Wistar rats, purchased from BRL (Fullinsdorf/BL, Switzerland), and WBN/Kob rats, purchased from SLC Inc. (Shizuoka, Japan), were specific pathogen-free. Rats were housed in groups of maximally 4 instandard cages (1,820 cm2 bottom area) and kept in our animal facility for various time periods between 1 week and 36 weeks (free access to standard rat chow and water; specific pathogen-free conditions; 20 degree C; day/night cycle simulated by artificial lighting of 50 lx from 7 a.m. to 7 p.m., dimmed in the remaining hours to almost complete darkness; air humidity 50 to 60%). Prior to surgery or sacrifice, the rats were fasted overnight (16 to18 h) with free access to water. All manipulations conformed with the Swiss Federal Guidelines on Animal Experiments and were approved by the local ethics committee.
Inflammation-dependent expression of SPARC during development of chronic pancreatitis in WBN/Kob rats and a microarray gene expression analysis.
Sex, Age, Specimen part, TimeView Samples
RNA-sequencing performed on petals and inflorescence of Arabidopsis plants. The study provides insight into the role of the TCP5 transcription factor and its molecular mechanism underlying petal growth, using knock-out, overexpression and induction lines on which RNA-sequencing was performed. Overall design: Analysis of differential gene expression using petals from TCP5 overexpression and knockout lines, as well as inflorescences of an inducible TCP5 mutant.
Novel functions of the Arabidopsis transcription factor TCP5 in petal development and ethylene biosynthesis.
Specimen part, SubjectView Samples
RNA-Sequencing analysis of 18 papillary thyroid carcinoma biopsies and of 4 healthy donors'' thyroids. In this analysis we assessed differential gene expression and investigated the mutational landscape in this tumor type. Analysis of gene fusion was also performed, leading to the identification of a novel chimeric transcript, potential driver in tumor initiation. Overall design: Total RNA isolated from 18 papillary thyroid carcinoma biopsies and 4 healthy donors'' thyroids.
New somatic mutations and WNK1-B4GALNT3 gene fusion in papillary thyroid carcinoma.
No sample metadata fieldsView Samples
Human intestinal macrophages contribute to tissue homeostasis in noninflamed mucosa through profound down-regulation of pro-inflammatory cytokine release. Here, we show that this down-regulation extends to Toll-like receptor (TLR)-induced cytokine release, as intestinal macrophages expressed TLR3-TLR9 but did not release cytokines in response to TLR-specific ligands. Likely contributing to this unique functional profile, intestinal macrophages expressed markedly down-regulated adapter proteins MyD88 and Toll interleukin receptor 1 domain-containing adapter-inducing interferon beta, which together mediate all TLR MyD88-dependent and -independent NF-kappaB signaling, did not phosphorylate NF-kappaB p65 or Smad-induced IkappaBalpha, and did not translocate NF-kappaB into the nucleus. Importantly, transforming growth factor-beta released from intestinal extracellular matrix (stroma) induced identical down-regulation in the NF-kappaB signaling and function of blood monocytes, the exclusive source of intestinal macrophages. Our findings implicate stromal transforming growth factor-beta-induced dysregulation of NF-kappaB proteins and Smad signaling in the differentiation of pro-inflammatory blood monocytes into noninflammatory intestinal macrophages.
Inflammation anergy in human intestinal macrophages is due to Smad-induced IkappaBalpha expression and NF-kappaB inactivation.
Specimen partView Samples