Photocoagulation and fluid-gas exchange for persistent macular hole.
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Drainage↗
Biomedical subjects
T Ohno
Publications and source records attributed to T Ohno.
Prurigo nodularis associated with advanced gastric cancer: report of a case.
In a male Japanese patient, prurigo nodularis (PN) appeared in association with gastric cancer. The cutaneous pruriginous lesions dramatically improved soon after total gastrectomy without any treatment for the skin lesions. Peripheral eosinophilia seen before the operation also rapidly disappeared. These data suggest that some cytokines involved in gastric cancer might have played an important role in the development of PN in our patient.
Adenocarcinoma↗
Quantification of the CD55 and CD59, membrane inhibitors of complement on HIV-1 particles as a function of complement-mediated virolysis.
Previous studies have demonstrated that the murine monoclonal antibody (MoAb) NM-01 activates the human complement classical pathway resulting in lysis of human immunodeficiency virus (HIV). The present study was performed to determine the availability of the V3-loop of gp120 relative to the complement regulatory proteins, CD55 (DAF) and CD59 (HRF20) molecules on HIV. The results demonstrate that CD55 and CD59 exist on HIV virions, along with gp120 molecules. These findings suggest that activation of human complement on free viral particles is induced by MoAb NM-01 and that this occurs regardless of the presence of CD55 and CD59 molecules. The destruction of viral particles was demonstrated by a decrease in infectivity. The involvement of human complement in this process was confirmed with an immunoelectron microscopy technique by the presence of a human C9 to prove membrane attack complex (MAC). The results indicate that NM-01 can induce complement activation because of the ratios of CD55 and CD59 to gp120 molecules on HIV virions. The availability of the gp120 V3 domain on the virion is sufficient for binding of NM-01 and thereby the formation of MAC that results in virolysis.
Antibodies, Monoclonal↗
Reduced liver function is the trigger for renal sodium retention following portal vein ligation in the rat.
Sodium retention along with peripheral vasodilation are features of prehepatic portal hypertension. In several models of experimental liver damage, sodium retention occurs only when hepatic function, measured by the aminopyrine breath test (ABT-k), falls below a critical threshold. The relationship between renal sodium handling, ABT-k and systemic and renal haemodynamics in partial portal vein ligated (PVL) rats was examined to test hypothesis that peripheral vasodilation was responsible for initiating sodium retention. Haemodynamic measurements were conducted early after surgery in portal hypertensive rats with and without sodium retention and in sham-operated controls. Compared with control, both PVL groups of rats had elevated portal pressure and lower peripheral vascular resistance (P < 0.05). Sodium retaining-PVL rats had both lower ABT-k (0.95 +/- 0.05 vs 1.38 +/- 0.06 x 10(-2)/min; P < 0.05) and higher sodium balance (1.38 +/- 0.09 vs 0.43 +/- 0.09 mmol/day; P < 0.05) than non-sodium retaining PVL rats. No differences in plasma renin activity or noradrenaline concentrations were observed. In a separate group of rats, hydralazine-induced pheripheral vasodilation did not induce sodium retention. These results suggest that the presence of peripheral vasodilation alone is not sufficient to trigger a sodium-retaining status. A factor, probably liver function-dependent, acting directly on renal tubules may be necessary for changes in renal sodium handling in this model.
Animals↗
Genotype, serum level of hepatitis C virus RNA and liver histology as predictors of response to interferon-alpha 2a therapy in Japanese patients with chronic hepatitis C.
To determine whether pretreatment HCV-RNA level, hepatitis C virus genotypes, alanine aminotransferase and histology correlate with subsequent response to interferon-alpha therapy or not, serum HCV-RNA levels and genotype were determined by branched DNA signal amplification assay and genotype-specific polymerase chain reaction in 43 patients with chronic active hepatitis C. Response to recombinant interferon-alpha 2a (504 million units in total) was defined as complete and sustained CR-->SR, n = 12), complete response followed by relapse (CR-->Rel, n = 17), and no response (NR, n = 10), excluding dropouts (n = 4). Patients who showed CR-->SR had a lower HCV-RNA level (0.438 x 10(6) eq/ml) compared to CR-->Rel (2.452 x 10(6) eq/ml, p = 0.008) and NR (4.882 x 10(6) eq/ml, p = 0.009). A higher proportion of patients with CR-->SR had type 2a HCV (67%) compared to the CR-->Rel (28%) and the NR (0%). There was a trend for type 1b hepatitis C virus infection to have higher serum HCV-RNA levels. There was no correlation between pretreatment HCV-RNA level and alanine aminotransferase. However, no relation between pretreatment HCV-RNA level and liver histology was observed; a high proportion of patients with CAH2a showed CR-->SR, compared to those with CAH2b (p = 0.001). Moreover, the patients with CAH2b who had low level hepatitis C virus viremia did not show CR-->SR. These data indicate that pre-treatment serum HCV-RNA levels, genotype and liver histology are good predictors of subsequent response to interferon-alpha therapy in Japanese patients with chronic hepatitis C virus infection.
