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F Taguchi

Publications and source records attributed to F Taguchi.

At least 73 records · Page 4Linked to original sources

[Techno-Stress; techno-centered and techno-phobia].

The "Techno-Stress" is a sociological new concept, hypothesized by Craig Brod and it includes clinically "Techno-Centered" and "Techno-Phobia". Based on 34 cases with mental disorders or psychosomatic diseases, we evaluated symptomatically these categories from standpoint of computer operating works. Fourteen cases represented severe problems in human relationship and they adapted excessively to computer operation. This group was thought as "Techno-Centered" and 50% of them were diagnosed as narcissistic, obsessive and schizophreniform personality. Twenty cases with maladaptation to computer operation were characterized as strict or avoidant personality and this group was evaluated as "Techno-Phobia". The "Techno-Phobia" was thought as simple adjustment disorder caused by new technology, on the other hand, the cases of "Techno-Centered" were seemed to be well-adapted to social skill only superficially, but psychological disturbance should be severer than "Techno-Phobia".

Adult↗

Recognition signal for the C-terminal processing protease of D1 precursor protein in the photosystem II reaction center. An analysis using synthetic oligopeptides.

Synthetic oligopeptides of different chain lengths of 11 to 38 amino acids, corresponding to the carboxyl-terminal sequence of D1 precursor protein of the photosystem II reaction center, were subjected to a proteolytic cleavage by a processing enzyme isolated from spinach, in order to analyze the recognition signal. Practically the same Km and Vmax values were obtained for the oligopeptides consisting of more than 19 amino acids; a decrease in affinity, without affecting the Vmax value, was observed for the peptide consisting of 16 amino acids; no detectable activity was found for the peptide with 11 amino acids. When Asp-342 (12th residue from C-terminus) was replaced with Asn, for the peptide consisting of 16 amino acids, the enzymatic activity was completely abolished. In contrast, replacing Asp-342 with Glu had little effect. The efficiency of these oligopeptides as a substrate mentioned above, together with their effectiveness as an inhibitor, clearly demonstrated that the negative charge on Asp-342 plays a crucial role in the recognition, i.e., binding and cleavage, of the substrate by the processing enzyme, and suggested that the carboxyl-terminal extension consisting of 9 amino acids, by itself is not important in the binding.

Amino Acid Sequence↗

CD7+ stem cell leukemia/lymphoma. Features of a subgroup without circulating blast cells.

Recent advances in immunology have clarified the cellular origin of hematopoietic neoplasms. Blast cells with a CD7+ CD4- CD8- phenotype are demonstrated to originate from malignant pluripotent hematopoietic stem cells. In this article, the authors describe three rare cases, designated as a lymphoma type of CD7+ stem cell leukemia/lymphoma, with clinical features described below. All three patients were admitted with non-Hodgkin lymphoma with a 2-month to 4-month history of lymphadenopathy. Histologic examination of lymph nodes showed lymphoblastic lymphoma (LBL) in all patients. Bone marrow blast cells had an immunophenotype consistent with CD7+ CD4- CD8- acute leukemia, although abnormal cells were not observed in the peripheral blood during the course of the disease. One patient had a recurrence in the bone marrow, with myeloperoxidase-positive blast cells expressing myeloid differentiation antigens. Chromosomal analysis detected a common abnormal karyotype initially and at relapse. Furthermore, the same T-cell receptor gene rearrangement was found initially and at relapse, suggesting that these blast cells originated from the same pluripotent leukemic clone. Additional studies on more patients are required to determine the clinical significance of this group, including the difference from CD7+ stem cell leukemia/lymphoma with circulating blast cells (leukemic type) or LBL.

Acute Disease↗

Origin of JC polyomavirus variants associated with progressive multifocal leukoencephalopathy.

JC polyomavirus (JCV) DNAs from the urine of nonimmunocompromised individuals (designated archetypal isolates) regularly contain a regulatory sequence that may have generated various regulatory sequences of JCV isolates derived from the brain of patients with progressive multifocal leukoencephalopathy (PML). In this report, we constructed a phylogenetic tree for 14 isolates (7 archetypes and 7 PML types) from DNA sequence data on the VP1 (major capsid protein) gene. According to the phylogenetic tree, the 14 isolates diverged into types A and B, each of which contained archetypal and PML-type isolates. Each type further diverged into several groups containing archetypal and PML-type isolates. We conclude that PML-type isolates are polyphyletic in their origin and do not constitute a unique lineage. This conclusion suggests that PML-type JCV isolates are generated from archetypal strains during persistence in the hosts. Furthermore, the present phylogenetic analysis indicates that an ancestral JCV carried the archetypal regulatory sequence and that this structure has been conserved in the course of JCV evolution.

