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Biomedical subjects

K Hoshi

Publications and source records attributed to K Hoshi.

At least 19 recordsLinked to original sources
PubMed1999

Nuclear vitamin K2 binding protein in human osteoblasts: homologue to glyceraldehyde-3-phosphate dehydrogenase.

The importance of vitamin K in bone metabolism has been suggested previously. The binding protein of vitamin K2 (menatetrenone, 2-methyl-3-all-trans-tetraphenyl-1,4-naphthoquinone, menaquinone-4), found in nuclear extract of human osteoblasts, binds to vitamin K1 and K2, but not K3. Since the binding protein does not bind to other steroids or vitamins, such as hydrocortisone, vitamin A, 1,25(OH)2vitamin D3, trolox (a derivative of vitamin E), and warfarin, a specific binding protein to vitamin K1 and vitamin K2 in osteoblasts was suggested. The size of the specific binding protein was revealed to be 6S by sucrose density gradient and about 40,000 daltons by SDS-PAGE. Twenty amino acid residues from the N-terminal were the same as human glyceraldehyde-3-phosphate dehydrogenase (GAPDH), but the 21st residue, alanine, was replaced with serine. The binding protein was precipitated with anti-human GAPDH antibody, and authentic human GAPDH could bind vitamin K2. We propose that the nuclear binding protein for vitamin K2 exists in nuclei similarly to other vitamin receptors and that the molecular structure is very close to human GAPDH.

Amino Acid Sequence↗
PubMed1999

Creutzfeldt-Jakob disease with florid-type plaques after cadaveric dura mater grafting.

BACKGROUND: Many reported cases of iatrogenic Creutzfeldt-Jakob disease (CJD) developed after grafting cadaveric dura mater contaminated with CJD prions (dura-associated CJD). They are known to be clinicopathologically similar to sporadic CJD. We report herein 2 autopsy cases of dura-associated CJD with atypical clinicopathological features. PATIENTS: Two patients presented with progressive ataxia and mental deterioration 10 or 11 years after neurosurgical treatment with cadaveric dural grafting, which led to their deaths at 8 and 17 months, respectively, after onset. RESULTS: The cases were clinically atypical in exhibiting no or late occurrence of myoclonus and periodic synchronous discharges on electroencephalographic studies. They were pathologically unique in several aspects. The most striking feature was the presence of many prion protein (PrP) plaques in multiple areas in the brain. Some of them were the "florid" type surrounded by a zone of spongiform changes known to be a hallmark for the new variant CJD. The distribution of spongiform degeneration was also unique in that it was intense in the thalamus, basal ganglia, and the dentate nuclei of the cerebellum but milder in the cerebrum. There were no mutations in the PrP gene of the patients. There was no major difference in the size and glycoform pattern between the abnormal isoform of PrP extracted from the brain tissue from the dura-associated cases of CJD and that from a sporadic case of CJD. CONCLUSIONS: These 2 cases are clinicopathologically distinct from typical dura-associated cases of CJD. They may be a subtype with florid-type plaques in dura-associated CJD.

Aged↗
PubMed1999

Amniotic fluid alpha-fetoprotein testing in native Japanese women.

Owing to differences in maternal serum alpha-fetoprotein, human chorionic gonadotrophin and oestriol levels between native Japanese and Caucasian women screened in this laboratory, a study was conducted to measure amniotic fluid alpha-fetoprotein (AFAFP) levels in native Japanese pregnancies. When the native Japanese AFAFP levels were compared with a United States (non-Black) population, the Japanese medians did not decrease as rapidly over the 14 to 22 weeks of gestation period investigated. At 14 weeks, the difference was negligible, graduating to a difference of 20 per cent by 22 weeks' gestation. Native Japanese pregnancy AFAFP levels should be interpreted based upon population data from that group alone. From these findings, prenatal screening laboratories should be encouraged to collect preliminary data for comparison before screening is initiated for a defined ethnic group.

Amniocentesis↗
PubMed1999

Effect of sperm immobilisation and demembranation on the oocyte activation rate in the mouse.

