Acquired B character in a "A" group subject (a case report).
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Biomedical subjects
Publications and source records attributed to S Prakash.
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The RAD10 gene is one of several genes in Saccharomyces cerevisiae required for incision of u.v.-irradiated or cross-linked DNA. We have determined the nucleotide sequence of the RAD10 gene and its flanking regions. The RAD10 nucleotide sequence presented here differs significantly from that recently reported. The RAD10 protein predicted from the nucleotide sequence contains 210 amino acids with a calculated mol. wt. of 24 310. The middle portion of the RAD10 protein, which is highly basic and also contains eight of the total of 10 tyrosine residues present in the protein, may be involved in DNA binding by ionic interactions and tyrosine intercalation between the bases of DNA. A genomic deletion of the entire RAD10 gene does not affect viability; however, the rad10 deletion mutant is highly u.v. sensitive.
The RAD3 gene of Saccharomyces cerevisiae is required for excision of pyrimidine dimers and is essential for viability. We present the nucleotide sequence of the RAD3 protein coding region and its flanking regions, and the deduced primary structure of the RAD3 protein. In addition, we have mapped the 5' end of RAD3 mRNA. The predicted RAD3 protein contains 778 amino acids with a calculated molecular weight of 89,779. A segment of the RAD3 protein shares homology with several adenine nucleotide binding proteins, suggesting that RAD3 protein may react with ATP. The twenty carboxyl terminal amino acids of RAD3 protein are predominantly acidic; however, deletion of this acidic region has no obvious effect on viability or DNA repair.
The RAD1 and RAD3 genes of Saccharomyces cerevisiae are required for excision repair of UV damaged DNA. In addition, the RAD3 gene is essential since rad3 deletions are recessive lethals. We have examined the induction of the RAD1 and RAD3 genes by DNA damage and during the cell division cycle. We have made fusions of the RAD1 and RAD3 genes with the Escherichia coli lacZ gene encoding beta-galactosidase. Beta-galactosidase activity was measured in a Rad+ yeast strain containing the RAD1-lacZ or the RAD3-lacZ fusion, either in a multicopy replicating plasmid or as a single copy integrant resulting from transformation with an integrating plasmid which transforms yeast by homologous recombination in the yeast genome. No induction of beta-galactosidase activity occurred after ultraviolet light (UV) or 4-nitroquinoline-1-oxide (NQO) treatment. Haploid cells of mating type a were synchronized by treatment with alpha factor and beta-galactosidase activity was determined during different cell cycle stages. No change in beta-galactosidase activity was observed in the strain containing the RAD1-lacZ or the RAD3-lacZ fusion integrated in the yeast genome.
We have cloned the RAD10 gene of Saccharomyces cerevisiae and physically mapped it to a 1.0-kb DNA fragment. Strains containing disruptions of the RAD10 gene were found to show enhanced UV sensitivity compared with the previously characterized rad10-1 or rad10-2 mutants. The UV sensitivity of the disruption mutant is comparable to the highly UV sensitive rad1-19, rad2-delta, and rad3-2 mutants.
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We have cloned CDC9, the structural gene for Saccharomyces cerevisiae DNA ligase, and investigated its transcriptional regulation both as a function of cell cycle stage and after UV irradiation. The steady-state level of DNA ligase mRNA increases at least fourfold in late G1, after the completion of start but before S phase. This high level of CDC9 mRNA then decays with an apparent half-life of ca. 20 min and remains at a low basal level throughout the rest of the cell cycle. The accumulation of CDC9 mRNA in late G1 is dependent upon the completion of start but not the CDC7 and CDC8 functions. Exposure of cells to UV light elicits an eightfold increase in DNA ligase mRNA levels.
