A new translocation (4;12)(q21;q15) after combined immunosuppressive therapy in a case of hypoplastic myelodysplastic syndrome with translocation (12;15)(q23;q12)
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Anemia, Refractory↗
Biomedical subjects
T Matsuo
Publications and source records attributed to T Matsuo.
Regional bond strengths of self-etching/self-priming adhesive systems.
The purpose of this study was to measure the regional tensile bond strengths (TBS) at various portions of human tooth enamel and dentin, and to observe the resin-dentin interfaces of two commercially available self-etching/self-priming adhesive systems by scanning electron microscopy (SEM). Twelve extracted human cuspid teeth were used to measure TBS and four additional teeth were used for scanning electron microscopy (SEM). Outer enamel and dentin were removed from the labial tooth surfaces to form a long cavity preparation into middle dentin extending from the mid-crown to the apex of the root within the same tooth. Either Clearfil Liner Bond 2 (LB 2, Kuraray) or Fluoro Bond (FB, Shofu) was bonded to the surfaces, and covered with resin-composite. The resin-bonded teeth were serially sliced at right angles to the long axis of the tooth, and the bonded surfaces were trimmed to give a bonded cross-sectional surface area of 1 mm2 for TBS tests. LB 2 and FB showed significantly higher TBS in coronal, cervical and middle root dentin than that in enamel and apical root dentin. SEM showed that the thickness of the hybrid layer of both systems was about 1.0 microm in coronal, cervical and middle root dentin, and less than 0.5 microm in apical root dentin. These results suggested that the self-etching/self-priming systems produce good adhesion in coronal, cervical and middle root dentin by creating thin hybrid and transitional layers, but bonding to enamel and apical root dentin should be improved.
Acid Etching, Dental↗
Nuclear factor kappa B dependent induction of gamma glutamylcysteine synthetase by ionizing radiation in T98G human glioblastoma cells.
Glioblastoma is one of the most malignant of all neoplasms, and often shows resistance to chemotherapy and radiation therapy. Ionizing radiation activates transcriptional factors, such as nuclear factor kappa-B (NF-kappa B). Previously we found that glutathione (GSH) synthesis is induced by cytokines mediated by NF-kappa B (Urata et al. J. Biol. Chem., 1996). Here, we present direct evidence that NF-kappa B activated by ionizing radiation induces the expression of gamma-glutamylcysteine synthetase (gamma-GCS), the rate limiting enzyme of GSH synthesis, using T98G human glioblastoma cells. T98G cells have approximately 14-times the level of intracellular GSH of NB9 cells, radiation-sensitive neuroblastoma cells. In T98G cells, 30-Gy of ionizing radiation was required for the activation of NF-kappa B on an electrophoretic mobility shift assay and the induction of gamma-GCS mRNA on Northern blots and a nuclear run-on assay. However, when T98G cells were treated with buthionine sulfoximine, 3-Gy of ionizing radiation stimulated the DNA-binding activity of NF-kappa B and the expression of gamma-GCS. We constructed chimeric genes containing various regions of gamma-GCS promoter gene and the coding region for Luciferase. T98G cells transiently transfected with a plasmid containing the gamma-GCS promoter-luciferase construct showed increased luciferase activity when treated with ionizing radiation. The luciferase activity stimulated by ionizing radiation was found in the gamma-GCS promoter containing the NF-kappa B binding site, whereas not in that containing its mutated site. These results suggest that GSH synthesis is upregulated by ionizing radiation mediated by NF-kappa B and a high concentration of GSH in T98G cells causes downregulation of the NF-kappa B-DNA binding activity in response to ionizing radiation. The irresponsiveness of the intracellular signal transduction cascade to irradiation may be a factor in the resistance of T98G cells to radiation therapy.
Acetylcysteine↗
Direct binding between two PDZ domain proteins Canoe and ZO-1 and their roles in regulation of the jun N-terminal kinase pathway in Drosophila morphogenesis.
During Drosophila embryogenesis, the ventral epidermis dorsally expands and the left and right epithelial sheets meet and fuse along the dorsal midline. For this dorsal closure to occur, two PDZ domain proteins, Cno and ZO-1, are required. The dorsal epidermis remains open when the expression of ZO-1 and Cno are reduced simultaneously by hypomorphic mutations in the relevant loci. ZO-1 and Cno colocalize at adherens junctions in embryonic epithelia, and form a protein complex upon binding to each other. Genetic analysis showed that Cno is involved in the Jun N-terminal kinase (JNK) pathway for dorsal closure, as a modulator acting upstream of, or in parallel with, the small GTPase Drac1. The ZO-1-Cno complex may be involved in dynamic changes in cytoskeletal organization and cell adhesion during morphogenetic events associated with dorsal closure in the Drosophila embryo.
