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Biomedical subjects

A Kato

Publications and source records attributed to A Kato.

At least 289 records · Page 16Linked to original sources
PubMed1998

[Mantle cell lymphoma with marked lymphocytosis at the presentation and with discordant morphology between the lymph node and peripheral blood].

A 72-year-old man was referred to our hospital because of lymphadenopathy, splenomegaly, and leukocytosis. His WBC count was 54,300/microliter, with 89.6% atypical lymphocytes two to three times the diameter of red blood cells, cleaved nuclei, and one or two nucleoli. A lymph node specimen revealed a vaguely nodular pattern, and the diagnosis of mantle cell lymphoma (MCL) was made. The lymphoma cells appeared smaller and more mature than the leukemic cells. The phenotype of the peripheral blood and the lymph node cells was CD5+ CD10- CD19+ CD20+ and the same rearranged JH bands were detected, suggesting that their lymphocytes were of the same origin. In addition, the phenotype of the leukemic cells was CD23+ CD38+ CD43- CD44+ FMC-7+ micro+ chi+. Cytogenetic analysis revealed complex anomalies but not t(11; 14). Cyclin D1 protein was not detected. Because the lymphocyte morphology of the peripheral blood and lymph nodes was discordant, we speculated that variant large cells had proliferated mainly in the peripheral blood. The patient achieved a partial response after 6 courses of CHOP regimen, and was then placed on a COP regimen. He seemed to have MCL, but the following findings were unusual: marked lymphocytosis at initial presentation, discordant morphology, CD5+ CD10- CD23+ CD43- phenotype with neither t(11; 14) or cyclin D1 over-expression.

Aged↗
PubMed1998

A possible mechanism of eighteen patient deaths caused by interactions of sorivudine, a new antiviral drug, with oral 5-fluorouracil prodrugs.

A toxicokinetic study was performed using rats to investigate the possible mechanism of 18 acute deaths in Japanese patients with cancer and herpes zoster by interactions of the new oral antiviral drug, sorivudine (SRV), with one of the oral 5-fluorouracil (5-FU) prodrugs within 40 days after approval of the use of SRV. Tegafur, an anticancer 5-FU prodrug suggested to be used by most of the patients who died, and SRV were orally administered to rats simultaneously once daily. All of these rats died within 10 days, whereas rats given SRV or tegafur alone under the same dosage conditions showed no appreciable change over 20 days compared with controls. In the rats given both drugs, bone marrow and intestinal membrane mucosa were greatly damaged at an early stage of the coadministration, and before death, the animals showed marked decreases in white blood cell and platelet counts, diarrhea with bloody flux, and severe anorexia, as was also manifested by the patients who subsequently died. In the rats given both drugs for 6 days, extremely enhanced 5-FU levels were observed from the first day of administration in plasma and in all tissues examined, including bone marrow and intestines. The extreme enhancement of the tissue 5-FU levels was attributable to the facile inactivation by (E)-5-(2-bromovinyl)uracil (BVU) of hepatic dihydropyrimidine dehydrogenase (DPD), a key enzyme regulating the systemic 5-FU level in the rat and human. BVU, a major metabolite formed from SRV by gut flora, was found at considerable levels in the liver of rats orally administered SRV alone or SRV and tegafur, and there was a marked decrease in hepatic DPD activity. In the presence of NADPH, DPD purified from rat liver cytosol was rapidly and irreversibly inactivated by [14C]BVU as a suicide inhibitor with concomitant incorporation of the radioactivity into the enzyme protein, although SRV showed no inhibitory effect on DPD under the same conditions. Human liver DPD was recently demonstrated by us to be inactivated with BVU in a manner very similar to rat DPD.

Animals↗
PubMed1998

Scalp localization using a simple algorithm.

