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Biomedical subjects

A Honda

Publications and source records attributed to A Honda.

At least 73 records · Page 4Linked to original sources
PubMed1999

Plasma levels of mevalonate and 7alpha-hydroxy-4-cholesten-3-one in chronic liver disease.

BACKGROUND AND AIMS: Cholesterol levels in blood tend to be preserved despite hepatic impairment, in contrast to albumin levels and other markers of liver function in patients with liver cirrhosis (LC). We reported previously that the levels of plasma mevalonate (MVA) and 7alpha-hydroxy-4-cholesten-3-one (7alpha3one) closely reflect hepatic synthetic rates of cholesterol and bile acids. The aim of this study was to examine the association between hepatic cholesterogenesis and bile acid synthesis in hepatocellular impairment using these indices. METHODS: The plasma indices were measured in patients with LC (n = 38) or chronic hepatitis (CH; n = 11) and in normal controls (n = 22). The severity of LC was assessed by the Child-Pugh score. RESULTS: There were no significant differences in plasma MVA levels between CH, LC and control groups. However, plasma 7alpha3one levels were significantly lower in LC than in CH and control groups (P< 0.01). While MVA levels did not correlate with the Child-Pugh score, there was a significant correlation between 7alpha3one level and Child-Pugh score (P< 0.005). The plasma 7alpha3one level in controls correlated positively with MVA levels (P< 0.01); however, there was no significant correlation between these indices in CH and LC. CONCLUSION: In chronic liver disease, there was a tendency for hepatic cholesterogenesis to be sustained in the face of hepatocellular impairment, while bile acid synthesis declined in parallel with the severity of impairment.

Bile Acids and Salts↗
PubMed1999

Isolation from tobacco mosaic virus-infected tobacco of a solubilized template-specific RNA-dependent RNA polymerase containing a 126K/183K protein heterodimer.

The complete nucleotide sequence was determined for the putative RNA polymerase (183K protein) gene of tobacco mosaic virus (TMV) OM strain, which differed from the related strain, vulgare, by 51 positions in its nucleotide sequence and 6 residues in its amino acid sequence. Three segments of this 183K protein, each containing the sequence motif of methyltransferase (M), helicase (H), or RNA-dependent RNA polymerase (P), were expressed in Escherichia coli as fusion proteins with hexahistidine tags, and domain-specific antibodies were raised against purified His-tagged M and P polypeptides. By immunoaffinity purification, a template-specific RNA-dependent RNA polymerase containing a heterodimer of the full-length 183K and 126K (an amino-terminal-proximal portion of the 183K protein) viral proteins was isolated. We propose that the TMV RNA polymerase for minus-strand RNA synthesis is composed of one molecule each of the 183- and 126-kDa proteins, possibly together with two or more host proteins.

Base Sequence↗
PubMed1999

Real time image processing with an analog vision chip system.

A linear analog network model is proposed to characterize the function of the outer retinal circuit in terms of the standard regularization theory. Inspired by the function and the architecture of the model, a vision chip has been designed using analog CMOS Very Large Scale Integrated circuit technology. In the chip, sample/hold amplifier circuits are incorporated to compensate for statistic transistor mismatches. Accordingly, extremely low noise outputs were obtained from the chip. Using the chip and a zero-crossing detector, edges of given images were effectively extracted in indoor illumination.

Adaptation, Ocular↗
PubMed1999

Detection of mutations in the enhancer 2/core promoter region of hepatitis B virus in patients with chronic hepatitis B virus infection: comparison with mutations in precore and core regions in relation to clinical status.

To investigate the meaning of the mutations in the enhancer 2/core promoter (Enh2/CP) region of hepatitis B virus (HBV) during the chronic HBV infection, mutations were examined in the Enh2/ CP region (carboxyl half of X region) and their correlation with mutations in the precore and core regions in relation to the presence of chronic liver disease. The entire nucleotide sequences of the Enh2/CP region were determined by direct sequencing of the amplified products derived from 30 cases with chronic HBV infection. The results were compared to the mutations in the precore and core regions. In the Enh2/CP region, 91 generally scattered nucleotide substitutions were detected. There were 11 substitutions in the 10 asymptomatic healthy carriers (mean, 1.1/case) and 80 in the 20 chronic liver disease patients (4.0/case). The most frequent substitutions from A to T at nucleotide 1764 and from G to A at nucleotide 1766 were seen in none of the 10 asymptomatic carriers and in 14 (70%) of the 20 chronic liver disease patients. Comparisons of mutations in the precore and core regions revealed that 14 of 16 patients with mutations in the core region had the mutations in the Enh2/CP region and/or a precore stop codon mutation. These data suggest that mutations in the Enh2/CP and precore regions may affect the expression of the core and HBeAg peptides and might be involved in the pathogenesis of chronic liver disease.

