表紙・目次 『第15回CEReS国際シンポジウム「環境リモートセンシングのこれま での成果とさらなる挑戦」』 2009年12月15日～16日 於千葉大学

Held on 15-16 December, 2009, Chiba Universit

Cathepsin K transgenic mice (black bars) and wild-type mice (white bars) were administered either saline or bleomycin for 1, 2, 3, and 4 weeks

Subsequently, mice were euthanized and lungs were lavaged as described in Materials and Methods. Total BAL fluid cell numbers (A), alveolar macrophages (B), exudate macrophages (C), neutrophils (D) and lymphocytes (E) were ascertained from Pappenheim-stained cytospin preparations of BAL fluid. The data are shown as mean ± SD of at least n = 5 mice per group and time point. No statistical significances were noted between wild-type and Cathepsin K transgenic mice.<p><b>Copyright information:</b></p><p>Taken from "Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis"</p><p>http://respiratory-research.com/content/9/1/54</p><p>Respiratory Research 2008;9(1):54-54.</p><p>Published online 18 Jul 2008</p><p>PMCID:PMC2490691.</p><p></p

Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis-2

Nized and BAL cells (A, B), freshly isolated type II alveolar epithelial cells (A, C), lung homogenate (A, D), and concentrated BAL fluid supernatant (E) were prepared for analysis of cath K mRNA by real-time RT-PCR (A) and western blotting (B-E). (A), data are given as fold change in cathepsin K mRNA of bleomycin-challenged cath K tg mice compared to wild-type mice. (F) Gelatin zymography employing concentrated BAL fluid protein from mock- or bleomycin-treated wild-type mice and cath K tg mice. Data are shown as mean ± SD of n = 3 determinations. (B-F), data represent at least n = 3–5 independent analyses. * indicates < 0.05 versus bleomycin-treated wild-type mice at day 14 post-treatment.<p><b>Copyright information:</b></p><p>Taken from "Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis"</p><p>http://respiratory-research.com/content/9/1/54</p><p>Respiratory Research 2008;9(1):54-54.</p><p>Published online 18 Jul 2008</p><p>PMCID:PMC2490691.</p><p></p

Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis-1

Ks. Subsequently, mice were euthanized and lungs were processed for quantitative assessment of collagen content by hydroxyproline assay, as described in Materials and Methods. The data are shown as mean ± SD of at least n = 10 mice per group and time point. * indicates < 0.05 compared to wild-type mice. + indicates significant increase (p < 0.05) compared to mock-treated wild-type mice.<p><b>Copyright information:</b></p><p>Taken from "Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis"</p><p>http://respiratory-research.com/content/9/1/54</p><p>Respiratory Research 2008;9(1):54-54.</p><p>Published online 18 Jul 2008</p><p>PMCID:PMC2490691.</p><p></p

Mutation Analysis of <em>BRCA1, BRCA2, PALB2</em> and <em>BRD7</em> in a Hospital-Based Series of German Patients with Triple-Negative Breast Cancer

<div><p>Triple-negative breast cancer (TNBC) is an aggressive form of breast carcinoma with a poor prognosis. Recent evidence suggests that some patients with TNBC harbour germ-line mutations in DNA repair genes which may render their tumours susceptible to novel therapies such as treatment with PARP inhibitors. In the present study, we have investigated a hospital-based series of 40 German patients with TNBC for the presence of germ-line mutations in <em>BRCA1</em>, <em>BRCA2</em>, <em>PALB2</em>, and <em>BRD7</em> genes. Microfluidic array PCR and next-generation sequencing was used for <em>BRCA1</em> and <em>BRCA2</em> analysis while conventional high-resolution melting and Sanger sequencing was applied to study the coding regions of <em>PALB2</em> and <em>BRD7</em>, respectively. Truncating mutations in <em>BRCA1</em> were found in six patients, and truncating mutations in <em>BRCA2</em> and <em>PALB2</em> were detected in one patient each, whereas no truncating mutation was identified in <em>BRD7</em>. One patient was a double heterozygote for the <em>PALB2</em> mutation, c.758insT, and a <em>BRCA1</em> mutation, c.927delA. Our results confirm in a hospital-based setting that a substantial proportion of German TNBC patients (17.5%) harbour germ-line mutations in genes involved in homology-directed DNA repair, with a preponderance of <em>BRCA1</em> mutations. Triple-negative breast cancer should be considered as an additional criterion for future genetic counselling and diagnostic sequencing.</p> </div

Double heterozygosity for <i>BRCA1</i> and <i>PALB2</i> mutations.

<p>A case with digenic mutations in <i>BRCA1</i> (left) and <i>PALB2</i> (right). Left: Heterozygosity for mutation c.927delA in exon 10 of the <i>BRCA1</i> gene. Right: Heterozygosity for mutation c.758insT in exon 4 of the <i>PALB2</i> gene. The sense strand is shown in both electropherograms.</p

Truncating mutations in <i>BRCA1</i>, <i>BRCA2</i> and <i>PALB2</i> among 40 TNBC patients.

<p>Truncating mutations in <i>BRCA1</i>, <i>BRCA2</i> and <i>PALB2</i> among 40 TNBC patients. Mutations were designated according to the improved mutation nomenclature recommended by the Human Genome Variation Society (<a href="http://www.hgvs.org/mutnomen/" target="_blank">www.hgvs.org/mutnomen/</a>). AD = age at diagnosis, BC = breast cancer, OC = ovarian cancer, IHC = immunohistochemistry, n.a. = not applicable.</p>*<p>BIC database as from Sep 29, 2010 (<a href="http://research.nhgri.nih.gov/projects/bic/Member/index.shtml" target="_blank">http://research.nhgri.nih.gov/projects/bic/Member/index.shtml</a>), accessed on July 10, 2012.</p