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Biomedical subjects

N Mori

Publications and source records attributed to N Mori.

At least 307 records · Page 17Linked to original sources
PubMed1996

Lipid profile of Helicobacter spp.: presence of cholesteryl glucoside as a characteristic feature.

The lipid and fatty acid profiles of eight Helicobacter spp. (H. nemestrinae, H. acinonyx, H. canis, Helicobacter sp. strain CLO-3, "H. rappini" [Flexispira rappini], H. pametensis, Helicobacter sp. strain Bird-B, and Helicobacter sp. strain Bird-C) and the fatty acid profiles of five additional species (H. pylori, H. felis, H. muridarum, H. mustelae, and H. fennelliae) were analyzed and compared. A heterologous fatty acid profile was observed among the Helicobacter spp., and on that basis the species could be divided into two groups. Group A had 19-carbon cyclopropane fatty acid (19:0cyc) and tetradecanoic acid (14:0) as the major fatty acids, and group B characteristically lacked the 19:0cyc and had hexadecanoic acid (16:0) and octadecenoic (18:1) acids as the major fatty acids. The species of group A are primarily gastric colonizers, and those of group B are primarily intestinal colonizers. Seven of the eight species studied showed the unusual and characteristic presence of cholesteryl glucosides (CGs), and most of these seven showed a very large amount (9.7 to 27.4% of the weight of total extractable lipid). The types of CGs and their distribution in different species were as follows: cholesteryl-6-O-acyl-alpha-D-glucopyranoside (cholesteryl-6-O-tetradecanoyl-alpha-D-glucopyranoside in H. nemestrinae and mainly cholesteryl-6-O-dodecanoyl-alpha-D-glucopyranoside in "H. rappini"), cholesteryl-alpha-D-glucopyranoside (H. nemestrinae, H. acinonyx, H. canis, Helicobacter sp. strain CLO-3, and "H. rappini"), and cholesteryl-6-O-phosphatidyl-alpha-D-glucopyranoside (H. nemestrinae, H. acinonyx, H. canis, and Helicobacter sp. strain CLO-3). Besides this, we could also detect cholesteryl acyl glucoside in H. acinonyx, cholesteryl glucoside in Helicobacter sp. strains Bird-B and -C, and cholesteryl phosphatidyl glucoside in "H. rappini" and Helicobacter sp. strain Bird-C. A selective accumulation of free cholesterol was observed in the neutral lipid fractions. On the basis of the detection of CGs in 11 of the 13 species studied so far, the presence of CGs appears to be a characteristic feature of the genus Helicobacter. In view of this and also because of a simple and rapid detection method described herein, the CGs can be used as a valuable chemotaxonomic marker.

Cholesterol↗
PubMed1996

Outward K+ current in epithelial cells isolated from intermediate portion of endolymphatic sac of guinea pigs.

Ion currents in epithelial cells isolated from the intermediate portion of endolymphatic sac (ES) in guinea pigs were investigated with the use of the whole cell patch-clamp technique. Depolarizing voltage steps from a holding potential of -60 mV induced a time- and voltage-dependent outward current, which is comparable to that of delayed rectifying K+ currents. The average resting membrane potential in the current-clamp mode was -54.8 +/- 11 mV (n = 45), which was similar to the value of zero current potential (-55.6 +/- 0.8 mV, n = 32) obtained from current-voltage (I-V) relationships of outward currents in voltage-clamp mode. The I-V relationship of the tail current exhibited a reversal potential (Erev) of -78.1 +/- 0.9 mV (n = 19) in standard external solution. The Erev of the outward current was linearly related to the logarithm of extracellular K+ concentrations. The slope was 48 mV per 10-fold change in extracellular K+ concentrations. The time constants of K+ current activation, inactivation, and K+ tail current deactivation were voltage dependent. The steady-state activation and inactivation of K+ current exhibited a sigmoidal relationship to voltage. The 50% maximal activation voltage and slope factor were -21 and 11 mV (n = 8), respectively. The 50% maximal inactivation voltage and slope factor were -45 and 13 mV (n = 7), respectively. The K+ current was blocked by externally applied 1 mM 4-aminopyridine (4-AP), 5 mM Ba2+ and 20 mM tetraethylammonium chloride (TEA). The sensitivity of the current to 4-AP and Ba2+ was higher than that to TEA. Elimination of external Ca2+ and increase of internal Ca2+ failed to significantly change the current, suggesting that the K+ current may be Ca2+ independent. The results show that epithelial cells in the intermediate portion of the ES possess a delayed-rectifier K+ current, which may be involved in membrane stability or in the ion balance between the cytosol and the extracellular environment.