To analyse the effect of the state of the sperm plasma membrane on oocyte activation rate following intracytoplasmic sperm injection (ICSI), three types of human and mouse spermatozoa (intact, immobilised and Triton X-100 treated) were individually injected into mouse oocytes. At 30, 60 and 120 min after injection, maternal chromosomes and sperm nuclei within oocytes were examined. Following human sperm injection, the fastest and the most efficient oocyte activation and sperm head decondensation occurred when the spermatozoa were treated with Triton X-100. Intact spermatozoa were the least effective in activating oocytes. Thus, the rate of mouse oocyte activation following human sperm injection is greatly influenced by the state of the sperm plasma membrane during injection. When mouse spermatozoa were injected into mouse oocytes, the rates of oocyte activation and sperm head decondensation within activated oocytes were the same irrespective of the type of sperm treatment prior to injection. We witnessed that live human spermatozoa injected into moue oocytes often kept moving very actively within the ooplasm for more than 60 min, whereas motile mouse spermatozoa usually became immotile within 20 min after injection into the ooplasm. In 0.002% Triton X-100 solution, mouse spermatozoa are immobilised faster than human spermatozoa. These facts seem to suggest that human sperm plasma membranes are physically and biochemically more stable than those of mouse spermatozoa. Perhaps the physical and chemical properties of the sperm plasma membrane vary from species to species. For those species whose spermatozoa have 'stable' plasma membranes, prior removal or 'damage' of sperm plasma membranes would increase the success rate of ICSI.

Animals↗
PubMed1999

Incidence rate of Creutzfeldt-Jakob disease in Japan.

BACKGROUND: The objective of this study is to clarify the incidence rate of Creutzfeldt-Jakob disease (CJD) during the last decade in Japan. METHODS: A nationwide mail survey was conducted in all hospitals with a minimum bed capacity of 100 and having at least one of three departments: neurology, psychiatry, and neuropathology. The survey required the patient's sex, date of birth, date of diagnosis, diagnostic criteria, medical history and CJD incidence in the family. RESULTS: From 493 hospitals throughout the country, 821 patients with CJD were reported from January 1985 through March 1996. The annual incidence rate was 0.49 per million population for males and 0.68 for females. The age-specific incidence rate was highest among those 70-79 years of age, followed by the 60-69, and 50-59 age groups. The incidence and mortality increased during the observed period; however, the incidence rate among younger generations did not rise. CONCLUSION: A nationwide incidence survey of CJD in Japan revealed the incidence and distribution of the disease over the recent decade. It was found that the incidence and mortality rates had increased during the observed period.

Adolescent↗
PubMed1999

Serum levels of circulating adhesion molecules after coronary angioplasty.

The activation of platelets, leukocytes, and vascular endothelial cells mediated by cell adhesion molecules may play a role in the mechanism of restenosis, which is still a significant complication after coronary angioplasty. We observed serial changes in the circulating soluble forms of adhesion molecules in 25 patients with coronary artery disease who underwent coronary angioplasty for a single lesion of the left anterior descending artery. Serum levels of sICAM-1 (p < 0.05) and sP-selectin (p < 0.05) were significantly increased immediately after angioplasty in the coronary sinus blood samples. These increases continued during the 48-hour observation period, and the maximum increase was seen 48 h after angioplasty for sICAM-1 (p < 0.01) and 24 h after angioplasty for sP-selectin (p < 0. 01). The level of sL-selectin increased 24 h (p < 0.01) and 48 h (p < 0.001) after angioplasty. These changes were not observed in the peripheral blood samples. The sE-selectin level did not change after angioplasty. A multiple regression analysis showed that the late loss index obtained from quantitative angiographic (QCA) analysis was correlated with the changes in sICAM-1 (r = 0.31, p < 0.05), sL-selectin (r = 0.28, p < 0.05), and sP-selectin (r = 0.26, p < 0. 05) 48 h after angioplasty in the coronary sinus blood samples, but was not correlated with procedural variables, other QCA variables, or the change in the sL-selectin level. The measurements of these adhesion molecule levels may help to evaluate traumatic vessel wall injury and inflammation at the intervention site after coronary angioplasty.

Analysis of Variance↗
PubMed1999

The primary calcification in bones follows removal of decorin and fusion of collagen fibrils.