Animals↗
Hemostatic activation and cardiac events after the 1995 Hanshin-Awaji earthquake.
Earthquake-induced stress seems to induce rheological deterioration associated with high blood pressure, an increase of blood viscosity due to hemoconcentration and an increase of the fibrinogen level. These changes lead to prolonged endothelial cell injury and accelerate fibrin turnover as the result of a high D-dimer level. An increase of these acute changes caused by mental and physical stress after an earthquake might trigger obstructive thrombus in coronary arteries in the elderly.
Disasters↗
Schwartz-Matsuo syndrome in retinal detachment with tears of the nonpigmented epithelium of the ciliary body.
PURPOSE: To elucidate clinical features of Schwartz-Matsuo syndrome (photoreceptor outer segment glaucoma) occurring in retinal detachment with tears of the nonpigmented epithelium of the pars plana or plicata of the ciliary body. METHODS: We reviewed retrospectively medical records of 17 consecutive patients (18 eyes) with retinal detachment caused by tears of the nonpigmented epithelium of pars plana (10 eyes) and pars plicata (8 eyes) of the ciliary body. RESULTS: Aqueous cells, ranging from 1+ to 3+, were found in 15 eyes, in contrast with no cells in the other 3 eyes. Eleven of the 15 eyes with aqueous cells showed circadian fluctuation of the intraocular pressure with a range, 4 mmHg or wider compared with the range in the fellow eye, but only 4 of these 11 eyes had a maximum pressure of 21 mmHg or higher. Photoreceptor outer segments were detected in the aqueous humor of 8 eyes out of 14 eyes with aqueous cells in which aqueous tap was done. The remaining 6 eyes had too small a number of aqueous cells for electron microscopy. CONCLUSION: Marked fluctuation of the intraocular pressure compared with the fellow eye, which was not necessarily associated with its rise, was found in retinal detachment with tears of the nonpigmented epithelium of the ciliary body, and should be included as one of key features for diagnosis of Schwartz-Matsuo syndrome.
Adolescent↗
Genetic variation in the promoter region of the beta-fibrinogen gene is associated with ischemic stroke in a Japanese population.
Evidence suggests that an allelic variation in the beta fibrinogen gene may confer an increased risk of coronary artery disease and stroke. The role of the beta fibrinogen gene polymorphism and fibrinogen levels in ischemic stroke has not been determined in Japanese, who are more prone to stroke than to coronary artery disease compared with Caucasians. We investigated the associations between ischemic stroke, plasma fibrinogen level, and a HaeIII restriction fragment length polymorphism (G/A(-455)) located at -455 bp from the start of transcription of the beta fibrinogen gene in 85 hypertensive patients with ischemic stroke (stroke group), 85 hypertensive patients without ischemic stroke (nonstroke group) and in 84 normotensive subjects matched for age, sex, and smoking status recruited at an annual health examination (normotensive group). The frequency of non-cutting allele (designated A(-455) allele) in the control group was 0.07 [95% CI: 0.03-0.11]; this value was significantly lower than that previously reported in Caucasians (0.19-0.26). The A(-455) allele frequency of the nonstroke group and stroke group were 0.08 [95% CI: 0.04-0.12] and 0.15 [95% CI: 0.10-0.21]. A(-455) allele frequency of the stroke group was significantly higher than that of the control group chi2 = 5.63, P= 0.018) and the nonstroke group chi2 = 4.00, P= 0.043). The mean +/- SD fibrinogen level was significantly higher in the stroke group than that in the normotensive group (277 +9/- 64 mg/dl versus 257 +/- 52 mg/dl, P < 0.03), but that of the nonstroke group was not significantly different compared with both normotensive and stroke groups. In conclusion, the positive association between the fibrinogen genotype G/A(-455) and ischemic stroke in hypertensive patients was independent of other risk factors. These results suggest that fibrinogen A(-455) allele may be an independent risk factor for ischemic stroke in the Japanese population.
Age Factors↗
Effect of an anticoagulant (heparin versus nafamostat mesilate) on the extrinsic coagulation pathway in chronic hemodialysis.
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Adult↗
Plasma levels of natriuretic peptides and adrenomedullin in elderly hypertensive patients: relationships to 24 h blood pressure.