Base Sequence↗

DNA-sequence rearrangement required for the adaptation of JC polyomavirus to growth in a human neuroblastoma cell line (IMR-32).

Infection of a human neuroblastoma cell line (IMR-32) with the JC polyomavirus (JCV) strain Mad-1 with subsequent serial passage results in the generation of a virus adapted to growth in IMR-32 (K. Akatani, M. Imai, M. Kimura, K. Nagashima, and N. Ikegami, J. Med. Virol., in press). To understand the basis of this adaptation, we molecularly cloned JCV DNAs from the adapted virus. The cloned JCV DNAs consisted of essentially three species (M1-IMRa, -IMRb, and -IMRc) with rearranged regulatory regions. Two TATA sequences are present in the regulatory region of the parental virus Mad-1, but one distal from the origin of replication was commonly deleted in M1-IMRa, -IMRb, and -IMRc. We showed that these regulatory regions were required for the efficient growth of JCV in IMR-32. Various JCV strains should be propagated in IMR-32, if their regulatory regions are replaced with those defined in this study. Since it is difficult to propagate JCV in cells other than primary human fetal glial cells, this system may be useful for structural and immunological studies of JCV.

Adaptation, Biological↗

Fusogenic properties of uncleaved spike protein of murine coronavirus JHMV.

We have tested the fusogenic properties of cleaved and uncleaved spike (S) protein of murine coronavirus (MCV) JHMV variant cl-2 by expressing the S protein by recombinant vaccinia viruses (RVVs). The amino acid sequence of the putative cleavage site of cl-2 S protein, Arg-Arg-Ala-Arg-Arg, was replaced by Arg-Thr-Ala-Leu-Glu by in vitro mutagenesis of cl-2 S gene. The RVVs having cl-2 S gene [RVV t(+)] or mutated cl-2 S gene [RVV t(-)] were tested for their ability to induce fusion as well as cleavability in DBT cells. After inoculation with RVV t(+) onto DBT cells, the fusion formation was first observed at 8 h postinoculation (p.i.) and spread throughout the whole culture by 24 h. In cells infected with RVV t(-), fusion appeared by 2 h and most of cells were fused by 30 h p.i. The S protein and its cleavage products were detected in DBT cells expressing wild type S protein. However, no cleavage products of the S protein were detected in RVV t(-) infected cells producing mutated S protein, even though fusion was clearly visible. These results suggest that the cleavage event of JHMV-S protein of MCV is not a prerequisite for fusion formation, but that it enhances fusion.

Amino Acid Sequence↗

Experiments on maternal and paternal transmission of Creutzfeldt-Jakob disease in mice.

No transmission of Creutzfeldt-Jakob disease in mice was observed in 75 offspring born to CJD agent-inoculated females or to normal females mated with inoculated males and in 19 normal offspring maintained by foster nursing with the inoculated mothers. The fertility of young adult female mice was lost by the 57th day after the inoculation, whereas the reproductivity of male mice was maintained over 106 days after the inoculation.

Aging↗

Isolation of a subclonal cell line of PC12 transfected with dexamethasone-regulated ras oncogene: morphological differentiation, biochemical properties, and tumorigenicity.