We have developed a simple algorithm for scalp localization for craniotomy. Using a series of CT/MRI data, the point on the scalp closest to the center of the lesion (T) is determined by our program. A plane (plane R) is defined by three points: bilateral auditory meati and T. Point S is the intersection of three planes: the plane R, the scalp surface and the midsagittal plane. The distance from either S or the ipsilateral external auditory meatus to T is measured along the scalp surface on the plane R. The distance from the nasion to S along the scalp surface on the midsagittal plane is also measured. To determine the craniotomy site, these distances are measured directly on a patient's scalp in the operating room. This simple and accurate method for scalp localization could be used by installing our program in conventional CT/MR scanners.

Aged↗
PubMed1998

Seasonal increase in specific IgE in serum induced by natural Japanese cedar pollen exposure in asymptomatic and symptomatic sensitized individuals.

The aim of this study was to determine whether there is a difference in the specific IgE response to pollen exposure between asymptomatic and symptomatic subjects who were already sensitized to Japanese cedar pollen. Sixty-four subjects with detectable serum levels of cedar pollen-specific IgE, which were apparent even before the pollen season in 1997, were enrolled in the study. Thirty-five had typical symptoms of seasonal allergic rhinitis during the pollen season in 1997 (symptomatic group) and the remainder had no seasonal aggravation during the pollen season in 1997 (asymptomatic group). Serum samples were collected twice from each subject, before and during the pollen season in 1997, to determine specific IgE by the lumiward immunoassay system. In both groups, the serum levels of specific IgE during the pollen season were significantly higher than those before the pollen season, and the rates of seasonal increase in specific IgE did not differ significantly between the groups. In conclusion, the specific IgE response during the pollen season is not a hallmark of clinical allergy and does not discriminate between symptomatic and asymptomatic individuals sensitive to the pollen.

Allergens↗
PubMed1998

[Terminal home care "Ikigai no Yoake--The real aim of our life"--case report].

It is difficult to provide home care especially for terminal cancer patients as their physical conditions deteriorate due to the cancer. It is important to enhance the will of home care providers to make this possible. Although a universal method has been worked out, personal and religious beliefs have made it difficult to create an effective method. We would like to introduce our experience in the paper entitled "Ikigai no Yoake" and subtitled "Influence of scientific study of reincarnation on view of life" by Fumihiko Ida of Fukushima University. It has encouraged home care providers and made it possible to provide home care to terminal patients along with benefits.

Advance Directives↗
PubMed1998

[Benefits and problems of "home care score"--discussion of deviation from home care].

Care ability is the most important factor in providing home care. This ability to care can be classified into family care and community care. The "Home care score" is a system developed through the comprehensive scientific study on long life by the Ministry of Health and Welfare in order to evaluate such care ability. We have scored 71 patients since August 1997 until February 1998, and we found benefits and problems with the system. Here are the benefits: (1) General evaluation can be made on status of patients and home care providers. (2) Comparison of large numbers of patients can be easily made. (3) Helpful to work out practical support. On the other hand, the system has the following problems: (1) Scoring can differ by subjective evaluation. (2) Difficulty to reflect status of disease deterioration and so on. The factors of deviation from home care are: (1) of disease. (2) Loss of desire to provide care. We believe it is important for the home care nurse to intervene so that the will to provide care will not weaken until the end.

Aged↗
PubMed1997

Enzymatic synthesis of the glycosides of calystegines B1 and B2 and their glycosidase inhibitory activities.

Several glycosides of calystegines B1 and B2 were synthesized by use of rice alpha-glucosidase and the whole cells of Rhodotorula lactosa, and their glycosidase inhibitory activities were investigated. Incubation of mixture of calystegine B1 and maltose with rice alpha-glucosidase gave 3-O-alpha-D-glucopyranosylcalystegine B1 (2, 11.3%). An enzymatic beta-transglucosylation reaction of calystegines B1 or B2 with cellobiose using the whole cells of R. lactosa gave 3-O-beta-D-glucopyranosylcalystegine B1 (1) (0.9%) or 4-O-beta-D-glucopyranosylcalystegine B2 (3, 11.2%), respectively, while similar beta-transgalactosylation of calystegine B2 from lactose gave 4-O-beta-D-galactopyranosylcalystegine B2 (4, 10.1%). The glycosylation of calystegines B1 and B2 markedly decreased or abolished their inhibition against beta-glucosidase, alpha- or beta-galactosidase. Compound 4 however retained more or less the potency of calystegine B2 against trehalase. Interestingly, compound 1 was a noncompetitive inhibitor of rice alpha-glucosidase, with a Ki value of 0.9 +/- 0.1 microM.

