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

For the stimulation of research on scleroderma and the prophylaxis of occupational scleroderma-like diseases and the prevention of iatrogenic injuries, respect., it is important to know the inducing environmental substances. Plastics (vinyl chloride, epoxy resins), solvents (chlorinated, aromatic and aliphatic hydrocarbons), drugs (bleomycin, pentazocine), cocaine (abuse) and contaminated rapeseed oil are more or less able to induce scleroderma-like diseases. Vinyl chloride disease is the best known among these. The toxic oil syndrome represents the most inglorious example of the recent time. Paraffin and silicon can act as adjuvants and induce a progressive systemic sclerosis. In our studies it could be shown, that silica is able to induce not only a silicosis, but also a true progressive systemic sclerosis after long term exposure. Acknowledgment of such cases as an occupational disease is justified and regulated by law in the German Democratic Republic.
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PMID:[Scleroderma and scleroderma-like diseases caused by environmental pollutants]. 242 99

A case of generalised scleroderma is reported in a dental technician exposed to the risk of silicosis. A study of the occupational toxic risks in this patient showed pulmonary overload with silica and metallic particles composed of chromium, cobalt and tungsten. The job also involved the handling of vinyl chloride and its stable polymer. This chemical is known to give rise to scleroderma-type skin disease. The relationship between these occupational factors leads to a difficult physio-pathological problem and justifies preventative measures, even though they may be costly and demanding.
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PMID:[Erasmus syndrome in a dental technician. Importance of the prevention of occupational hazards]. 666 4

Arteriopathies of occupational diseases predominate in the upper limbs and are usually expressed as Raynaud's phenomenon ("white finger"), sometimes complicated by digital gangrene. Hand-arm vibration disease, hypothenar hammer syndrome, exposure to silica even without silicosis and vinyl chloride intoxication are the principal causes of occupational diseases acknowledged as such by the laws. In a personal series of 60 patients with complicated upper limb arteriopathies, 25% had a recognized occupational disease. Since December 1992, Erasmus' syndrome and systemic scleroderma due to silica without silicosis have been accepted in France as being occupational diseases. The therapeutic problems are discussed, notably the surgical indications in hypothenar hammer syndrome, the possible medical treatments of finger necrosis occurring in Erasmus' syndrome and, in particular, the role played by spinal cord neurostimulation.
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PMID:[Arteriopathies as occupational diseases]. 823 49

We analyze mechanisms of moral disengagement used to eliminate moral consequences by industries whose products or production practices are harmful to human health. Moral disengagement removes the restraint of self-censure from harmful practices. Moral self-sanctions can be selectively disengaged from harmful activities by investing them with socially worthy purposes, sanitizing and exonerating them, displacing and diffusing responsibility, minimizing or disputing harmful consequences, making advantageous comparisons, and disparaging and blaming critics and victims. Internal industry documents and public statements related to the research activities of these industries were coded for modes of moral disengagement by the tobacco, lead, vinyl chloride (VC), and silicosis-producing industries. All but one of the modes of moral disengagement were used by each of these industries. We present possible safeguards designed to protect the integrity of research.
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PMID:Moral disengagement in the corporate world. 1924 52

Activation of the inflammasome generates the pro-inflammatory cytokines interleukin-1 beta and -18, which are important mediators of inflammation. Abnormal activation of the inflammasome leads to many inflammatory diseases, including gout, silicosis, neurodegeneration, and genetically inherited periodic fever syndromes. Therefore, identification of small molecule inhibitors that target the inflammasome is an important step toward developing effective therapeutics for the treatment of inflammation. Here, we show that the herbal NF-kappaB inhibitory compound parthenolide inhibits the activity of multiple inflammasomes in macrophages by directly inhibiting the protease activity of caspase-1. Additional investigations of other NF-kappaB inhibitors revealed that the synthetic I kappaB kinase-beta inhibitor Bay 11-7082 and structurally related vinyl sulfone compounds selectively inhibit NLRP3 inflammasome activity in macrophages independent of their inhibitory effect on NF-kappaB activity. In vitro assays of the effect of parthenolide and Bay 11-7082 on the ATPase activity of NLRP3 demonstrated that both compounds inhibit the ATPase activity of NLRP3, suggesting that the inhibitory effect of these compounds on inflammasome activity could be mediated in part through their effect on the ATPase activity of NLRP3. Our results thus elucidate the molecular mechanism for the therapeutic anti-inflammatory activity of parthenolide and identify vinyl sulfones as a new class of potential therapeutics that target the NLRP3 inflammasome.
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PMID:Anti-inflammatory compounds parthenolide and Bay 11-7082 are direct inhibitors of the inflammasome. 2009 58