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K Quade

Publications and source records attributed to K Quade.

14 recordsLinked to original sources
PubMed2005

An evaluation of the acute impact of pursed lips breathing on walking distance in nonspontaneous pursed lips breathing chronic obstructive pulmonary disease patients.

This study was designed to test the effects of pursed lips breathing (PLB) during exercise in patients with chronic obstructive pulmonary disease (COPD) who did not spontaneously perform PLB. Sixty-nine COPD patients, mean FEV1 (SD) 1.09 (0.5), age 68 (51-83) were recruited to the study. They performed three incremental shuttle walk tests (ISWT). The first walk was designed to identify natural PLBs and the next two walks were performed in a random order; ISWT + PLB or ISWT whilst breathing normally. Measures of respiratory rate (RR), breathlessness and oxygen saturation were taken before and after walks. Data was analysed using the t-test. Fifteen patients demonstrated PLB on baseline ISWT and were therefore excluded from further walking tests although baseline data was included in the analysis. There was no significant difference between walks, mean (SD), 298.5 (173.7) PLB and non-PLB; 292.5 (161.9) nor any difference in dyspnoea. There was a significant reduction in end exercise RR and recovery time with PLB, mean difference (95% CI); 6.2 (4.5-7.9) and 24.9 (2.8-47.0) seconds, respectively. Patients who showed a good response with the PLB walk (41%) had significantly higher baseline breathlessness, Borg score, mean (SD), 1.5 (1.0) versus 0.74 (0.96) (P = 0.02). Natural PLB patients demonstrated lower exercise tolerance on the baseline walk (P = 0.01) and a trend towards greater resting breathlessness than those who did not. This study shows PLB during exercise and recovery results in lower post exercise RR and speeds return to pre exercise breathlessness, compared with exercise and non-PLB. Reductions in RR appear to be greatest in those patients with resting breathlessness.

Aged↗
PubMed1992

Integration of hepatitis B virus DNA through a mutational hot spot within the cohesive region in a case of hepatocellular carcinoma.

Integrated hepatitis B virus (HBV) DNA previously cloned from a hepatocellular carcinoma genomic library derived from a Japanese patient was characterized further. Sequence analysis of restriction fragments bearing the virus-host junctions defined 3125 nucleotides of essentially un-rearranged HBV DNA of the adr subtype with the right junction mapping within the cohesive region at position 1970 and the left within the pre-core at position 1886. The right viral-host junction contains a 7 bp repeat (TGTAGGC) and a possible 2 bp inversion. The integrated HBV DNA includes the complete open reading frames for core, pre-S, S and polymerase and a 3' truncated X gene, and lacks most of the pre-core. Integration has occurred at a mutational hot spot of the viral genome and appears to be located in a region of semi-repetitive genomic DNA 3' to the beta-globin gene cluster.

Base Sequence↗
PubMed1983

Virus gene expression in rat cells transformed by avian myelocytomatosis virus strain MC29 and avian erythroblastosis virus.

Virus gene expression in rat cells transformed by either avian myelocytomatosis virus strain MC29 or avian erythroblastosis virus has been studied by biological and biochemical methods. In the clones examined, virus-specific sequences were found to be transcribed into RNA and, in most clones, the characteristic gag-related proteins could be identified. The transformed rat cells were fused to permissive chick cells and the rescued virus was shown to transform both chick embryo fibroblasts and the appropriate haemopoietic cell type in chick bone marrow cultures. These results clearly demonstrate that, as with the non-defective avian sarcoma viruses, the genetic information responsible for transformation by the defective avian leukaemia viruses can be expressed in non-permissive mammalian host cells as well as in permissive avian cells.

Alpharetrovirus↗
PubMed1982

Expression of the ASV src gene in hybrids between normal and virally transformed cells: specific suppression occurs in some hybrids but not others.

Somatic cell hybrids have been made between clones of rat cells transformed by avian sarcoma virus and rat or mouse cells that are untransformed. Intraspecies hybrids were either predominantly morphologically normal or predominantly transformed, some clones that formed transformed intraspecies hybrids yielding normal interspecies hybrids. Untransformed hybrids usually showed no detectable alteration in the structure or location of the integrated provirus, but viral RNA and pp60src kinase activities were much reduced. No decrease in viral gene expression was seen in transformed hybrids. Thus hybrid suppression of viral transformation, mediated in trans by the untransformed parent, is a specific event that depends on both untransformed and transformed parental parameters.

Animals↗
PubMed1981

Revertants of rats cells transformed by avian erythroblastosis virus.

Morphological revertants of the avian erythroblastosis virus (AEV)-transformed rat cell line ATla were isolated and characterised. The revertants are similar to the uninfected parental rat cell line in that they have regained an organized cytoskeleton and they are no longer capable of anchorage-independent growth. The pattern of integrated viral DNA in the revertants is indistinguishable from that of the transformed parent. However, the revertants do not express the integrated viral genome at either the mRNA or protein level. Phenotypic reversion thus is probably .due to reduced transcription of the AEV-transforming gene below a threshold necessary to induce morphological transformation.

Alpharetrovirus↗
PubMed1973

Physiocochemical studies on L-cell virions.

The L-cell virion (LCV) has been purified from supernatant fluids of mouse L cells grown in suspension culture. The virion is similar to other RNA tumor viruses by several criteria: (i) the density of the virion is 1.16 g/cm(3); (ii) the virion appears as a rounded membranous particle with an outer diameter of 146.7 +/- 11.8 nm, and contains knobs (7-nm diameter) over its surface; (iii) 15 polypeptides (ranging in molecular weight from 7,000 to 110,000) are detectable after electrophoresis of virion protein in sodium dodecyl sulfate-polyacrylamide gels; (iv) three species of RNA can be isolated-high molecular weight (80 to 88s) (50%), 7s (35%) and 4s (15%); (v) heat denaturation of the high-molecular-weight RNA yields a heterogeneous population of molecules (20 to 35s) as well as a 7s and 4s species. Despite the general similarity to infectious RNA tumor viruses, LCV is apparently defective as evidenced by the fact that it does not induce tumors in animals or transform normal mouse cells in vitro (Kindig and Kirsten [17]). The defective nature of the LCV might be related to the fact that assays for DNA polymerase in the virion showed only a negligible activity when compared to Rous sarcoma virus.

Adenosine↗
PubMedDate not supplied

Increased MHC H-2K gene transcription in cultured mouse embryo cells after adenovirus infection.

The class I major histocompatibility complex (MHC) antigens are highly polymorphic cell-surface proteins whose expression is essential for the cellular immune response against virus-infected, abnormal and foreign cells. Transformation of primary rat cell cultures by the oncogenic adenovirus 12 (Ad12) results in suppression of the transplantation antigens, thus enabling the transformed cells to escape the immune response and efficiently form tumours in vivo. In contrast, transformation of the same cells with the non-oncogenic adenovirus 5 (Ad5) does not suppress the transplantation antigens and, consequently, they elicit an effective (MHC-restricted) immune response. Here, however, we show that infection of mouse embryo cells with both viruses initially increases the level of transcripts from the H-2Kb transplantation antigen gene. Both the adenovirus E1a (12S RNA) and E1b genes are required for activation of the H-2K gene and measurement of the relative rate of transcription indicates that the increase in the level of H-2K messenger RNA following infection is at least in part due to a gene-specific transcriptional activation. The newly transcribed H-2Kb mRNA is then properly transported to the cytoplasm.

Adenoviruses, Human↗