Two cell lines, designated HTZ and HT3, were nolated from two transplanted hamster sarcomas induced by bovine papillomavirus type I (BPV-I) and studied after 50 to 60 subcultures. Cells are tumorigenic for hamsters and showed no detectable viral capsid protein synthesis by immunofluorescence technique. Cells contained multiple copies of the entire BPV-I genome, 100 to 500 and 10 t o 100 per diploid amount of HT2 and HT3 cell DNA, respectively, as determined by blot hybridization experiments. In unrestricted cell DNA, viral genomes migrated as free single viral DNA molecules and slow migrating species. HT2 cell DNA restricted by single cut enzymes for BPV-I DNA (Eco RI and Bam HI endonucleases) yielded only one viral genome unit length DNA molecule, indicating that the slow migrating species could correspond to free oligomeric or catenated molecules. Patterns of HT3 cell DNA restricted by Eco RI or Barn HI enzymes showed the presence of additional bands, suggesting that the slow migrating species could correspond t o viral DNA sequences integrated in cell DNA. Up to five polypeptides (I90 K, 125 K, 59 K, 33 K, 30 K) were reproducibly precipitated from[3SS]-methionine-or 32P -labelled HT2 or HT3 cell extracts by sera from hamsters bearing HT2 or HT3 cellinduced tumors and by sera from pikas bearing BPV-I induced fibrosarcomas. Polypeptides with similar molecular weights were detected by HT2 sera in a SV40 tumor hamster cell line (TSV5 CI.2) and in a rat cell line transformed in vitro by SV40 DNA form I (VI I FI Cl. I).The I90 K polypeptide was also detected in a normal hamster embryo cell strain (EH). Conversely, a pool of SV40 tumor hamster sera precipitated the 59 K and the 33 K polypeptides from HTZ cells. The polypeptides thus identified are most probably transformation-related cell proteins. Whether or not their synthesis is related t o the expression of some BPV-I transforming genes remains to be established.

BackgroundChicken meat and eggs can be a source of human zoonotic pathogens, especially Salmonella species. These food items contain a potential hazard for humans. Chickens lines differ in susceptibility for Salmonella and can harbor Salmonella pathogens without showing clinical signs of illness. Many investigations including genomic studies have examined the mechanisms how chickens react to infection. Apart from the innate immune response, many physiological mechanisms and pathways are reported to be involved in the chicken host response to Salmonella infection. The objective of this study was to perform a meta-analysis of diverse experiments to identify general and host specific mechanisms to the Salmonella challenge.ResultsDiverse chicken lines differing in susceptibility to Salmonella infection were challenged with different Salmonella serovars at several time points. Various tissues were sampled at different time points post-infection, and resulting host transcriptional differences investigated using different microarray platforms. The meta-analysis was performed with the R-package metaMA to create lists of differentially regulated genes. These gene lists showed many similarities for different chicken breeds and tissues, and also for different Salmonella serovars measured at different times post infection. Functional biological analysis of these differentially expressed gene lists revealed several common mechanisms for the chicken host response to Salmonella infection. The meta-analysis-specific genes (i.e. genes found differentially expressed only in the meta-analysis) confirmed and expanded the biological functional mechanisms.ConclusionsThe meta-analysis combination of heterogeneous expression profiling data provided useful insights into the common metabolic pathways and functions of different chicken lines infected with different Salmonella serovars.

Ingenuity Pathway Analysis indicated that hsa-miR-99b and hsa-miR-125a could be associated with the phenotypes manifested by p.F508del patients. Here we provide novel elements in the mechanism of hsa-miR-99b and hsa-miR-125a biogenesis, and for the role of CFTR and DeltaF508-CFTR on the expression of this miRNA cluster. These findings augment existing data implicating miRNAs as putative CF modifiers.