Animals↗
PubMed1996

Systemic scleroderma and perforating granuloma annulare: differential diagnosis from calcinosis.

BACKGROUND: Systemic scleroderma is a disorder of unknown etiology with skin sclerosis. Its major histological features are swollen and homogenized collagen bundles. OBJECTIVE AND METHODS: We describe 2 patients with systemic sclerosis who have multiple umbilicated nodules indistinguishable from calcinosis cutis. RESULTS: Histological examinations including Von Kossa staining revealed features of perforating granuloma annulare, but not of calcinosis cutis. CONCLUSION: The association may not be fortuitous but both diseases may be etiologically related.

Adult↗
PubMed1996

Expression of perforin in nasal lymphoma. Additional evidence of its natural killer cell derivation.

Eight patients with nasal lymphoma in whom fresh-frozen tissues were available were studied to elucidate the nature of the lymphoma cells. Two cases were diagnosed as diffuse, large cell lymphoma, and the remaining six cases as diffuse, mixed cell types. Immunohistochemical studies revealed that all of the cases were positive for perforin, which is a specific marker for cytotoxic T or natural killer (NK) cells. As all of the cases were CD8 negative, the perforin-positive finding further confirmed the concept that nasal lymphoma is a distinct neoplastic entity derived from NK or NK-related cells. Light microscopic immunohistochemical studies revealed that these nasal lymphoma cases could be classified into Leu19(CD56)+Leu4(CD3)+ (two cases) and Leu19(CD56)+Leu4(CD3)- (six cases) types according to the phenotypes of the proliferating cells. However, simultaneous staining for perforin and Leu4 (CD3) using immunoelectron microscopy on the Leu19+Leu4+ cases showed that the perforin-positive cells were different from the Leu4-positive cells. This finding suggests that the Leu4-positive cells are not neoplastic NK cells but reactive T cells. Six cases were positive for EBER-1 by in situ hybridization analysis. This finding reconfirms the previous studies that Epstein-Barr virus plays a significant role in the pathogenesis of nasal lymphoma.

Adult↗
PubMed1996

[A clinical evaluation of fluconazole in deep seated fungal infections associated with hematological disorders].

The effectiveness of fluconazole on deep seated fungal infections associated with hematological disorders was evaluated in a multicenter clinical study. The underlying diseases included acute myeloblastic leukemia, acute lymphocytic leukemia, malignant lymphoma, adult T cell leukemia, multiple myeloma and others. Fluconazole (FLCZ) was administrated 100-400 mg/day intravenously or orally to 79 patients with systemic fungal infections complicated with hematological disorders and it was possible to evaluate clinical efficacies in 60 patients. 27 patients were diagnosed as having determinate systemic fungal infections and 33 patients suspected fungal infections. The clinical efficacies were 81.5% (22/27) in patients with diagnosed fungal infections and 57.6% (19/33) in patients with suspected fungal infections. The overall clinical efficacy was 68.3% (41/60). No side effects such as gastrointestinal symptoms, vascular pain and renal dysfunction were observed in this study. As for abnormal laboratory test, transient increases in GOT, GPT, Al-P, LDH, serum Na, Cl and decrease in serum K were observed in 9 patients (11.4%). These results indicated that FLCZ has a high therapeutic efficacy on deep seated fungal infections in patients with hematological disorders.