Alanine Transaminase↗
Prediction of adult height in healthy Japanese children.
Longitudinal records from 13,707 children (6749 boys and 6958 girls), aged 6-17 years, were fitted by a smoothing cubic spline function, and the factors influencing changes in height SD score (SDS) during puberty were analysed. Height SDS at 6 years correlated closely with final height SDS. However, short children at 6 years of age tended to increase their height SDS at final height, whereas tall children at the same age tended to decrease their final height SDS for children with the same prepubertal height, the later that pubertal maturation occurred, the greater was the final height achieved. As short children entered puberty relatively late and tall children entered puberty relatively early, height SDS tended to approach 0 SD during puberty. A prediction function obtained by multiple regression analysis using height SDS at 6 years, the percentage by which the child is overweight at 6 years, age at onset of the pubertal growth spurt (PGS) and height at onset of the PGS provides a reasonable model for the prediction of final height SDS without the need to estimate bone age.
Adolescent↗
A modular family 19 chitinase found in the prokaryotic organism Streptomyces griseus HUT 6037.
The specificity of chitinase C-1 of Streptomyces griseus HUT 6037 for the hydrolysis of the beta-1,4-glycosidic linkages in partially acetylated chitosan is different from that of other microbial chitinases. In order to study the primary structure of this unique chitinase, the chiC gene specifying chitinase C-1 was cloned and its nucleotide sequence was determined. The gene encodes a polypeptide of 294 amino acids with a calculated size of 31.4 kDa. Comparison of the amino acid sequence of the deduced polypeptide with that of other proteins revealed a C-terminal catalytic domain displaying considerable sequence similarity to the catalytic domain of plant class I, II, and IV chitinases which form glycosyl hydrolase family 19. The N-terminal domain of the deduced polypeptide exhibits sequence similarity to substrate-binding domains of several microbial chitinases and cellulases but not to the chitin-binding domains of plant chitinases. The previously purified chitinase C-1 from S. griseus is suggested to be generated by proteolytic removal of the N-terminal chitin-binding domain and corresponds to the catalytic domain of the chitinase encoded by the chiC gene. High-performance liquid chromatography analysis of the hydrolysis products from N-acetyl chitotetraose revealed that chitinase C-1 catalyzes hydrolysis of the glycosidic bond with inversion of the anomeric configuration, in agreement with the previously reported inverting mechanism of plant class I chitinases. This is the first report of a family 19 chitinase found in an organism other than higher plants.
Amino Acid Sequence↗
Dermatofibrosarcoma protuberans. CT findings with pathologic correlation in 6 cases.
PURPOSE: To characterize the CT findings of dermatofibrosarcoma protuberans. MATERIAL AND METHODS: CT and pathologic specimens of 6 patients with dermatofibrosarcoma protuberans (5 in the trunk and 1 in the leg) were retrospectively reviewed. RESULTS: CT clearly defined the tumors in the dermis and subcutaneous tissue with a characteristic, if not pathognomonic, protrusion. On postcontrast CT, 3 tumors showed marginal enhancement and central low density, while the others showed homogeneous enhancement. Pathologically, the marginal enhancement on CT corresponded to fibrosarcomatous changes, and the central low density to necrosis. The tumors with homogeneous enhancement had no sarcomatous changes. CONCLUSION: CT allows detection and precise anatomic localization of dermatofibrosarcoma protuberans. Marginal enhancement with central low density on CT may suggest a relatively poor prognosis.
Adult↗
Preparation and pharmacological evaluation of 1-(1,4-benzoquinon-2-yl)-1,2,3,4-tetrahydronaphthalenes as potent cerebral protective agents.
Two new series of 1-(1,4-benzoquinon-2-yl)-1,2,3,4-tetrahydronaphthalenes (3,4) were synthesized for evaluation of their pharmacological activities. These compounds showed significant anti-lipid peroxidation (ALP) activities with rat brain homogenate and some of them possessed a protective effect against hypobaric hypoxia in mice.
Animals↗
Failure of the oxytocin-induced increase in secretion of urinary kallikrein in young spontaneously hypertensive rats.
