1,721,134 research outputs found
Methacoline Responsiveness and airway parenchymal interdipendence in the decorin deficient mouse.
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Changes in Smad expression and subcellular localization in bleomycin-induced pulmonary fibrosis.
No full textAdministration of bleomycin (BM) produces inflammation and fibrosis of the lung in humans and experimental animals. The molecular defects by which BM induces these pathological effects have not been studied in detail. We studied the expression of Smad family proteins, key molecules involved in mediating transforming growth factor (TGF)-_ signaling from the cell membrane to the nucleus, during the early and late phases of BM-induced fibrogenesis. Pulmonary fibrosis was induced in male Sprague-Dawley rats by a single intratracheal injection (1.5 units) of BM. Control rats received saline. Rats were killed at 3, 5, 7, 14, and 28 days after BM, cytosolic and nuclear proteins were extracted and isolated from lung tissues,
and Smad proteins were probed with specific antibodies. In BMexposed lung tissue, compared with control, Smad3 decreased persistently in the cytosol and increased transiently in the nucleus. There was a persistent increase in phosphorylation and nuclear accumulation of Smad2/3. Smad4 was increased transiently in both the cytosol and nucleus. A significant and progressive decrease in the expression of Smad7, the endogenous inhibitor of TGF-_/Smad signaling, was observed after BM instillation. Collectively, our results indicate that
an imbalance between agonistic Smads2–4 and antagonistic Smad7 may result in the unchecked activation of an autocrine TGF-_ loop, which contributes to the pathogenesis of BM-induced pulmonary fibrosis
Tidal airway closure in asthma and COPD
Full text linkFunctional closure of small airways can occur during tidal breathingabove functional residual capacity (FRC) both in asthma and chronicobstructive pulmonary disease (COPD) patients, especially during ex-acerbations. Such event has several noxious consequences on gas ex-change, airway hyperresponsiveness and mechanical stress and strainwithin lung tissue and airway wall, mostly due to increase in ventila-tion heterogeneity. The availability of simple functional tests based onsequential measurements of lung volumes (i.e., FRC), by plethysmog-raphy and dilutional techniques may reveal and monitor easily tidalairway closure that can be and should be treated with the aim of abol-ishing or at least reducing this dangerous condition
Airway obstruction or closure during bronchoconstricction in asthma: can we preconize it?
No full textSevere acute respiratory syndrome coronavirus 2 infection in those on mepolizumab therapy
No full textHeart and lung in the old age. The association between COPD and cardiovascular diseases: How much and how
No full textThe association COPD-Cardiovascular diseases (CVD) - in particular heart failure - is a wellknown phenomenon that invest COPD of a new clinical dimension. Given the high occurrence of both diseases, their association - also due to common risk factors - is not surprising. An additive contribution to this association is given by: the Aging effect (progressive development of a pro-inflammatory and pro-thrombotic state), the COPD effect (the emphysema impaired the systolic ventricular function; the increasing of the systemic inflammation through a mechanism of overspill; neuro-umoral activation). A particular attention to the cardiac function should be used in exacerbations of COPD. Due to the peculiar diagnostic, prognostic and therapeutics problems, the association between COPD and CVD cannot be ignored by the future guidelines, taking into account that in the general population the cardiovascular mortality is reducing, whether in COPD patients it is increasing
Alpha1-antitrypsin Deficiecy and nephropathy
No full textGlomerulonephritis occurring in association with alpha(1)-antitrypsin deficiency has been sporadically reported in the literature but it is assumed to be a rare and poorly investigated disease. The complete pathologic pattern of glomerular lesions has not yet been established. The aim of our work was to investigate the correlation between the extent of antiprotease deficiency and the expression of nephropathy evaluated in two groups of patients (47 heterozygotic subjects with the PiMZ phenotype and 12 homozygotic subjects with the PiZZ phenotype) by a noninvasive approach with urinalyses and proteinuria measurement. No statistical differences between proteinuria in the two groups were observed suggesting that nephropathy is not a direct and single expression of the protein deficiency
Interrelazione tra deficit funzionale di 1-ANTITRIPSINA ed iperreattività delle vie aeree.
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