Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Background and objective: Generally, a disease-specific health-related quality of life (HRQOL) measurement is more useful than generic measures in assessing perceived physical and mental health characteristic of a particular disease. The idiopathic pulmonary fibrosis (IPF)-specific version of St. George's Respiratory Questionnaire (SGRQ-I) has been recently developed for patients with IPF. We proposed to evaluate associations between the SGRQ-I and other clinical indices, as well as its prognostic value in patients with IPF. Methods: Fifty-two patients with IPF were recruited in this prospective cohort study. HRQOL was assessed using the SGRQ-I and the Medical Outcomes Study 36-item Short Form, dyspnea using the modified Medical Research Council (mMRC) dyspnea scale, and psychological status using the Hospital Anxiety and Depression Scale (HADS). We then evaluated the relationship between the SGRQ-I and other clinical measures, as well as one-year clinical deterioration defined as a hospital admission due to respiratory exacerbation or all-cause death. Results: Stepwise multiple-regression analyses revealed that the mMRC dyspnea scale, the HADS anxiety or depression, and minimum oxygen saturation during a six-minute walk test significantly contributed to the Total and three components of the SGRQ-I. In multivariate Cox proportional-hazards analyses, the Total score of SGRQ-I predicted clinical deterioration independent of forced vital capacity, the six-minute walk distance, or partial pressure of arterial oxygen on room air. Conclusions: The SGRQ-I is a multidisciplinary instrument representing physical, functional and psychological impairments in patients with IPF. The SGRQ-I is a significant predictor of short-term disease progression independent of physiological measurements. (Sarcoidosis Vasc Diffuse Lung Dis 2017; 34: 226-235).
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PMID:The association between health-related quality of life and disease progression in idiopathic pulmonary fibrosis: a prospective cohort study. 3247 50

Background: Exercise training have been shown to be the effective approach for functional outcomes in interstitial lung diseases (ILD). In many studies, the duration of exercise programs (EPs) varies between 8-12 weeks. However, the optimal duration of EPs is still unknown. Objective: In our prospective non-controlled study, we aimed to compare the results of the 8th week with the results of the 12th week of the PR programs applied to the patients with ILD. Methods: A total of 14 patients [Age; 63(53,70) years, body mass index: 28(25,32) kg/m2, disease duration; 1.5 (1,4) years] with ILD [11 idiopathic pulmonary fibrosis, 2 sarcoidosis (stage 3 and 4) and 1 nonspecific interstitial pneumonia] were included in the study. 6-minute walk test, pulmonary function test, arterial blood gas analysis, mMRC dyspnea scale, quality of life questionnaires and hospital anxiety depression scale were performed at before and 8 and 12 weeks after the program. Results: 6-minute walk distance, dyspnea, anxiety, depression and quality of life improved both at 8th and 12th week after EP when compared the with the initial assessment(P<0.05). When compared with 8th week; mMRC dyspnea score, 6-minute walk distance and quality of life scores significantly improved at 12th weeks (P=0.046, P=0.016, P<0.05, respectively). Conclusions: Prolonging duration of the EPs results in more improvement in functional outcomes in patients with ILD. However, it has no effect on pulmonary functions and arterial blood gas results. (Sarcoidosis Vasc Diffuse Lung Dis 2018; 35: 299-307).
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PMID:A comparison trial of eight weeks versus twelve weeks of exercise program in interstitial lung diseases. 3247 17

Pirfenidone (PFD), a pyridone compound, is well recognized as an antifibrotic agent tailored for the treatment of idiopathic pulmonary fibrosis. Recently, through its anti-inflammatory and anti-oxidant effects, PFD based clinical trial has also been launched for the treatment of coronavirus disease (COVID-19). To what extent this drug can perturb membrane ion currents remains largely unknown. Herein, the exposure to PFD was observed to depress the amplitude of hyperpolarization-activated cation current (Ih) in combination with a considerable slowing in the activation time of the current in pituitary GH3 cells. In the continued presence of ivabradine or zatebradine, subsequent application of PFD decreased Ih amplitude further. The presence of PFD resulted in a leftward shift in Ih activation curve without changes in the gating charge. The addition of this compound also led to a reduction in area of voltage-dependent hysteresis evoked by long-lasting inverted triangular (downsloping and upsloping) ramp pulse. Neither the amplitude of M-type nor erg-mediated K+ current was altered by its presence. In whole-cell potential recordings, addition of PFD reduced the firing frequency, and this effect was accompanied by the depression in the amplitude of sag voltage elicited by hyperpolarizing current stimulus. Overall, this study highlights evidence that PFD is capable of perturbing specific ionic currents, revealing a potential additional impact on functional activities of different excitable cells.
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PMID:Effective block by pirfenidone, an antifibrotic pyridone compound (5-methyl-1-phenylpyridin-2[H-1]-one), on hyperpolarization-activated cation current: An additional but distinctive target. 3252 5

Idiopathic pulmonary fibrosis (IPF) is a fatal fibrosing interstitial lung disease with limited therapeutic options and a median survival of 3 years after diagnosis. Dysregulated epithelial regeneration is key event involved in initiating and sustaining IPF. The type II alveolar epithelial cells (AECIIs) play a crucial role for epithelial regeneration and stabilisation of alveoli. Loss of cell apical-basal polarity contributes to fibrosis. AECII has apical-basal polarity, but it is poorly understood whether AECII apical-basal polarity loss is involved in fibrosis. Bleomycin is a traditional inducer of pulmonary fibrosis. Here firstly we observed that bleomycin induced apical-basal polarity loss in cultured AECIIs. Next, cell polarity proteins lethal (2) giant larvae 1 (Lgl1), PAR-3A, aPKC and PAR-6B were investigated. We found bleomycin induced increases of Lgl1 protein and decreases of PAR-3A protein, and bleomycin-induced PAR-3A depression was mediated by increased-Lgl1. Then Lgl1 siRNA was transfected into AECIIs. Lgl1 siRNA prevented apical-basal polarity loss in bleomycin-treated AECIIs. At last, Lgl1-conditional knockout mice were applied in making animal models. Bleomycin induced pulmonary fibrosis, but this was attenuated in Lgl1-conditional knockout mice. Together, these data indicated that bleomycin mediated AECII apical-basal polarity loss which contributed to experimental pulmonary fibrosis. Inhibition of Lgl1 should be a potential therapeutic strategy for the disease.
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PMID:Bleomycin induced apical-basal polarity loss in alveolar epithelial cell contributes to experimental pulmonary fibrosis. 3297 Nov 16


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