Urinary kallikrein excretion during oxytocin (OT) infusion were studied in anesthetized (sodium pentobarbital, 50 mg/kg, i.p.) young (4-weeks-old) spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). OT-infusion (30 nmol/kg/30 min) to WKY significantly increased urinary excretion of the active kallikrein from the basal levels (25.4 +/- 5.6 10(-2) x AU/15 min, n = 5) to 37.3 +/- 5.0 10(-2) x AU/15 min (P < 0.05, n = 5) and 50.7 +/- 17.1 10(-2) x AU/15 min (P < 0.05, n = 5) 15 and 30 min after the start of OT-infusion, respectively. In SHR, OT-infusion did not increase the urinary excretion of active kallikrein, but did decrease the urine volume and sodium excretion. The concentration of the active kallikrein in the kidney of WKY was not changed by OT-infusion, but that of SHR was slightly increased. The OT-infusion resulted in significantly higher concentrations of the active kallikrein in SHR kidney than in WKY kidney. These results suggest that less excretion of urinary kallikrein in SHR during OT-infusion may be attributable to a lower response in the secretion of kallikrein from the kidney.
Animals↗
Spheroid cultures of human hepatoblastoma cells (HuH-6 line) and their application for cytotoxicity assay of alcohols.
Spheroid cultures of human hepatoblastoma cells (HuH-6 line) were established by rotating 3 x 10(6) cells/3 ml culture medium in 25-ml Erlenmeyer flasks on a gyratory shaker. The size of the spheroids rapidly increased until 4 days of culture, and thereafter their size gradually increased until 8 days of culture. A considerable amount of lactate dehydrogenase (LDH) was detected in the culture medium at 24h after seeding because of cell damage by subculturing, but thereafter the amount released was small, indicating that the spheroids were in healthy condition. Albumin production, one of the differentiated functions of hepatocytes, was higher in spheroid cultures than in monolayer cultures. Using this spheroid culture model, the cytotoxic effects of alcohols on HuH-6 cells were studied by measuring the activity of LDH released in the medium from damaged cells. The results indicate that the increasing order of toxicity of the alcohols was as follows: methanol < ethanol < propanol.
Albumins↗
Comparison of various methods of assaying the cytotoxic effects of ethanol on human hepatoblastoma cells (HUH-6 line).
The sensitivity of five kinds of cytotoxicity assays using ethanol on human hepatoblastoma cells (HUH-6 line), which were cultured as monolayers or spheroids, was compared. Ethanol was chosen as a test because it acts on cell membranes directly without being metabolized and exerts its cytotoxicity. The assay methods used were as follows: 3- (4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase (LDH), colony formation, cell growth and DNA assays. The sensitivity of the assays was: LDH < DNA < cell growth < MTT < colony formation. LDH assay had the advantage that the same culture could be used for multiple assays, but when a small number of cells were assayed, no significant increase in the release of LDH was detected in the assay cultures compared with the control cultures. Although the DNA and cell growth assays were more sensitive than the LDH assay, the extent of cell damage may be underestimated because the damaged cells and DNA present in the cultures are included in the assay samples. On the other hand, both MTT and colony formation assays showed a high sensitivity. The MTT assay was done within 24 h after ethanol was added to the cultures and was applicable to both monolayer and spheroid cultures, while the colony formation assay required 1-2 weeks and it was applicable only to monolayer cultures. Taken together, the MTT assay was the most suitable method to evaluate the cytotoxic effects of ethanol on HUH-6 cells cultured as either monolayers or spheroids.
Cell Survival↗
Evaluation of cardiac sympathetic nervous function by 123I-metaiodobenzylguanidine scintigraphy in insulin-treated non-insulin dependent diabetics with hypoglycemia unawareness.
The association between the lack of adrenergic symptoms during hypoglycemia and myocardial 123I-metaiodobenzylguanidine (MIBG) accumulation was investigated in 12 insulin-treated non-insulin-dependent diabetes mellitus (NIDDM) patients who had no evidence of heart disease. These patients were divided into 2 groups according to the presence (group A) or absence (group B) of adrenergic symptoms during hypoglycemia. Autonomic function tests revealed significantly severe autonomic dysfunction in group B compared to that in group A. Insulin infusion test indicated no significant difference in the catecholamine response between the two groups. 123I-MIBG scintigraphy showed that the heart/mediastinum ratio of MIBG uptake was significantly lower, and scintigraphic defect was greater in group B than in group A. There were no significant differences in the washout rate between the two groups. These results suggested that the lack of adrenergic symptoms during hypoglycemia may be associated with cardiac sympathetic nervous dysfunction in insulin-treated NIDDM patients, and this dysfunction is mainly due to cardiac sympathetic denervation.
3-Iodobenzylguanidine↗
Fatty acid profiles of phospholipids in brown adipose tissue from rats during cold acclimation and repetitive intermittent immobilization: with special reference to docosahexaenoic acid.
