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Biomedical subjects

R Fukuda

Publications and source records attributed to R Fukuda.

At least 127 records · Page 7Linked to original sources
PubMed1994

[Pure red cell aplasia induced by erythromycin and furosemide effects on in vitro erythroid colony forming unit (CFU-E)].

A 84-year-old man was treated with antibiotics including erythromycin and a diuretic (furosemide) because of acute heart failure and pneumonia. During the treatment, he developed moderate anemia (Hb 8.7g/dl). His anemia improved after the treatment. He again developed marked anemia (Hb 6.3g/dl) during the second treatment with erythromycin and furosemide and received blood transfusions. Bone marrow aspiration study revealed severe erythroid hypoplasia (0.2%). He was referred to our hospital, but he was not treated because his hemoglobin levels and reticulocyte count increased (80%) and his bone marrow showed increased erythroblasts (41.5%). His anemia gradually improved without any treatment. We diagnosed the case as drug-induced pure red cell aplasia (PRCA). We cultured bone marrow cells obtained from the present case and four normal healthy volunteers by a plasma clot method to determine the effects of two drugs on the number of erythroid colony forming unit (CFU-E). Furosemide strongly inhibited the CFU-E colony formation in the patient, but the inhibition effect of erythromycin was moderate. Furthermore, CFU-E was markedly suppressed by a combination of erythromycin and furosemide in both patient and control materials. These results indicate that both furosemide and erythromycin were related to the occurrence of PRCA in this patient.

Aged↗
PubMed1993

An influenza virus temperature-sensitive mutant defective in the nuclear-cytoplasmic transport of the negative-sense viral RNAs.

An influenza A virus mutant ts-51, which contains a temperature-sensitive (ts) defect in the genome encoding the M1 and M2 proteins, was characterized. Nucleotide sequencing of the M segment revealed a predicted single amino acid change of phenylalanine to serine at amino acid position 79 in the M1 protein. The nuclear-cytoplasmic transport of the negative-sense viral RNAs (vRNAs) was then investigated using an in situ hybridization technique. At 6 hr after the ts-51 virus infection, approximately 95% of the vRNAs were accumulated in the nucleus at a non-permissive temperature, when approximately 50% of the vRNAs were transported into the cytoplasm in the wild-type virus-infected cells. The M1 protein of the ts-51 virus was also accumulated in the nucleus under the same conditions. Therefore, the M1 protein of the ts-51 virus may be associated with the vRNPs, but the possible M1-vRNP complex thus formed was defective in the nuclear-cytoplasmic transport and the single amino acid change in the M1 protein was responsible for this defect.

Base Sequence↗
PubMed1993

A study of the association between schizophrenia and the dopamine D3 receptor gene.

A study of the genetic association between schizophrenia and a BalI polymorphism in exon 1 of the dopamine D3 (DRD3) gene, a candidate gene for schizophrenia, was conducted. The polymorphism was examined in 91 patients whose symptoms satisfied DSM-III-R for schizophrenia and 90 controls. There were no significant differences between the groups in allele frequencies or genotype counts. Contrary to a previous report, the patients were no more likely to be homozygous than controls. Moreover, no association with the presence of illness could be demonstrated when the patients were grouped according to sex, age of onset, history of admission to psychiatric institutions or positive family history.

Adult↗
PubMed1993

No evidence for a point mutation at codon 713 and 717 of amyloid precursor protein gene in Japanese schizophrenics.

A point mutation at codon 717 of amyloid precursor protein (APP) gene has been demonstrated to play an important pathogenic role in some cases of familial Alzheimer's disease (FAD). Recently, a single case of chronic schizophrenia with a point mutation at codon 713 of APP gene which sits very close to the mutation in FAD was reported. We screened for these two kinds of mutations in 39 schizophrenic patients using polymerase chain reaction (PCR) and restriction enzyme technique. A mutation of codon 713 creates a MaeIII restriction site and that of codon 717 creates a BclI site. Enzyme digestion with amplified PCR product revealed no restriction site in all subjects. None of our subjects had either of these two kinds of mutations. Our findings support the hypothesis that the case of a mutation at codon 713 of APP gene is a natural non-pathogenic variant and, as well as a mutation at codon 717, has no relation with the genetic predisposition to schizophrenia.

Adult↗
PubMed1993

Inflammation of the liver causes mutations in duck hepatitis B virus genome.

To investigate whether hepatitis causes mutation in the viral genome, DNA sequences in the pre-core region of duck hepatitis B virus (DHBV) DNA were analyzed in both ducks with hepatitis and without hepatitis. Five DHBV carrier ducks were injected with DHBV particle proteins purified from duck serum with Freund's complete adjuvant (FCA) intrahepatically from 14 day posthatch for 9 weeks (immunized group). Serum was drawn at the end of the 1st and 4th week after the 1st injection of DHBV particle protein and ducks were killed at the end of the 9th week to obtain the liver. Another five ducks without treatment were used as controls. All ducks of the immunized group showed moderate to severe hepatitis at the 9th week. All ducks in the immunized group showed one mutation except one duck that showed two mutations only at the 9th week. Mutations were observed in the 5th, 13th, 21st, 22nd, and 28th codon of the pre-core region. All of them were point mutation at the 3rd base in the triplets. The frequency of mutation was different in each duck from 20% to 60% but not 100%. There was no mutations in ducks in control group. These results suggest that hepatitis causes mutation in the pre-core lesion genome of duck hepatitis B virus.

