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N Fujiwara

Publications and source records attributed to N Fujiwara.

At least 91 records · Page 5Linked to original sources
PubMed1997

[Distribution of antigenic glycolipids among Mycobacterium tuberculosis strains and their contribution to virulence].

Tuberculosis is a chronic disease caused by Mycobacterium tuberculosis infection. The major pathological changes are immunologically hypersensitive granuloma formation due to the local proliferation or infiltration of immune cells. However, the mechanism for the development of the disease has not yet been fully understood. The first step of infection in intracellular survival in the phagocytic cells and this process has been reported to be regulated by cell surface glycolipid virulence factors. As genetical heterogeneity of M. tuberculosis among strains has been reported recently based on DNA fragmentation pattern, I have examined the distribution of cell surface glycolipids (cord factor, sulfolipids and penta acyl trehaloses) among the virulent (M. tuberculosis H37Rv and M. tuberculosis Aoyama B) and virulent (M. tuberculosis H37Ra) strains by two dimensional thin-layer chromatography of silica gel. Seven characteristic glycolipid components of the virulent strains were detected and separated by thin-layer chromatography of silica gel. Each glycolipid was identified by fast-atom-bombardment mass-spectrometry (FAB/MS) analysis of the intact lipid and gas-chromatography mass-spectrometry (GC/MS) analysis of the fatty acid or the carbohydrate moiety. As the result, molecular weight (m/z, 1,200-3,000) of each glycolipid was determined clearly by FAB/MS analysis. The structure of fatty acids (C16-C40) or mycolic acids (C76-C88) were determined by GC/MS analysis. Cord factor (TDM, trehalose 6,6'-dimycolate) and trehalose 6-monomycolate (TMM) showed strong granuloma forming activity, but other glycolipids practically did not. On the other hand, cord factor and trehalose 6-monomycolate showed phagocytosis inhibition (but showed promotion in the presence of complement) and marked inhibition of phagosome-lysosome fusion, while sulfolipids showed strong phagocytosis promotion and marked inhibition of phagosome-lysosome fusion. Penta acyl trehaloses showed phagocytosis promotion but no effect on phagosome-lysosome fusion. Cord factor and trehalose 6-monomycolate existed ubiquitously among virulent and avirulent strains, while sulfolipids and penta acyl trehaloses were detected in only virulent strains (M. tuberculosis H37Rv and M. tuberculosis Aoyama B). These results indicate that the existence of these toxic glycolipids contributes to the virulence of M. tuberculosis, profoundly. It is suggested that these glycolipids play an important role as virulence factors in the early stage of infection and expression of pathogenicity.

Antigens, Bacterial↗
PubMed1997

[Effectiveness of percutaneous transluminal angioplasty and intra-arterial papaverine infusion for symptomatic vasospasm after subarachnoid hemorrhage].

PURPOSE: To evaluate the clinical effectiveness of PTA and/ or intra-arterial infusion of papaverine (PPV) for the treatment of symptomatic vasospasm after subarachnoid hemorrhage. MATERIALS AND METHODS: From September 1989 to March 1996, twenty patients with symptomatic vasospasm were treated by PTA and/or intra-arterial infusion of PPV. Nine of the patients were treated by only PTA, eight by only PPV infusion, and three by both PTA and PPV infusion. Early clinical results were evaluated within 48 hours after treatment. Changes in the mean flow velocity (MFV) of the M1 segment as determined by TCD before and after treatment were also evaluated. RESULTS: Six of the nine patients (66.7%) treated only by PTA, six of the eight patients (75%) treated only by PPV, and all three patients (100%) treated by both PTA and PPV infusion showed improvement of neurological deficits within 48 hours after treatments. CONCLUSION: PTA was effective for main trunk vasospasm, while PPV infusion was more effective for peripheral severe vasospasm in recovery from neurological deterioration after subarachnoid hemorrhage. Use of both treatments further increased the effectiveness.

Adult↗
PubMed1996

Quinazoline derivatives suppress nitric oxide production by macrophages through inhibition of NOS II gene expression.