The effects of cold acclimation and repetitive intermittent immobilization were examined on fatty acid (FA) compositions in phospholipids of rat interscapular brown adipose tissue (BAT) and plasma. As previously reported, cold acclimation and intermittent immobilization increased the degree of unsaturation as a whole in FAs of BAT but not in plasma. N-3 polyunsaturated docosahexaenoic acid (22-6; DHA) decreased in cold acclimation but increased in intermittent immobilization in phospholipids of BAT. DHA was decreased in phospholipids of plasma in both groups. Considering our previous findings that the in vitro thermogenic response of BAT was suppressed in cold acclimation and enhanced in intermittent immobilization, it was inferred that DHA in BAT is involved in the regulation of thermogenic function of this tissue.
Acclimatization↗
Expression of N-ras gene in gliomas.
Expression of N-ras gene was examined by northern blot analysis in two cases of astrocytoma (grade II), four cases of glioblastoma multiforme (six samples including two recurrent tumors), and normal brain tissues. Expression of N-ras gene was only found in the two recurrent glioblastoma multiforme samples. Southern blot analysis found no significant difference in copy numbers of N-ras gene in pre- and post-recurrence samples. The histological diagnosis of the two recurrent tumors was glioblastoma multiforme at both first recurrent presentation. However, the tumors had progressed during recurrence, because of worsened histological findings, such as increased cellularity, pleomorphism, and vascularity. These tumors recurred at very short intervals. Enhanced expression of N-ras gene by disorder of transcription may be a factor in the progression of glioblastoma multiforme.
Astrocytoma↗
[A case of rheumatoid arthritis associated with multiple myeloma].
Previous reports have stressed the association between autoimmune disease and lympho-proliferative neoplasm. Here we report a patient in whom multiple myeloma developed about 30 years after the onset of rheumatoid arthritis. A 79 year-old woman with an about 30-year history of rheumatoid arthritis was admitted because of lumbago in December, 1993. Laboratory findings revealed M-proteinemia (IgA 2,380 mg/dl, IgG 728 mg/dl, IgM 51 mg/dl) and serum immunoelectrophoresis showed monoclonal IgA with lambda type light chain. Bone marrow aspirate contained 66.0% plasma cells. Serological tests of rheumatoid factor were positive. X-ray findings revealed radiolucent myelomatous foci in the skull and typical destructive changes of rheumatoid arthritis in multiple joint. From these findings, IgA lambda-type multiple myeloma with rheumatoid arthritis was diagnosed. Although the pathogenesis of the association between rheumatoid arthritis and multiple myeloma is unknown, prolonged antigenic stimulation manifested by rheumatoid arthritis is considered to be a possible pathogenetic factor in the development of multiple myeloma.
Aged↗
Age-related alteration of pancreatic beta-cell function. Increased proinsulin and proinsulin-to-insulin molar ratio in elderly, but not in obese, subjects without glucose intolerance.
OBJECTIVE: To determine the secretion of insulin, C-peptide, and proinsulin after oral glucose loading in healthy elderly subjects compared with middle-aged subjects with and without obesity and with NIDDM. RESEARCH DESIGN AND METHODS: Subjects fell into four groups: nonobese middle-aged normal control subjects (CNT group; n = 38, 40-64 years old); obese normal subjects (OB group; n = 18, 40-64 years old); nonobese NIDDM subjects (NIDDM group; n = 28, 40-64 years old); and nonobese elderly subjects (OL group; n = 17, 65-92 years old). Insulin, C-peptide, and proinsulin were determined by radioimmunoassay in plasma samples taken at 0, 30, 60, and 120 min during a 75-g oral glucose tolerance test (OGTT). RESULTS: There were no differences in plasma glucose during the OGTT among the three nondiabetic groups. Hyperinsulinemia was significant in the OB and NIDDM groups but not in the OL group. On the other hand, absolute hyperproinsulinemia was significant in the OL and NIDDM groups compared with the CNT group. Increased proinsulin was rather dominant in the OL group, especially late after glucose loading. Molar ratios of proinsulin to insulin or C-peptide thus were significantly higher in the OL and NIDDM groups. CONCLUSIONS: Alteration of pancreatic beta-cell function independent of that seen with NIDDM occurred in relation to aging. This may be a predisposing factor to the development of impaired glucose tolerance or NIDDM in elderly subjects, that is, independent of obesity.
Adult↗
PRAD1/Cyclin D1 gene overexpression in mantle cell lymphoma.
The t(11;14) (q13;q32) translocation and its molecular counterpart Bcl-1 rearrangement are consistent features of mantle cell lymphoma (MCL). This translocation activates the PRAD1/cyclin D1 gene that is considered to be the Bcl-1 oncogene. PRAD1/cyclin D1 gene overexpression is closely associated with MCL. The PRAD1/cyclin D1 protein is localized to the nucleus, and the strong correlation between PRAD1/cyclin D1 and MCL is also found in the protein level. This finding indicates that PRAD1/cyclin D1 expression is a highly specific and sensitive molecular marker for MCL. This gene may function as an oncogene in the malignant transformation of cells.
Cyclin D1↗