[Effect of roxithromycin treatment on the IL-4, IL-5, and IFN-gamma production system induced by mite antigen].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Aoki.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We reported a 73-year-old man with pure akinesia syndrome who showed severe acquired stuttering and paradoxical kinesia on speech. He was evaluated in another hospital for bradykinesia and frozen gait at age of 67 when his cranial MRI disclosed ischemic changes in bilateral basal ganglia and periventricular deep white matter. The treatment with L-dopa and L-threo DOPS was not effective. His symptoms were slowly progressive and got worse gradually. At age of 72, he began to have difficulty in speech due to severe acquired stuttering, and one year later, he visited our hospital. The diagnosis of pure akinesia syndrome was made because of akinesia, micrographia, marked frozen gait with paradoxical kinesia and disturbance of postural reflex without tremor and rigidity. His speech showed severe acquired stuttering with marked blocking and repetition of initial phonemes at the beginning of speech. But intelligible speech recurred with pointing the characters by his finger or with writing an initial letter of word, although his speech was small and monotonous. Surface EMG findings of muscles participating speech in acquired stuttering showed the similar tonic discharge to those of muscles of lower extremity in frozen gait. These results implied that freezing phenomenon and festination of muscles participating speech in our patient may result in acquired stuttering.
Explore the source record for details and available documents.
To evaluate thrombopoiesis in thrombocytopenic disorders, we simultaneously determined reticulated platelet counts in whole blood by FACScan flow cytometry and serum thrombopoietin (TPO) concentrations by a sensitive sandwich ELISA. The subjects were 40 healthy volunteers and 45 thrombocytopenic patients. In idiopathic thrombocytopenic purpura (ITP), the percentage of reticulated platelets was significantly elevated (5.61 +/- 2.02%: mean +/- SD) relative to normal controls (2.17 +/- 0.90%), but serum TPO concentrations (1.91 +/- 1.27 fmol/l) did not differ significantly from the normal range (1.43 +/- 0.62 fmol/l). The patients with aplastic anemia (AA) had decreased reticulated platelet counts and markedly increased serum TPO concentrations (13.65 +/- 10.64 fmol/l). In thrombocytopenic patients with liver cirrhosis (LC), the absolute number of reticulated platelets (1.65 +/- 1.11 x 10(9)/l) decreased similarly that in AA. However, serum TPO concentrations (1.38 +/- 0.50 fmol/l) did not increase in contrast to AA. Our findings suggested a possible dual mechanism of thrombocytopenia in LC; that is, thrombocytopenia in LC results from the decreased TPO production primarily in the liver adding to an increase in platelet sequestration in the spleen.
Mitral valve aneurysm is defined as a localized protrusion of the valve with a different radius from that of the remaining portion of the valve. The medical records and pathological findings of seven patients with mitral valve aneurysm [aged 48-69 years (mean 64), 4 males] and the pathological findings of other 29 Japanese cases were reviewed. All seven patients were diagnosed pathologically as infective endocarditis, but two patients had no documentation of clinical symptoms suggestive of infective endocarditis (latent infective endocarditis). The underlying lesion of the heart was aortic valve disease and/or fibrosal degeneration of the mitral valve. Only 29 of 36 Japanese case reports stated a precise description of the valve pathology. Of these 29 cases, 23 were associated with infective endocarditis, two with rheumatic valvular disease with fusion and/or shrinkage of the chordae tendineae, three with mitral valve prolapse or myxomatous degeneration of the mitral valve, and one with aortitis syndrome. Neovascularization was described in eight cases. Neovascularization with thick wall should be considered as post-inflammatory vascularization. This review indicates that patients with latent infective endocarditis and mitral valve aneurysm should be considered as potential candidates for valve surgery.
The isolation of adenovirus type 7 (Ad7) has been rare in Japan in the past. However since April, 1995, many isolates of Ad 7 have been reported. In order to find the cause of Ad 7 re-emergence in Japan, we investigated the genome sequences of Ad 7 by analyzing the hexon hypervariable regions (HVRs). HVRs of genomes isolated before and after this prevalence showed little change and were closely related with each other. It was concluded that adenovirus hexon which contains HVRs is conserved in the same serotype of any genome type. At present, virus genome typing seems more suitable for comparing the differences of genomes than sequencing.
Combination adjuvant therapy with intravenous dimethyl triazeno imidazole carboxamide (DTIC), 1-[4-amino-2-methyl-5-pyrimidinyl]-methyl-3-[2-chloroethyl]-3-nitrosoure a hydrochloride (ACNU) and vincristine (VCR) and local injection of interferon-beta (IFN-beta) (DAV + IFN-beta therapy) has been widely applied to treat malignant melanoma, and its therapeutic effect is accepted in Japan. Natural killer (NK) activity, CD4+ and CD8+ T cell counts, CD4/CD8 ratio, and white blood cell counts were analyzed before and after DAV + IFN-beta therapy in order to validate its efficacy. After DAV + IFN-beta therapy, the CD4/CD8 ratio was elevated; however, numbers of both CD4+ and CD8+ T cells and NK activity were consecutively depressed. Peripheral lymphocytes were also decreased, possibly by myelosuppression due to the DAV therapy. The posttreatment suppression of NK activity appeared in spite of the administration of IFN-beta. It is suggested that a more effective adjuvant immunomodulator should be introduced to improve the therapeutic effect of the combination adjuvant chemotherapy in malignant melanoma.
