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Biomedical subjects

T Minami

Publications and source records attributed to T Minami.

At least 55 records · Page 3Linked to original sources

High accumulations of calcium and phosphorus in women's pubic symphysis.

To elucidate compositional changes of the pubic symphysis (PS) by aging, elements of pubic symphysis (PSs) removed from 26 cadavers were determined by inductively coupled plasma atomic-emission spectrometry. It was found that the relative contents (RCs) of calcium and phosphorus in women's PSs were about three- and five-fold amounts as compared with those in men's PSs, respectively. In contrast, the RCs of sulfur, magnesium, sodium, and iron in women's PSs were somewhat lower than those in men's PSs. The accumulations of calcium (Ca) and phosphorus (P) in women's PSs occurred mainly beyond the age of 70-yr-old, but did not occur in men's PSs.

Adult

High accumulation of elements in the human femoral artery.

The relative contents (RCs) of elements in the femoral arteries as well as the thoracic aorta, coronary, basilar, and radial arteries from 26 subjects within the age range between 55 and 92 yr old, were analyzed by inductively coupled plasma atomic emission spectrometry. The RCs of calcium and phosphorus in the femoral arteries started to increase before the age of 60 yr. The RCs of magnesium increased after the age of 70 yr. However, the RCs of sulfur did not change significantly within the age range between 55 and 92 yr. With regard to localization of the mineral accumulations in the femoral arterial wall, it was found that the accumulations of calcium and phosphorus occurred only in the tunica media, only in the tunica intima, or in both the tunica media and the tunica intima. The manner of accumulation of calcium and phosphorus in the femoral arterial wall was different from that in the aortic wall. The average RCs of calcium in the 26 specimens were the highest in the femoral artery, followed in descending order by the thoracic aorta, coronary, basilar, and radial arteries. The average RCs of phosphorus were highest in the thoracic aorta, followed by the coronary, femoral, basilar, and radial arteries. It is noted that the accumulation of mineral elements never occurred uniformly in all the arteries.

Aged

Phospholipase A2 stimulates rat gastric epithelial cell line (RGM-1) migration.

OBJECTIVE AND METHODS: The effect of phospholipase A2 (PLA2) and its phospholipid metabolites on gastric epithelial migration was examined using an in vitro wounding model of confluent monolayers of rat gastric epithelial cell line RGM-1. RESULTS: Lysophosphatidylcholine (lysoPC) (0.01 100 ng/ml) as well as PLA2 (0.01-100 mU/ml) dose-dependently increased the cell migration. Lysophosphatidic acid (10 ng/ml) also increased the migration, but no significant increase in migration was observed when stimulated by lysophosphatidylethanolamine (10 ng/ml) or lysophosphatidylserine (10 ng/ml). Addition of 4-bromophenacyl bromide (BPB), a PLA2 inhibitor, completely blocked the effect of PLA2. However, addition of piroxicam (a cyclooxygenase inhibitor) or nordihydroguaiaretic acid (a lipoxygenase inhibitor) had no significant effect. Combination of PLA2 (10 mU/ml) with lysoPC (10 ng/ml) had no additive effect on migration. Moreover, lysoPC levels were increased in the cells after incubation with PLA2 (10 mU/ml). After pretreatment of RGM-1 cells with replication-inhibiting doses of mitomycin C. PLA2 and lysoPC still increased the cell migration. CONCLUSIONS: These data suggest that PLA2 may, independently of proliferation, increase gastric epithelial migration mainly via lysoPC production.

Acetophenones

Trace element composition and histological analysis of rat bones from the space shuttle.

The physiological and pharmacobiological changes associated with space flight are of greater concern. Exposure to a weightless environment has been shown to have numerous effects on body composition and organ functions. Alterations include decreases in muscle and liver mass, changes in bone structure and integrity, and changes in cardiovascular functions. Zero-gravity in particular has been reported to inhibit several physiological processes of bone formation, retard bone growth and impair the mechanical properties of bones. This report examines the effect of 14 days of spaceflight on the bone trace element compositions of rapidly growing rats. Marked changes of bone trace element contents were found in either weight-bearing bones or non-weight-bearing bones, depending on the metal species. Histological examination revealed an irregular thickening of the endosteal surface of the cortical bone (thoracic vertebrae) of the in-flight rat, whereas it was uniform in the ground control. We suggest that the microgravity environment causes several bone alternations, such as abnormal trace element compositions and defects in vertebral maturation.