Animals↗
PubMed1997

Bactericidal action of lysozymes attached with various sizes of hydrophobic peptides to the C-terminal using genetic modification.

The genetic modification of lysozyme was attempted to improve the bactericidal activity against Gram-negative bacteria E. coli. The different lengths of hydrophobic peptides were attached to the C-terminus of the hen egg white lysozyme to investigate the most effective length of the hydrophobic peptides for killing bacteria. The oligonucleotides encoding Phe-Val-Pro (H3), Phe-Phe-Val-Ala-Pro (H5) and Phe-Phe-Val-Ala-Ile-Ile-Pro (H7) were fused to the C-terminus Leu 129 of lysozyme cDNA. The reconstructed cDNAs were inserted into the yeast expression vector. The hydrophobic peptide-fused lysozymes were secreted in the yeast carrying the reconstructed cDNA. Although the hydrophobic peptide-fused lysozymes retained 75 80% lytic activity of the wild-type protein, the bactericidal action to E. coli was greatly increased with the length of hydrophobic peptides. These results suggest that the hydrophobic peptides play an important role in killing Gram-negative bacteria. To elucidate the role of catalytic domain in bactericidal action of the hydrophobic fusion lysozyme (H5-Lz), the mutant hydrophobic lysozyme (H5/E35A-Lz) whose glutamic acid was substituted with alanine at the position 35 was constructed to diminish the catalytic activity. The mutant hydrophobic lysozyme (H5/E35A-Lz) was greatly lost the bactericidal action to E. coli, suggesting that not only the length of hydrophobic peptide fused to C-terminus but also the catalytic domain is important for the bactericidal action of the hydrophobic peptide-fused lysozyme.

Anti-Bacterial Agents↗
PubMed1997

Phosphorylation of the Sendai virus M protein is not essential for virus replication either in vitro or in vivo.

A large proportion of intracellular Sendai virus (SeV) M proteins is phosphorylated, but in mature virions the M protein is not phosphorylated or dephosphorylated. Phosphorylated M protein in cells is bound to the cytoskeletal components more firmly than unphosphorylated M protein. Thus it has been hypothesized that M protein phosphorylation plays an important role in the virus life cycle, especially in the step of maturation. Here, a transient expression-mutation experiment of the M gene demonstrated that a change of the Ser residue at the 70th position from the N-terminus to Ala (S70A) totally abolished M protein phosphorylation, strongly suggesting that this residue is phosphorylated. The mutated M gene was then placed in the corresponding region in the cDNA plasmid which generates a full-length antigenome SeV RNA, and a mutant SeV M-S70A was successfully recovered from the cDNA. This mutant virus was indeed defective in M protein phosphorylation but did not differ at all from the wild-type SeV recovered from the parental cDNA either in the replication kinetics and plaque morphology in cultured cells or in in vivo replication and pathogenicity for mice. We thus concluded that no phosphorylation of the M protein was required for SeV replication either in vitro or in vivo.

Animals↗
PubMed1997

Specific alpha-galactosidase inhibitors, N-methylcalystegines--structure/activity relationships of calystegines from Lycium chinense.