We have isolated and characterized a new subclonal cell line designated as MR31, which was obtained by transfection of PC12 cells with a glucocorticoid-regulated ras oncogene. The mRNA derived from the c-Ha-ras gene was proved to be expressed on exposure of the MR31 cells to dexamethasone, the highest value being attained at 8 h. MR31 cells rapidly extended neurite-like processes within 24 h in response to dexamethasone as well as nerve growth factor (NGF). The time of onset of neurite outgrowth induced by dexamethasone corresponded to the time when the highest ras mRNA level was observed. The catecholamine content of MR31 cells was found to be twice that of PC12 cells. A time course study on the effects of dexamethasone or NGF on cells showed that the former caused an increase in dopamine, a major catecholamine, to twofold the control level at 48 h after the treatment, while the latter caused a decrease in the dopamine level. These effects on catecholamines were almost the same in MR31 and PC12 cells. The acetylcholinesterase activity of MR31 cells was enhanced by both dexamethasone and NGF, whereas that of PC12 cells was enhanced by NGF, but not by dexamethasone. The changes in acetylcholinesterase activity were correlated with neurite outgrowth. Electron-microscopically, MR31 cells were not different from PC12 cells. MR31 cells exhibited extremely decreased tumorigenicity as compared with PC12 cells. The morphological and biochemical properties of MR31 cells remained constant, even after repeated passages.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Brain-gut response to stress and cholinergic stimulation in irritable bowel syndrome. A preliminary study.

To investigate the influence of the brain-gut interactions on the pathophysiology of irritable bowel syndrome (IBS), we compared such patients (n = 10) with healthy control subjects (n = 11) by measuring the pressure of the colon and small intestine simultaneously with analysis of power spectrum of the electroencephalography (EEG) under mental stress and administration of neostigmine. Stress slightly increased the colonic motility index, reduced the percentage of alpha power, and increased the percentage of beta and theta power of the EEG in the patients with IBS more than in the controls (p < 0.05). The patients with IBS had a longer phase II (p < 0.01) and shorter phase I (p < 0.02) of fasting duodenal motor activity than the controls. Neostigmine (10 micrograms/kg) caused a significant difference in the colonic motility index (p < 0.01) and power spectra of EEG (p < 0.05) in the patients with IBS compared to the controls. Significant positive correlation was detected between colonic motility and power spectral change induced by stress (r = 0.46, p < 0.05) or neostigmine (r = 0.51, p < 0.01). These results suggest that patients with IBS have exaggerated responsivity of the gut and the brain to mental stress and cholinergic stimulation. Moreover, there is a possibility that these exaggerated responses are related.

Abdominal Pain↗

Expression of the S1 and S2 subunits of murine coronavirus JHMV spike protein by a vaccinia virus transient expression system.

The spike (S) protein of murine coronavirus JHMV, variant cl-2, comprises two polypeptides, N-terminal S1 (with an N-terminal signal peptide) and C-terminal S2 (with a C-terminal transmembrane domain). In order to express these subunits, we constructed three different vaccinia virus transfer vectors (VV-TVs) containing cDNAs encoding the S1 protein without a transmembrane domain (pSFS1utt), the S1 protein with a C-terminal transmembrane domain derived from S2 (pSFS1tmd) or the S2 protein with an N-terminal signal peptide derived from S1 (pSFssS2). The S1 and S2 proteins were expressed in DBT cells by infection with vaccinia virus and transfection of these VV-TVs. In cells transfected with the pSFS1utt and pSFS1tmd, 96K and 106K proteins, respectively, were detected by Western blotting. The ssS2 protein expressed by pSFssS2 was 96K, which was slightly larger than the authentic S2 protein. The S1utt and S1tmd proteins were shown by binding studies using a panel of monoclonal antibodies to be antigenically indistinguishable from the authentic S1 protein. The S1tmd and ssS2 proteins were detected on the cell surface by immunofluorescence, whereas the S1utt protein was not. However, when the S1utt protein was expressed together with the ssS2 protein, the S1utt was detected on the cell membrane. This suggested that the S1utt was associated with ssS2 on the cell membrane. These observations indicate that the expressed S1 and S2 proteins associated in a similar manner to the authentic S1 and S2 proteins produced in DBT cells infected with cl-2. However, cell fusion was not observed in cells expressing either S1 or S2 nor in cells coexpressing both S1 and S2, although the whole S protein expressed by VV-TV did induce fusion.

Amino Acid Sequence↗

Neutralization and fusion inhibition activities of monoclonal antibodies specific for the S1 subunit of the spike protein of neurovirulent murine coronavirus JHMV c1-2 variant.