We assessed the difference between transcortical sensory aphasia (TCSA) following the left frontal lesions (F-TCSA) and TCSA following the left posterior lesions (P-TCSA). All the patients were right-handed and the 7 patients had the lesions in the only frontal lobe and the 10 patients had the lesions only in the left temporo-parieto-occipital regions. We administered pointing tasks, using 90 line drawings representing single nouns. We presented 6 line drawings a pointing board, and we used two kinds of pointing boards: one showed the line drawings each belonging to different categories (random categorized pointing task), the other showed the line drawings each belonging to only either two different categories (two categorized pointing task) and we presented 15 pointing boards each alternatively. The result was that regarding the patients of P-TCSA showed different number of correct answers between the random categorized pointing task and the two categorized pointing task with statistical significance. Regarding the patients of F-TCSA showed no difference between them. The results indicated that disturbance of P-TCSA on the pointing task was the disturbance of semantic process per se. And the disturbance of F-TCSA on the pointing task was that of not only semantic process but also the whole process including comprehending the presented words, searching the line drawings, comparing the line drawings with the presented word and final selection, which demanded persistent multiple memory process consistent with working memory.
To examine whether there is a circadian variation in skin blood flow response to passive heat stress and maximal skin blood flow, which was measured by local warming to 42 degrees C for 45 min, we studied six men at an ambient temperature of 28 degrees C at four different times of day [0400-0700 (morning), 1000-1300 (daytime), 1600-1900 (evening), and 2200-0100 hours (night)], each time of day being examined on separate days. Heat stress at rest was performed by immersing the legs below the knee in hot water (42 degrees C) for 60 min. The esophageal temperature (Tes) at rest was significantly higher in the evening than in the morning. The maximal skin blood flow (SkBFmax) on both sites, back and forearm, did not show a significant difference among the four times of day. The variation in Tes thresholds for cutaneous vasodilation to heat stress was similar to the circadian rhythm in resting Tes. The relationship of the percentage of SkBFmax (%SkBF) with Tes was significantly lower in the morning than in the evening. The results suggest that the maximal skin blood flow during local warming does not show variation over the day, but the sensitivity of vasodilation to passive heat stress shows a circadian variation.
Binding of Escherichia coli chaperonin, GroEL, to substrate proteins with non-native structure, reduced alpha-lactalbumin (rLA) and denatured pepsin, were analyzed by isothermal titration calorimetry at various temperatures in the presence of salt (0.2 M KCl). Both proteins bound to GroEL with 1:1 stoichiometry and micromolar affinity at all temperatures tested. However, thermodynamic properties of their binding to GroEL are remarkably different from each other. While heat capacity changes (DeltaCp) of rLA-GroEL binding showed large negative values, -4.19 kJ mol-1 K-1, that of denatured pepsin-GroEL binding was only -0.2 kJ mol-1 K-1. These values strongly indicate that the hydrophobic interaction is a major force of rLA-GroEL binding but not so for denatured pepsin-GroEL binding. When salt was omitted from the solution, the affinity and DeltaCp of the rLA-GroEL binding reaction were not significantly changed whereas denatured pepsin lost affinity to GroEL. Thus, in the non-native protein-GroEL binding reaction, thermodynamic properties, as well as the effect of salt, differ from protein to protein and hydrophobic interaction may not always be a major driving force.
We present a gene-culture coevolutionary model for brother-sister mating in the human. It is shown that cultural--as opposed to innate--determination of mate preference may evolve, provided the inbreeding depression is sufficiently high. At this coevolutionary equilibrium, sib mating is avoided because of cultural pressures.
Bone morphogenetic proteins (BMPs) belong to the transforming growth factor-beta (TGF-beta) family and have been identified as factors that stimulate bone formation in vivo. They turned out to be multifunctional molecules regulating the growth, differentiation, and apoptosis in various target cells. Some BMPs and their receptors (BMPRs) are expressed on prostate cancer cells. We have reported previously that BMPR-IB mRNA expression is highest in the prostate, a characteristic that is not shared by the other BMPRs, BMPR-IA and BMPR-II. However, the amounts of BMPR-IB mRNA were significantly low in prostate tissues after androgen withdrawal therapy. They were also low in prostate cancer cell lines. Semiquantitative RT-PCR showed that BMPR-IB mRNA was induced by androgen in the androgen-sensitive human prostatic cancer cell line LNCaP, whereas the expression of BMPR-IA and BMPR-II mRNAs was not affected by androgen. When the recombinant human BMP-2 was added to the LNCaP cells in the presence of androgen, cell growth was inhibited. In contrast, the growth rate was increased by the addition of the same ligand when the cells were cultured in the absence of androgen; under this condition, the amounts of BMPR-IB mRNA were decreased significantly. These observations showed that the amounts of BMPR-IB, but not those of BMPR-IA, were regulated by androgen and further suggest that BMPR-IA and BMPR-IB differentially modulate prostate cancer cell growth in response to BMP under different hormonal conditions; BMPR-IA elicits growth stimulation, and BMPR-IB conveys a negative regulatory signal in response to BMP-2.