An examination of the roots of Lycium chinense (Solanaceae) has resulted in the discovery of 14 calystegines, a cycloheptane bearing an amino group and three hydroxyl groups, and two polyhydroxylated piperidine alkaloids. Calystegines A7 and B5, in addition to the previously known calystegines A3, A5, A6, B1, B2, B3, B4, C1, C2 and N1, were isolated and determined as 1alpha,2beta,4alpha-trihydroxy-nortropane and 1alpha,2alpha,4alpha,7alpha-tetrahydroxy-nort ropane, respectively. L. chinense also had two polyhydroxytropanes bearing a methyl group on the nitrogen atom, unlike the previously reported nortropane alkaloids. They were established as N-methylcalystegines B2 and C1, and their N-methyl groups were found to be axially oriented from NOE experiments. 1Beta-amino-3beta,4beta,5alpha-trihydroxycyclohepta ne was also present in L. chinense and may be a biosynthetic precursor of the calystegines that occur in this plant. Two polyhydroxypiperidine alkaloids, fagomine and 6-deoxyfagomine, were isolated. Calystegine B2 is a potent competitive inhibitor of almond beta-glucosidase (Ki = 1.9 microM) and coffee bean alpha-galactosidase (Ki = 0.86 microM), while N-methylcalystegine B2 was a more potent competitive inhibitor of the latter enzyme (Ki = 0.47 microM) than the parent compound but showed a marked lack of inhibitory activities towards most other glycosidases. Since this compound is a very specific inhibitor of alpha-galactosidase and inhibits rat liver lysosomal alpha-galactosidase with a Ki of 1.8 microM, it may provide a useful experimental model for the lysosomal storage disorder, Fabry's disease. The addition of a hydroxyl group at C6exo, as in calystegines B1 and C1, enhances the inhibitory potential towards beta-glucosidase and beta-galactosidase but markedly lowers or abolishes inhibition towards alpha-galactosidase. Hence, the N-methylation of calystegine C1 did not enhance its inhibition of alpha-galactosidase. The chemical N-methylation of calystegines A3 and B4 markedly enhanced inhibition of coffee bean alpha-galactosidase, with Ki values of 5.2 microM and 36 microM, respectively, but almost eliminated their inhibitory potential towards beta-glucosidase and trehalase, respectively. Thus, methylation of the nitrogen atom significantly altered the specificity of the inhibitors.

Animals↗
PubMed1997

Clonal HTLV-I-infected CD4+ T-lymphocytes and non-clonal non-HTLV-I-infected giant cells in incipient ATLL with Hodgkin-like histologic features.

Lymph nodes from the incipient or early neoplastic phase of adult T-cell leukemia/lymphoma (ATLL) histologically resemble Hodgkin's disease. Integrated proviral human T-lymphotrophic virus type I (HTLV-I) has been demonstrated in such lesions. We studied 18 patients with this disease, and about half of the cases developed typical ATLL within 2 or 3 years. In all cases, either mono- or oligoclonal cell populations with proviral HTLV-I DNA were detected by Southern blot analysis and/or inverse polymerase chain reaction (IPCR). In addition, either a mono- or oligoclonal rearrangement of T-cell receptor genes was demonstrated. Giant cells with Reed-Sternberg-like histological features revealed CD15 and CD30 positivity. The background infiltrating lymphocytes represented either no or only minimal nuclear abnormalities with a CD4+ T-cell phenotype. In less than half of all cases, Epstein-Barr virus (EBV) infected the giant cells. A mixed EBV-A and -B type was found in 3, and a multiple genotype of EBV lymphocyte-determined membrane antigen (LYDMA) was found in 6 cases. These results could have been due to the immunodeficient status of the patients. A single-cell PCR of the giant cell, B cell, CD4+ or CD8+ T cells could be performed after cell sorting in 4 cases. HTLV-I infection was frequently found in the CD4+ T cells, but in neither the giant cells nor the B cells. The CD4+ T cells exhibited clonality. The giant cells showed various PCR products of IgH, and also expressed recombination activating genes (RAG). In summary, the giant cells were reactive cells, which resembled the immature B-lineage cells, while HTLV-I infected the CD4+ T cells, which demonstrated clonality. Based on these above findings, we consider CD4+ cells to play an important role in ATLL tumorigenesis.

