Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q99581 (FEV)
 3,296 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eupnea is normal breathing. If eupnea fails, as in severe hypoxia or ischemia, gasping is recruited. Gasping can serve as a powerful mechanism for autoresuscitation. A failure of autoresuscitation has been proposed as a basis of the sudden infant death syndrome. In an in vitro preparation, endogenous serotonin is reported to be essential for expression of gasping. Using an in situ preparation of the Pet-1 knockout mouse, we evaluated such a critical role for serotonin. In this mouse, the number of serotonergic neurons is reduced by 85-90% compared with animals without this homozygous genetic defect. Despite this reduction in the number of serotonergic neurons, phrenic discharge in eupnea and gasping of Pet-1 knockout mice was not different from that of wild-type mice. Indeed, gasping continued unabated, even after administration of methysergide, a blocker of many types of receptors for serotonin, to Pet-1 knockout mice. We conclude that serotonin is not critical for expression of gasping. The proposal for such a critical role, on the basis of observations in the in vitro slice preparation, may reflect the minimal functional neuronal tissue and neurotransmitters in this preparation, such that the role of any remaining neurotransmitters is magnified. Also, rhythmic activity of the in vitro slice preparation has been characterized as eupnea or gasping solely on the basis of activity of the hypoglossal nerve or massed neuronal activities of the ventrolateral medulla. The accuracy of this method of classification has not been established.
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PMID:Genesis of gasping is independent of levels of serotonin in the Pet-1 knockout mouse. 1921 35

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