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Biomedical subjects

M Otsuki

Publications and source records attributed to M Otsuki.

At least 73 records · Page 4Linked to original sources
PubMed2000

[Interchangeability of resin composites and bonding agents based on bis-GMA or UDMA].

Recently, dentin bonding systems have been released separately from the resin composites, because the adhesive systems have been quickly improved. Since the merit of each material should be effectively utilized for each clinical case, the bonding systems and resin composites produced by different manufacturers may be combined according to the clinical purpose. The current restorative resins are basically categorized into two groups according to the main resin monomer, bis-GMA or UDMA resins. The purpose of this study was to evaluate the interchangeability between the bonding systems and resin composites, which were made by different manufacturers. Two bonding systems and five resin composites based on bis-GMA or UDMA were used in this study. The evaluation was performed by the tensile bond strength, fracture modes, and SEM observation, using the dentin surface of freshly-extracted bovine teeth. The highest bond strength (19.2 MPa) was shown by the combination of LBII sigma and AP-X. The bond strengths of nine other combinations were not statistically different (p > 0.05). There were many cohesive failures in dentin or resin composite, using all combinations. From the results, it was concluded that the interchangeability of the resin composites and bonding systems should be clinically acceptable.

Animals↗
PubMed2000

[A case of agnosia for streets and houses unaccompanied by prosopagnosia of familiar faces due to the right occipital lobe infarction].

We reported a patient who showed agnosia for streets and homes unaccompanied by prosopagnosia of familiar faces following infarction in the right occipital lobe. A 70-years-old right-handed man admitted to our department because of sudden development of visual impairment. He had left hemianopsia, left unilateral spatial neglect and slight visual memory disturbance but no other neurological abnormalities. His verbal memory was maintained intact. He was, however, unable to distinguish the sceneries of buildings and streets regardless of their familiarities and often got lost in the hospital. His topographical abilities in map-sketching and route-description were partially impaired depending upon the familiarity of targets; the disability was observed toward unfamiliar targets. His ability in facial recognition was also partially impaired depending upon the familiarity of persons. The patient was unable to distinguish faces of unfamiliar persons, such as nurses and doctors whom he met following stroke, whereas he was able to distinguish faces of familiar persons, such as his family and friends. The brain MRI demonstrated infarction in the right medial occipital lobe including parahippocampal gyrus, lingual gyrus and fusiform gyrus. In general, the manifestation of agnosia for streets and houses is associated with prosopagnosia. The present case, however, exhibited only the former in association with the partial manifestation of the latter. The fact suggests that those two are independent syndromes. The present case also showed a dissociation in the abilities of topographical and facial recognition according to the familiarity of targets. The process for the retrieval and reference of acquired information and that for the acquirement of new visual information may work in an independent manner.

Aged↗
PubMed1999

Identification and characterization of a new phospholipase C-like protein, PLC-L(2).

We have isolated a cDNA encoding a novel protein, PLC-L(2), with homology to the phospholipase C-like protein PLC-L and delta-type phospholipase C. PLC-L(2) contains a relatively well-conserved PH domain, PLC catalytic region, and X and Y domains. However, it did not have PLC activity. This inactivation was thought to be caused by the replacement of two amino acids that are essential for PLC activity, His356 and Tyr552, with Thr and Phe in the X and Y domain. PLC-L(2) has a wide distribution with strong expression in skeletal muscle and mapped to chromosome 3p24-25. The PH domain of PLC-L(2) bound strongly to PI(4,5)P(2) and Ins(1,4,5)P(3), and moderately to PI(4)P and PI(3,4,5)P(3). PLC-L(2) predominantly localized to perinuclear areas in both myoblast and myotube C2C12 cells. Ectopically expressed GFP-PLC-L(2) also mainly localized in perinuclear areas, including endoplasmic reticulum in COS 7 cells. Furthermore, the expression of GFP-PH showed the same intracellular distribution as the full-length PLC-L(2). All these results suggest that PLC-L(2) plays an important role in the regulation of Ins(1,4, 5)P(3) around the endoplasmic reticulum on which the Ins(1,4,5)P(3) receptor exists.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Short- and long-term results of endoscopic variceal ligation for esophageal varices compared with injection sclerotherapy.