Aged↗
PubMed1996

Poor correlation between clonal immunoglobulin gene rearrangement and immunoglobulin gene transcription in Hodgkin's disease.

It recently has been suggested that some cases of Hodgkin's disease (HD) are derived from B lymphocytes. We therefore examined immunoglobulin heavy chain gene rearrangement and transcription by polymerase chain reaction in 30 cases of HD and compared them with 25 cases of non-Hodgkin's B-cell lymphoma. Clonal VDJ gene rearrangements were observed in 6 cases of HD. Of these 6 cases, clonal VDJ gene transcription was found by RNA-dependent polymerase chain reaction in only 2 cases. One of these 2 cases histologically showed composite lymphoma of HD and diffuse large B cell lymphoma. We performed in situ hybridization with a clonal VDJ gene probe in this case to determine the localization of the genetic clonality. The large lymphoma cells reacted positively, but Hodgkin's and Reed-Sternberg cells showed only nonspecific staining. No discrepancy between immunoglobulin gene rearrangement and transcription was observed in 24 of the 25 cases of non-Hodgkin's B-cell lymphoma. The discordance between clonal gene rearrangement and transcription in HD contrasts sharply with the high correlation of those processes in non-Hodgkin's B-cell lymphoma.

Gene Rearrangement↗
PubMed1995

SCG10 expresses growth-associated manner in developing rat brain, but shows a different pattern to p19/stathmin or GAP-43.

The gene encoding SCG10 was originally isolated as a neuronal marker from neural crest derivatives, implying that this protein may contribute to fundamental neuronal properties. To examine the developmental change of SCG10 expression in brain, immunoblot analysis and in situ hybridization were performed in embryonic day 15 (E15), E19, postnatal day 0 (P0), P6, P14, P30 and P90 rat brains. The distribution of SCG10 mRNA was compared to those of its homologue, p19/stathmin, and the well-characterized growth-associated protein GAP-43. Overall expression of SCG10 in brain reached a peak at E19 and decreased gradually by P30 to the adult level. The expression pattern of SCG10 in E15 whole body was identical with that of GAP-43; both mRNAs were specifically detected in developing neuronal structures. p19/stathmin mRNA, on the other hand, showed widespread expression throughout the whole body. Expression patterns of the three mRNAs overlapped in many structures in the perinatal brain, yet each showed unique expression during postnatal development. For example, in the developing cerebellum, strong GAP-43 expression was found in the external granule cells, which are presumably extending parallel fibers, while SCG10 strongly hybridized in the internal granule cells which have reached their final position and begun dendrite outgrowth. The unique transient expression of p19/stathmin was found in the subventricular zone in the cortex, the white matter in the cerebellum, the optic nerve layer of the superior colliculus and the inner edge of the dentate granule layer in the hippocampus. Considering the timing, all of these areas are known to produce neurons or glia. This is consistent with the suggestion that p19/stathmin is related to differentiation. SCG10 may be a new member of growth-associated proteins and this protein may contribute to neurite extension in perinatal brain as does GAP-43. However, the differential expression between SCG10 and GAP-43 in later developmental stages suggests their diverse functions, which indicates these proteins may play different roles during postnatal brain development.

Animals↗
PubMed1995

Liposome-entrapped phenytoin locally suppresses amygdaloid epileptogenic focus created by db-cAMP/EDTA in rats.