We have found three novel quinazolidine derivatives which inhibit the formation of nitrite dose-dependently in a murine macrophage cell line, RAW264.7. The decreased nitrite formation was due not to the inhibition of nitric oxide synthase activity but to suppression of NOS II mRNA and protein expression. In rat vascular smooth muscle cells (VSMC), however, these compounds rather enhanced NOS II mRNA. These compounds also prevented LPS-stimulated heme oxygenase-1 (HO-1) and cyclooxygenase-2 (COX-2) gene expression in RAW264.7 cells, but again not in VSMC. The three quinazolidine derivatives specifically inhibit gene expression of NOS II, HO-1 and COX-2 only in macrophage cells, indicating that they are selective inhibitors of inducible gene expression in macrophages.

Animals↗
PubMed1996

Thy-1-mediated phosphatidylinositol turnover in cultured rat glomerular mesangial cell.

Thy-1 glycoprotein is expressed in rat glomerular mesangial cells, and anti-Thy-1 nephritis induced by anti-Thy-1 antibodies is a model of human renal diseases. In this study, we examined Thy-1-mediated biological reactions in cultured rat glomerular mesangial cells utilizing two anti-Thy-1 monoclonal antibodies (mAbs), 1-22-3 and OX-7. Incubation of the cells with these mAbs resulted in increased inositol trisphosphate (IP3) levels. The rise in IP3 produced by mAb 1-22-3 was greater than that produced by mAb OX-7 at the same dose. Incubation of mesangial cells with these mAbs resulted in an increase in the intracellular free calcium concentration ([Ca2+]i). mAb 1-22-3 induced a sustained increase in [Ca2+]i, while that induced by mAb OX-7 lasted 1-2 min, then decreased to the basal level. An transient increase in [Ca2+]i was also observed in Ca(2+)-free medium, indicating that these [Ca2+]i increases are due to release of Ca2+ from internal stores by IP3 without calcium flux across cell membrane. When cells were pretreated with protein tyrosine kinase (PTK) inhibitors (herbimycin A or genistein), Thy-1-mediated increases in [Ca2+]i were inhibited. These data suggest that Thy-1 induces the production of IP3 (including inositol 1,4,5-triphosphate, an intracellular Ca(2+)-releasing factor) and that PTKs may contribute to the Thy-1-mediated elevation of [Ca2+]i which presumably results from phospholipase C activation following Thy-1-mediated signaling in rat mesangial cells.

Animals↗
PubMed1996

Pain-related and cognitive components of somatosensory evoked potentials following CO2 laser stimulation in man.

We recorded cortical potentials evoked by painful CO2 laser stimulation (pain SEP) employing an oddball paradigm in an effort to demonstrate event-related potentials (ERP) associated with pain. In 12 healthy subjects, frequent (standard) pain stimuli (probability 0.8) were delivered to one side of the dorsum of the left hand while rare (target) pain stimuli (probability 0.2) were delivered to the other side of the same hand. Subjects were instructed to perform either a mental count or button press in response to the target stimuli. Two early components (N2 and P2) of the pain SEP demonstrated a Cz maximal distribution, and showed no difference in latency, amplitude or scalp topography between the oddball conditions or between response tasks. In addition, another positive component (P3) following the P2 was recorded maximally at Pz only in response to the target stimuli with a peak latency of 593 msec for the count task and 560 msec for the button press task. Its scalp topography was the same as that for electric and auditory P3. The longer latency of pain P3 can be explained not only by its slower impulse conduction but also by the effects of task difficulty in the oddball paradigm employing the pain stimulus compared with electric and auditory stimulus paradigms. It is concluded that the P3 for the pain modality is mainly related to a cognitive process and corresponds to the P3 of electric and auditory evoked responses, whereas both N2 and P2 are mainly pain-related components.

Adult↗
PubMed1996

Tachyphylaxis to furosemide in isolated airways of guinea pigs.