Animals

Absence of prostaglandin E2-induced hyperalgesia in NMDA receptor epsilon subunit knockout mice.

1. We have previously found that intrathecal administration of prostaglandins E2 (PGE2) and D2 (PGD2) into conscious mice induced hyperalgesia by the hot plate test. The present study investigated the involvement of N-methyl-D-aspartate (NMDA) receptor in the prostaglandin-induced hyperalgesia by use of mice tacking NMDA receptor epsilon 1, epsilon 4, or epsilon 1/epsilon 4 subunits. 2. PGE2 induced hyperalgesia over a wide range of doses from 50 pg to 500 ng kg-1 in wild-type mice. But PGE2 could not induce hyperalgesia in epsilon 1, epsilon 4, or epsilon 1/epsilon 4 subunit knockout mice. 3. The NMDA receptor antagonist D-(-)-2-amino-5-phosphonovaleric acid (D-AP5), the non-NMDA receptor antagonist 7-D-glutamylaminomethyl sulphonic acid (GAMS), and the nitric oxide synthase inhibitor N epsilon-nitro-L-arginine methyl ester (L-NAME) inhibited the PGE2-induced hyperalgesia in wild-type mice. 4. PGD2 induced hyperalgesia at doses of 25 ng to 250 ng kg-1 in both wild-type and epsilon 1/epsilon 4 subunit knockout mice. The substance P receptor antagonist OP 96.345 blocked the PGD2-induced hyperalgesia in wild-type and epsilon 1/epsilon 4 subunit knockout mice. 5. These results demonstrate that the pathways leading to hyperalgesia are different between PGD2 and PGE2, and that both epsilon 1 and epsilon 4 subunits of the NMDA receptor are involved in the PGE2-induced hyperalgesia.

Animals

Characterization of nociceptin hyperalgesia and allodynia in conscious mice.

1. Intrathecal (i.t.) administration of nociceptin and high doses of morphine induced allodynia in response to innocuous tactile stimuli, and i.t. nociceptin evoked hyperalgesia in response to noxious thermal stimuli in conscious mice. Here we have characterized the nociceptin-induced allodynia and compared it with the morphine-induced allodynia and the nociceptin-evoked hyperalgesia. 2. Nociceptin-induced allodynia was evoked by the first stimulus 5 min after i.t. injection, reached a maximum at 10 min, and continued for a 50 min experimental period. Dose-dependency of the allodynia showed a bell-shaped pattern from 50 pg to 5 ng kg-1, and the maximum effect was observed at 2.5 ng kg-1. 3. Morphine-induced allodynia reached the maximum effect at 15 min and declined progressively until cessation by 40-50 min. The dose-response curve showed a bell-shaped pattern, similar to that induced by nociceptin, with a maximum effect at 0.5 mg kg-1, five orders of magnitude higher than that of nociceptin. 4. The allodynia evoked by nociceptin and morphine were dose-dependently blocked by glycine, D(-)-2-amino-5-phosphonovaleric acid (D-AP5, an N-methyl-D-aspartate (NMDA) receptor antagonist), gamma-D-glutamylaminomethyl sulphonic acid (GAMS, a non-NMDA receptor antagonist) and methylene blue (a soluble guanylate cyclase inhibitor), but were not affected by muscimol (a gamma-aminobutyric acidA (GABAA) receptor agonist) and baclofen (a GABAB receptor agonist). 5. Morphine did not inhibit forskolin-stimulated cyclicAMP formation in cultured cells expressing the nociceptin receptor. 6. Nociceptin-induced hyperalgesia was evoked 10-15 min after i.t. injection. Nociceptin produced a monophasic hyperalgesic action over a wide range of doses from 5 fg to 50 ng kg-1. The nociceptin-induced hyperalgesia was blocked by glycine only among the agents examined. 7. None of the pain responses evoked by nociceptin and morphine were blocked by naloxone. 8. These results demonstrate that, whereas the mechanisms of the nociceptin-induced allodynia and hyperalgesia are evidently distinct, they involve a common neurochemical event beginning with the disinhibition of the inhibitory glycinergic response. Morphine may induce allodynia through a pathway common to nociceptin, but the nociceptin receptor does not mediate the action of high doses of morphine.

