Biomedical subjects

H Mitani

Publications and source records attributed to H Mitani.

At least 91 records · Page 5Linked to original sources

PubMed1998

Diurnal variation in tooth movement in response to orthodontic force in rats.

The purpose of this study was to determine whether there is any difference in orthodontic tooth movement when the orthodontic force is applied at different times of the day. Twenty-four rats were divided into three experimental groups based on the time of day that maxillary expansive force was applied; i.e., the force was applied continuously throughout the entire experimental period of 21 days in animals in the whole-day group; animals in the dark-period group and the light-period group received force only during the dark period (19:00-07:00) or the light period (07:00-19:00), respectively. Maxillary expansion in the light-period group was about 2 times greater than that in the dark-period group on day 21. There was no significant difference in expansion between the light-period group and the whole-day group. An experiment that used chronologic labeling with NTA-Pb revealed that there was greater formation of new bone on the tension side in the light-period group than in the dark-period group. There was no significant difference in the width of the palate among the three groups. These results indicate that there is a diurnal variation in tooth movement in response to orthodontic external force and that the application of force during the animal's rest period may be more effective than that while it is active.

Analysis of Variance↗

PubMed1998

Generation of metastatic variants of Eker renal carcinoma cell lines for experimental investigation of renal cancer metastasis.

We and others have demonstrated that a mutation in Tsc2 is the rate-limiting step for renal carcinogenesis in the Eker rat model. Although inactivation of Tsc2 results in development of renal tumors, it is not sufficient for metastatic renal cell carcinomas (RCs) in the Eker rat. To investigate the additional genetic event(s) necessary for cancer metastasis, we have established highly metastatic S-Lk9d-SLM cell lines from a non-metastatic RC cell line (Lk9dL) by co-implantation with a foreign body (gelatin sponge). Since these cell lines were remarkably different in metastatic performance (all and none, respectively) despite having the same genetic background, they should be useful experimental tools to investigate metastasis-promoting events in renal carcinogenesis.

Animals↗

PubMed1998

Specific induction of hepatocellular adenomas by transplacental administration of ENU in the tsc2 gene mutant (Eker) rat.

Eker rats develop dominantly inherited renal carcinomas (RCs), with hereditary mutation, and following somatic mutation (Knudson's second hit) at tuberous sclerosis gene (Tsc2). We document the effect of transplacental administration of N-ethyl-N-nitrosourea to Eker (Eker/+) and non-Eker (+/+) rats (same genetic background). Although we observed no difference in the number of preneoplastic GST-P positive foci between Eker and non-Eker rats, interestingly we observed the specific development of hepatocellular adenomas only in Eker rats. The Tsc2 gene mutation might thus influence the phenotype of preneoplastic initiated hepatocytes.

Adenoma, Liver Cell↗

PubMed1998

Use of selectively colored stereolithography for diagnosis of impacted supernumerary teeth for a patient with cleidocranial dysplasia.

The objective of the present study was to develop a three-dimensional method of locating the position of impacted supernumerary teeth in a patient with cleidocranial dysplasia. Stereolithographies of the patient's teeth and maxillofacial structure were prepared, coloring the teeth red. This model established accurate tooth malposition and provided support for selection of surgical exposure for extraction and traction of the impacted teeth. Selectively colored stereolithography is expected to be useful in a number of diverse situations.

Adolescent↗

PubMed1998

Repair of (6-4) photoproducts in cultured goldfish cells at confluence or treated with H2O2.

Previously we reported that fluorescent light (FL) illumination prior to UV irradiation (FL preillumination) had multiple effects on the repair of cyclobutane pyrimidine dimers (CPD) and (6-4) photoproducts ([6-4] PD) in cultured goldfish cells (RBCF-1) at the exponentially growing phase. In this study, it is shown that even under the confluent condition of RBCF-1 cells, FL preillumination increased the disappearance of (6-4) PD in the dark. In addition, both at confluence and at the exponentially growing phase, the disappearance of (6-4) PD after PR treatment was increased by FL preillumination to RBCF-1 cells. Moreover, it was found that H2O2 pretreatment, followed by UV irradiation, of the exponentially growing cells also enhanced the disappearance of (6-4) PD in the dark and by photorepair treatment. The degree of enhancement by H2O2 pretreatment was almost the same as that by FL preillumination.