OBJECTIVE: The aim of this study was to investigate the relationships between levels of natriuretic peptides and adrenomedullin and 24 h blood pressure levels in elderly hypertensives. DESIGN AND METHODS: We performed both 24 h ambulatory blood pressure monitoring and measurement of plasma levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and adrenomedullin in 118 asymptomatic hypertensive elderly (> 60 years old) patients. We classified the subjects into groups with isolated clinic hypertension (n = 40) and sustained hypertension (n = 78). We also measured the levels of these peptides in 37 elderly normotensive subjects. RESULTS: Plasma ANP and BNP levels were slightly increased in patients with isolated clinic hypertension compared with elderly normotensives. Among the hypertensives, plasma ANP and BNP levels were more closely related to 24 h blood pressure levels than to office blood pressure levels. Sustained hypertensives showed significantly increased plasma levels of ANP and BNP compared with isolated clinic hypertensives, while adrenomedullin levels were similar in the two groups. Elderly hypertensives with left ventricular hypertrophy detected by electrocardiography had significantly higher levels of ANP and BNP, and higher BNP/ANP ratios than those without left ventricular hypertrophy, while there was no significant difference in adrenomedullin levels between the two groups. CONCLUSIONS: Our results suggest that measurements of ANP and BNP may be useful in detecting left ventricular hypertrophy and in differentiating isolated clinic hypertension from sustained hypertension in elderly hypertensive patients.
Adrenomedullin↗
Augmentation of the inhibitory effect of FK480, a CCK-A receptor antagonist, on pancreatic exocrine secretion by achlorhydria.
The effect of intraluminal acid and cholecystokinin (CCK) receptor blockade on the pancreatic secretory response was examined in rats. Blockade of gastric acid secretion by YM022 (CCK-B receptor antagonist) or famotidine (histamine-2 receptor antagonist) resulted in a significant suppression of casein-stimulated pancreatic exocrine secretion as determined by juice volume and amylase secretion. Ligation of the gastric pylorus, which leads to complete prevention of gastric acid from entering the duodenum, also suppressed pancreatic exocrine secretion. FK480 (CCK-A receptor antagonist) inhibited pancreatic exocrine secretion dose dependently at doses of 0.01-1.0 mg/kg. When submaximal doses of FK480 and YM022 were treated concomitantly, pancreatic exocrine secretion was inhibited more profoundly than when treated solely. Hydrochloric acid (HCl; 0.05 N), injected into the duodenum, stimulated pancreatic exocrine secretion to a level comparable to that exhibited by intraduodenal casein. This effect of HCl was inhibited by FK480 (1.0 mg/kg) but not by YM022 (1.0 mg/kg). These findings suggest that inhibition of gastric acid secretion leads to the suppression of pancreatic exocrine secretion through mechanisms mediated by CCK-A receptors.
Achlorhydria↗
Two types of initial ocular manifestations in intraocular-central nervous system lymphoma.
PURPOSE: To study initial ocular manifestations of ocular-central nervous system (CNS) lymphoma. METHODS: The authors reviewed medical records of 10 consecutive patients with intraocular-CNS lymphoma seen at Okayama University Hospital during 16 years from 1981 to 1996. RESULTS: Three patients showed only vitreous opacity as an initial sign, whereas five other patients had typical yellowish-white infiltrates at the sub-retinal pigment epithelial (sub-RPE) level without vitreous opacity. Both manifestations were found in two patients. In seven patients, ocular symptoms developed first, followed by brain lesions. In contrast, in three patients the initial presentation was brain tumor, for which they received chemotherapy; subsequently, vitreous opacity without sub-RPE infiltrates developed. The diagnosis was made by vitrectomy in four patients, three of whom had also undergone brain biopsy; by aqueous tap in one; and by brain biopsy in one. The other four patients were diagnosed clinically, and one of them was confirmed later to have lymphoma by autopsy. CONCLUSIONS: The initial ocular manifestations of intraocular-CNS lymphoma were of two types, sub-RPE infiltrates and vitreous opacity. Keeping these two manifestations in mind will help physicians consider a diagnosis of intraocular-CNS lymphoma earlier.
Adult↗
Human T-lymphotropic virus type-I infection, antibody titers and cause-specific mortality among atomic-bomb survivors.