Adolescent↗
PubMed1999

Bile acid synthesis in the Smith-Lemli-Opitz syndrome: effects of dehydrocholesterols on cholesterol 7alpha-hydroxylase and 27-hydroxylase activities in rat liver.

The Smith-Lemli-Opitz syndrome (SLOS) is a congenital birth defect syndrome caused by a deficiency of 3beta-hydroxysterol Delta(7)-reductase, the final enzyme in the cholesterol biosynthetic pathway. The patients have reduced plasma and tissue cholesterol concentrations with the accumulation of 7-dehydrocholesterol and 8-dehydrocholesterol. Bile acid synthesis is reduced and unnatural cholenoic and cholestenoic acids have been identified in some SLOS patients. To explore the mechanism of the abnormal bile acid production, the activities of key enzymes in classic and alternative bile acid biosynthetic pathways (microsomal cholesterol 7alpha-hydroxylase and mitochondrial sterol 27-hydroxylase) were measured in liver biopsy specimens from two mildly affected SLOS patients. The effects of 7- and 8-dehydrocholesterols on these two enzyme activities were studied by using liver from SLOS model rats that were treated with the Delta(7)-reductase inhibitor (BM15.766) for 4 months and were comparable with more severe SLOS phenotype in plasma and hepatic sterol compositions. In the SLOS patients, cholesterol 7alpha-hydroxylase and sterol 27-hydroxylase were not defective. In BM15.766-treated rats, both enzyme activities were lower than those in control rats and they were competitively inhibited by 7- and 8-dehydrocholesterols. Rat microsomal cholesterol 7alpha-hydroxylase did not transform 7-dehydrocholesterol or 8-dehydrocholesterol into 7alpha-hydroxylated sterols. In contrast, rat mitochondrial sterol 27-hydroxylase catalyzed 27-hydroxylation of 7- and 8-dehydrocholesterols, which were partially converted to 3beta-hydroxycholestadienoic acids. Addition of microsomes to the mitochondrial 27-hydroxylase assay mixture reduced 27-hydroxydehydrocholesterol concentrations, which suggested that 27-hydroxydehydrocholesterols were further metabolized by microsomal enzymes. These results suggest that reduced normal bile acid production is characteristic of severe SLOS phenotype and is caused not only by depletion of hepatic cholesterol but also by competitive inhibition of cholesterol 7alpha-hydroxylase and sterol 27-hydroxylase activities by accumulated 7- and 8-dehydrocholesterols. Unnatural bile acids are synthesized mainly by the alternative pathway via mitochondrial sterol 27-hydroxylase in SLOS.

Animals↗
PubMed1998

phd1+, a histone deacetylase gene of Schizosaccharomyces pombe, is required for the meiotic cell cycle and resistance to trichostatin A.

A gene named phd1+ encoding a protein highly homologous to the yeast and human histone deacetylases, such as Saccharomyces cerevisiae Rpd3p and human HDAC1, was cloned from Schizosaccharomyces pombe. The immune complex isolated from S. pombe cells expressing Phd1 fused to the FLAG epitope showed histone deacetylase activity, which was inhibited by trichostatin A (TSA), a specific inhibitor of histone deacetylase. The null mutation of phd1+ resulted in a marked decrease in the total cellular histone deacetylase activity and an increase in the sensitivity to TSA. Although the phd1 disruptant showed no obvious defect in the mitotic cell cycle or mating, both homothallic haploid and heterothallic diploid cells failed to form spores in the absence of phd1+. These results indicate that phd1+ encodes a histone deacetylase, which is involved in the meiotic cell cycle in S. pombe.