Animals↗

PubMed1997

Hyperlipidemia enhancement of renal preneoplasia but not tumor formation is due to elevated apoptosis in the Eker rat.

The influence of a high-fat diet on the appearance of renal tumors was assessed in the Eker rat model of hereditary renal carcinoma. Examination of H&E-stained sections showed a significant increase in the number of microscopic solid adenomas in the high-fat group compared with the low-fat group, whereas there was no significant difference in the number of macroscopic tumors between the two groups. Where had the tumor buds gone? Staining for apoptotic bodies occasionally revealed apoptosis in and around the microscopic adenomas. In addition, an Eker rat renal tumor-derived cell line showed apoptosis when it was cultured with high concentrations of native and acetylated low-density lipoprotein. These findings suggested that tumor buds repeatedly appeared and disappeared in Eker rats on a high-fat diet.

Adenoma↗

PubMed1997

Transgenic rescue from embryonic lethality and renal carcinogenesis in the Eker rat model by introduction of a wild-type Tsc2 gene.

We recently reported that a germ-line insertion in the rat homologue of the human tuberous sclerosis gene (TSC2) gives rise to dominantly inherited cancer in the Eker rat model. In this study, we constructed transgenic Eker rats with introduction of a wild-type Tsc2 gene to ascertain whether suppression of the Eker phenotype is possible. Rescue from embryonic lethality of mutant homozygotes (Eker/Eker) and suppression of N-ethyl-N-nitrosourea-induced renal carcinogenesis in heterozygotes (Eker/+) were both observed, defining the germ-line Tsc2 mutation in the Eker rat as embryonal lethal and tumor predisposing mutation. To the best of our knowledge, this is the first report of rescue from a naturally occurring dominantly inherited cancer. This transgenic rescue system will be useful to analyze Tsc2 gene function, its relation to tumorigenesis in vivo, and genetic-environmental interactions in carcinogenesis.

Animals↗

PubMed1997

Localization of types I, II and III collagen and glycosaminoglycans in the mandibular condyle of growing monkeys: an immunohistochemical study.

In order to analyse the regional and age-related variations of primate condyles, immunohistochemical techniques were used to examine the localization of types I, II and III collagen and a variety of glycosaminoglycans in distinct anteroposterior regions of the mandibular condyle of two growing female rhesus monkeys (Macaca mulatta). In the juvenile monkey staining for types I and III collagen was weak in the fibrous tissue layer, intense in the pre-cartilaginous tissue layer and faint in the cartilaginous tissue layer; staining was significantly more intense in the posterosuperior and posterior regions than in the anterior region. Similarly, staining for cartilage-characteristic extracellular matrices, including type II collagen and keratan sulfate, was intense in the cartilaginous tissue layer of the posterior condyle. In contrast, in the late-adolescent monkey staining for the extracellular matrices was more intense in the anterior half of the condyle (i.e. from the anterior to the posterosuperior region) than in the posterior region, and most intense in the posterosuperior region. The results demonstrate that marked regional differences exist in the phenotypic expression of the extracellular matrices in the mandibular condyles of growing monkeys and that these differences vary between different developmental stages. The variations probably reflect the predominance of competing growth and articulatory functions in the mandibular condyles.

Aging↗

PubMed1997

Localization of types I, II and X collagen and osteocalcin in intramembranous, endochondral and chondroid bone of rats.