There have been few longitudinal studies on the long-term health effects of human T-lymphotropic virus type-I (HTLV-I) infection. The authors performed a cohort study of HTLV-I infection and cause-specific mortality in 3,090 atomic-bomb survivors in Nagasaki, Japan, who were followed from 1985-1987 to 1995. The prevalence of HTLV-I seropositivity in men and women was 99/1,196 (8.3%) and 171/1,894 (9.0%), respectively. During a median follow-up of 8.9 years, 448 deaths occurred. There was one nonfatal case of adult T-cell leukemia/lymphoma (incidence rate = 0.46 cases/1,000 person-years; 95% confidence interval [CI] 0.01-2.6). After adjustment for sex, age and other potential confounders, significantly increased risk among HTLV-I carriers was observed for deaths from all causes (rate ratio [RR] = 1.41), all cancers (RR = 1.64), liver cancer (RR = 3.04), and heart diseases (RR = 2.22). The association of anti-HTLV-I seropositivity with mortality from all non-neoplastic diseases (RR = 1.40) and chronic liver diseases (RR = 5.03) was of borderline significance. Possible confounding by blood transfusions and hepatitis C/B (HCV/HBV) viral infections could not be precluded in this study. However, even after liver cancer and chronic liver diseases were excluded, mortality rate was still increased among HTLV-I carriers (RR = 1.32, 95% CI 0.99-1.78), especially among those with high antibody titers (RR = 1.56, 95% CI 0.99-2.46, P for trend = 0.04). These findings may support the idea that HTLV-I infection exerts adverse effects on mortality from causes other than adult T-cell leukemia/lymphoma. Further studies on confounding by HCV/HBV infections and the interaction between HCV/HBV and HTLV-I may be required to analyze the increased mortality from liver cancer and chronic liver diseases.
Adult↗
Case report: a patient who developed an amoebic liver abscess during treatment with interferon.
A 65-year-old female received recombinant interferon (IFN) alpha-2b daily for the treatment of chronic hepatitis C. Fever (39 degrees C or higher) developed 14 days after the start of administration. Abdominal computed tomography suggested multiple liver abscesses, which had not been detected before IFN administration. An autopsy revealed an amoebic liver abscess. A subclinical infection of Entamoeba histolytica in this case developed into amoebic liver abscess during IFN administration.
Aged↗
Fosfomycin reduces CD15s-related antigen expression of Streptococcus pyogenes.
We have previously shown the immunological mimicry of human sialyl-Lewis(x) (CD15s) by a surface antigen of Streptococcus pyogenes. This mimicking surface antigen may act as a ligand to the selectin family and may induce antibody production against CD15s on host cells, suggesting a possible role in the pathogenesis of S. pyogenes. In this study, the effects of antibiotics on the CD15s-related antigen expression of S. pyogenes were examined at a concentration below the MIC (sub-MIC). The amounts of CD15s on the surfaces of S. pyogenes cells and on the surfaces of S. pyogenes biofilms were determined by a whole-cell enzyme-linked immunosorbent assay and by laser scanning fluorescence microscopy, respectively, by using an anti-CD15s monoclonal antibody. At the sub-MICs, fosfomycin (1R,2S-1,2-epoxypropyl phosphonic acid), its enantiomer (1S,2R-1,2-epoxypropyl phosphonic acid), and benzylpenicillin significantly inhibited the CD15s expression of all strains studied. The effects of fosfomycin and its enantiomer on biofilms were also observed by scanning electron microscopy. Incubation of S. pyogenes with the sub-MIC of fosfomycin or its enantiomer, which has no antibacterial activity, reduced the amount of CD15s on the biofilm surface and made it smooth. These results suggest that fosfomycin or its enantiomer might be useful for preventing S. pyogenes adherence to human CD15s receptors and the resulting immunological pathogenicity.
Anti-Bacterial Agents↗
Transplanted and repopulated retinal pigment epithelial cells on damaged Bruch's membrane in rabbits.
AIMS: The authors studied how artificially damaged Bruch's membrane influenced growth and differentiation of transplanted embryonic retinal pigment epithelial (RPE) cells and of host RPE cells in rabbits. METHODS: Embryonic RPE cells obtained from pigmented rabbits were transplanted into the subretinal space of adult albino rabbits. The host RPE was removed with a silicone cannula, and Bruch's membrane was damaged by scratching with a microhooked 27 gauge needle under the detached retina in closed vitrectomy. The transplantation sites were examined 3, 7, and 14 days after surgery by light and electron microscopy. RESULTS: Varying degrees of damage in Bruch's membrane were observed. Pigmented and hypopigmented RPE cells showed a normal polarity and tight junctions were seen at the sites of mild to moderate damage 3-7 days after the surgery. In contrast, fibroblast-like cells with no such features of RPE cells formed multiple layers at the sites of severe damage involving the full thickness of Bruch's membrane and the choriocapillaris even 14 days after the surgery. Without transplantation, host RPE cells repopulated the damaged areas in the same way as transplanted RPE cells. CONCLUSIONS: Transplanted embryonic RPE cells as well as host RPE cells grew and differentiated on the moderately damaged Bruch's membrane, while the severely damaged Bruch's membrane did not allow differentiation of RPE cells although these cells could grow and cover the damaged areas.