This in vitro study was conducted to determine whether tachyphylaxis of guinea pig airway to furosemide occurs under conditions that produce tachyphylaxis to the beta 2-adrenoceptor agonist, salbutamol. Isometric tension was measured in tracheal rings bathed in HEPES buffer from 4-6 d newborn guinea pigs of either sex, and 6 wk old males. Paired rings were first incubated with furosemide, 30 or 300 microM, or control for 60 min, washed, then constricted with 3 microM acetylcholine. At stable contraction, relaxation to furosemide (30 microM-1 mM) was measured. For comparison, similar experiments were performed with 10 microM salbutamol incubation for 30 min. 86Rb uptake, a marker for K+ transport and Na-K-Cl cotransport activity, was also measured in these airway segments. Pre-exposure to these airway relaxants did not affect contractile force generation by acetylcholine. Tracheal desensitization to both salbutamol and furosemide was observed. Partial recovery of furosemide induced relaxation was seen one hour after desensitization. Pre-exposure to 300 microM furosemide did not inhibit the decrease in 86Rb uptake normally observed with furosemide. In summary, we found that: 1) tachyphylaxis of guinea pig airway relaxation occurred with both salbutamol and furosemide under similar experimental conditions; however 2) inhibition of 86Rb uptake by furosemide was not affected by prior exposure. Taken together, these results suggest that furosemide induced airway relaxation could be affected by repeated or prolonged exposure, but this response may not be associated with changes in furosemide-sensitive Na-K-Cl cotransporter activity.

Albuterol↗
PubMed1996

Septal structure of incomplete interlobar fissures of the lung.

RATIONALE AND OBJECTIVES: Some septal structures have been observed in the areas of incomplete interlobar fissures (IIFs) in resected lungs. We describe the anatomy of IIFs with or without the presence of septal structures. METHODS: Twenty fused areas from 16 autopsy cases were examined histologically. Other septal structures outside the areas of IIFs also were examined. RESULTS: In 10 of the 20 fused areas, there was a mixture of septal structures with and without defects. In the remaining 10, there were no septal structures. The septal structures consisted of two inner layers from both lobes. Other septal structures examined were the same as ones observed in the IIFs. CONCLUSION: Linear shadows seen at interlobar fissures and on computed tomography scans do not necessarily depict the presence of complete interlobar fissures. The absence of linear shadows does not necessarily imply the absence of septal structures.

Bronchi↗
PubMed1996

Effect of a nitric oxide synthase inhibitor, S-ethylisothiourea, on cultured cells and cardiovascular functions of normal and lipopolysaccharide-treated rabbits.

Nitric oxide (NO) is synthesized from L-arginine by three isoforms of NO synthase (NOS). It is essential to suppress the function of the inducible isoform (macNOS) for amelioration of some inflammatory diseases in which the cytotoxic effect of NO is involved. S-Ethylsiothiourea (S-EIU) was reported to be a potent and specific inhibitor of macNOS. We also confirmed that it rather specifically inhibited the activity of the purified macNOS and the formation of nitrite by RAW264.7 cells compared to NG-monomethyl-L-arginine (L-NMA) and NG-nitro-L-arginine (L-NNA), the other isoforms being less effective. S-EIU suppressed the release of nitrite and lactate dehydrogenase from rat vascular smooth muscle cells treated with interleukin-1 beta and forskolin more potently than L-NMA or L-NNA. S-EIU also slightly suppressed internucleosomal DNA cleavage in pancreatic beta-cells induced by NO produced by macNOS. Intravenous administration of either S-EIU at 0.1 mg/kg/min or L-NMA at 1 mg/kg/min increased the blood pressure but decreased the heart rate in normal rabbits, while aminoguanidine at 1 mg/kg/min affected neither cardiovascular function. These inhibitors at these doses caused recovery of the blood pressure in lipopolysaccharide-treated rabbits that exhibited lowered blood pressure similar to that in the case of septic shock. Although S-EIU seemed not to be an adequate inhibitor for therapeutic use in vivo due to its side effects on cardiovascular functions, it is one of the most potent inhibitors of macNOS among reported inhibitors in vitro.