Status epilepticus was induced in rats by injecting a combination of dibutyryl-cAMP (db-cAMP) and ethylenediaminetetraacetic acid (EDTA) into the amygdala (AM), and the effect of phenytoin (PHT), entrapped in liposomes (PHT-L) and given intravenously at 40 mg/kg, on the spiking activity of the AM epileptogenic focus was examined. Electroencephalograms were recorded from the db-cAMP/EDTA-injected AM and the bilateral sensorimotor cortices. One dose of PHT-L, given 30 min after intra-AM db-cAMP, produced immediate and transient seizure suppression, but did not suppress the sequential spiking activity, which lasted for more than 5 h. In contrast, two doses of PHT-L, given 30 and 60 min after intra-AM db-cAMP/EDTA, produced delayed and local suppression of AM discharges, and immediate and transient seizure suppression was also observed. The AM discharges began to be suppressed about 100 min after the second injection of PHT-L injection, with no overt change occurring in cortical spiking activity. This was followed by total seizure suppression about 170 min after the second PHT-L injection. This effect was not observed after one or two injections of PHT alone. When horseradish peroxidase (HRP), to which the blood-brain barrier is impermeable, was entrapped in liposomes (HRP-L) and given intravenously 30 min after intra-AM db-cAMP/EDTA, an accumulation of HRP was found in the db-cAMP/EDTA-injected AM in 2 of the 5 animals tested. With 2 doses of HRP-L given 30 and 60 min after intra-AM db-cAMP/EDTA, the local augmentation of HRP in the AM was found in all 5 of the 5 animals tested. Our findings suggest that: (1) the AM epileptogenic focus created by db-cAMP/EDTA has a high affinity for liposomes, and this factor participates in the local suppression of AM discharges by PHT-L, and (2) two injections of PHT-L are required for the AM to gather an effective amount of PHT-L.

Amygdala↗
PubMed1995

Apoptosis susceptibility genes on mouse chromosome 9 (Rapop2) and chromosome 3 (Rapop3).

The strain distribution pattern of susceptibility to thymocyte apoptosis induced by ionizing radiation in 20 CcS/Dem recombinant congenic (RC) strains derived from the strains BALB/cHeA (susceptible) and STS/A (resistant) indicates that this trait is controlled by several genes. Recently, we mapped a novel apoptosis susceptibility gene Rapop1 (radiation-induced apoptosis 1) to chromosome 16 (N. Mori et al., 1995, Genomics 25: 604-614). In the present study, the analysis of F2 crosses between the resistant RC strain CcS-8 and the susceptible strain BALB/cHeA or the highly susceptible RC strain CsS-10 demonstrated two additional apoptosis susceptibility genes, Rapop2 and Rapop3, located in the proximal region of chromosome 9 and the telomeric region of chromosome 3, respectively. The possible candidate genes for these loci are discussed.

Analysis of Variance↗
PubMed1995

Cloning, expression, and chromosomal localization of a novel cadherin-related protein, protocadherin-3.

To study the diversity of the protocadherin family, the cDNA clones for a novel protocadherin were isolated by screening rat brain cDNA libraries with a cDNA fragment obtained by PCR, and some of the properties were then characterized. The overall structure of the protein defined by the clone is similar to that of previously identified protocadherins; however, the cytoplasmic domain is distinct from those of previously cloned protocadherins or any other protein sequences in the data bank. We named this protocad herin-3 (Pcdh3) since this is the third protocadherin of which the entire coding sequence has been determined. Most of the deduced amino acid sequences of other cDNA clones obtained by the screening show high homology with but are distinct from that of Pcdh3, indicating that most of these sequences correspond to homologous but different protocadherins. These results demonstrate that Pcdh3 and the protocadherins defined by these clones constitute a protocadherin subfamily. Chromosome mapping indicates that mouse Pcdh3 is located in a specific region of mouse chromosome 18, close to the location of previously cloned protocadherins, suggesting that various protocadherins form a cluster in this region. In situ hybridization results showed that Pcdh3 and its related proteins were expressed at various areas in brain. The expressed Pcdh3 protein from the cDNA in mouse L cells was about 100 kDa in molecular weight and was localized at cell-cell contact sites. In contrast to the classical cadherins, however, the expressed Pcdh3 was sensitive to trypsin even in the presence of Ca2+, and the transfectants did not show strong Ca(2+)-dependent cell aggregation activity. These results indicate the structural and possibly functional diversity of the protocadherin family and suggest a distinctive biological role for Pcdh3.

Amino Acid Sequence↗
PubMed1995

Different effect of hippocampal granule cell destruction on amygdaloid kindling in Sprague-Dawley and Wistar rats.

