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Biomedical subjects

N Mori

Publications and source records attributed to N Mori.

At least 271 records · Page 15Linked to original sources
PubMed1997

Variation in coxII intron in the wild ancestral species of wheat.

To study the maternal lineage and evolution of polyploid species of wheat, variation in mitochondrial DNA was investigated in Triticum and Aegilops by PCR-aided RFLP analysis. A 1.3 kb region containing the intron of coxII was studied using 20 accessions from five species of Sitopsis section of Aegilops, one species of Einkorn wheat, four species of tetraploid wheat, and one species of common wheat. Only three restriction site changes and a single deletion/insertion were found among 884 restriction fragments surveyed. This fact suggests the highly conserved nature of this region within Triticum and Aegilops. Four haplo-types were recognized in coxII intron. A parsimonious relationship indicated that three haplo-types were independently derived from one prototype which was found in wild Einkorn and Aegilops species except for Ae. speltoides. All but one accession of Ae. speltoides possessed a derivative haplo-type, common in Timopheevi wheat. The result supported the hypothesis that Ae. speltoides donated the G genome to Timopheevi wheat; however did not agree with that Ae. speltoides was the B genome donor to the Emmer and common wheat.

Biological Evolution↗
PubMed1997

[Case report: lung abscess caused by Streptococcus agalactiae].

Streptococcus agalactiae is a well-recognized cause of neonatal sepsis and meningitis. In adults, infections by S. agalactiae are rare. We report an adult case of lung abscess and pyogenic spondylitis caused by S. agalactiae. A 51-year-old male was admitted to our hospital because of an abnormal shadow in the chest and lumbago on May 25, 1995. He was diagnosed as lung abscess from the chest roentgenogram and CT scan and the subcutaneous pus was aspirated. The pus culture was only positive for S. agalactiae. He was treated with IPM/CS 1 g/day and CLDM 1.2 g/day and the abscess was drained. MRI showed his lumbago was caused by pyogenic spondylitis. The underlying disease of this case was diabetes mellitus. He recovered from the infections with in about 10 weeks of antibiotic treatment.

Humans↗
PubMed1997

A new hereditary cataract mouse with lens rupture.

A new cataract model originated in a recombinant inbred (RI) strain, CXS4 or CXSD (D), between BALB/cHeA(BALB/c or C) and STS/A(STS or S) mice. Opacity appeared as a white pinpoint focus in unpigmented eyes of albino mice from 5 weeks old. All the mice were bilaterally affected by 14 weeks old. They were fully viable and fertile. There was no sex difference in incidence of cataract. Histologically, the 3-4 months old mice showed vacuoles in the lens cortex. The vacuoles were spread all over the lens cortex in advanced cases. Ruptures of the lens nucleus to the vitreous chamber was a typical occurrence. For elucidation of the mode of inheritance, F1 hybrids (CXD and SXD) and backcross progenies [(CXD)F1XD and (SXD)F1XD] were analysed. No affected mice were observed in F1 hybrids. In backcross progenies, the segregation ratio of affected and normal mice was close to 1:1 in both matings. We conclude that the cataract is inherited by an autosomal single recessive gene. This mutant gene is provisionally named 'lens rupture 2' (gene symbol 1r2, Mouse Genome Database Accession No. MGD-JNUM-37399). The new cataract model mouse will be a good tool for the genetic analysis and molecular biological study of cataractogenesis.

Age Factors↗
PubMed1997

Purification and properties of a new enzyme, D-carnitine dehydrogenase, from Agrobacterium sp. 525a.

A new enzyme, D-carnitine dehydrogenase from Agrobacterium sp. 525a, was purified by DEAE-Toyopearl, ammonium sulfate fractionation, Sephadex G-75, affinity chromatography, and Mono Q and TSK-gel filtration column chromatography. The enzyme had the molecular mass of 89 kDa and consisted of three identical subunits. The optimum pH for the oxidation reaction was 9.3. The Michaelis constants for D-carnitine and NAD+ were 3.1 and 0.07 mM, respectively. The N-terminal 20 amino acids were sequenced.

Alcohol Oxidoreductases↗
PubMed1997

Transactivation of the interleukin-1 alpha promoter by human T-cell leukemia virus.