We assessed the efficacy and safety of endoscopic therapy for esophageal varices in Japanese patients comparing the results of ligation therapy performed in 101 patients with those of sclerotherapy with paravariceal injection of polidocanol in 40 patients. Both therapies were effective in controlling active hemorrhages. Hemostasis rates at the first endoscopic session were 100% in both groups and rebleeding rates were 40.0% in the sclerotherapy and 29.6% in the ligation group. Variceal eradication was achieved equally in both groups in approximately 90% of the patients. However, the ligation achieved eradication more quickly in fewer endoscopic sessions than did the sclerotherapy (mean; 2.1 vs. 3.7 sessions, P < 0.01). Complications such as rebleeding and intramural hematomas were less common in the ligation group. These results indicate some advantages of the ligation over the sclerotherapy. A disadvantage of the ligation therapy is that recurrence occurs more quickly than in the sclerotherapy, although the difference was not statistically significant.

Endoscopy↗
PubMed1999

Role of beta1 integrins in adhesion and invasion of hepatocellular carcinoma cells.

To investigate the role of integrins in hepatocellular carcinoma (HCC) invasion, we analyzed the relationship between the expression and activity of beta1 integrins and the invasive ability of multiple HCC cell lines. Human HCC cell lines, PLC/PRF/5, Hep3B, HepG2, HLE, HuH7, and C3A cells, had high expression of beta1 and alpha6 subunits, and various levels of alpha1, alpha2, alpha3, and alpha5 expression as determined by cell surface flow cytometry. Activity of beta1 integrins was evaluated by cell adhesion to collagen, fibronectin, and laminin in the presence or absence of the stimulatory anti-beta1 monoclonal antibody (mAb) TS2/16. Different types of HCC cells showed various levels of constitutive activity of beta1 integrins as assessed by the TS2/16 requirement in cell adhesion. TS2/16 rapidly stimulated constitutively inactive or partially active beta1 integrins to fully active states, and as the result, the levels of cell adhesion to each ligand correlated with the expression levels of corresponding beta1 integrins. Thus, in the presence of TS2/16 stimulation, the levels of cell adhesion to collagen, fibronectin, and laminin correlated predominantly with the expression levels of alpha2, alpha5, and alpha6, respectively. Remarkably, as a result of in vitro chemoinvasion assay, the levels of constitutive activity of beta1 integrins correlated with the invasive ability of HCC cells. The inhibitory anti-beta1 mAb 13 almost completely blocked the invasion of PLC/PRF/5 and Hep3B cells that are the most invasive HCC cell lines. Alternatively, the stimulatory anti-beta1 mAb TS2/16 strongly inhibited the invasion. These results not only show an essential role of beta1 integrins in invasion of HCC cells but also suggest subtle regulatory mechanisms of cell invasion.

Antibodies, Monoclonal↗
PubMed1999

Metabolic abnormalities in the genetically obese and diabetic Otsuka Long-Evans Tokushima Fatty rat can be prevented and reversed by alpha-glucosidase inhibitor.

The recently developed Otsuka Long-Evans Tokushima Fatty (OLETF) rat is known to develop insulinopenic diabetes after a prolonged period in a condition resembling non-insulin-dependent diabetes mellitus (NIDDM). We examined the effect of pharmacological intervention with a potent intestinal alpha-glucosidase inhibitor, acarbose, on the metabolic and histopathologic changes in this rat model. The first two groups of rats received an acarbose-rich diet (150 mg/100 g normal chow) from 12 weeks of age (ie, before the onset of diabetes) or from 28 weeks of age (ie, after the onset of diabetes), while a third group received the acarbose-rich diet for the initial 16 weeks only (from 12 to 28 weeks of age). A control group received standard rat chow. Acarbose-fed rats gained less weight or lost weight despite increased food intake when switched to the acarbose-rich diet. Acarbose also reduced visceral adipose depots and fasting triglyceride (TG), glucose, and insulin levels. At the end of the study at 72 weeks, the pancreatic wet weight and insulin content were significantly higher in the treated groups versus control rats. The morphological changes observed in control rats, such as atrophy of the pancreas and reduced number and size of islets, were not present in acarbose-treated rats. Rats fed acarbose from 12 to 28 weeks of age gradually gained weight after switching to standard chow, and hyperinsulinemia, hyperglycemia, and hyperlipidemia appeared (in that order). The pancreatic insulin content in these rats was significantly higher and the visceral adipose depot was significantly smaller than in control rats. Our study demonstrates that acarbose prevented and reversed the metabolic derangement and histopathological changes in genetically diabetic rats. Moreover, treatment with acarbose even for a short period produced a marked delay in the development of insulin insensitivity and frank diabetes.

