PubMed Health⌕ Search

Biomedical subjects

M Shinjoh

Publications and source records attributed to M Shinjoh.

11 recordsLinked to original sources
PubMed2001

Genetic analysis of an influenza B virus isolated from a patient with encephalopathy in Japan.

An influenza B virus, B/Saga/S172/99 (SAG99), was isolated from the nasopharynx of a patient with encephalopathy/encephalitis in Japan in 1999. To clarify the molecular characteristics of this virus, detailed analysis of the gene segments coding for the hemagglutinin (HA), neuraminidase (NA), nucleoprotein (NP), matrix protein (M) and non-structural protein (NS) was undertaken. All five genes of SAG99 showed high nucleotide and predicted amino acid similarities with those of recent non-encephalopathic strains isolated in the same epidemic season. Subsequent phylogenetic analysis revealed that all five gene segments of SAG99 analyzed in the present study were most similar to those of the recent Yamagata/16/88-like viruses. The hemagglutinin and neuraminidase proteins of SAG99 were each distinguished from those of recent epidemic strains by one characteristic amino acid substitution. These substitutions were not found in the previously reported encephalopathy/encephalitis-derived influenza B viruses, and we could not find any common characteristic amino acid changes in SAG99 and these viruses. Similarly, among the internal proteins studied, only the M2 protein of SAG99 was found to contain a single novel amino acid change when compared with other recent isolates. Thus, it was apparent that SAG99 contained very few amino acid differences when compared with other epidemic viruses. The association of recent B/Yamagata/16/88-like viruses with encephalitis/encephalopathy observed in the present study and previously suggest that these viruses may have a higher potential for causing neurological complications in certain individuals.

Child↗
PubMed2000

Influenza A-associated encephalopathy with bilateral thalamic necrosis in Japan.

Two cases of acute encephalopathy in young children clearly showed evidence of influenza A virus infection and bilateral thalamic lesions. Influenza-associated encephalopathy with bilateral thalamic lesions has mostly been reported in Japan; it differs from Reye's syndrome in several respects. Other factors in addition to influenza virus infection may have contributed to the etiology of encephalopathy in our case patients.

Brain Diseases↗
PubMed2000

Phylogenetic analysis of the three polymerase genes (PB1, PB2 and PA) of influenza B virus.

Phylogenetic patterns of the three polymerase (PB2, PB1 and PA) genes of a total of 20 influenza B viruses isolated during a 58 year period, 1940-1998, were analysed in detail in a parallel manner. All three polymerase genes consistently showed evolutionary divergence into two major distinct lineages and their amino acid profiles demonstrated conserved lineage-specific substitutions. Dendrogram topologies of the PB2 and PB1 genes were very similar and contrasted with that of the PA gene. It was of particular interest to reveal that even though the PA gene evolved into two major lineages, that of three recent Asian Victoria/1/87-like strains formed a branch cluster located in the same lineage as that of recent Yamagata/16/88-like isolates. Differences in the phylogenetic pathways of three polymerase genes were not only a reflection of genetic reassortment between co-circulating influenza B viruses, but also an indication that the polymerase genes were not co-evolving as a unit. As a result, comparison of the phylogenetic patterns of the three polymerase genes with previously determined patterns of the HA, NP, M and NS genes of 18 viruses defined the existence of eight distinct genome constellations. Also, similar phylogenetic profiles among the PA, NP and M genes, as well as between the PB2 and PB1 genes, were observed, suggesting possible functional interactions among these proteins. Completion of evolutionary analysis of the six internal genes and the HA gene of influenza B viruses revealed frequent genetic reassortment among co-circulating variable strains and suggested co-dependent evolution of genes.

Amino Acid Sequence↗
PubMed2000

In vitro growth profiles of respiratory syncytial virus in the presence of influenza virus.

To elucidate epidemiological interference between respiratory syncytial (RSV) and influenza viruses, the influence of influenza A (HlN1) virus on the growth of RSV was examined. Although RSV grew in MDCK cells, coinfection with influenza A virus led to a reduction of progeny RSV. The degree of growth interference depended on the time of infection with influenza A virus post infection (p.i.) with RSV. In fact, infection with influenza A virus 12 hrs p.i. with RSV did not influence growth of the latter virus. On the contrary, growth suppression of influenza A virus by RSV was observed when the coinfection began at the later stages of RSV infection. Suppression of the growth of RSV by influenza A infection was further demonstrated at the level of viral protein synthesis. An indirect immunofluorescence (IF) test revealed that a large proportion of infected cells synthesized both RSV and influenza A virus antigens. Scanning electron microscopic (SEM) examination demonstrated that influenza A and RSV virions possessing surface antigens specific for each virus were selectively released from dually infected cells. In the present study, we proved for the first time that the growth of RSV is blocked by competitive infection with influenza A virus in a susceptible cell population, competitive protein synthesis and selective budding of RSV and influenza viruses from the same infected cells.