The expression of interleukin-1 alpha (IL-1 alpha) appears to be tightly regulated, as the levels of constitutive expression in normal cells is extremely low. In contrast to normal hematopoietic cells, human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines constitutively produce high levels of IL-1 alpha mRNA and secret this cytokine into the culture medium. IL-1-alpha mRNA is also expressed in fresh leukemic cells of adult T-cell leukemia/lymphoma (ATLL) patients. HTLV-I-induced IL-1 alpha might explain some symptoms observed in ATLL. In this regard, molecular dissection of the IL-1 alpha gene transcriptional regulation is of primary importance. In this review, the transcriptional regulation of IL-1 alpha gene expression and the possible role of the NF-kappaB pathway are discussed in the light of our current understanding of IL-1 alpha gene regulation by HTLV-I and HTLV-II Tax proteins, which are viral transcriptional transactivators.

Animals↗
PubMed1997

[The mechanism of formation of the otoconia in the utricular supporting cells of the guinea pig].

The mechanism of formation of the otocania in the utricular supporting cells of the guinea pig was investigated by means of an organ culture system using the potassium pyroantimonate (PA) precipitation method. The utricular otoconia and the secretory granules and mitochondria in the utricular supporting cells immediately after removal from the animal were positive to PA. When the specimens were treated with ethylene-glycol-0, 0-bis (2-aminoethyl)-N, N, N', N'-tetraacetic acid (EGTA) as a chelater prior to the PA staining, almost all deposits disappeared. This indicates that calcium is the main ion precipitated by the PA method. The utricules of the guinea pig were exposed to 30 mg of streptomycin sulfate per ml for 3 days in culture. The number of large lysosomes which contained vesicles and myeloid bodies in the supporting cells increased. On the other hand, the secretory granules were reduced in the cytoplasm of the supporting cells. Acid phosphatase activity in the lysosomes and the Golgi apparatus decreased. As a result of the PA treatment, these large lysosomes, especially the vesicles which were in them, contained a large quantity of calcium ion. From these findings, I conclude that the mechanism of formation of otoconia is as follows: The area of formation of otoconia is the supporting cells. Globular substances are the precursors of otoconia, and they contain calcium ion which was taken into the supporting cells. These globular substances are made in close relationship among the endplasmic reticula, secretory granules and lysosomes. They are secreted from the supporting cells and form the mature otoconia on the otoconial membrane.

Animals↗
PubMed1997

[Generalization mechanisms of limbic seizures].

It is well known that complex partial seizures of temporal origin may evolve into secondarily generalized convulsive seizures. For this reason, amygdaloid kindling, which begins with limbic seizures and culminates in secondarily generalized convulsions, is considered to be a useful model for examination of mechanisms underlying the development of convulsive seizures originating from a non-motor structure such as the amygdala. Recent observations made in our laboratory are relevant to anatomic network underlying expression and the generalization of amygdala-onset seizures. Specifically, functional roles played by the substantia innominata, massa inter-media of the thalamus and caudate-putamen in secondary generalization were examined in rats. Obtained results suggest: (1) the substantia innominata may mediate ictal linkage between the kindled amygdala and the iplilateral cortical motor mechanism, with secondary recruitment of the contralateral cortical motor mechanism, although the kindled amygdala can directly gain access to the contralateral hemispheric motor mechanism without participation of the substantia innominata; (2) the thalamus may be conceived to be a direct extension of the cortical motor mechanism; and (3) the caudate-putamen regulates the function of cerebral motor mechanisms responsible for the expression of generalized convulsive seizures, although the caudate-putamen may partly participate in the termination of seizures.

Animals↗
PubMed1997

[Two-peak monoclonal protein (IgA kappa and IgG kappa) in non-Hodgkin lymphoma].

A 72-year-old man was admitted because of general weakness. On physical examination, marked splenomegaly was found. Blood tests revealed anemia, thrombocytopenia and two-peak hypergammaglobulinemia composed of kappa type IgG and IgA monoclonal proteins. Peripheral blood and bone marrow (BM) contained abnormal lymphocytes including plasmacytoid lymphocytes and/or plasma cells. Pathological examination of the biopsied BM showed non-Hodgkin lymphoma consistent with the lymphoplasmacytoid type. Immunohistochemical staining revealed two different populations of cells, one with IgG and the other with IgA; no cell stained both and no solitary cluster of either IgG or IgA positive cell was seen. The surface phenotype of the lymphoma cells was CD19+, CD20+, HLADR+. Double immunofluorescence staining of the BM smear showed IgG or IgA positive plasma cells, whereas small lymphocytes were negative for IgG and IgA. Analysis of immunoglobulin genes in the BM cells showed 2 rearranged bands in each of heavy chain genes and kappa light chain genes. The patient was treated with modified MVCP therapy and the two monoclonal proteins decreased in parallel with the improvement of splenomegaly. These findings strongly suggest that the two-peak monoclonal protein was produced by monoclonal lymphoma cells. The patients has been disease-free without any therapy since August, 1995.

