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)

We describe the first case of bilateral hypothenar hammer syndrome (HHS) followed by systemic sclerosis (SSc) that was associated with silica exposure (Erasmus syndrome). The patient was a woman smoothing tiles in an earthenware factory who presented with bilateral digital ischemia associated with Raynaud's phenomenon. HHS was diagnosed, based on an angiographic study showing aneurysm of the ulnar arteries and occlusions of multiple digital arteries. Pulmonary silicosis was also diagnosed on pulmonary tomodensitometry. Two years later digital swelling with acroosteolysis developed. The FANA test was positive (titer 1:640) and anticentromere antibody tests were also positive. Esophageal manometry showed dysmotility of the lower esophagus. These findings were consistent with a diagnosis of SSc.
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PMID:Hypothenar hammer syndrome followed by systemic sclerosis. 1155 Sep 91

Inhibition of poly(ADP-ribosyl)ation in oxidative stress-related pathologies has recently emerged as a very effective anti-inflammatory intervention in animal models of arthritis, colitis, diabetes and shock. Recent data from three laboratories also support the role of poly(ADP-ribose) polymerase-1 (PARP-1) activation in asthma. Similarly to other inflammatory conditions, the protective effects of PARP inhibition and the PARP-1 knock out phenotype in asthma models have been attributed to inhibition of inflammatory signal transduction (mainly via NF-kappaB) and of oxidative stress-induced cell dysfunction and tissue injury. Here I discuss the complex role of poly(ADP-ribosyl)ation in the regulation of inflammatory cell migration, chemokine and cytokine production and expression of other inflammatory mediators (inducible nitric oxide synthase, matrix metalloproteinases) in asthma. The role of PARP-1 in other oxidative stress-related lung diseases such as asbestosis, silicosis, acute respiratory distress syndrome and ischemia-reperfusion injury is also reviewed.
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PMID:Poly(ADP-ribosyl)ation in asthma and other lung diseases. 1591 36

The aim of this study was to evaluate the oxidative status in patients with silicosis by detecting dynamic thiol disulfide homeostasis (TDH), ischemia-modified albumin level (IMA) catalase (CAT) activity, and the correlation of these markers with pulmonary function tests. Male ceramic workers with silicosis (n = 91) and healthy individuals (n = 47) were recruited for the study. Radiographic abnormalities of pneumoconiosis were classified into three profusion categories (categories 1, 2, and 3), and patients with silicosis, those with category 1, were defined as group 1 and those with category 2 or 3 were defined as group 2. Plasma levels of native thiol (NT), total thiol (TT), disulfide (Ds), IMA, and CAT activities were determined. Pulmonary function tests of groups were compared. NT, TT, and NT/TT ratios were significantly lower in groups 1 and 2 than the control group (p < 0.05). These did not differ between patients with silicosis (groups 1 and 2) and control group (p = 0.421). Ds/NT and Ds/TT ratios were significantly higher in group 2 than the control group (p < 0.05). NT, TT, and Ds did not differ significantly between groups 1 and 2. The oxidant biomarker IMA was higher (p < 0.001), and the antioxidant parameters albumin and CAT were lower in groups 1 and 2 (p < 0.001) compared with the control group. The mean FEV1act, FVCact, forced expiratory volume in 1 second/forced vital capacity (%), and value of 25-75 percent maximum expiratory flow were significantly lower in groups 1 and 2 than control group. We have used a novel colorimetric method to assess TDH in patients with silicosis. Alteration of plasma thiol/disulfide homeostasis and IMA levels might be novel indicators of oxidative stress in silicosis.
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PMID:Alteration of thiol disulfide homeostasis and ischemia-modified albumin levels as indicators of oxidative status in patients with silicosis. 3330 88