Animals

Inhibition of nociceptin-induced allodynia in conscious mice by prostaglandin D2.

1. We recently showed that intrathecal administration of nociceptin induced allodynia by innocuous tactile stimuli and hyperalgesia by noxious thermal stimuli in conscious mice. In the present study, we examined the effect of prostaglandins on nociceptin-induced allodynia and hyperalgesia. 2. Prostaglandin D2 (PGD2) blocked the allodynia induced by nociceptin in a dose-dependent manner with an IC50 of 26 ng kg(-1), but did not affect the nociceptin-induced hyperalgesia at doses up to 500 ng kg(-1). BW 245C (an agonist for PGD (DP) receptor) blocked the allodynia with an IC50 of 83 ng kg(-1). 3. The blockade of nociceptin-induced allodynia by PGD2 was reversed by the potent and selective DP-receptor antagonist BW A868C in a dose-dependent manner with an ED50 of 42.8 ng kg(-1). 4. Glycine (500 ng kg[-1]) almost completely blocked the nociceptin-induced allodynia. A synergistic effect on the inhibition of nociceptin-evoked allodynia was observed between glycine and PGD2 at below effective doses. 5. Dibutyryl cyclic AMP, but not dibutyryl cyclic GMP, blocked the nociceptin-induced allodynia with an IC50 of 2.9 microg kg(-1). 6. PGE2, PGF2alpha, butaprost (an EP2 agonist) and cicaprost (a PGI receptor agonist) did not affect the nociceptin-induced allodynia. 7. These results demonstrate that PGD2 inhibits the nociceptin-evoked allodynia through DP receptors in the spinal cord and that glycine may be involved in this inhibition.

Animals

Inhibition of [3H]MK-801 binding by ferrous (II) but not ferric (III) ions in a manner different from that by sodium nitroprusside (II) in rat brain synaptic membranes.

The addition of sodium nitroprusside (SNP) significantly inhibited binding of (+)-5- [3H]methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine ([3H]MK-801) to an ion channel associated with the N-methyl-D-aspartate (NMDA) receptor in a concentration-dependent manner at concentrations of >1 microM in rat brain synaptic membranes not extensively washed. However, neither S-nitroso-N-acetylpenicillamine nor S-nitroso-L-glutathione inhibited binding even at 100 microM. Of the two compounds structurally related to SNP (II), similarly potent inhibition was induced by potassium ferrocyanide (II) but not by potassium ferricyanide (III). In addition, ferrous chloride (II) induced much more potent inhibition of binding than ferric chloride (III), at a similar concentration range. In contrast, iron chelators prevented the inhibition by ferrous chloride (II) without markedly affecting that by SNP (II) and potassium ferrocyanide (II). Pretreatment with ferrous chloride (II) also led to potent inhibition of [3H]MK-801 binding in a manner insensitive to subsequent addition of the iron chelators. Pretreatment with Triton X-100 resulted in significant potentiation of the ability of ferrous chloride (II) to inhibit [3H]MK-801 binding irrespective of the addition of agonists, moreover, although binding of other radioligands to the non-NMDA receptors was unaltered after pretreatment first with Triton X-100 and then with ferrous chloride (II). These results suggest that ferrous ions (II) may interfere selectively with opening processes of the NMDA channel through mechanisms entirely different from those underlying the inhibition by both SNP (II) and potassium ferrocyanide (II) in rat brain.

Animals

Identification of essential amino acids in the Streptococcus mutans glucosyltransferases.