Aged↗
PubMed1997

[Immunohistochemical and immunogenetic analysis of ocular adnexal lymphoid proliferations].

We examined 20 cases (21 specimens) of ocular adnexal lymphoid proliferations, using the histological, immunohistochemical and molecular genetic methods. The latter two protocols were performed to detect the light chains restriction of immunoglobulin with peroxidase-antiperoxidase (PAP) methods, and the clonality of immunoglobulin heavy chain gene with the hemi-nested polymerase chain reaction (PCR) method, respectively. Although in 8 cases it could not be morphologically determined whether they were neoplastic or not, clonality was revealed in 1 case with immunohistochemistry and in 4 cases with PCR. Two cases showed discordant results between immunohistochemistry and PCR probably due to somatic mutation of the framework region of the immunoglobulin heavy chain gene. Therefore, we, concluded that examination with these methods contribute to a better understanding of the nature of the ocular adnexal lymphoid proliferations. Furthermore, the immunoglobulin gene PCR method is very useful in practical examination, as it can be used with formalin-fixed paraffin-embedded specimens.

Adult↗
PubMed1997

Subclinical vestibulo-cerebellar, anterior cerebellar lobe and spinocerebellar effects in lead workers in relation to concurrent and past exposure.

By computerized static posturography, the subclinical effects of past and concurrent lead absorption on the vestibulo-cerebellum (lower vermis), anterior cerebellar lobe and spinocerebellar afferent pathway were examined in 49 male chemical factory workers exposed to lead stearate (lead workers). Their concurrent blood lead (BPb) concentrations ranged from 7 to 36 (mean 18.0) microgram/100 g. In the past, their maximum BPb ranged from 11 to 113 (mean 47.7) micrograms/100 g; mean BPb was 7-52 (mean 23.5) micrograms/100 g; and cumulative BPb, defined as mean BPb x years of exposure, was 15-1268 (mean 390.6) micrograms.year/100 g. Control subjects were 23 healthy male workers who had never been occupationally exposed to lead. The postural sway of high (2-4 Hz) and low (1 Hz or less) frequencies with eyes open for lead workers was significantly greater than that for controls in the medio-lateral (right-left) and anterior-posterior directions. Similarly, the sway of high and low frequencies with eyes closed was significantly larger in lead workers than in controls in the medio-lateral direction. Results of stepwise multiple regression analysis indicated that the sway with frequencies of 0.5-2 Hz with eyes open was related to concurrent BPb in the anterior-posterior direction. With eyes closed the sway of high frequency was significantly related to mean BPb in the past in the medio-lateral direction. The pattern of the changes suggests that the vestibulo-cerebellum, anterior cerebellar lobe and spinocerebellar pathway are asymptomatically affected by lead. It appears that the change in the vestibulo-cerebellum reflects concurrent lead absorption, while on the other hand, that in the anterior cerebellar lobe reflects past lead absorption.

Adult↗
PubMed1997

[Neuronal growth-associated proteins in neural plasticity and brain aging].

This review summarizes current issues on neuronal structural plasticity and its molecular marker genes in the aged brain. Neuronal growth-associated proteins (nGAPs) are introduced as potential markers of neuronal structural plasticity in the brain. The expression of genes encoding nGAPs such as GAP-43, SCG10 and stathmin is increased following striatal and hippocampal neuronal deafferentation lesions in the adult rat brain. In aged brains, the magnitude of neuronal plasticity is reduced and nGAP gene induction is limited at least in part, while the kinetics of the response remains unchanged in comparison to young brains. These results suggest that nGAPs serve as molecular markers of neuronal structural plasticity in the aging brain and that neuronal plasticity decreases, at least in certain neuronal circuits, during aging. The expression of genes encoding SCG10, stathmin and GAP-43 is also altered in age-related neurodegenerative conditions such as Alzheimer's disease in humans. Thus, studies of nGAPs are important for the elucidation of the mechanisms of the reduction of neuronal structural plasticity in aged brains.