Acarbose↗
PubMed1999

Pharmacologic profile of TS-941, a new benzodiazepine derivative cholecystokinin-receptor antagonist, in in vitro isolated rat pancreatic acini.

We investigated the pharmacologic characteristics of a newly developed benzodiazepine derivative (S)-(-)-N-[2,3-dihydro-2-oxo-5-phenyl-1-[(1H-tetrazol-5-yl)methyl] -1H-1,4-benzodiazepine-3-yl]-2-indolecarboxamide (TS-941), a cholecystokinin type A (CCK-A)-receptor antagonist, in the isolated rat pancreatic acini and compared with those of well-known CCK-A-receptor antagonists, devazepide and loxiglumide. TS-941 inhibited CCK-8-stimulated amylase release concentration dependently, as did devazepide and loxiglumide, with a half-maximal inhibition (IC50) at 78.6 +/- 10.3 nM. TS-941 was approximately 23 times less potent than devazepide (IC50, 3.4 +/- 0.3 nM), but was 50 times more potent than loxiglumide (IC50, 3,966 +/- 544 nM) in inhibiting 100 pM CCK-8-stimulated amylase release from rat pancreatic acini. TS-941 had a fivefold lower selectivity than devazepide for pancreatic CCK (CCK-A) over brain CCK (CCK-B) receptors but fourfold greater than loxiglumide when IC50 values for inhibition of [125I]CCK-8 binding in isolated acini and cerebral cortex were compared. The antagonism produced by TS-941 was specific for CCK in that the effects of other receptor secretagogues or agents bypassing receptors were not altered. TS-941 caused a parallel rightward shift of the entire dose-response curve for CCK-8-stimulated amylase release without altering the maximal increase, as did devazepide and loxiglumide. TS-941, whether added at the beginning or 20 min after the CCK-8 stimulation, inhibited amylase release. TS-941 caused a concentration-dependent residual inhibition of the action of CCK-8. The acini, once incubated with a high concentration of TS-941 (10 microM; 127 times IC50) for 30 min, was 10-fold less sensitive to CCK-8 than the acini preincubated without TS-941, whereas the sensitivity and the responsiveness to CCK-8 stimulation of those incubated with a low concentration of TS-941 (1.0 microM) were similar to the control acini. These results indicate that TS-941 is a potent, competitive, and selective CCK-A receptor antagonist for the pancreas.

Amylases↗
PubMed1999

Genotypes of alcohol-metabolizing enzymes in relation to alcoholic chronic pancreatitis in Japan.