Chondroid bone is a unique calcified tissue intermediate between bone and cartilage. To clarify its characteristics, we examined the distributions of the ECMs associated with chondrogenic differentiation and matrix calcification in the chondroid bone of the rat glenoid fossa, and compared them to those in two typical bone tissues, alveolar bone of the maxilla (intramembranous bone) and the growth plate of long bone (endochrondral bone), using immunofluorescence techniques. Morphologically, the glenoid fossa consisted of the fibrous, progenitor and cartilaginous cell layers and the cartilaginous cell layer was further divided into the superficial non-hypertrophic layers (secondary cartilage) and the deep hypertrophic cell layers (chondroid bone). The co-distribution of type I and type II collagens was observed in secondary cartilage and chondroid bone, whereas type X collagen was restricted to the pericellular matrix of hypertrophied cells (chondroid bone). Osteocalcin, which was absent from the calcified cartilage of endochondral bone formation, was also present in the ECM of the chondroid bone, but not in cells. These results demonstrate that chondroid bone of rats, which is adjacent to secondary-type cartilage in the glenoid fossa, has phenotypic expressions associated with both hypertrophied chondrocytes and osteocytes.

Animals↗

PubMed1997

Effects of bisphosphonates on alkaline phosphatase activity, mineralization, and prostaglandin E2 synthesis in the clonal osteoblast-like cell line MC3T3-E1.

The effects of 3 bisphosphonates, AHBuBP, AHPrBP, and Cl2MBP on cell growth, alkaline phosphatase (ALP) activity, mineralization, and prostaglandin E2 (PGE2) synthesis in the clonal osteoblast-like cell line MC3T3-E1 were studied. These bisphosphonates had essentially similar effects on growth and the osteoblastic functions of the cells, i.e., they had no inhibitory effects on cell growth except at higher concentrations, they increased ALP activity, and inhibited PGE2 production. In the presence of AHBuBP, ALP activity was higher than that in the control after day 6 of culture. Lower concentrations of AHBuBP slightly facilitated mineralization by the cells. It is probable that bisphosphonates enhance the functions of osteoblasts in certain concentration and that the inhibition of endogenous PGE2 production may be involved in the mechanism of action of bisphosphonates.

Alendronate↗

PubMed1997

Factors affecting hypertrophic scar development in median sternotomy incisions for congenital cardiac surgery.

BACKGROUND: Even after successful operations on children, unattractive postoperative scars are often distressing to patients and their parents. There are no reports about the factors affecting keloid or hypertrophic scar (HS) development after congenital cardiac surgery. STUDY DESIGN: Postoperative scars were studied in 75 patients 3 months after congenital cardiac surgery by median skin incision. The mean age of the 51 males and 24 females was 2.7 +/- 2.3 years (range, 2 days-12 years). The scars were evaluated according to degree of redness, expressed as redness score, and skin blood flow, as measured by laser Doppler imaging. Skin blood flow ratio was calculated as blood flow at the scar divided by blood flow below the navel. After surgery, 40 patients received 5 mg/kg/day of tranilast, which inhibits the collagen synthesis of keloid fibroblasts. RESULTS: None of the 75 patients had keloid formation and 21 (28%) developed HS after operation. Mean age of patients with HS (HS (+) group) was 4.4 +/- 3.3 years and that of patients with no HS development (HS (-) group) was 1.5 +/- 1.9 years (p < 0.01). There were no significant differences between these two groups in gender or in pre- or postoperative cyanosis. Hypertrophic scar (+) patients exhibited significantly higher skin blood flow ratios than HS (-) patients (2.7 +/- 1.3 versus 1.4 +/- 0.6; p < 0.001). Hypertrophic scar was seen in 11 of 40 tranilast administered patients (28%) and in 10 of 34 patients not receiving tranilast (29%) (NS). Hypertrophic scar was less apparent in the patients who received tranilast versus those who did not; redness scores were 29.5 +/- 16.5 and 51.6 +/- 14.9, respectively (p < 0.01). CONCLUSIONS: These data suggest that age and skin blood flow ratio were the factors affecting HS development. Postoperative use of tranilast did not affect the frequency of HS development but did reduce its redness.

Age Factors↗

PubMed1997

Facial growth of skeletal Class III malocclusion and the effects, limitations, and long-term dentofacial adaptations to chincap therapy.