Base Sequence↗
PubMed1998

Regulation of early cholesterol biosynthesis in rat liver: effects of sterols, bile acids, lovastatin, and BM 15.766 on 3-hydroxy-3-methylglutaryl coenzyme A synthase and acetoacetyl coenzyme A thiolase activities.

Cytosolic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase catalyzes the formation of HMG-CoA, the substrate for the rate-controlling enzyme in the cholesterol biosynthetic pathway. To explore the regulation in liver, we developed a new, accurate, and reliable reversed-phase ion-pair chromatographic assay that uses nonradioactive substrates and n-propionyl coenzyme A as an internal recovery standard. The hepatic activities were measured in rats treated with cholesterol, sitosterol, cholic acid, deoxycholic acid, ursodeoxycholic acid, cholestyramine, bile fistula, lovastatin, and BM 15.766, an inhibitor of 7-dehydrocholesterol delta7-reductase, and were compared with microsomal HMG-CoA reductase and cytosolic acetoacetyl coenzyme A (AcAc-CoA) thiolase activities. HMG-CoA synthase activity was effectively suppressed in synchrony with HMG-CoA reductase activity by treatments with cholesterol (-41%, P < .05), cholic acid (-72%, P < .005), and deoxycholic acid (-62%, P < .05). However, ursodeoxycholic acid increased activity 84% (P < .05) and intravenous sitosterol did not change activity. AcAc-CoA thiolase activities also paralleled HMG-CoA reductase and HMG-CoA synthase activities, but differences were not statistically significant. In contrast to inhibition, up-regulation of hepatic HMG-CoA synthase activities by cholestyramine, bile fistula, and lovastatin was much less than HMG-CoA reductase activities. In addition, BM 15.766 did not stimulate synthase activity, whereas lovastatin increased activity 2.4-fold. Thus, hepatic HMG-CoA synthase activity was regulated coordinately with HMG-CoA reductase, and responded more forcefully to regulatory stimuli than acetoacetyl-CoA thiolase activity but usually less than HMG-CoA reductase.

Acetyl-CoA C-Acetyltransferase↗
PubMed1998

Mapping of Rpb3 and Rpb5 contact sites on two large subunits, Rpb1 and Rpb2, of the RNA polymerase II from fission yeast.

[Rpb1 and Rpb2] Mapping of the contact sites on two large subunits of the fission yeast Schizosaccharomyces pombe RNA polymerase II with two small subunits, Rpb3 and Rpb5, was carried out using the two-hybrid screening system in the budding yeast Saccharomyces cerevisiae. Rpb5 was found to interact with any fragment of Rpb1 that contained the region H, which is conserved among the subunit 1 homologues of all RNA polymerases, including the beta' subunit of prokaryotic RNA polymerases. In agreement with the fact that Rpb5 is shared among all three forms of eukaryotic RNA polymerases, the region H of RNA polymerase I subunit 1 (Rpa190) was also found to interact with Rpb5. On the other hand, two-hybrid screening of Rpb2 fragments from RNA polymerase II indicated the presence of an Rpb3 contact site in the region H which is conserved among the subunit 2 homologues of all RNA polymerases, including the beta subunit of prokaryotic RNA polymerases. Possible functions of the regions H in the subunits 1 and 2 are discussed.

Binding Sites↗
PubMed1998

Molecular cloning of the chromosomal breakpoint in the LIS1 gene of a patient with isolated lissencephaly and balanced t(8;17).

Karyotypic analysis of a patient exhibiting a phenotype of isolated lissencephaly, and of her parents, revealed a de novo balanced translocation, t(8;17)(p11.2; p13.3). Since the lissencephaly (LIS1) gene was known to be located on 17p13.3, we investigated whether the translocation might involve this gene. We performed Southern analysis using cosmid clones that contained genomic sequences corresponding to LIS1, and found that the breakpoint was located within intron 1. As sequence analysis of the parental chromosomes in the vicinity of the breakpoint identified no additional putative transcripts, haploinsufficiency of the LIS1 gene is likely to be solely responsible for the patient's lissencephaly. Characterization of both breakpoints indicated a possible involvement of repetitive sequences in the recombigenic process that led to the translocation.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1998

Bone structural and metabolic changes at the end of pregnancy and lactation in rats.