The cleavage products of the spike (S) protein, the S1 and S2 subunits, of the highly neurovirulent murine coronavirus (MHV) JHMV c1-2 variant were identified by immunoprecipitation of virus-infected cell lysates after treatment with urea and 2-mercaptoethanol. By this method 14 monoclonal antibodies (MAbs) raised against the S protein of the c1-2 variant were revealed to react with the S1 subunit and one with the S2 subunit. These 14 MAbs were classified into the following three groups: (A) MAbs reactive to almost all MHV strains examined, (B) MAbs specific for the JHMV strain and (C) MAbs specific for a large S protein of the JHMV strain. All five MAbs classified in group B showed neutralization activity and four of them also showed fusion inhibition activity. Four of six MAbs in group C showed neutralizing activity to the c1-2 variant but not to the sp-4 variant, and most of them had no fusion inhibition activity. Western blot analyses showed that all of the MAbs, except for no. 2 in group A, failed to react with the denatured S and S1 proteins. All MAbs in groups A and C, with the exception of no. 19 in group A, reacted with the mildly denatured S proteins, whereas none of the MAbs in group B did. These results suggest that MAbs in group B recognized highly conformational epitopes which may be involved in the binding of virions to cellular receptors and the fusion activity of the virus.

Animals↗

Opsonisation of group B streptococci and restriction endonuclease digestion patterns of their chromosomal DNA.

Isolates of group B streptococci (GBS) from neonates with early-onset septicaemia are associated with particular restriction endonuclease digestion patterns (RDP types Ia-3 and III-3) of chromosomal DNA. Opsonophagocytosis of serotype Ia and serotype III GBS isolates was studied by the luminol-enhanced phagocytic chemiluminescence (CL) assay. Pools of serum containing GBS type-specific antibody levels equivalent to or just above levels typically found in sera from mothers of infected infants were used. CL intensities induced by GBS isolates of RDP types Ia-2, Ia-3 and III-3 were lower than those of the other RDP types of the same serotype. Opsonophagocytosis was more efficient with serum containing higher concentrations of type-specific antibodies but for RDP type III-3 strains these differences were much less marked than for other RDP types. CL intensity did not correlate with cell surface charge, hydrophobicity or sialic acid content of GBS. Results demonstrate that certain GBS RDP types are more resistant to opsonophagocytosis and suggest that potentially virulent strains with genetic homogeneity may exist.

Adult↗

Fusion formation by the uncleaved spike protein of murine coronavirus JHMV variant cl-2.

The fusogenic properties of the uncleaved spike (S) protein of murine coronavirus JHMV variant cl-2 were studied by expressing the S protein with a deleted putative cleavage site. The amino acid sequence of the putative cleavage site, Arg-Arg-Ala-Arg-Arg, was replaced by Arg-Thr-Ala-Leu-Glu by in vitro mutagenesis of the cl-2 S protein cDNA. Recombinant vaccinia viruses containing the cl-2 S cDNA [RVV t(+)] or the mutated cDNA [RVV t(-)] were constructed and monitored for fusion formation and cleavage of the expressed S proteins. When cultured DBT cells were infected with RVV t(+) at a multiplicity of infection of 0.5, fusion formation was first observed at 10 to 12 h postinoculation and spread throughout the whole culture by 20 to 24 h postinoculation. In cells infected with RVV t(-) under the same conditions, fusion formation appeared by 12 to 14 h. This result represented a 2- to 4-h delay in the onset of fusion, compared with its appearance in cells expressing the wild-type S protein. By 25 to 30 h, most of the cells infected by RVV t(-) had fused. By immunoprecipitation and Western blotting (immunoblotting), the 170-kDa S protein was detected in DBT cells expressing the wild-type S protein and the mutated S protein. However, interestingly, the cleavage products of the S protein, S1 and S2, were not detected in RVV t(-)-infected cells, producing the mutated S protein, even though fusion was clearly visible. Both products were, of course, detected in RVV t(+)-infected DBT cells, producing the wild-type S protein. The same results concerning the fusion formation and cleavage properties of the S proteins were reproduced by the transiently expressed S proteins. These results suggest that the cleavage event in the S protein of murine coronavirus JHMV is not a prerequisite for fusion formation but that it does facilitate fusion formation.

Amino Acid Sequence↗

Detection of mouse hepatitis virus by the polymerase chain reaction and its application to the rapid diagnosis of infection.