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We have reported that IL 2 is one of the essential helper factors in culture supernatants from concanavalin A-activated spleen cells or T cell hybridomas that support proliferation and immunoglobulin secretion in B cell cultures responding to anti-immunoglobulin. Here we show that cells in such cultures consume IL 2 and bear high affinity IL 2 receptors detected by binding of purified, radiolabeled IL 2. Induction of high affinity IL 2 receptors depends on addition of both anti-immunoglobulin and helper factors, and does not occur in cultures given only anti-Ig, only helper factors, concanavalin A plus helper factors, or LPS. The majority of IL 2 receptors are on cells that also bear endogenous membrane immunoglobulin, because they are found in the membrane immunoglobulin-positive fraction when cultured cells are separated by fluorescence sorting after overnight culture in the absence of anti-immunoglobulin to allow reexpression of membrane immunoglobulin.
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We have cloned the RAD2 gene of Saccharomyces cerevisiae and used it to determine the size and direction of its transcript and to make rad2 deletion mutants. The RAD2 gene encodes a 3.3-kb transcript and the direction of transcription is leftwards, from EcoRI towards Bg/II. Deletions of the RAD2 gene have no effect on viability of vegetative cells or spores, or on sporulation.
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Fifty-one North Indian patients with ankylosing spondylitis (AS) are described with mean age of onset 21.2 years and male to female ratio of 16:1. AS began with peripheral arthritis in 47%, low back pain in 41%, acute anterior uveitis in 10%, and heel pain in 2% of the patients. 76% of 51 patients had one of the extra-axial features of AS: peripheral arthritis (61%), heel pain (24%), anterior uveitis (22%), urethritis (12%), kidney disease (10%), mucosal ulcerations (6%), aortic incompetence (4%), and apical pulmonary fibrosis (4%). A majority (71%) of the patients with peripheral arthritis had mono- or oligoarthritis affecting mainly the lower limb joints. Two patients had coexistent rheumatoid arthritis also. HLA-B27 antigen was detected in 48 (94%) of 51 patients compared with 7 (6%) of 118 controls (relative risk 254; Fisher's exact p = 3.49(-29]. On comparing patients with juvenile onset AS and patients with adult onset disease we found peripheral arthritis to be more frequent at the beginning and during the course of disease in the former.
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Quantitative sacroiliac scintigraphy (QSS) was evaluated for the detection of sacroiliac (SI) joint disease before the appearance of radiographic/changes. QSS with fractional quantitation was done in 13 age- and sex-matched controls and 28 patients with different grades of radiographic sacroiliitis. The SI index of each joint was considered separately. The mean SI index values in patients with grade I radiographic sacroiliitis (1.54) and HLA-B27 positive patients with low back pain (1.50) were significantly (P less than 0.01) higher than the mean SI index of controls (1.22); but more than 50% of their SI index values were within the 97.5% confidence limits of the control range. The mean SI index values of patients with grade II (1.38) and grade III (1.34) radiographic sacroiliitis did not differ significantly from the mean SI index of controls (P greater than 0.05). Thus a large overlap between the normal and abnormal ranges of sacroiliac ratios limits the utility of quantitative sacroiliac scintigraphy for the early diagnosis of sacroiliac joint disease.
Thirty-six patients fulfilling the criteria for Reiter's disease were studied (29 men and 7 women; 4:1). The mean age of onset was 23.8 years; in 75% of patients the onset was in the second and third decades. Clinical manifestations included low back pain and stiffness (69%), non specific urethritis (53%), heel pain (44%), radiographic sacroiliitis (42%), conjunctivitis (39%), dysentery and diarrhoea (33%), mucosal ulcerations (17%) kidney disease (14%), anterior uveitis (19%), and keratoderma blennorrhagicum (8%). Peripheral arthritis was mono or oligoarthritis in 58% of patients, mainly affecting the large joints of lower extremities, and it was often asymmetric (mean degree of asymmetry = 0.37). HLA-B27 antigen was detected in 83% of 36 patients compared with 5.9% of 118 controls (relative risk 79, corrected Fisher's P = 7.719E-18).