OBJECTIVE: The objective of this study was to elucidate the net change of bone structure and metabolism in the lumbar trabecular bone of rats at the end of the pregnancy and lactation. STUDY DESIGN: Female virgin Sprague-Dawley rats aged 200 days were mated, and bone mineral density by dual-energy x-ray absorptiometry, bone histomorphometry, and serum bone metabolic markers were measured at the end of pregnancy (day 22 of pregnancy), after delivery (day 5 post partum), and at the end of lactation (day 21 post partum). RESULTS: At the end of pregnancy bone mineral density, bone volume, trabecular thickness, and serum calcium decreased; serum parathyroid hormone increased; and the histomorphometric parameters indicated that bone resorption were higher than those variables in nonpregnant rats, but bone formation was suppressed, as demonstrated by the low histomorphometric parameters and by the low serum alkaline phosphatase levels. After delivery the bone mineral density of nonlactating rats recovered rapidly, as in nonpregnant rats, but nonlactating rats showed more bone formation by histomorphometry than nonpregnant rats did. At the end of lactation, bone mineral density and serum calcium levels decreased considerably, and lactating rats showed substantial bone formation, bone resorption, and high serum alkaline phosphatase levels. The correlation between the number of pups (x) of the lactating and nonlactating groups and the bone mineral density (y, in grams per square centimeter) showed simple linear regression (y = -0.0067 . x +0.2517, r = 0.949, p < 0.0001). CONCLUSIONS: These results indicate that significant decreases occur in the trabecular bone of rats at the end of pregnancy and lactation and that lactational intensity is related to bone mineral density.

Absorptiometry, Photon↗
PubMed1998

Effect of long-term hormone replacement therapy on the bone in ovariectomized women with cancer.

OBJECTIVE: To evaluate longitudinally the effectiveness of long-term hormone replacement therapy (HRT) in preserving the bone mineral density (BMD) over a 5-year period in ovariectomized patients treated for gynecologic malignancies. METHODS: A total of 70 pre-menopausal women ovariectomized for gynecologic malignancies at our hospital were divided non-randomly into two groups: HRT (+) group (n = 59) and HRT (-) group (n = 11). HRT was administered in a sequential regimen of 0.625-1.25 mg conjugated estrogen for 24 days and 5-10 mg medroxyprogesterone acetate for 10 days. RESULTS: The BMD of the lumbar vertebrae decreased significantly in the HRT (-) group (pre-operative BMD was 91.8%, 91.0% and 91.3% at 1, 2 and 3 years post-ovariectomy), but no decrease in the BMD was observed in the HRT (+) group (pre-operative BMD was 98.4%, 99.0%, 99.4%, 98.8% and 98.7% at 1, 2, 3, 4 and 5 years post-ovariectomy); the difference in BMD between the two groups was statistically significant (P < 0.01). Serum alkaline phosphatase levels were significantly lower in the HRT (+) group than in the HRT (-) group (P < 0.01). There were four recurrences of cancer in the HRT (+) group. CONCLUSION: HRT appeared to have beneficial effects on bone metabolism by maintaining BMD for 5 years in ovariectomized patients for gynecologic malignancies.

Adult↗
PubMed1998

Lumbar bone mineral density changes during pregnancy and lactation.

OBJECTIVE: To elucidate the change of bone metabolism in the lumbar trabecular and its relationship with serum hormonal changes in pregnancy and lactation. STUDY DESIGN: In a cross-sectional study, we measured the bone mineral density (BMD) of 2-4 lumbar vertebrae of 571 puerperae at days 3-5 postpartum and 341 healthy, non-pregnant women (control subjects) of approximately the same age by dual energy X-ray absorptiometry. In a longitudinal study, we also measured the BMD of 111 puerperae at 3 and 6 months after delivery. RESULTS: The mean BMD at days 3-5 postpartum was significantly lower than that of the control (1.013+/-0.005 vs. 1.032+/-0.006 g/cm2, P = 0.019). The lactating group showed BMD decrement to 95.1+/-0.5% (n = 69) and 94.1+/-0.7% (n = 61) at 3 and 6 months postpartum, respectively, compared with days 3-5 postpartum, and the amenorrhea group showed the same tendency. The non-lactating group and resumption of menses group did not show a BMD decrement postpartum. In the lactating group, serum estradiol was significantly lower than in the non-lactating group at 3 months postpartum, serum prolactin and bone alkaline phosphatase levels were higher than in the non-lactating group at 3 and 6 months postpartum. CONCLUSIONS: Pregnancy may cause a decrease of lumbar BMD, and the lactation and amenorrhea also cause a decrease of BMD. In addition to lactation status, the ovarian dysfunction is one of the factors in bone loss during lactation.