Animals↗
Mechanisms of cardiac hypertrophy in canine volume overload.
This study tested whether the modest hypertrophy that develops in dogs in response to mitral regurgitation is due to a relatively small change in the rate of protein synthesis or, alternatively, is due to a decreased rate of protein degradation. After 3 mo of severe experimental mitral regurgitation, the left ventricular (LV) mass-to-body weight ratio increased by 23% compared with baseline values. This increase in LV mass occurred with a small, but not statistically significant, increase in the fractional rate of myosin heavy chain (MHC) synthesis (Ks), as measured using continuous infusion with [3H]leucine in dogs at 2 wk, 4 wk, and 3 mo after creation of severe mitral regurgitation. Translational efficiency was unaffected by mitral regurgitation as measured by the distribution of MHC mRNA in polysome gradients. Furthermore, there was no detectable increase in translational capacity as measured by either total RNA content or the rate of ribosome formation. These data indicate that translational mechanisms that accelerate the rate of cardiac protein synthesis are not responsive to the stimulus of mitral regurgitation. Most of the growth after mitral regurgitation was accounted for by a decrease in the fractional rate of protein degradation, calculated by subtracting fractional rates of protein accumulation at each time point from the corresponding Ks values. We conclude that 1) volume overload produced by severe mitral regurgitation does not trigger substantial increases in the rate of protein synthesis and 2) the modest increase in LV mass results primarily from a decrease in the rate of protein degradation.
Animals↗
Progressive subretinal fibrosis in patients with rheumatoid arthritis and renal dysfunction.
We present two patients (56-year-old and 71-year-old women) who developed subretinal fibrosis in parallel with exacerbation of rheumatoid arthritis and deteriorated renal function. The first patient developed subretinal fibrosis in the right eye, coupled with multifocal choroiditis and serous retinal detachment in both eyes, in the course of rapidly progressive glomerulonephritis complicated with rheumatoid arthritis. Antineutrophil cytoplasmic antibody was positive in a perinuclear pattern (pANCA) and the increased dose of prednisolone to 40 mg/day resulted in subsidence of the subretinal inflammation. The second patient developed subretinal fibrosis in the left eye with mottled retinal pigment epithelium of both eyes, in the course of rheumatoid arthritis and stable chronic renal failure. Although the manifestations of subretinal fibrosis and concurrent renal dysfunction were different between these two patients, subretinal fibrosis might be noted as a complication of rheumatoid arthritis and renal dysfunction.
Aged↗
Decrease in circulating and urine adrenomedullin concentrations in stroke-prone spontaneously hypertensive rats.
Adrenomedullin (AM) is a peptide with potent vasodilatory and hypotensive properties. Plasma AM levels in rats with experimentally induced hypertension, such as Dahl salt-sensitive rats and two-kidney, one-clip hypertensive rats, are higher than those in normotensive rats. We previously noted, however, that plasma AM levels in spontaneously hypertensive rats (SHR) are similar to those in Wistar-Kyoto rats. To define the role of AM in rats with severe hypertension, we investigated changes in circulating and tissue AM levels in stroke-prone spontaneously hypertensive rats (SHRSP/Izm). The immunoreactive rat AM levels in plasma, urine, and tissue measured with a sensitive radioimmunoassay, and the AM mRNA levels in various tissues in 15-wk-old SHRSP/Izm were compared with those in age-matched Wistar-Kyoto rats (WKY/Izm). The plasma and urinary AM levels in SHRSP/Izm were significantly lower than those in WKY/Izm [plasma AM, 2.14+/-0.06 (SE) vs. 3.24+/-0.16 fmol/ml, p< 0.001; urinary AM, 16.36+/-3.21 vs. 36.12+/-6.09 fmol/ml, p< 0.01]. A negative correlation was found between the plasma AM level and the systolic blood pressure in both SHRSP/Izm and WKY/Izm. Reverse-phase high-performance liquid chromatography showed that the molecular components of plasma immunoreactive AM in SHRSP/Izm were similar to those in WKY/Izm. Furthermore, tissue AM levels in various organs in SHRSP/Izm were not lower than those in WKY/Izm. In conclusion, low levels of circulating AM may contribute to the maintenance of high blood pressure in 15-wk-old SHRSP/Izm. These low plasma AM levels may be caused by accelerated metabolism of circulating AM in SHRSP/Izm.
Adrenomedullin↗