This article outlines the authors' research findings on the craniofacial growth of untreated skeletal Class III malocclusion, as well as the short-term and long-term effects of chincap orthopedic force for controlling Class III mandibular growth. Skeletal Class III malocclusion is believed to be the result of excessive growth of the mandible with respect to the maxilla and/or cranial base. The results of the authors' longitudinal studies show similar maxillary and mandibular incremental growth change during prepubertal, pubertal, and postpubertal periods when compared with Class I subjects. Therefore, it seems reasonable to assume that the skeletal framework of the Class III malocclusion must have been established before the prepubertal growth period. As for treatment with chincap appliances, the study on short-term and long-term effects indicate that, on average, the skeletal profile is greatly improved during the initial stages of chincap therapy. However, such changes are rarely maintained during pubertal growth period. Treatment with chincap appliances seldom alters the inherited prognathic characteristics of skeletal Class III profiles after completion of growth.

Adaptation, Physiological↗

PubMed1997

Photoreactivating enzyme for (6-4) photoproducts in cultured goldfish cells.

We previously reported that when cultured goldfish cells are illuminated with fluorescent light, photorepair ability for both cyclobutane pyrimidine dimers and (6-4) photoproducts increased. In the present study, it was found that the duration of the induced photorepair ability for cyclobutane pyrimidine dimers was longer than that for (6-4) photoproducts, suggesting the presence of different photolyases for repair of these two major forms of DNA damage. A gel shift assay was then performed to show the presence of protein(s) binding to (6-4) photoproducts and its dissociation from (6-4) photoproducts under fluorescent light illumination. In addition, at 8 h after fluorescent light illumination of the cell, the binding of protein(s) to (6-4) photoproducts increased. The restriction enzymes that have recognition sites containing TT or TC sequences failed to digest the UV-irradiated DNA photoreactivated by using Escherichia coli photolyase for cyclobutane pyrimidine dimers, indicating that restriction enzymes could not function because (6-4) photoproducts remained in recognition sites. But, when UV-irradiated DNA depleted of cyclobutane pyrimidine dimers was incubated with extract of cultured goldfish cells under fluorescent light illumination, it was digested with those restriction enzymes. These results suggested the presence of (6-4) photolyase in cultured goldfish cells as in Drosophila, Xenopus and Crotalus.

Animals↗

PubMed1997

Induction of apoptosis in cultured midbrain cells from embryonic mice.

Midbrain cells from embryonic mice were cultured at a high cell density for 4 days to observe proliferation and differentiation. Results indicate that UVC radiation caused dose-dependent inhibition of their proliferation and differentiation. Inhibitory effects of UVC radiation (per unit dose) were greater on cell differentiation than on proliferation. The percentage of apoptotic cells in the groups irradiated with 15 J/m2 became significantly higher than the control level 2 h after irradiation. The percentage of apoptotic cells increased with time in a dose-associated fashion and reached a maximum at about 7.5 h after irradiation. Then it decreased with time and returned to the control level at about 30 h after irradiation. Metabolic inhibitors could postpone occurrence of intermediate apoptosis (>2 h, but <20 h) if they were added at suitable times after irradiation but failed to prevent a delayed apoptosis (>24 h). Results showed that UVC radiation induced intermediate apoptosis which could be postponed by metabolic inhibitors, and that UVC could also induce delayed apoptosis with the addition of metabolic inhibitors. The result that UVC radiation could induce intermediate apoptosis in the midbrain cells was different from previous data obtained using cells of an established cell line. The implications of the results for the understanding of the mechanism involved are discussed.

Animals↗

PubMed1996

Inhibitory effect of fluvastatin at doses insufficient to lower serum lipids on the catheter-induced thickening of intima in rabbit femoral artery.