Animals↗
PubMed1993

Induction of programmed cell death (apoptosis) by influenza virus infection in tissue culture cells.

The process of cell death caused by influenza virus infection in cultured MDCK and HeLa cells was analysed. This infection gave rise to nuclear fragmentation and chromatin condensation accompanied by chromosomal DNA fragmentation into oligonucleosomes. Chromosomal DNA fragmentation progressed concomitantly with cell lysis of MDCK cells and HeLa cells, producing high and low yields of virus particles, respectively, indicating that the extent of cell lysis was not proportional to the virus production. The endonuclease inhibitor zinc blocked DNA fragmentation in MDCK cells. Cycloheximide inhibited DNA fragmentation as well as cell lysis. Inhibition occurred when the drug was added to the medium within 2 h after infection but not efficiently at 4 h or later. Infection induced the Fas Ag gene, which encodes a possible apoptosis-mediating molecule, in the early infectious stage followed by the expression of Fas Ag on the cell surface. These results suggested that influenza virus infection causes apoptotic death of cultured cells, and their fate might be determined at an early stage of the infection by induction of an apoptotic gene.

Animals↗
PubMed1993

Acquisition of CD13 and CD33 expression at relapse on acute myeloid leukemia cells with an unusual phenotype: MPO+CD13-CD33-.

A case of acute myeloid leukemia (AML) with an unusual phenotype which was negative for a panel of myeloid antigens determined by flow cytometry, but was strongly positive for myeloperoxidase has recently been reported. We herein describe a case of AML with this unusual phenotype at diagnosis; relapse occurred with the acquisition of CD13 and CD33 expressions. Morphological features of the blasts at relapse seemed to be more compatible with myeloblasts than those at diagnosis. These phenotypic and morphological changes are suggestive of asynchronous differentiation, clonal evolution or clonal change of leukemic cells.

Antigens, CD↗
PubMed1993

[Changes of bone marrow MRI pattern in aplastic anemia before and after bone marrow transplantation].

In order to evaluate the usefulness of magnetic resonance imaging (MRI) in estimating bone marrow cellularity, we performed T1-weighted MRI of the lumbar vertebral marrow in two patients with severe aplastic anemia, before and after bone marrow transplantation (BMT). High signal intensity was detected in the bone marrow before BMT, but the bone marrow pattern of MRI became normal after BMT. MRI seems to be effective for evaluating bone marrow cellularity and recovery, and for monitoring therapeutic effects in patients with aplastic anemia before and after treatment with BMT.

Adult↗
PubMed1993

[Refractory acute myelogenous leukemia successfully treated with a continuous infusion chemotherapy of low dose aclarubicin and cytosine arabinoside: a case report].

A 44-year-old female with refractory acute myelogeneous leukemia had experienced an early relapse after a third complete remission (CR) with combination chemotherapy (BHAC-AMP) using daily one-shot infusion of 20 mg aclarubicin (ACR). Further treatments including intermediate dose of cytosine arabinoside (Ara-C) were not effective. After treatment with a continuous administration of low dose ACR (9 mg/day) and Ara-C (21 mg/day) for 14 days she entered a fourth CR. The mechanism of this treatment relates to both cell-killing and differentiation effects on leukemic cells.

Aclarubicin↗
PubMed1993

[The effects of Ara-A on viral markers in duck hepatitis B virus carrier ducks].

Duck hepatitis B virus (DHBV) carrier ducks of one week old were injected with Ara-A (adenine arabinoside) of different dose including 2.5 (11 ducks), 5.0 (11), 10.0 (10) and 20.0 (10) mg/kg for 14 days. This antiviral effect showed dose-dependence up to 5.0 mg/kg and this dose seemed effective to obtain significant antiviral effect. Viral DNA and DNA polymerase activity were reduced significantly from the 1st week after starting the administration of Ara-A. This antiviral effect was maintained even at the 1st week after discontinuation of the drug. These findings were quite similar to those observed in HBV carriers. With the increasing necessity of Ara-A treatment in patients who will not respond to interferon therapy, DHBV seemed a suitable model for the investigation of the dose and antiviral effect of Ara-A treatment in humans.

Animals↗
PubMed1992

The sequential change of serum 2',5' oligoadenylate synthetase in different infectious patterns of duck hepatitis B virus in ducks in experimental transmission.

Duck hepatitis B virus (DHBV) shows clear age-dependent infectious patterns like that of Hepatitis B virus, and many factors have been assumed to have a role in the persistence of the infection. In the present study, the activities of the interferon-induced enzyme 2',5' oligoadenylate synthetase (2,5AS) were observed sequentially in the serum of ducks experimentally infected with DHBV on posthatch days 1, 7 and 14. These were compared with the infectious pattern to investigate whether the endogenous interferon response after infection in ducks of different ages has a major role in its determination. The infectious pattern of DHBV in 1-day-old ducks was persistent without hepatitis and the others were transient with hepatitis. Persistently infected ducks showed significantly lower activities of 2,5AS compared with those with transient hepatitis, which resulted in a rapid elimination of DHBV. Although 1-day-old ducks showed significantly high 2,5AS compared with non-infected ducks, interferon response alone appeared to be insufficient for the elimination of DHBV. The immune response seemed necessary for the complete elimination of DHBV by way of evoking hepatitis and stimulating more interferon response during the usual infectious course. The interferon system alone did not seem to have a critical role in determining the infectious pattern. Other factors, including the immune response to the virus, seemed to have a major role in this problem.

2',5'-Oligoadenylate Synthetase↗