To elucidate the mechanisms of primary calcification in bone, ultrastructural changes in collagen fibrils, as well as cytochemical alteration of proteoglycan, especially decorin, were investigated morphologically in 19-day postcoitum embryonic rat calvariae. Below the osteoblast layer, calcification of the osteoid area increased in direct proportion to its distance from the osteoblasts. In the uncalcified osteoid area, collagen fibrils near matrix vesicles possessed sharp contours and were a uniform 50 nm in diameter. Immunoelectron microscopy revealed decorin to be abundantly localized in the vicinity of the collagen fibrils. In the osteoid area undergoing the process of calcification, collagen fibrils tended to fuse side by side. Where calcification was progressed, this fusion was even more so. Some very large fibrils exhibited complicated contours, 400 nm or more in diameter. Although the calcification at this stage affected areas both inside and outside of the collagen fibrils, the interior areas manifested a lower density of calcification. The immunolocalization of decorin was also much decreased around these fibrils. Thus, primary calcification in bone matrix follows the removal of decorin and fusion of collagen fibrils. This phenomenon may aid in the process of calcification and bone formation, because (1) inhibitors of calcification, such as decorin, are removed, (2) the fusion of collagen fibrils provides the room necessary for rapid growth of mineral crystals, and (3) the soft elastic bone matrix containing abundant fused collagen fibrils less subjective to calcification is safe for both maternal and embryonic bodies and is convenient for subsequent bone remodeling.

Animals↗
PubMed1999

Changes in serum levels of type I collagen-related proteins after surgically induced menopause and correlations with bone loss in the lumbar spine.

The purpose of this prospective study was to characterize the changes in serum levels of two proteins produced during the synthesis and degradation of type I collagen, i.e., the carboxyterminal propeptide of type I procollagen (PICP) and the pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), respectively, after oophorectomy, and to assess the degree of correlation between changes in the serum values of these proteins and changes in bone mineral density (BMD) of the lumbar spine. Serum levels of PICP, ICTP and bone gla protein (BGP) were determined in 18 women before oophorectomy (baseline) and at 7 days, and 1, 2, 3, 6, 9 and 12 months post-oophorectomy (PO). The BMD of the lumbar spine was measured at baseline, and at 6 months and 12 months PO. ICTP had increased significantly at 7 days PO and peaked between 1 and 3 months PO. PICP and BGP had increased significantly at 2 months PO and remained at high levels thereafter. The percent changes in lumbar BMD from baseline values (% CFB) at 6 months and at 12 months PO were significantly correlated with % CFB in ICTP, but not with % CFB in PICP or BGP. Accordingly, bone resorption is a main determinant of bone mineral loss after oophorectomy and the change in recently-developed bone resorption markers, such as ICTP, is of clinical utility in predicting a degree of subsequent bone loss after surgical menopause.

Adult↗
PubMed1999

Prenatal confirmation of the translocation between chromosome 15 and Y-chromosome by fluorescence in situ hybridization.

A 30-year-old woman and her husband visited our hospital with habitual abortion as the complaint. Chromosome examination revealed a normal 46, XX for her and 46, XY, 15, der (15) t (Y; 15) (q12; p12) for him. After her pregnancy amniocentesis was performed. The karyotype was 46, XX, 15, der (15) t (Y; 15) (q12; p12) pat. ish der (15) (DYZ1+). A female baby was delivered. The growth of the baby was normal at 12 months of age.

Abortion, Habitual↗
PubMed1998

Fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, scavenges free radicals and inhibits lipid peroxidation in rat liver microsomes.

We investigated the effect of fluvastatin sodium (fluvastatin) and pravastatin, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, on the formation of thiobarbituric acid reactive substances both in vivo and in vitro in rat liver microsomes and on active oxygen species. Oral administration of fluvastatin at low doses (3.13 and 6.25 mg/kg) inhibited the formation of thiobarbituric acid reactive substances in rat liver microsomes, but high doses (12.5 and 25 mg/kg) did not change the formation of thiobarbituric acid reactive substances. Fluvastatin at any dose used had no effect on the content of cytochrome P-450 and the activity of NADPH-cytochrome P-450 reductase. In in vitro experiments, concentrations of fluvastatin ranging from 1 x 10(-6) - 1 x 10(-4) M markedly inhibited NADPH-dependent lipid peroxidation in liver microsomes, but pravastatin weakly inhibited lipid peroxidation. The order of magnitude of inhibition of each drug on in vitro lipid peroxidation was butylated hydroxytoluene > probucol > or = fluvastatin > pravastatin. Moreover, fluvastatin chemically scavenged active oxygen species such as hydroxyl radicals and superoxide anion generated by the Fenton reaction and by the xanthine-xanthine oxidase system, respectively, but pravastatin showed no scavenging of superoxide anion. These results indicate that the suppression of in vivo and in vitro lipid peroxidation in liver microsomes may be, at least in part, due to the scavenging by fluvastatin of free radicals.

