Int J Clin Exp Patho
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Int J Clin Exp Patho · Jan 2012
Idiopathic pulmonary fibrosis: immunohistochemical analysis provides fresh insights into lung tissue remodelling with implications for novel prognostic markers.
This study explored the cellular and biological interrelationships involved in Idiopathic Pulmonary Fibrosis (IPF) lung tissue remodelling using immunohistochemical analysis. ⋯ The pathogenesis of IPF is complex and involves multiple factors, possibly including EMT. Histological analysis suggests TGF-β-stimulated myofib rob lasts initiate a contractile response within established fibroblastic foci while proliferating ATII cells attempt to instigate alveolar epithelium repair. Marker expression (N-cadherin and Ki-67) correlation with histological disease activity (as reflected by fibroblastic foci extent) may emerge as future prognostic indicators for IPF.
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Int J Clin Exp Patho · Jan 2012
The cell death of C6 astrocytoma cells induced by oridonin and its mechanism.
Many studies have shown that oridonin, a compound purified from Rabdosia rubescens, was able to suppress proliferation and induce apoptosis in many cell types. In this study, In order to investigate the proliferation suppression and apoptosis-inducing effect of oridonin on Rat C6 astrocytoma cells, we treated C6 cells with different concentrations of oridonin for various time intervals. Oridonin concentration-time viability curve were used to test the effect of oridonin on the C6 cells. ⋯ Hochest 33258 staining and flow cytometry revealed that oridonin induced apoptosis and arrested the entry into G2/M phase of C6 cells. According to the results of Western blot, oridonin down-regulated Bcl-2, up-regulated Bax protein, and activated caspase-3 in the oridonin-treated C6 cells. All together, our results suggested that oridonin can cause the suppression of proliferation in C6 astrocytoma cells and the cell death induced by oridonin might be associated with mitochondria- mediated apoptosis by activating caspase-3.
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Int J Clin Exp Patho · Apr 2011
Somatic mutations of the EGF receptor and their signal transducers affect the efficacy of EGF receptor-specific tyrosine kinase inhibitors.
Non-small cell lung cancer (NSCLC) is a major subtype of lung cancer that has been the most common and most fatal cancer worldwide. Gefitinib (Iressa) and erlotinib (Tarceva) specific tyrosine kinase inhibitors (TKI) for the epidermal growth factor receptor (EGFR), have been demonstrated to be effective for some NSCLC patients and are pioneering molecular-targeted drugs used in the clinic for cancer. ⋯ Moreover, problems of acquired resistance after long-term treatment with the drugs have emerged. In this review, I summarize the current understanding of the EGFR-activated signal transduction pathway, which plays important roles in tumorigenesis, and of the molecular mechanisms that determine the sensitivity toward EGFR-TKI.
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Carney complex is a syndrome that may include cardiac and mucocutaneous myxomas, spotting skin pigmentation, and endocrine lesions. Many patients with Carney complex have been shown to have a stop codon mutation in the PRKAR1A gene in the 17q22-24 region. Here we present the case of a 57 year-old man with multiple skin lesions and cardiac myxomas. ⋯ A germline missense mutation was identified at exon 1A. This is the first report of this mutation, and one of the few reported missense mutation associated with Carney complex. This finding strengthens the argument that there are alternative ways in which the protein kinase A 1-alpha subunit plays a role in tumorigenesis.
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Int J Clin Exp Patho · Jan 2008
Gut hyperpermiability after ischemia and reperfusion: attenuation with adrenomedullin and its binding protein treatment.
Ischemia bowel remains a critical problem resulting in up to 80% mortality. The loss of gut barrier function plays an important role. Our previous studies have shown that administration of adrenomedullin (AM), a novel vasoactive peptide, and its binding protein (AMBP-1), reduces the systemic inflammatory response and organ injury after systemic ischemia induced by hemorrhagic shock. ⋯ Treatment with AM/AMBP-1 dramatically improved I/R-induced intestinal mucosal damages, attenuated remote organ injury, and downregulated gene expression and protein levels of TNF-alpha in the small intestine. In conclusion, AM/AMBP-1 attenuates structural and functional damages to the intestinal mucosa, and it appears to be a novel treatment for reperfusion injury after gut ischemia. The beneficial effect of AM/AMBP-1 on gut barrier function after I/R is associated with downregulation of TNF-alpha.