The hippocampal granule cells receive major inputs via the perforant path from other limbic structures such as the amygdala (AM). In this study, we examined Sprague-Dawley (SD) and Wistar rats, the effect of bilateral destructions of the hippocampal granule cells on the process of AM kindling and kindled AM seizures after completion of kindling. The granule cells were selectively and completely destroyed bilaterally by intra-hippocampal injections of colchicine. The left AM was used as the primary kindling site and the right AM as the secondary site. In SD rats, prior destruction of the granule cells caused a marked delay in the seizure development of both the primary AM kindling and subsequent secondary AM kindling. However, once AM kindling was established in SD rats, the destruction of granule cells was totally ineffective in preventing kindled seizures. In Wistar rats, unlike SD rats, prior destruction of the granule cells failed to change the rate of kindling at the primary and secondary sites. However, Wistar rats showed a transient and marked regression of kindled seizures when the granule cells were destroyed after the completion of AM kindling. In both strains, granule cell destruction had no effect on the re-establishment of kindled seizures at the time of primary-site re-test. These findings suggest that hippocampal granule cells of SD and Wistar rats play different roles in AM kindling.

Amygdala↗
PubMed1995

Anaplastic large cell lymphomas expressing the novel chimeric protein p80NPM/ALK: a distinct clinicopathologic entity.

Anaplastic large cell lymphoma (ALCL) is a subtype of non-Hodgkin's lymphoma characterized by the CD30+ large neoplastic cells and sometimes carries a t(2;5)(p23;q35). Recently, we found a novel hyperphosphorylated 80-kD protein tyrosine kinase, p80, in ALCLs with t(2;5). Subsequent cDNA cloning showed p80 to be a fusion protein of two genes, the novel tyrosine kinase gene and the nucleophosmin gene, in accordance with the sequence of the NPM/ALK gene (Morris et al, Science 263:1281, 1994). Meanwhile, the clinicopathologic features of p80-carrying ALCLs have remained unclear. Paraffin sections of 105 cases of ALCL were immunostained using anti-p80 antibody, and 30 of them were shown to express p80. Clinicopathologic comparison between p80-positive and -negative ALCLs showed that p80-positive cases occurred in a far younger patient age group (16.2 +/- 12.9 years; p80-negative cases, 51.0 +/- 22.3 years; P < .0001) and the patients showed a far better 5-year survival rate (79.8%; p80-negative group, 32.9%; P < .01). These data showed that p80-positive ALCL is a distinct entity both clinically and pathogenetically and should be differentiated from p80-negative ALCL.

Adolescent↗
PubMed1995

Production of interleukin 8 in adult T-cell leukemia cells: possible transactivation of the interleukin 8 gene by human T-cell leukemia virus type I tax.

Interleukin 8 (IL-8) mRNA was detected in peripheral leukemic cells obtained from adult T-cell leukemia patients, as well as in cultured human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines (HUT-102, MT-1, SALT-3, and SKT-1B). With the use of ELISA, IL-8 protein was also detected in the culture medium of these cells and in the extracellular fluids of patients. Furthermore, we demonstrated that the HTLV-I-derived transactivator protein, tax, could stimulate endogenous IL-8 gene expression in an uninfected T-cell line (Jurkat) and in a rheumatoid synovial cell line (E-11). Induction of IL-8 by tax at protein level was also demonstrated in transfected cells. We found that the IL-8 NF-kappa B-binding site specifically formed a complex with NF-kappa B-containing nuclear extracts from HTLV-I-infected T-cell lines and freshly isolated leukemic cells from adult T-cell leukemia patients. Finally, transfection of HTLV-I tax into Jurkat cells resulted in induction of specific binding of nuclear extracts to the NF-kappa B sequence. These results suggest that the HTLV-I tax gene may transactivate the IL-8 gene through the kappa B site in HTLV-I-infected cells and that constitutive expression of the IL-8 gene may play a role in HTLV-I-associated pathogenesis.

Acute Disease↗