The anti-atherosclerotic effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors at doses insufficient to lower serum cholesterol was investigated in rabbit femoral artery denuded by balloon catheter. Fluvastatin and pravastatin were given orally at doses of 4 and 8 mg/kg per day, respectively, for 2 weeks after the catheterization. There was little change in serum cholesterol, triglyceride and phospholipid by chronic treatment with the drugs. The cross-sectional area of the intima, expressed as relative values to media (I/M ratio), was increased by the catheterization, showing intimal thickening in the denuded arteries. The I/M ratio was reduced by fluvastatin but not pravastatin: 0.327 +/- 0.060 for control, 0.116 +/- 0.035 for 4 mg/kg fluvastatin, 0.088 +/- 0.027 for 8 mg/kg fluvastatin and 0.22 +/- 0.069 for 8 mg/kg pravastatin. Fluvastatin (8 mg/kg)-induced effect on the I/M ratio, was prevented by the combined administration with 40 mg/kg per day mevalonate, a metabolite in the HMG-CoA reductase pathway. These results suggest that fluvastatin inhibits intimal thickening after catheterization-induced injury through percutaneous transluminal coronary angioplasty (PTCA) and that the inhibition is presumably attributed to reduced migration and proliferation of smooth muscle cells but not secondarily to a lowering of serum lipid.

Animals↗

PubMed1996

Effects of UVC irradiation on cultured mouse embryonic limb bud cells.

Effects of UVC irradiation (UVC) at a dose range from 0 to 30 J/m(2) were investigated on the cultured embryonic limb bud cells (LBC), isolated from fore- and hindlimbs of day 11 mouse embryos. Although dose-dependent inhibition was found for both cellular proliferation and chondrogenesis, the chondrogenic proteoglycan (PG) synthesis was more sensitive to UVC than cellular proliferation when compared at ID(50), the inhibitory dose that reduced assessment value by 50% of the control. No significant difference in induction and repair kinetics of UV-induced cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts ((6-4)PPs) were found between LBC and NIH3T3 mouse cell line. The fluorescent light (FL) treatment of LBC pre or post UVC irradiation did not affect repair kinetics of CPDs and (6-4)PPs, cellular proliferation, formation of PG-producing nodule and the PG synthesis.

3T3 Cells↗

PubMed1996

Effect of nipradilol on silent myocardial ischemia, plasma beta-endorphin, and bradykinin in chronic stable angina.

HYPOTHESIS: This study was undertaken to investigate the effect of nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS: Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS: Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and nipradilol phases of the study. However, during the nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION: Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.

Adrenergic alpha-Antagonists↗

PubMed1996

Age-related changes in the localization of glycosaminoglycans in condylar cartilage of the mandible in rats.

There is little information available regarding the morphological and biomolecular characteristics of mandibular condylar cartilage. The purpose of this study was to determine the age-related changes in the morphology and immunolocalization of glycosaminoglycans (GAGs) in mandibular condyles. The mandibular condylar cartilages from 4-, 8-, 16-, 32-, and 64-week-old Wistar male rats were examined to verify the localization of chondroitin-4-sulfate (Ch-4S), chondroitin-6-sulfate (Ch-6S) and keratan sulfate (KS) using an indirect immunofluorescent technique with three monoclonal antibodies for glycosaminoglycans, 2-B-6, 3-B-3 and 5-D-4, respectively. Morphologically, the condylar cartilage was a growth cartilage during growing periods, began to differentiate into articular cartilage from the central area of 16-week-old condyles, and became mature articular cartilage at 32 weeks of age. A regional difference was found in the morphological features and distribution of GAGs between the anterior, central, postero-superior and posterior areas of the condyles at each age. The immunohistochemical localizations of these three glycosaminoglycans showed age-related, morphology-dependent changes, from growth cartilage to articular cartilage-like cartilage. Immunoreactions for all of the antibodies decreased progressively with age in the interterritorial matrix, while the pericellular and territorial matrix in the condylar cartilage of the mandible maintained relatively higher immunoreactivity. In conclusion, age-related and regional differences in the localization of glycosaminoglycans Ch-4S, Ch-6S, and KS were found in the mandibular condyles in rats, and these changes are believed to be related to functional and developmental requirements.

Aging↗