Aging↗
PubMed1997

[Self-efficacy and related factors related in Parkinson's disease patients].

This study was designed to assess self-efficacy and the factors leading to higher self-efficacy in Parkinson's disease patients, as measured by General Self-Efficacy Scale (GSES). Questionnaires were mailed to patients with Parkinson's disease in Tokyo. This study surveyed 73 male and 70 female patients. Approximately 66.5% of the patients fell into the low self-efficacy group. Data was divided into 3 groups (high, moderate and low) and evaluated statistically. Approximately 66.5% of the patients fell into the low self-efficacy group. Patients in the high self-efficacy group exhibited the following features: Males: 1) The male patients in the high self-efficacy group tended to belong to more groups and had less trouble than any other groups in coping with their daily lives; 2) they generally had people to turn to for mental support outside their families, and for their daily life inside or outside their families; 3) they also felt confident that they had sufficient understanding of better life styles and how to exercise. Females: 1) The female patients in the high self-efficacy group tended to go out more often than any other groups and had places to go where they could practice hobbies and exercise; 2) they generally had people outside their families to turn to for mental support; 3) their subjective symptoms, such as freezing and dysarthria, tend to be less acute than in the moderate or low self-efficacy patients. 4) had les trouble than any other groups in coping with their housing accommodations; 5) they also felt confident that they understood how to exercise. In order to increase self-efficacy among Parkinson's disease patients, this study suggests that support, both social and psychological, and providing health education, are important.

Aged↗
PubMed1996

N-Shc: a neural-specific adapter molecule that mediates signaling from neurotrophin/Trk to Ras/MAPK pathway.

Shc has been implicated in a variety of growth factor- and cytokine receptor-signaling through its specific binding to phosphotyrosine residues of the activated receptors. In neuronal cells, such as PC12, Shc has been shown to be involved in Ras-dependent MAP kinase activation following Trk receptor stimulation with NGF. While the ubiquitous role of Shc as an adaptor molecule in signal transduction is increasing in both neuronal and non-neuronal cells and tissues, the expression level of Shc is surprisingly low in the brain. We demonstrated here the isolation of a neural-specific member of the Shc family. This novel protein, named N-Shc (neuronal Shc), contains two potential phosphotyrosine-binding domains, PTB and SH2, and is expressed exclusively in the brain; whereas Shc is present in all other non-neuronal tissues. As in Shc, N-Shc can bind activated EGF receptor, become tyrosine phosphorylated, and form a complex with Grb2 adapter protein following EGF stimulation. Furthermore, N-Shc can bind activated TrkB receptor following the stimulation with brain-derived neurotrophic factor (BDNF), which is the most abundant neurotrophin in the brain. These data suggest that N-Shc, rather than Shc, mediates neurotrophin and other neuronal signalings in the central nervous system.

3T3 Cells↗
PubMed1996

Interleukin-10 gene expression in adult T-cell leukemia.

We studied the serum levels of interleukin-10 (IL-10), in patients with adult T-cell leukemia (ATL) caused by human T-cell leukemia virus type I (HTLV-I) infection. Elevated IL-10 levels were observed in 33 of 45 patients with ATL. Fresh leukemic cells from ATL patients as well as HTLV-I-infected T-cell lines MT-2, SLB-1, and C10/MJ expressed IL-10 mRNA by reverse transcription-polymerase chain reaction analysis, whereas IL-10 mRNA was not detected in normal peripheral mononuclear cells and an uninfected T-cell line Jurkat. IL-10 protein was also detected in the culture medium of leukemic cells from ATL patients as well as these HTLV-I-infected cell lines, and in the extracellular fluids of ATL patients. Interestingly, MT-4 cells, which did not express Tax although transformed by HTLV-I, did not express IL-10 at either the mRNA or protein level. To elucidate the role of the HTLV-I encoded transactivator Tax in IL-10 gene expression, Jurkat cells were transfected with a Tax expression plasmid. In transiently transfected Jurkat cells, endogenous IL-10 mRNA expression was induced by Tax. Stably transfected Jurkat cell lines expressed IL-10 mRNA and secreted IL-10 protein into the culture medium. The nuclear factor (NF)-kappa B pathway is a target for Tax transactivation. We treated MT-2 cells with phosphorothioate antisense oligonucleotides to the p65 subunit of NF-kappa B. A reduction in the expression of p65 was accompanied by a reduction in IL-10 gene expression and IL-10 production. We showed that the IL-10 kappa B-like sites ( kappa B1,-2,034 to -2,025; kappa B2, -1,961 to -1,952; kappa B3, -452 to -443) specifically formed a complex with NF-kappa B-containing nuclear extract from MT-2 cells and that NF-kappa B bound with the highest affinity to the kappa B2 element (kappa B2 > kappa B3 > kappa B1). These data suggest a general role for NF-kappa B activation in the induction of IL-10 gene transcription. Activation of IL-10 in HTLV-I-infected cells may contribute to the pathology associated with HTLV-I infection.

