Biomedical subjects
Publications and source records attributed to T Azuma.
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The prevalence of RA in Japan has been reported to be approximately 0.3% of general population and the ratio of male to female patients is 1 to 4. The course of RA is classified into 3 types, those are monocyclic, polycyclic and progressive. The polycyclic and progressive courses of RA would have been ameliorated by the recent progress of medical and surgical treatment and an increased number of patients in monocyclic course would be expected. The mortality rate among RA patients is higher than that of population control. There are causes of death directly related to rheumatoid process itself and resulted from drug treatment. The former includes secondary amyloidosis and basilar impression and the latter includes infection, renal failure and GI bleeding.
To study the distribution of somatic mutation, we determined nucleotide sequences of rearranged lambda 1-chain genomic DNA from four hybridomas obtained from C57BL/6 mice that had been immunized with (4-hydroxy-3-nitrophenyl)acetyl-conjugated chicken gamma globulin. In total, 114 nucleotide substitutions were observed, with neither insertion nor deletion. Sixty-one mutations occurred in the variable-joining region genes (V lambda 1-J lambda 1) and 49 in joining-constant (J lambda 1-C lambda 1) introns. Although frequency decreased with distance from the V lambda 1-J lambda 1 coding region, somatic mutations occurred in the entire J lambda 1-C lambda 1 intron and even in the C lambda 1 region. We found four nucleotide substitutions in C lambda 1 genes, all of which were replacement mutations. Therefore, the mechanism responsible for somatic mutation is operative into the C lambda 1 exons. Nucleotide sequences of rearranged but inactive lambda 2-chain genes from two hybridomas were also examined and compared with those of lambda 1-chain genes. The clustering of replacement mutations in complementarity-determining regions in the inactive lambda 2-chain genes similar to the active lambda 1-chain genes suggested a mechanism that induces somatic mutation preferentially in this region even in the absence of antigenic selection.
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MLR in various combinations with class I H-2 disparity revealed that there are three patterns of MLR in the aspect of responding T subset (CD4 vs CD8) dominance. Irrespective of the CD8 vs CD4 dominance, a single i.v. administration of class I-disparate allogeneic spleen cells resulted in almost complete abrogation of anti-class I proliferative capacity of both CD4+ and CD8+ T cells in six combinations. The suppression of proliferative responses was correlated with the striking reduction in the ability to produce IL-2 upon stimulation with the relevant class I alloantigens. In contrast, i.v. presensitized recipient mice exhibiting only marginal MLR/Il-2 production could generate comparable magnitudes of anti-allo class I CTL as well as graft rejection responses to those induced by normal unpresensitized mice. The administration in vivo of anti-CD4 antibody along with the i.v. presensitization not only suppressed the generation of CTL responses by spleen cells but also induced appreciable prolongation of allo-class I-disparate skin grafts under conditions in which neither alone did it. These results demonstrate that 1) the suppression of graft rejection responses is not necessarily reflected on the reduction of MLR; 2) CD8+ CTL precursors responsible for graft rejection can be activated by either allo-class I-reactive CD8+ or CD4+ Th cells; 3) i.v. presensitization induces functional elimination of CD8+ and CD4+ proliferative/IL-2-producing T cells but not of CD8+ CTL precursors and CD4+ Th whose capacity is expressed by assistance of CTL induction but not by their own proliferation. Thus, this study illustrates the heterogeneity of class I alloantigen-reactive CD4+ T cells in the aspect of their capacity to proliferate themselves vs contribute to CTL induction as well as graft rejection.
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The effects of L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), an unnatural norepinephrine precursor, on alpha 2-adrenergic receptors in platelet membranes were investigated in a patient with familial amyloidotic polyneuropathy, two patients with multiple system atrophy, and two patients with Parkinson's disease. Each patient was treated for at least six months. While L-threo-DOPS alone, or in combination with decarboxylase inhibitor benserazide hydrochloride, produced sustained increase in plasma norepinephrine and clinical improvement, it did not induce a change in the number of alpha 2-adrenergic receptors in platelet membranes.
A patient with motor neuron disease and tonic pupil who had an antinuclear antibody (Ab) in the serum and oligoclonal pattern in IgG in the CSF is described. Sera and CSF from this patient and controls (37 sera and 30 CSF) were screened for an antineuronal Ab using immunoblotting. Only the serum and CSF from this patient contained an Ab to a 70-kD protein in the human spinal cord but not in the human muscle or cerebellar cortex. This patient's serum immunohistochemically stained human and Japanese monkey anterior horn cells but not Japanese monkey dorsal root ganglion.
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Two cases of primary lung cancer with initial symptoms due to metastasis to the eye or the orbit are reported. Case 1 had orbital metastasis, while case 2 had intraocular metastasis. It has been reported that the survival period is short after the metastasis was found. In our cases, the survived periods for case 1 and case 2 were 3.5 months and one month, respectively.
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