Animals↗
PubMed1999

[A case of influenza A virus associated encephalopathy with bilateral thalamic hemorrhage].

A three-year old girl was hospitalized in a semi-conscious state following a febrile convulsion. She did not recover despite treatment and died 16 days after admission. Influenza A virus (H3N2) was detected from a throat swab from the patient, and serum hemagglutinin-inhibiting antibodies to the virus elevated from less than 8 to 256. Brain CT revealed bilateral thalamic hemorrhage and peripheral low density. Subarachnoid hemorrhage was also observed thereafter. Based on clinical manifestations and neuroimaging, this patient was diagnosed as an atypical case of acute necrotizing encephalopathy associated with influenza A virus infection. Such rapid progressive encephalopathies may occur due to intracranial vascular injury including vasculitis or spasms. Although it is clear that influenza A virus triggered this case, we cannot confirm that it was a pathogen. Also, it might be advisable to consider other possible contributing factors such as drugs administered before hospitalization.

Brain Diseases↗
PubMed1995

Cloning and nucleotide sequencing of the membrane-bound L-sorbosone dehydrogenase gene of Acetobacter liquefaciens IFO 12258 and its expression in Gluconobacter oxydans.

Cloning and expression of the gene encoding Acetobacter liquefaciens IFO 12258 membrane-bound L-sorbosone dehydrogenase (SNDH) were studied. A genomic library of A. liquefaciens IFO 12258 was constructed with the mobilizable cosmid vector pVK102 (mob+) in Escherichia coli S17-1 (Tra+). The library was transferred by conjugal mating into Gluconobacter oxydans OX4, a mutant of G. oxydans IFO 3293 that accumulates L-sorbosone in the presence of L-sorbose. The transconjugants were screened for SNDH activity by performing a direct expression assay. One clone harboring plasmid p7A6 converted L-sorbosone to 2-keto-L-gulonic acid (2KGA) more rapidly than its host did and also converted L-sorbose to 2KGA with no accumulation of L-sorbosone. The insert (25 kb) of p7A6 was shortened to a 3.1-kb fragment, in which one open reading frame (1,347 bp) was found and was shown to encode a polypeptide with a molecular weight of 48,222. The SNDH gene was introduced into the 2KGA-producing strain G. oxydans IFO 3293 and its derivatives, which contained membrane-bound L-sorbose dehydrogenase. The cloned SNDH was correctly located in the membrane of the host. The membrane fraction of the clone exhibited almost stoichiometric formation of 2KGA from L-sorbosone and L-sorbose. Resting cells of the clones produced 2KGA very efficiently from L-sorbosone and L-sorbose, but not from D-sorbitol; the conversion yield from L-sorbosone was improved from approximately 25 to 83%, whereas the yield from L-sorbose was increased from 68 to 81%. Under fermentation conditions, cloning did not obviously improve the yield of 2KGA from L-sorbose.

Acetobacter↗
PubMed1995

Cloning and Nucleotide Sequencing of the Membrane-Bound l-Sorbosone Dehydrogenase Gene of Acetobacter liquefaciens IFO 12258 and Its Expression in Gluconobacter oxydans.

Volume 61, no. 2, p. 419, column 1, lines 15-19: this sentence should read as follows. "The alcohol dehydrogenase and glucose dehydrogenase have a common region reported to be related to pyrroloquinoline quinone binding (2, 10), but SNDH does not contain such a region, indicating that SNDH is not a quinoprotein." Page 419, column 2, line 12: "(Table 4)" should read "(Table 3)." [This corrects the article on p. 413 in vol. 61.].

Journal Article↗
PubMed1991

Vascular smooth muscle contraction induced by Na+ channel activators, veratridine and batrachotoxin.

The effects of the sodium channel activators veratridine and batrachotoxin on isolated rat aorta were investigated. Veratridine caused gradual contraction, independent of the presence of endothelium, with an EC50 of 35 microM. Batrachotoxin (1 microM) also induced contraction. Both effects were completely inhibited by the sodium channel blocker tetrodotoxin (1 microM). The veratridine (60 microM)-induced contraction was inhibited by nifedipine (0.1 microM). In the absence of extracellular Ca2+, veratridine (60 microM) did not cause contraction. Sodium nitroprusside (80 nM), acetylcholine (10 microM) and isoproterenol (1 microM) caused relaxation of rings precontracted with veratridine (60 microM). An inhibitor of endothelium-derived relaxing factor (EDRF) synthase, N omega-nitro-L-arginine methyl ester (L-NAME) (0.65 mM), enhanced the veratridine-induced contraction in rings with an intact endothelium, which suggests that EDRF was being released during the veratridine-induced contraction. These results show that the activation of sodium channels on smooth muscle cells induces a contraction that is probably mediated by Ca2+ influx through voltage-dependent Ca2+ channels.

Animals↗