Adult↗
PubMed1996

The effects of N-methyl-D-aspartate (NMDA) and its competitive antagonist, 3-(2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP), injected into caudate-putamen on kindled amygdaloid seizures in rats.

N-methyl-D-aspartate (NMDA) is an agonist of NMDA receptors and 3-(2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP) is an NMDA receptor antagonist. NMDA (1 or 2 nmol per side) or CPP (2.5 or 10 nmol per side) was injected into the bilateral caudate-putamen of amygdaloid-kindled rats. In addition, CPP (10 nmol) was ipsilaterally or contralaterally injected into the unilateral caudate-putamen. Either 20 min after NMDA or 60 min after CPP, the kindled amygdala was stimulated at the generalized seizure triggering threshold. In a few animals tested, injection of NMDA into the bilateral caudate-putamen produced transient spiking activity, with no clinical manifestations. This feature began about 5 min after the injection and lasted about 10 s. When these animals were excluded from the statistical analysis, NMDA in the caudate-putamen showed a weak and non-significant anticonvulsant action. Injection of CPP into the bilateral caudate-putamen caused no ictal change, but markedly suppressed the kindled seizures. Injection of CPP into the unilateral caudate-putamen, regardless of the site, did not cause any ictal change, or affect the stimulation of the amygdala. These findings suggest that: (1) NMDA receptors in the caudate-putamen facilitate the development of kindled amygdaloid seizures; (2) activation of NMDA receptors in the bilateral, but not in the unilateral, caudate-putamen is required for the generalization and expression of kindled amygdaloid seizures.

Amygdala↗
PubMed1996

Acute lymphoblastic leukemia of childhood: identification of two distinct regions of deletion on the short arm of chromosome 12 in the region of TEL and KIP1.

Cytogenetic analysis of acute lymphoblastic leukemia (ALL) of childhood identified nonrandom chromosomal abnormalities of the short arm of chromosome 12. The alterations include deletions that are thought to be indicative of the presence of a tumor suppressor gene that is mutated on the remaining allele. To refine further the chromosomal localization of this gene, we analyzed the loss of heterozygosity (LOH) of chromosome 12 in 100 primary ALL samples using 22 polymorphic markers and identified two distinct smallest common deleted regions on chromosome 12p13. One region is flanked by D12S77 and D12S98 and has a size of 4 cM. Twenty-six percent of informative patients showed LOH in this region. This region may contain the TEL gene. The other region is flanked by D12S269 and D12S308 including the KIP1 gene. Forty-four percent of informative patients showed LOH in this second region. Mutational analysis of KIP1 using polymerase chain reaction-single-strand conformation polymorphism analysis and Southern blot analysis showed no homozygous deletions and point mutations suggesting that the altered gene in this second region is not the KIP1. Clinical data showed that LOH of 12p was demonstrated more frequently in precursor-B ALLs (32 of 80; 40%) than in T-ALLs (1 of 20; 5%) (P = .0027). Furthermore, patients with 12p LOH were younger (P = .013), with a lower DNA index (P = .046), but they had the same survival rates at 3 years. In summary, these data suggest that two different tumor suppressor genes are on chromosome arm 12p, which act separately in the development of childhood precursor-B ALLs. One of the tumor suppressor genes is in the region the KIP1 gene, but our data suggest this gene is not abnormal. The other target is in the region of the TEL gene; and this candidate deserves further study.

Cell Cycle Proteins↗