Early transcriptional response in the jejunum of germ-free piglets after oral infection with virulent rotavirus

Germ-free piglets were orally infected with virulent rotavirus to collect jejunal mucosal scrapings at 12 and 18 hours post infection (two piglets per time point). IFN-gamma mRNA expression was stimulated in the mucosa of all four infected piglets, indicating that they all responded to the rotavirus infection. RNA pools prepared from two infected piglets were used to compare whole mucosal gene expression at 12 and 18 hpi to expression in uninfected germ-free piglets (n = 3) using a porcine intestinal cDNA microarray. Microarray analysis identified 13 down-regulated and 17 up-regulated genes. Northern blot analysis of a selected group of genes confirmed the data of the microarray. Genes were functionally clustered in interferon-regulated genes, proliferation/differentiation genes, apoptosis genes, cytoskeleton genes, signal transduction genes, and enterocyte digestive, absorptive, and transport genes. Down-regulation of the transport gene cluster reflected in part the loss of rotavirus-infected enterocytes from the villous tips. Data mining suggested that several genes were regulated in lower- or mid-villus immature enterocytes and goblet cells, probably to support repair of the damaged epithelial cell layer at the villous tips. Furthermore, up-regulation was observed for IFN-γ induced guanylate binding protein 2, a protein that effectively inhibited VSV and EMCV replication in vitro (Arch Virol 150:1213–1220, 2005). This protein may play a role in the small intestine’s innate defense against enteric viruses like rotavirus

Neuromusculoskeletal disorders in the neck and upper extremities among drivers of all-terrain vehicles – a case series

BACKGROUND: The purpose of this study was to investigate whether professional drivers of all-terrain vehicles (ATVs) with neck pain have a different array of neuromusculoskeletal disorders in the neck and upper extremities than a referent group with neck pain from the general population. It is hypothesized that exposure to shock-type vibration and unfavorable working postures in ATVs have the capacity to cause peripheral nervous lesions. METHODS: This study was based on a case series analyzed according to a case-case comparison design. The study population consisted of 60 male subjects, including professional drivers of forest machines (n = 15), snowmobiles (n = 15), snowgroomers (n = 15) and referents from the general population (n = 15) all of whom had reported neck pain in a questionnaire and underwent an extensive physical examination of the neck and upper extremities. Based on symptom history, symptoms and signs, and in some cases chemical, electroneurographical and radiological findings, subjects were classified as having a nociceptive or neuropathic disorder or a mix of these types. RESULTS: The occurrence of asymmetrical and focal neuropathies (peripheral nervous lesion), pure or in a mix with a nociceptive disorder was common among cases in the ATV driver groups (47%–79%). This contrasted with the referents that were less often classified as having asymmetrical and focal neuropathy (27%), but instead had more nociceptive disorders. The difference was most pronounced among drivers of snowgroomers, while drivers of forest machines were more frequently classified as having a nociceptive disorder originating in the muscles. CONCLUSION: This study found a high prevalence of assymetrical and focal neuropathies among drivers with pain in the neck, operating various ATVs. It seems as if exposure to shock-type whole-body vibration (WBV) and appurtenant unfavorable postures in ATVs may be associated to peripheral nervous lesions

SAMMSON fosters cancer cell fitness by concertedly enhancing mitochondrial and cytosolic translation

Synchronization of mitochondrial and cytoplasmic translation rates is critical for the maintenance of cellular fitness, with cancer cells being especially vulnerable to translational uncoupling. Although alterations of cytosolic protein synthesis are common in human cancer, compensating mechanisms in mitochondrial translation remain elusive. Here we show that the malignant long non-coding RNA (lncRNA) SAMMSON promotes a balanced increase in ribosomal RNA (rRNA) maturation and protein synthesis in the cytosol and mitochondria by modulating the localization of CARF, an RNA-binding protein that sequesters the exo-ribonuclease XRN2 in the nucleoplasm, which under normal circumstances limits nucleolar rRNA maturation. SAMMSON interferes with XRN2 binding to CARF in the nucleus by favoring the formation of an aberrant cytoplasmic RNA-protein complex containing CARF and p32, a mitochondrial protein required for the processing of the mitochondrial rRNAs. These data highlight how a single oncogenic lncRNA can simultaneously modulate RNA-protein complex formation in two distinct cellular compartments to promote cell growth