Animals↗
PubMed1998

Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty.

BACKGROUND: The Cutting Balloon is a novel dilatation catheter for coronary angioplasty (InterVentional Technologies Inc). It produces longitudinal, microsurgical incisions in the vessel wall before the actual dilatation. It is assumed that these controlled surgical incisions relieve hoop stress and reduce vessel wall injury and eventually restenosis. However, no clinical indicator to support the theory of reduced injury has been described. Certain clusters of differentiation (eg, CD11, CD18 on the leukocytes) are implicated in leukocyte adhesion, increased permeability, and opsonization. Therefore, they might serve as clinical indicators of the injury level of the vessels after angioplasty. METHODS AND RESULTS: We randomly selected 64 patients with isolated left anterior descending coronary artery disease for either Cutting Balloon angioplasty or conventional balloon angioplasty. The expression of CD18 and CD11b on the surface of neutrophils was determined by flow cytometric analysis. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) were also measured. The expression of both the CD18 and CD11b in the coronary sinus blood gradually increased and reached its maximum at 48 hours after angioplasty. The sICAM-1 levels in the coronary sinus serum also increased after angioplasty. Percentage increases of CD18 and CD11b expression and the increase of the sICAM-1 levels at 48 hours after angioplasty (as ratios to baseline values before angioplasty) were less in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group (CD18, 1.10+/-0.05 versus 1.31+/-0.05, P<0.05; CD11b, 1.23+/-0.06 versus 1.72+/-0.10, P<0.001; sICAM-1, 1.12+/-0.05 versus 1.25+/-0.02, P<0.05). In all patients, the late lumen loss at follow-up angiogram positively correlated with the increased levels of CD11b (R=0.59, P<0.001) and sICAM-1 (R=0.38, P<0.05) at 48 hours after angioplasty. CONCLUSIONS: Balloon angioplasty upregulated Mac-1 (CD11b/CD18) on the surface of the neutrophils and increased sICAM-1 levels in association with late loss increase. These changes were significantly smaller in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group. This suggests that Cutting Balloon angioplasty may produce less vessel wall injury and, consequently, less neutrophil activation, which may account for the lower rate of restenosis.

CD18 Antigens↗
PubMed1998

Intracellular retention and degradation of tissue-nonspecific alkaline phosphatase with a Gly317-->Asp substitution associated with lethal hypophosphatasia.

One point mutation which converts glycine-317 to aspartate of tissue-nonspecific alkaline phosphatase (TNSALP) was reported to be associated with lethal hypophosphatasia (Greenberg, C. R., et al. Genomics 17, 215-217, 1993). In order to define the molecular defect of TNSALP underlying the pathogenesis of hypophosphatasia, we have examined the biosynthesis of TNSALP with a Gly317-->Asp substitution. When expressed in COS-1 cells, the mutant did not exhibit alkaline phosphatase activity at all, indicating that the replacement of glycine-317 with aspartate abolishes the catalytic activity of TNSALP. Pulse-chase experiments showed that the newly synthesized mutant failed to acquire Endo H-resistance and to reach the cell surface. Interestingly, this TNSALP mutant was found to form a disulfide-bonded high-molecular-mass aggregate and was rapidly degraded within the cell, though the mutant protein was modified by glycosylphosphatidylinositol (GPI). Lactacystin, an inhibitor of the proteasome, obstructed the degradation of the mutant protein, suggesting the involvement of proteasome as a part of quality control of TNSALP.

Alkaline Phosphatase↗
PubMed1998

Morphological examination of bone synthesis via direct administration of basic fibroblast growth factor into rat bone marrow.

Woven bone induced by direct injection of basic fibroblast growth factor (bFGF) into rat bone marrow was examined. On the first day after injection, fibrous tissues formed in the treated region of the bone marrow. Tissue-nonspecific alkaline phosphatase (TNAPase)-immunopositive osteoblastic cells and osteopontin immunopositive-extracellular matrices were observed in the fibrous tissues, indicating bone induction. On the fifth day, the bFGF-induced bone was found broadly in the bone marrow. In the originally existing bone, osteopontin-immunoreactivity was observed at cement lines, but not in the fully calcified matrix, whereas the woven bone displayed immunoreactivity throughout the matrix. Numerous TRAPase-positive osteoclasts were present on the surfaces of the woven bone, but no obvious cement line was observed. Therefore, both bone formation and resorption appeared highly active, without normal cellular coupling equilibrated between bone formation and resorption performed by osteoblasts and osteoclasts. On the tenth day, the bFGF-induced bone was almost replaced by bone marrow. Thus, bone formation actively occurred in the first half of the experimental period, whereas bone resorption came to be predominant thereafter. This study demonstrated that bFGF stimulates bone formation, which, however, is subject to subsequent resorption, probably due in part to the absence of coordinated cellular coupling between osteoclasts and osteoblasts.