A comparison of the amino acid sequences of the glucosyltransferases (GTFs) of mutans streptococci with those from the alpha-amylase family of enzymes revealed a number of conserved amino acid positions which have been implicated as essential in catalysis. Utilizing a site-directed mutagenesis approach with the GTF-I enzyme of Streptococcus mutans GS-5, we identified three of these conserved amino acid positions, Asp413, Trp491, and His561, as being important in enzymatic activity. Mutagenesis of Asp413 to Thr resulted in a GTF which expressed only about 12% of the wild-type activity. In contrast, mutagenesis of Asp411 did not inhibit enzyme activity. In addition, the D413T mutant was less stable than was the parental enzyme when expressed in Escherichia coli. Moreover, conversion of Trp491 or His561 to either Gly or Ala resulted in enzymes devoid of GTF activity, indicating the essential nature of these two amino acids for activity. Furthermore, mutagenesis of the four Tyr residues present at positions 169 to 172 which are part of a subdomain with homology to the direct repeating sequences present in the glucan-binding domain of the GTFs had little overall effect on enzymatic activity, although the glucan products appeared to be less adhesive. These results are discussed relative to the mechanisms of catalysis proposed for the GTFs and related enzymes.

Amino Acid Sequence

Alveolar bone loss in rats infected with a strain of Prevotella intermedia and Fusobacterium nucleatum isolated from a child with prepubertal periodontitis.

Prevotella intermedia and fusobacterium nucleatum are associated with various forms of periodontal disease. The purpose of the present study was to infect the clinical isolates of these periodontopathic bacteria and to induce a significant loss of alveolar bone in specific pathogen-free (SPF) rats in the absence of ligatures. P. intermedia YKD8 and F. nucleatum YKZ5 were isolated from a prepubertal periodontitis patient, while P. gingivalis MWB13 was from a patient with juvenile periodontitis. At first, SPF Sprague-Dawley rats (70 days of age, male) were infected with A. viscosus Ny1R and subsequently superinfected with P. gingivalis MWB13, P. intermedia YKD8, or F. nucleatum YKZ5, respectively. The control group was infected with A. viscosus Ny1R alone. All rats were killed and periodontal bone levels were assessed morphometrically 135 days after the first infection with A. viscosus. P. intermedia YKD8 was recovered frequently from rats, with serum antibody levels remaining highly elevated throughout the experiment. Significant loss of alveolar bone was found in rats infected with P. intermedia YKD8, the virulence of which was equivalent to that of P. gingivalis MWB13. F. nucleatum YKZ5 also induced alveolar bone loss, but not significantly when compared with rats infected with A. viscosus Ny1R alone.

Aggregatibacter actinomycetemcomitans

Bleeding in portal hypertensive gastropathy evaluated in terms of gastric mucosal microcirculation and coagulation-fibrinolysis system.

Gastric intramucosal bleeding in portal hypertensive gastropathy was investigated in terms of gastric mucosal microcirculation, coagulation-fibrinolysis factors, and local fibrinolysis in patients with liver cirrhosis. The gastric mucosa was examined by endoscopy, and the patients were classified into two groups with or without bleeding. Gastric mucosal blood flow was measured simultaneously with coagulation-fibrinolysis factors or local fibrinolysis in both groups. As gastric mucosal blood flow, the gastric mucosal blood volume (IHb) and the oxygenated hemoglobin concentration (ISO2) were determined by the organ reflection spectrum method. Coagulation-fibrinolysis factors were measured in the blood. For evaluation of local fibrinolysis, gastric biopsy specimens were placed on a standard fibrin plate, and the fibrinolysis area was measured. Compared with the non-bleeding group, the bleeding group showed increased IHb and decreased ISO2 (p < 0.05), suggesting marked congestion of blood flow. Gastric intramucosal bleeding was frequently observed in patients with marked congestion of blood flow and markedly abnormal values of coagulation-fibrinolysis factors. Gastric local fibrinolysis was also significantly enhanced in the bleeding group (p < 0.05). In addition, local fibrinolysis was correlated positively with the gastric mucosal blood volume (r = 0.68, p < 0.05) and negatively with the oxygenated hemoglobin concentration (r = -0.58, p < 0.05). These results suggest the following mechanism of gastric mucosal bleeding in liver cirrhosis and portal hypertension. Congestion of gastric mucosal blood flow is present in liver cirrhosis and portal hypertension. An increase in the microvascular pressure and hypoxia cause release of tissue plasminogen activators from gastric mucosal cells and vascular endothelial cells. As a result, gastric local fibrinolysis is enhanced, causing gastric mucosal bleeding.

Adult

Immunohistochemical localization of group II phospholipase A2 in colonic mucosa of patients with inflammatory bowel disease.

