silicosis/phosphatase

Cytochemical tuberculin-associated shifts along with their prognostic evaluation were studied in 30 patients with silicosis and silicotuberculosis with intrathoracic adenopathy. The study revealed that a decrease of alkaline phosphatase activity of neutrophils, alpha-glycerophosphate dehydrogenase

Protein Expression Profile in Rat Silicosis Model Reveals Upregulation of PTPN2 and Its Inhibitory Effect on Epithelial-Mesenchymal Transition by Dephosphorylation of STAT3.

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Silicosis is a chronic occupational lung disease caused by long-term inhalation ofcrystalline silica particulates. We created a rat model that closely approximates the exposure and development of silicosis in humans. Isobaric tags for relative and absolute quantitation (iTRAQ) technologies weused to

[The importance of assessing angiotensin-converting activity in silicosis patients].

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The macrophage cells have an essential role in the pathogenesis of silicosis. After the endocytosis of silica grains, the lung macrophage demonstrates an active state, associated with high levels of lysosomal enzymes, expressed also in serum. A similar active state of macrophages is evident in

Lung alkaline phosphatase as a marker of fibrosis in chronic interstitial disorders.

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Alkaline phosphatase (ALP) in lung lavage fluids is a marker of tissue damage and type II cell proliferation. Type II pneumocytes are extensively involved in fibrosis. The aim of our study was to verify whether local ALP activity can be held as a marker of fibrosis in chronic interstitial lung

Global DNA methylation and PTEN hypermethylation alterations in lung tissues from human silicosis.

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BACKGROUND Silicosis is a respiratory disease caused by long-term silica dust exposure. Our previous study has demonstrated that silica mediates the activation of phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/serine or threonine kinase

Rho GDP dissociation inhibitor α silencing attenuates silicosis by inhibiting RhoA/Rho kinase signalling.

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Transforming growth factor-β1 (TGF-β1) alters the fibroblast phenotype by promoting transdifferentiation into myofibroblasts, which exhibit the ability to promote collagen synthesis and extracellular matrix (ECM) deposition, thereby playing a significant role in the pathology of silicosis. In this

Histoenzymology of the lung. II. The behaviour of lung hydrolytic enzymes during some experimental pulmonary processes.

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The enzymic activity of acid alkaline phosphatases, of alanyl- and leucine-aminopeptidases, of beta-galactosidase and beta-glucuronidase, and of Tween-60-esterase was tested in the rabbit lung tissue during the following experimental processes: a) the sensitization with Freund adjuvant containing

Coelonin, an Anti-Inflammation Active Component of Bletilla striata and Its Potential Mechanism.

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Ethanol extract of Bletilla striata has remarkable anti-inflammatory and anti-pulmonary fibrosis activities in the rat silicosis model. However, its active substances and molecular mechanism are still unclear. To uncover the active ingredients and potential molecular mechanism of the

[Cytoenzymological, immunological and scanning electron microscopic studies on 49 cases (author's transl)].

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Light cytology, enzymology, immunofluorescence and scanning electron microscopy have been performed on 49 bronchoalveolar fluids recovered by bronchoscopic lavage. The patients had the following lung diseases: infectious pneumonitis (19 cases), pulmonary fibrosis (13 cases) including 5 sarcoïdosis,

[Histochemical mechanisms in etiology of pulmonary fibrosis after short-term exposure to a mixture of dust and quartz from copper mine].

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The authors induced pulmonary silicosis in albino rats by the intratracheal method with 50 mg mixed middling slime from Panaguiriste and quartz dust, dissolved in I ml physiological solution. The animals received a single treatment and were killed on 90th day of the experiment. Some intime

Pulmonary inflammation in rats after intratracheal instillation of quartz, amorphous SiO2, carbon black, and coal dust and the influence of poly-2-vinylpyridine-N-oxide (PVNO).

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Effects of poly-2-vinylpyridine-N-oxide (PVNO) were investigated in numerous in vivo and in vitro studies published in the nineteen sixties and seventies. These studies showed that PVNO inhibited development of fibrosis from quartz dust and improved lung clearance of quartz after inhalation

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