The modulating effects of nitric oxide (NO) and reactive oxygen species on cocaine-induced hepatotoxicity were examined by measuring plasma alanine aminotransferase activity and by carrying out histological studies. Liver injury was induced by a single injection of cocaine in adult male ICR mice. Pretreatment with aminoguanidine (an inhibitor of NO synthase), N-methyl-D-glucamine dithiocarbamate complex with iron ion (II) (Fe2+(MGD)2, a trapping reagent of NO) or deferoxamine complex with iron ion (III) (Fe3+-deferoxamine, a scavenger of NO) produced a marked inhibition of the hepatotoxicity induced by cocaine. In addition, pretreatment with allopurinol (an inhibitor of xanthine oxidase) and 1,3-dimethylthiourea (a scavenger of hydroxyl radical) also produced a potent inhibition. These findings suggest that a hydroxyl radical produced by the reaction of NO and superoxide anion (O2-) via peroxynitrite may be involved in the pathogenesis of cocaine hepatotoxicity.
Upon the addition of histidine and histamine, the copper containing monoamine oxidase (MAO) catalyzes the oxidation of L-ascorbic acid (AsA) by dissolved oxygen, in which the consumed oxygen was finally converted to hydrogen peroxide, according to Michaelis-Menten kinetics (Km) = 1.97 mM, upon the addition of 5 x 10(-5) M L-histidine at 35 degrees C and pH 8.5). The amount of oxygen consumption depended on the amount of histidine and histamine added, and specific responses over other amines were observed when the oxygen electrode modified with immobilized MAO membrane was used in the 0.1 M Tris buffer containing AsA. The calibration curves of L-histidine and histamine at 4 mM AsA exhibit linearity in the concentration range from 5 x 10(-7) to 5 x 10(-5) M L-histidine and 5 x 10(-6) to 1 x 10(-8) M histamine, with detection limit of 3 x 10(-7) M L-histidine and 3 x 10(-6) M histamine, respectively. The ESR signal of copper(II) in active site of MAO at 77K was apparently changed upon the addition of L-histidine and histamine indicating that exogenous histidine and histamine bound to the copper site of enzyme and lead to the structural change in active site.
Explore the source record for details and available documents.
Human Translin is a novel DNA end binding protein that specifically recognizes consensus sequences at the breakpoint junctions in chromosomal translocations, mostly involving immunoglobulin (Ig)/T-cell receptor gene segments, in human lymphoid neoplasms. We have recently cloned a full-length human Translin cDNA using peptide sequence information obtained from the purified protein. From comparisons of the amino acid sequences in humans and other vertebrates, we conclude that Translin has been highly conserved during evolution, especially at the leucine zipper motif and the basic region, which is thought to be the DNA binding domain. Analysis of the human and mouse Translin genes revealed that they have identical genomic structures consisting of six exons, five introns, and a GC-rich upstream region. In situ hybridization and physical mapping of somatic cell hybrids allowed localization of the gene to human chromosome 2q21.1.
BACKGROUND: Intimal lesions observed in the coronary arteries (CAs) of patients who have suffered episodes of Kawasaki disease (KD) raise concern about the premature development of arteriosclerosis. Accordingly, we investigated endothelial function in the epicardial and resistance CAs after KD during long-term observation. METHODS AND RESULTS: We assessed the responses of left epicardial and resistance CAs to serial intracoronary infusions of acetylcholine (final concentrations, 0.1 and 1 micromol/L) and nitroglycerin in subjects by using quantitative angiography and a Doppler flow wire system. Three age-matched groups were evaluated: 8 control subjects (group 1), 10 KD patients with normal left CA from the onset (group 2), and 8 KD patients with a persistent or regressed aneurysm in the left anterior descending CA (LAD) (group 3). Acetylcholine (1 micromol/L) changed the LAD area to 114.0+/-2.6%, 72.7+/-3.9% (P<.05 versus group 1), and 88.9+/-4.3% (P<.05 versus groups 1 and 2) of baseline in groups 1, 2, and 3, respectively, with a similar degree of increased coronary blood flow in each group. Nitroglycerin increased the LAD area to 143.5+/-7.7%, 132.3+/-1.9%, and 120.8+/-5.6% (P<.05 versus group 1), respectively. CONCLUSIONS: Results demonstrate a persistent endothelial dysfunction in the epicardial but not resistance CAs in patients after KD and enhanced stiffness of persistent or regressed aneurysms. The concern over early arteriosclerosis warrants the surveillance of KD patients from childhood to adulthood.