Eight different strains of mouse hepatitis virus (MHV) were analyzed by the polymerase chain reaction (PCR) to see whether two sets of oligonucleotides, which were synthesized based on the published nucleotide sequence of MHV-JHM mRNAs 6 and 7, could be used as universal primers for amplification. Total RNA extracted from virus-infected cells or virus-infected culture fluids was transcribed into cDNA by using reverse transcriptase and oligo(dT) as primer, then the cDNA transcripts were amplified by PCR. The MHV-specific fragments of 199-bp and 241-bp were obtained from all eight strains irrespective of nucleotide differences in the primer regions. The same fragments were also amplified from RNA derived from the liver and brain of MHV-JHM-infected mice as soon as day 1 after intraperitoneal injection, even from the liver from which the virus was not detected. Results of PCR amplification from the liver RNA extracts became positive when more than 10(-2)PFU of MHV-JHM was contained in the PCR reaction mixture. In contrast, anti-MHV antibody was not detected by enzyme-linked immunosorbent assay until day 6 after inoculation. These results suggest that PCR is a very sensitive method to identify a variety of MHV infections in laboratory animals, especially at the early phase of infection.

Animals↗

Deletion of chromosome 6q in two cases of acute myeloblastic leukemia and a review of the literature.

Two cases of acute myeloblastic leukemia (AML M2) associated with a deletion of chromosome 6q are described. One was a 38-year-old man with constitutional inversion of chromosome 9, and another was a 57-year-old female atomic-bomb survivor. The karyotype of these patients were 46,XY,del(6)(q12q14),inv(9)(p11q13), and 47,XX,6q-,+min, respectively. In both cases c-myb protooncogene, which is located in chromosome 6q, was neither deleted nor rearranged, and c-myb messenger RNA level was not elevated. These results suggest that c-myb is not involved in the leukemogenesis of AML with 6q- as well as lymphoid malignancies with 6q-. Out of 23 AML cases with 6q- reviewed, 6 cases had erythroleukemia, and 4 developed in Down syndrome patients.

Adult↗

Molecular cloning and expression of a spike protein of neurovirulent murine coronavirus JHMV variant cl-2.

A cDNA encoding the spike (S) protein of the neurovirulent murine coronavirus JHMV variant cl-2 was isolated and sequenced. Analysis of the cDNA revealed that the S protein consists of 1376 amino acids, as does the S protein of mouse hepatitis virus 4. We inserted the cDNA into the genome of vaccinia virus to obtain a recombinant vaccinia virus (rVV). The S protein expressed in RK13 cells infected by the rVV was shown to be electrophoretically and immunologically indistinguishable from the S protein produced in DBT cells infected with cl-2 virus. RVV infection of rats and mice induced S protein-specific antibody production detectable by immunofluorescence and neutralization. Moreover, the S protein expressed by the rVV induced syncytium formation not only in mouse DBT and L cells, which are susceptible to cl-2 virus infection, but also in rabbit RK13 cells, which are not susceptible to cl-2 virus infection. This result suggests the possibility that RK13 cells have binding sites for the cl-2 virus S protein.

Amino Acid Sequence↗

An endoscopic study of antibiotic-associated hemorrhagic colitis.

Colonoscopy was performed on acute stage within 72 hours from onset in 48 patients with antibiotic-associated hemorrhagic colitis (AAHC). From our observations we have developed a new endoscopic classification of AAHC and investigated the incidence of each finding in further detail. We have classified in principle the endoscopic findings of the 48 subjects into two groups: major and minor ones respectively. Category of major findings were: 1) diffuse mucosal hemorrhage (100%); 2) spotty mucosal hemorrhage (100%), and 3) linear mucosal hemorrhage (22.9%), while minor findings were: 1) irregular ulcers in 10.4%; 2) aphthoid ulcers in 6.3%, and 3) linear erosions or ulcers in 4%. Minor findings were ulcers or erosions present over the hemorrhagic mucosa associated with the moderate degree of inflammation. A histopathologic study of colon biopsy specimens from 24 patients with AAHC showed hemorrhage and inflammatory cell infiltration in the lamina propria mucosae varying from mild to moderate in extent. It was concluded that AAHC was a colonic mucosal hemorrhagic disease caused by the destruction of mucosal vessels from unknown causes and in this disease mild to moderate inflammation was partially followed by ulceration over the edematous and hemorrhagic mucosa of the colon.

Adolescent↗