Long-term consumption of large amounts of alcohol is the main cause of chronic pancreatitis. All heavy drinkers, however, do not contract chronic pancreatitis. Although genetic predisposition to alcoholism and alcoholic liver disease has been reported, genetic susceptibility to alcoholic pancreatitis is still a matter of debate. To determine the relation between genotypes of alcohol-metabolizing enzymes and chronic alcoholic pancreatitis, we examined genotype patterns of aldehyde dehydrogenase 2 (ALDH 2), alcohol dehydrogenase 2 (ADH 2) and cytochrome P-4502E1 (CYP2E1) in 54 patients with chronic alcoholic pancreatitis who were diagnosed in general hospitals in all over Japan and compared with those in 30 patients with chronic nonalcoholic pancreatitis or in 46 alcoholics with normal pancreatic function. There were no significant differences in the distribution of genotypes of ALDH 2 and CYP2E1 among those three groups. As for the ADH 2 genotype, distribution of 2(1)/2(1), 2(1)/2(2), and 2(2)/2(2) was 35%, 30%, and 35% in alcoholics with normal pancreatic function; 4%, 39%, and 57% in the chronic alcoholic pancreatitis group; and 0%, 50%, and 50% in the chronic nonalcoholic pancreatitis group, respectively. The frequency of ADH 2(2) allele was significantly higher in the chronic alcoholic pancreatitis group, compared with alcoholics with normal pancreatic function; but, it was not significantly different from that in the chronic nonalcoholic pancreatitis group. We also examined the relation between pancreatic fibrosis or pancreatitis histologically diagnosed and genotypes of alcohol-metabolizing enzymes in alcoholic autopsy cases. Twenty of 31 cases showed moderate or severe pancreatic fibrosis and showed intralobular + interlobular fibrosis, which is characteristic in alcoholic pancreatitis or intralobular fibrosis. ADH 2(2) allele tended to show a high frequency in the intralobular + interlobular fibrosis group, compared with that in the intralobular fibrosis group (75.0% vs. 41.7%, p < 0.1). The chronic pancreatitis group had a significantly higher frequency of the ADH 2(2) allele than that in cases without such findings (87.5% vs. 58.7%, p < 0.05). However, the ALDH 2 and CYP2E1 genotypes showed no significant relation to the findings of pancreatic fibrosis or histological pancreatitis. These data suggest that the risk of chronic alcoholic pancreatitis diagnosed clinically and pathologically seems to be associated with the ADH 2(2) allele in the genotypes of alcohol-metabolizing enzymes.

Alcohol Dehydrogenase↗
PubMed1999

Recurrent subcutaneous abscess of the sternal region in ulcerative colitis.

An 18-yr-old female patient with extensive ulcerative colitis suffered from several episodes of recurrent aseptic subcutaneous abscesses of the sternal region with a course paralleling that of her colitis. The abscess seemed to occur secondarily to osteomyelitis of the sternum, which is a manifestation of the synovitis, acne, pustulosis, hyperostosis, and osteomyelitis (SAPHO) syndrome.

Abscess↗
PubMed1999

Asymptomatic amebic colitis in a homosexual man.

We describe case of a 75-yr-old Japanese homosexual man who was diagnosed as having amebic colitis. The present case is unique in that invasive amebiasis has occurred in a homosexual man, because Entamoeba histolytica in homosexual patients is considered to be a nonpathogenic and commensal organism in western countries, and that the patient has not complained of any gastrointestinal symptoms associated with minute colonic lesion of an isolated cecal ulcer. This report indicates that the absence of gastrointestinal symptoms does not rule out invasive amebiasis. Therefore, once the ameba is identified in stool specimens, even in homosexual men, it is important to differentiate pathogenic from nonpathogenic species irrespective of whether the patient is symptomatic, and to treat the patient infected with pathogenic species. By means of this strategy, we can prevent pathogenic ameba from spreading in the community.

Aged↗
PubMed1999

Pure apraxic agraphia with abnormal writing stroke sequences: report of a Japanese patient with a left superior parietal haemorrhage.

A 67 year old Japanese male patient had pure agraphia after a haemorrhage in the left superior parietal lobule. He developed difficulty in letter formation but showed no linguistic errors, consistent with the criteria of apraxic agraphia. He manifested a selective disorder of sequencing writing strokes, although he was able to orally state the correct sequences. The patient's complete recovery after 1 month, without new learning, showed that he had manifested a selective disorder of writing stroke sequences. These findings indicate that the final stage of the execution of writing according to acquired sequential memory shown as a stroke sequence can be selectively disturbed, and should be considered to be distinct from the ability of character imagery and the knowledge of the writing stroke sequence itself. This case also indicates that the left superior parietal lobule plays an important part in the execution of writing.

Aged↗