OBJECTIVES AND METHODS: We previously reported the increased contents of group II phospholipase A2 (PLA2) in inflamed colonic mucosa of patients with Crohn's disease and ulcerative colitis (UC). However, the cellular source of the increased group II PLA2 has remained to be clarified. In the present study, we examined immunohistochemical localization of group II PLA2 in inflamed colonic mucosal biopsy samples obtained from eight patients with Crohn's disease, seven with UC, and in normal colonic mucosa of six control subjects without inflammatory bowel disease using a monoclonal antibody raised against human group II PLA2. RESULTS: and CONCLUSIONS: On immunoblot analysis using the antibody, a single band was detected on each lane containing colonic mucosal homogenates from a control subject, a Crohn's disease patient, or a UC patient at the same position as human group II PLA2 purified from ileal mucosa. The results of immunohistochemistry showed that colonic epithelial cells in inflamed mucosa obtained from all active Crohn's disease patients examined (n = 4) contained immunoreactive group II PLA2. In four of seven patients with active UC, group II PLA2 immunoreactivity was similarly positive. No apparent group II PLA2 immunoreactivity was detected in all colonic mucosal biopsy samples obtained from inactive Crohn's disease patients (n = 4) and control subjects. The present study supports the presence of group II PLA2 in colonic epithelial cells in actively inflamed mucosa of patients with Crohn's disease and UC, which suggests that epithelial cells may serve as the cellular source of increased group II PLA2 content in inflamed colonic mucosa of these patients.

Adolescent

Liver cytosolic aldehyde dehydrogenase (ALDH1) polymorphism and its inheritance in Wistar rats.

Rats are very important experimental animal to study alcohol related problems. Liver aldehyde dehydrogenases (ALDHs) which metabolize aldehydes are reported to have several isozymes which are distributed in mitochondrial, microsomal and cytosolic fractions. However, there is discrepancy on reports concerning properties of cytosolic ALDH from normal liver. We report here the liver cytosolic ALDH (ALDH1) polymorphism and its inheritance in Wistar rats. Isoelectrophoretic focusing technique reveals the three ALDH1 phenotypes (termed AA, AC and CC) which are inherited in accordance with Mendelian fashion, indicating the existence of two alleles, ALDH1A and ALDH1C. In the range of pI 5.3 to 5.8, the AA phenotype possesses a major anodic band with pI 5.3 and CC phenotype also has a cathodic pI 5.8 band. In contrast, AC phenotype exhibits five bands with pIs of 5.3, 5.4, 5.5, 5.7 and 5.8. Intensity of these bands gradually diminishes from the main band with pI 5.5 to the both opposite ends. These findings suggest that AC phenotype as well as AA and CC types has a structure of tetramer which consist of the combination of subunit of the A and C gene products.

Aldehyde Dehydrogenase

[Sexual differences of the bone mineral content and density of human calcanei].

To examine whether there were sexual differences of human calcanei, the bone mineral content, bone mineral density and bone mass were determined by inductively coupled plasma atomic emission spectrometry, dual energy x-ray absorptiometry, and the principal of Archimedes, respectively. Inductively coupled plasma atomic emission spectrometry indicated that the average relative contents of calcium and phosphorus in the man's calcanei were one and a half folds higher than those in the woman's calcanei over 40 years old. Dual energy x-ray absorptiometry showed that the average bone mineral density of the man's calcanei was two times higher than that of the woman's ones over 40 years old. In addition, the average calcanean volume of the man was about one and a half folds larger than that of the woman over 40 years old.

Absorptiometry, Photon

[The significance of arterial chemotherapy for multiple hepatic metastases from colorectal carcinoma].

We studied 54 patients with multiple (more than 5 nodules) hepatic metastases from colorectal carcinoma retrospectively. Twelve cases in the non-chemotherapy group had a 0% one-year survival rate and 3.0 months of 50% survival period; 15 patients in the general chemotherapy group had 23.4% and 5.1 months respectively. In contrast, 27 subjects in the arterial chemotherapy group showed 48.3% and 11.5 months respectively (p < 0.05). Five cases that received hepatectomy were all alive but the prognosis remains unclear. It is suggested that long survivors with multiple metastases from colorectal cancer need radical resection of primary lesion and intrahepatic arterial chemotherapy.

Adult