Adolescent↗
PubMed1997

vesl, a gene encoding VASP/Ena family related protein, is upregulated during seizure, long-term potentiation and synaptogenesis.

We have isolated a novel cDNA, vesl, that was induced during convulsive seizure in the rat hippocampus. The vesl gene encodes a protein of 186 amino acids that has significant homology to the EVH1 domain of the VASP/Ena family of proteins implicated in the control of microfilament dynamics. The expression of vesl mRNA was induced in the granule cell layer during persistent long-term potentiation (LTP) of the dentate gyrus in an NMDA receptor-dependent manner. Furthermore, vesl mRNA was expressed at a high level during hippocampal synaptogenesis. We suggest that the Vesl protein may be involved in the structural changes that occur at synapses during long-lasting neuronal plasticity and development.

Amino Acid Sequence↗
PubMed1997

Targeting of endopeptidase 24.16 to different subcellular compartments by alternative promoter usage.

Endopeptidase 24.16 or mitochondrial oligopeptidase, abbreviated here as EP 24.16 (MOP), is a thiol- and metal-dependent oligopeptidase that is found in multiple intracellular compartments in mammalian cells. From an analysis of the corresponding gene, we found that the distribution of the enzyme to appropriate subcellular locations is achieved by the use of alternative sites for the initiation of transcription. The pig EP 24.16 (MOP) gene spans over 100 kilobases and is organized into 16 exons. The core protein sequence is encoded by exons 5-16 which match perfectly with exons 2-13 of the gene for endopeptidase 24.15, another member of the thimet oligopeptidase family. These two sets of 11 exons share the same splice sites, suggesting a common ancestor. Multiple species of mRNA for EP 24.16 (MOP) were detected by the 5'-rapid amplification of cDNA ends and they were shown to have been generated from a single gene by alternative choices of sites for the initiation of transcription and splicing. Two types of transcript were prepared, corresponding to transcription from distal and proximal sites. Their expression in vitro in COS-1 cells indicated that they encoded two isoforms (long and short) which differed only at their amino termini: the long form contained a cleavable mitochondrial targeting sequence and was directed to mitochondria; the short form, lacking such a signal sequence, remained in the cytosol. The complex structure of the EP 24.16 (MOP) gene thus allows, by alternative promoter usage, a fine transcriptional regulation of coordinate expression, in the different subcellular compartments, of the two isoforms arising from a single gene.

Amino Acid Sequence↗
PubMed1997

Human lymphotoxin mutein lacks hypotensive activity but has higher in vivo antitumor activity than lymphotoxin or tumor necrosis factor.

A serious drawback of tumor necrosis factor alpha (TNF) as a clinical antitumor agent is that it also has hypotensive activity. To overcome this problem, derivatives of its sister cytokine lymphotoxin (TNF-beta or LT) were prepared. One of them, mutein 2 (Mut2) has a deletion of amino acids 1-7 but contains substituted amino acids, Met-Phe-Pro at positions 8-10 of the mature human LT. This mutein has no hypotensive activity at the maximum dose (10 mg/kg) tested on rats. In contrast, a much lower dose (1 mg/kg) of TNF and LT caused a significant blood pressure drop. In vivo studies revealed that Mut2 was more effective than TNF or LT against MethA (a mouse tumor line) as judged by the therapeutic ratio [calculated as LD50 (dose that kills 50% of the animals)/ED50 (dose that reduces the tumor size by 50%)]. With five other different mouse tumors and two different human tumors, Mut2 was also effective and the effectiveness was comparable or superior to that of TNF or LT. These results suggest the possibility that this derivative may be usable as a clinical antitumor agent without the serious side effects associated with TNF.

Animals↗
PubMed1997

Inactivation of the cyclin D-dependent kinase in the rat fibroblast cell line, 3Y1, induced by contact inhibition.

