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71.
Sheldon M. Cooper Karen Roessner John A. Ferriss Gregory Baigent Antony C. Bakke 《Arthritis \u0026amp; Rheumatology》1987,30(10):1089-1096
Patients with very active rheumatoid arthritis that was being treated only with nonsteroidal antiinflammatory drugs had increased numbers of peripheral blood OKM1 + lymphocytes. In 3 patients, 90° light scatter analysis revealed a double lymphocyte peak. When sorted, the high scatter peak contained a large percentage of granular lymphocytes. Patients with mild-to-moderately active rheumatoid arthritis had normal levels of OKM1 + lymphocytes, but when the drugs were discontinued, the activity of the disease and the numbers of OKM1 + cells increased. Administration of piroxicam was associated with clinical improvement and a decrease in levels of OKM1 + cells. OKM1 + granular lymphocytes are increased in some rheumatoid arthritis patients, and their numbers may correlate with clinical disease activity and/or therapy. 相似文献
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Zehnder D Landray MJ Wheeler DC Fraser W Blackwell L Nuttall S Hughes SV Townend J Ferro C Baigent C Hewison M 《Nephron. Clinical practice》2007,107(3):c109-c116
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Marek’s disease virus (MDV) is a cell-associated alphaherpesvirus that induces rapid-onset T-cell lymphomas in poultry. MDV
isolates vary greatly in pathogenicity. While some of the strains such as CVI988 are non-pathogenic and are used as vaccines,
others such as RB-1B are highly oncogenic. Molecular determinants associated with differences in pathogenicity are not completely
understood. Comparison of the genome sequences of phenotypically different strains could help to identify molecular determinants
of pathogenicity. We have previously reported the construction of bacterial artificial chromosome (BAC) clones of RB-1B from
which fully infectious viruses could be reconstituted upon DNA transfection into chicken cells. MDV reconstituted from one
of these clones (pRB-1B-5) showed similar in vitro and in vivo replication kinetics and oncogenicity as the parental virus.
However, unlike the parental RB-1B virus, the BAC-derived virus showed inability to spread between birds. In order to identify
the unique determinants for oncogenicity and the ‘‘non-spreading phenotype’’ of MDV derived from this clone, we determined
the full-length sequence of pRB-1B-5. Comparative sequence analysis with the published sequences of strains such as Md5, Md11,
and CVI988 identified frameshift mutations in RLORF1, protein kinase (UL13), and glycoproteins C (UL44) and D (US6). Comparison
of the sequences of these genes with the parental virus indicated that the RLORF1, UL44, and US6 mutations were also present
in the parental RB-1B stock of the virus. However with regard to UL13 mutation, the parental RB-1B stock appeared to be a
mixture of wild type and mutant viruses, indicating that the BAC cloning has selected a mutant clone. Although further studies
are needed to evaluate the role of these genes in the horizontal-spreading defective phenotype, our data clearly indicate
that mutations in these genes do not affect the oncogenicity of MDV. 相似文献
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