Acid Phosphatase↗
PubMed1998

Impaired endothelium-dependent acetylcholine-induced coronary artery relaxation in patients with high serum remnant lipoprotein particles.

Acetylcholine (Ach)-induced vascular relaxation is mediated by nitric oxide released from the endothelium. Hence, impaired Ach-induced relaxation reflects endothelial dysfunction. The action of lipoprotein lipase on chylomicrons and very low density lipoproteins produces remnant lipoproteins (RLP) rich in triglycerides (TG), cholesterol (C) and apolipoprotein E (apo E). Apo E on RLP serves as a ligand for uptake of RLP by macrophages, endothelial cells and other cells expressing the LDL receptor or the remnant receptor; uptake of RLP by vascular wall cells can promote atherosclerosis. Serum C, TG, Lp(a), apo E, apo A-I, apo B, HDL-C and RLP-C were measured in 652 patients who underwent diagnostic coronary angiography. Of these, 48 (32 males and 16 females, age 59 +/- 10 years) were suspected of having ischaemic heart disease because they had chest pain, but without angiographic evidence of atherosclerotic coronary artery disease defined as a discrete stenosis or intimal irregularity, and without any other known underlying heart disease. These were selected for acetylcholine provocation test in the left coronary artery. Nineteen of 48 patients had high RLP-C ( > or = 5 mg/dl, mean 8.7 +/- 3.1 mg/dl), 29 had normal RLP-C ( < or = 5 mg/dl, mean 2.4 +/- 0.4 mg/dl, P < 0.0001). The percent change (-, constriction, or +, dilation) in coronary artery diameter after intracoronary injection of Ach was smaller in the high RLP-C group, compared with the normal RLP-C group thus, in the left anterior descending artery, -33 +/- 23 vs -8 +/- 25 in the proximal segment (P <0.01), -30 +/- 37 vs -3 +/- 29 in the mid segment (P < 0.01), -17 +/- 47 vs 16 +/- 43 in the distal segment (P < 0.001); in the left circumflex artery, -29 +/- 46 vs -9 +/- 28 in the proximal segment (P < 0.01), -29 +/- 43 vs -5 +/- 34 in the mid segment (P < 0.01), -26 +/- 43 vs 10 +/- 31 in the distal segment (P < 0.001). There were no significant differences in other lipid levels. These results suggest that there is an association between high serum RLP-C and coronary vascular endothelial cell dysfunction and that RLP-C may be taken as a marker of early stage coronary artery atherosclerosis not detectable by angiography.

Acetylcholine↗
PubMed1998

Anti-angiogenic effect of TGFbeta in aqueous humor.

Neovascularization is mediated by various factors in ocular tissues. Recent studies have emphasized the role of vascular endothelial growth factor in the induction of angiogenesis. We have previously reported that aqueous humor (AH) suppressed vascular endothelial cell growth and angiogenesis. We speculated that the anti-angiogenic effect of AH is mediated by transforming growth factor beta (TGFbeta). In order to clarify the presence of TGFbeta in bovine AH, we applied it on the heparin-sepharose affinity column and prepared two fractions (bound and unbound fractions). We measured TGFbeta concentration in each fraction and examined how the anti-TGFbeta antibody decreased the inhibitory effect of AH on human umbilical vein endothelial cell growth and on in vitro angiogenesis. We found the presence of TGFbeta2, but not TGFbeta1, in the heparin bound fraction, and the inhibitory effect was detected in the heparin-bound fraction. Anti-TGFbeta antibody completely and dose-dependently extinguished the inhibitory effect of AH. We propose that the inhibitory effect of AH on endothelial cell growth and in vitro angiogenesis are both mediated by TGFbeta2. Our results indicate TGFbeta2 is normally present in AH and protects the eye tissue against abnormal neovascularization.

Animals↗