Transcripts from the Circadian Clock: Telling Time and Season

We all know it when we wake mere moments before an alarm clock is scheduled to wake us: our body clock made the alarm clock redundant. This phenomenon is driven by an endogenous timer known as the biological, or circadian clock. Each revolution of the Earth about its own axi

Cerebroventricular Microinjection (CVMI) into Adult Zebrafish Brain Is an Efficient Misexpression Method for Forebrain Ventricular Cells

The teleost fish Danio rerio (zebrafish) has a remarkable ability to generate newborn neurons in its brain at adult stages of its lifespan-a process called adult neurogenesis. This ability relies on proliferating ventricular progenitors and is in striking contrast to mammalian brains that have rather restricted capacity for adult neurogenesis. Therefore, investigating the zebrafish brain can help not only to elucidate the molecular mechanisms of widespread adult neurogenesis in a vertebrate species, but also to design therapies in humans with what we learn from this teleost. Yet, understanding the cellular behavior and molecular programs underlying different biological processes in the adult zebrafish brain requires techniques that allow manipulation of gene function. As a complementary method to the currently used misexpression techniques in zebrafish, such as transgenic approaches or electroporation-based delivery of DNA, we devised a cerebroventricular microinjection (CVMI)-assisted knockdown protocol that relies on vivo morpholino oligonucleotides, which do not require electroporation for cellular uptake. This rapid method allows uniform and efficient knockdown of genes in the ventricular cells of the zebrafish brain, which contain the neurogenic progenitors. We also provide data on the use of CVMI for growth factor administration to the brain – in our case FGF8, which modulates the proliferation rate of the ventricular cells. In this paper, we describe the CVMI method and discuss its potential uses in zebrafish

Redox-regulated expression of glycolytic enzymes in resting and proliferating rat thymocytes

AbstractResting rat thymocytes partially degrade glucose aerobically to CO2 and H2O and produce reactive peroxide anions. In contrast proliferating cells, due to enhanced induction of glycolytic enzymes, degrade glucose almost completely to lactate thus minimizing the production of reactive oxygen species. In this paper we show that under conditions of oxidative stress the induction of the glycolytic enzymes in cultured rat thymocytes is markedly reduced. Furthermore, transfection assays with a rat hepatoma cell line and Drosophila Schneider cells revealed that reactive oxygen intermediates dramatically decrease the transcriptional activities of the Sp1-dependent aldolase A and pyruvate kinase M2 promoters leading to reduced reporter gene expression. These results indicate that cellular redox changes can regulate gene expression by reversible oxidative inactivation of Sp1 binding.© 1997 Federation of European Biochemical Societies

...eine Soziologie, als ob Natur nicht zählen würde?

Die Differenz von Natur und Gesellschaft ist für die Soziologie von fundamentaler Bedeutung: Konstituiert sie doch von Anbeginn an Soziologie als Fach mit einem anderen Gegenstand als Naturwissenschaften und erzeugt diese Differenz durch weitere Differenzen der Erfahrung und des gesellschaftlichen Umgangs mit der Natur. Angesichts des Verlustes der gesicherten Grenzen zischen Natürlichem und Sozialem, zwischen Technischem und Sozialem, muss jedoch das sichere Terrain der vertrauten Soziologie verlassen werden. Der Beitrag führt ein in die Plenarveranstaltung des 28. Kongresses der Deutschen Gesellschaft für Soziologie "Soziologie der Natur". Die Diskussionen dort zeigen, dass die Mehrheit sich nicht dazu verleiten lassen will, der Natur und den Objekten Tür und Tor zur Soziologie zu öffnen. Jedoch wollen auch, vor allem die Jüngeren, sich mit einer Soziologie, in der Natur nicht zählt, nicht abfinden. (ICB2

Oncostatin M Mediates STAT3-Dependent Intestinal Epithelial Restitution via Increased Cell Proliferation, Decreased Apoptosis and Upregulation of SERPIN Family Members

Objective: Oncostatin M (OSM) is produced by activated T cells, monocytes, and dendritic cells and signals through two distinct receptor complexes consisting of gp130 and LIFR (I) or OSMR-beta and gp130 (II),respectively. Aim of this study was to analyze the role of OSM in intestinal epithelial cells (IEC) and intestinal inflammation. Methods: OSM expression and OSM receptor distribution was analyzed by PCR and immunohistochemistry experiments, signal transduction by immunoblotting. Gene expression studies were performed by microarray analysis and RT-PCR. Apoptosis was measured by caspases-3/7 activity. IEC migration and proliferation was studied in wounding and water soluble tetrazolium assays. Results: The IEC lines Caco-2, DLD-1, SW480, HCT116 and HT-29 express mRNA for the OSM receptor subunits gp130 and OSMR-b, while only HCT116, HT-29 and DLD-1 cells express LIFR mRNA. OSM binding to its receptor complex activates STAT1, STAT3, ERK-1/2, SAPK/JNK-1/2, and Akt. Microarray analysis revealed 79 genes that were significantly up-regulated (adj.-p <= 0.05) by OSM in IEC. Most up-regulated genes belong to the functional categories "immunity and defense'' (p=2.1x10(-7)),"apoptosis'' (p=3.7x10(-4)) and "JAK/STAT cascade'' (p=3.4x10(-6)). Members of the SERPIN gene family were among the most strongly up-regulated genes. OSM significantly increased STAT3- and MEK1-dependent IEC cell proliferation (p < 0.05) and wound healing (p=3.9x10(-5)). OSM protein expression was increased in colonic biopsies of patients with active inflammatory bowel disease (IBD). Conclusions: OSM promotes STAT3-dependent intestinal epithelial cell proliferation and wound healing in vitro. Considering the increased OSM expression in colonic biopsy specimens of patients with active IBD, OSM upregulation may modulate a barrier-protective host response in intestinal inflammation. Further in vivo studies are warranted to elucidate the exact role of OSM in intestinal inflammation and the potential of OSM as a drug target in IBD