy in the progression of pulmonary fibrosis diseases have been systematically analysed. It has provided a new insight into the therapeutic potential associated with autophagy in pulmonary fibrosis diseases. In conclusion, the targeting of autophagy might prove to be a prospective avenue for the therapeutic intervention of pulmonary fibrosis diseases.
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PMID:Autophagy, an important therapeutic target for pulmonary fibrosis diseases. 3187 97