Absorptiometry, Photon↗
PubMed1998

Guillain-Barré syndrome associated with IgG anti-GM1b antibody subsequent to Mycoplasma pneumoniae infection.

Sera from patients with Guillain-Barré syndrome (GBS) frequently have antibodies to various gangliosides. We report a girl with GBS after Mycoplasma pneumoniae infection who had serum IgG antibody to GM1b ganglioside as well as the cold agglutinins. The cold agglutinins are polyclonal IgM autoantibodies to 'I' antigen on erythrocytes. Ganglioside GM1b contains the terminal moiety shared with sialylated I antigen, a main receptor for M. pneumoniae. In this patient, the anti-GM1b antibody may be elicited in a similar mechanism producing anti-I antibody, and functioned in the development of GBS.

Agglutinins↗
PubMed1998

Decrease in the proportion of granulated CD56+ T-cells in patients with a history of recurrent abortion.

We investigated levels of CD56+ T-cells (CD3+ CD56+ cells) in peripheral circulation, which express one of the natural killer (NK) cell markers, by flow cytometry and with monoclonal antibodies in patients with a history of recurrent abortion. We compared these values with those obtained in normal women who were not pregnant as well as in normal pregnant subjects. The percentage of CD56+ T-cells in the peripheral blood of patients with a history of recurrent abortion was less than that in the non-pregnant or pregnant women. These results suggest that CD56+ T-cells with extrathymic properties may be associated with the maintenance of normal pregnancy in humans.

Abortion, Habitual↗
PubMed1998

Identification of the 5' terminal structure of influenza virus genome RNA by a newly developed enzymatic method.

A combination of T4 polynucleotide kinase, Escherichia coli alkaline phosphatase, yeast Saccharomyces cerevisiae capping enzyme consisting of alpha (RNA guanylyltransferase) and beta (RNA 5'-triphosphatase) subunits. and its alpha subunit without RNA 5'-phosphatase activity was used to establish a simple enzymatic method for determination of RNA species with 5'-hydroxyl, 5'-monophosphate, 5'-diphosphate or 5'-triphosphate termini. Using this method, we found that viral genome RNA (vRNA) segments of both A-type and C-type influenza viruses carry tri- or diphosphates at their 5' termini. The conclusion was based on the observations that: (i) 5' phosphorylation of vRNAs by T4 polynucleotide kinase takes place only after phosphatase treatment; and (ii) capping of vRNAs can be observed with both the intact yeast capping enzyme and its alpha subunit alone devoid of RNA 5'-triphosphatase activity; but (iii) the level of capping is higher for the alphabeta holoenzyme than the alpha subunit though the relative level varies depending on RNA preparations. The results support the de novo initiation for the RNA replication although transcription of influenza vRNAs is initiated by host cell capped RNAs as primers.

Acid Anhydride Hydrolases↗
PubMed1998

Isolated lissencephaly sequence with balanced chromosome translocation involving 17p13.3.

We describe a patient with isolated lissencephaly sequence (ILS) who had a de novo balanced translocation with breakpoint at 8p11.23 and 17p13.3. She developed infantile spasms and had severe developmental delay. There was no apparent deletion of 17p13.3 on fluorescence in situ hybridization (FISH) analysis. The breakpoint was located centromeric to the Miller-Dieker syndrome (MDS) marker (D17S379), and telomeric to the marker D17S1566, which is located centromeric to the LIS1 gene. This is the second reported case of ILS with balanced translocation. It is suspected that the breakpoint of 17p13.3 in this patient is located in the responsible gene for ILS.

Brain↗