Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological data show that chronic diseases of the respiratory apparatus have constantly increased over the last 20 years or so, often involving relatively young age classes. The increased survival rates due to chemotherapy also increase the importance of rehabilitation in such diseases. The officially accepted concept of a "global" rehabilitation is particularly significant in the case of patients of working age. The main rehabilitation procedures include chest physiotherapy, aerosol therapy, oxygen therapy (where selection criteria have been established and where there are new prospects related to long-term oxygen therapy), intermittent positive pressure breathing and physical retraining. Details on the methods of assessment and training and data concerning three groups of patients suffering from respectively chronic obstructive lung disease, silicosis and asbestosis, are given. The data show a general pattern of a decrease in ventilation (for an unchanged level of O2 uptake and CO2 output) and reflect a rise in muscular efficiency (exercising and respiratory) enabling the body to perform the same work load at a lower energy cost. The authors discuss the vocational rehabilitation of the patient with lung disease and illustrate the most useful procedures in the assessment of the subject, the environment and the place of work, including guidelines to achieve this. Rehabilitation treatment is also summarized into a number of stages, with the goals at different therapeutic levels and the ways to reach them.
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PMID:[Rehabilitation of the worker with bronchopneumopathy]. 648 73

Ventilatory responses to hypoxia (A) and hypercapnia (S) were measured in 127 healthy men (105 males and 22 females) by a dual control system for regulating Pa O2 and Pa CO2 simultaneously and independently of each other. The subjects were classified into groups according to sex, age, family history, and genetics (twins). Mean values for A were 138 +/- SD 93 liters/min.mmHg in group I (subjects without family history of chronic lung diseases) and 80 +/- 56 liters/min.mmHg in group II (sons of patients with chronic obstructive pulmonary disease or silicosis). The difference was highly significant (P less than 0.001). Mean S were 1.11 +/- 0.39 liters/min.mmHg-1 in group I and 1.16 +/- 0.48 liters/min.mmHg-1 in group H. The difference was not significant. Mean values for A and S in the aged males (mean age = 71.3 years) did not differ from those in 15 adult males (mean age = 29.5 years) and 60 young twins (mean age = 16.4 years). In every respect of age, sex, familial factors, and genetics, A and S were not interrelated. Mouth occlusion pressure (P0.1) was measured during air breathing and it correlated neither with A nor S. These results indicate 1) hypoxic and hypercapnic responses are not strongly related to each other, and 2) the aging process does not alter ventilatory responses to hypoxia and hypercapnia.
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PMID:Relationship between hypoxic and hypercapnic ventilatory responses in man. 730 42

Small particles of crystalline silicon dioxide (crystallites) are exceptionally toxic. Inhalation of quartz crystallites causes silicosis, a devastating lung disease afflicting miners, particularly coal and stone workers. Poly(vinylpyridine-N-oxide)s (PVPNOs) have been applied in the prevention and treatment of silicosis, but their mode of action has been obscure. Recently, the sites of inducible *NO synthase activation and of nitrotyrosine formation were associated anatomically with the pathological quartz particle-caused lesions in the lungs. It has been suggested that the *NO formed combines rapidly with O2*- to yield ONOO-, a potential mediator of lung injury following silica exposure. Here, we show that PVPNOs do not react with peroxynitrite but scavenge exceptionally rapidly CO3*- radicals, which are produced in the decomposition of ONOO- in bicarbonate solutions. The rate constant for the reaction of CO3*- with PVPNO was found to be independent of the type and size of PVPNO, i.e., k = (1.9 +/- 0.2) x 10(5) M(-1) s(-1) per monomer. In contrast, the rate constant for the reaction of CO3*- with the small molecule 4-methylpyridine N-oxide did not exceed 1 x 10(4) M(-1) s(-1). The underlying reason for the difference is that, in the dissolved polymeric PVPNOs, the electrostatic repulsion between the N-oxide zwitterions destabilizes them, increasing dramatically their pKa. The protonated N-oxides at physiological pH have abstractable hydrogen atoms and are expected to react rapidly with CO3*-, just as cyclic hydroxylamines do. It is also shown that PVPNO inhibits tyrosine nitration by peroxynitrite at pH 7.6 in the presence of excess of CO2 in a concentration-dependent manner. Hence, binding of PVPNO to the quartz particles and eliminating CO3*- could prevent the killing of macrophages, the associated release of macrophage-recruiting cytokines, and the amplification of the local concentration of *NO by the recruited macrophages. The latter causes necrosis of the macrophage-infiltrated lung tissue and, upon repair of the necrotic lesion, results in the growth of the dysfunctional fibrotic tissue, which is the hallmark of silicosis.
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PMID:Mode of action of poly(vinylpyridine-N-oxide) in preventing silicosis: effective scavenging of carbonate anion radical. 1641 60