Cyclin-dependent kinase (Cdk) inhibitory proteins are involved in cell cycle arrest induced by antiproliferating factors or chemicals. High cell density also induces cell cycle arrest in which the genomic DNA is unreplicated, even in the presence of a mitotic dose of growth factors; this is termed contact inhibition. Although the cell cycle of the rat fibroblast cell line, 3Y1, was arrested in quiescence by contact inhibition, the Cdk4 bound to its regulatory subunit, cyclin D1 or D3. However, these complexes were enzymatically inactive. Phosphorylation of the cyclin D1-bound Cdk4 by the Cdk-activating kinase could convert the inactive cyclin D1-Cdk4 complex into its active form in vitro, suggesting that threonine 172 of the Cdk4, of which phosphorylation is required for its activation, was in part unphosphorylated in contact-inhibited 3Y1 cells. Although MO15 was active in cell extracts prepared from the arrested 3Y1 cells, activation of bacterially produced Cdk4 in the cell extracts was inhibited. Removal of p27(kip1) from the cell extracts allowed the MO15 holoenzyme to phosphorylate the Cdk4 and in turn activate it, indicating that p27(kip1) plays a role in inhibiting the phosphorylation of Cdk4 by MO15 in the contact-inhibited 3Y1 cells.

Animals↗
PubMed1997

The paramyxovirus, Sendai virus, V protein encodes a luxury function required for viral pathogenesis.

The Sendai virus (SeV) V protein is characterized by the unique cysteine-rich domain in its carboxy-terminal half which is fused to the amino-terminal half of the P protein, but its function has remained enigmatic. The V protein-directing mRNA is generated by a remarkable process known as mRNA editing involving the pseudotemplated addition of a single G residue at a specific septinucleotide locus in the P gene, whereas the unedited exact copy encodes the P protein. Here, we introduced two nucleotide changes in the septinucleotide motif (UUUUCCC to UUCUUCC) in a full-length SeV cDNA and were able to recover a virus from the cDNA, which was devoid of mRNA editing and hence unable to synthesize the V protein. Compared with the parental wild-type virus with regard to gene expression, replication and cytopathogenicity in various cell lines in vitro, the V(-) virus was found to be either potentiated or comparable but never attenuated. The V(-) virus, however, showed markedly attenuated in vivo replication capacity in and pathogenicity for mice. Thus, though categorized as a nonessential gene product, SeV V protein encodes a luxury function required for in vivo pathogenicity.

Animals↗
PubMed1997

Comparison of the nucleotide sequence of enteroaggregative Escherichia coli heat-stable enterotoxin 1 genes among diarrhea-associated Escherichia coli.

The presence of the enteroaggregative Escherichia coli (EAggEC) heat-stable enterotoxin 1 (EAST1) gene was investigated in 15 strains each of EAggEC, enteropathogenic E. coli (EPEC), EPEC-related strains of non-EPEC serotypes, diffusely adhering E. coli (type 1 DAEC) that carries F1845 adhesive pili (or a related adhesin), and enteroinvasive E. coli (EIEC) by PCR and colony hybridization. The EAST1 gene or its homologue was present in 53.3% of EAggEC, 20% of EPEC, 13.3% of the EPEC-related strains, and 6.7% of type 1 DAEC, EIEC and E. coli unrelated with diarrhea had no gene with sequence similarity to the EAST1 gene. Comparison of the EAST1 gene sequences analyzed in this study as well as those reported previously showed that EAggEC (including strain O42, which was shown to be pathogenic in volunteer experiments), EPEC, type 1 DAEC, type 2 DAEC (which carries the 57-kDa outer membrane protein as an adhesin), and enterotoxigenic E. coli shared a common sequence. A variant type of the EAST1 gene sequence was present in the EAggEC strain 17-2 (initially characterized for the EAST1 gene) and in an EPEC-related strain of a non-EPEC serotype. These data suggest that the EAST1 gene or its variant is a virulence gene widely distributed among diarrhea-associated E. coli.

Amino Acid Sequence↗