Animals↗
PubMed1996

Relationship between induction of macrophage chemotactic factors and formation of granulomas caused by mycoloyl glycolipids from Rhodococcus ruber (Nocardia rubra).

Mycoloyl glycolipids cause granulomas in the lungs, liver, and spleen of mice, but the mechanism is not fully understood. To understand the role of macrophage chemotactic factors (MCFs) in granuloma formation, we prepared various mycoloyl glycolipids with different carbohydrate moieties: trehalose dimycolate (TDM), glucose mycolate (GM), mannose mycolate (MM), and fructose mycolate (FM) from Rhodococcus ruber, and examined the relationship between their MCF induction in peritoneal macrophages and the extent of granuloma formation. The molecular mass of each glycolipid was confirmed by fast-atom-bombardment mass-spectrometry. TDM or GM caused granulomas in the lungs, spleen, and liver of ICR mice, but MM and FM did not. The culture supernatant of peritoneal macrophages stimulated with TDM or GM increased macrophage migration, whereas MM and FM had no chemotactic activity. The activity of interleukin-1 (IL-1) in the supernatant was increased equally by each glycolipid and was therefore not related to chemotaxis. Tumor necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were not detected in the four supernatants. The TDM-induced MCF was heat-stable, trypsin-labile, and undialyzable. Furthermore, we separated two MCF active fractions from the supernatant of TDM-stimulated macrophages by gel filtration. These factors acted on macrophages but not on neutrophils. Our results suggested that macrophages recognize the sugar moieties of mycoloyl glycolipids and may, in response, generate a MCF that may play an important role in the macrophage or monocyte recruitment which is essential prior to granuloma formation.

Animals↗
PubMed1996

The effects of halothane on arginine-vasopressin-induced Ca2+ mobilization from the intracellular stores and the receptor-mediated Ca2+ entry from the extracellular space in single cultured smooth muscle cells of rat aorta.

Halothane has a direct action on vascular smooth muscle cells and causes relaxation of these cells, yet neither the mechanism nor the site of its action is completely understood. Using digital imaging microscopy with the Ca2+ indicator fura-2, the effects of halothane on the intracellular [Ca2+] dynamics induced by arginine vasopressin (AVP) in the perinuclear region and cytosol in single cultured smooth muscle cells of rat aorta were studied. Changes in intracellular [Ca2+] were expressed as percent increases in the ratios of fluorescence intensity at 500 nm excited by 340 nm and 380 nm. AVP (10(-7) M) elicited an initial transient increase in [Ca2+] in the perinuclear region higher than that in the cytosol in Ca(2+)-containing solution (346% +/- 21% and 213% +/- 22%, respectively). Halothane, 0.5%, attenuated the [Ca2+] increase induced by AVP in the perinuclear region and cytosol, and halothane, 1.0% and 2.0%, abolished the differential increase. Under the continuous application of AVP (10(-7) M), Ca2+ restoration in the medium after perfusion with Ca(2+)-free solution increased the perinuclear [Ca2+] more than the cytosolic [Ca2+]. Both were significantly attenuated by 2.0% halothane, but not by nicardipine (10(-5) M) or ryanodine (10(-6) M). Our results suggest that halothane may attenuate the Ca2+ release from the intracellular Ca2+ stores more than the receptor-mediated Ca2+ entry from the extracellular space in the AVP-induced response in these cells.

Anesthetics, Inhalation↗
PubMed1996

Regionally different elevation of intracellular free calcium in hippocampus of septic rat brain.

The effect of sepsis on cellular calcium homeostasis in the central nervous system (CNS) was investigated using hippocampal slices of rats in which sepsis was induced by cecal ligation and puncture (CLP). Hippocampal slices were prepared from septic or sham-operated rats at 24 h after abdominal surgery. The basal intracellular calcium ([Ca2+]i) and its response to oxygen-glucose deprivation in hippocampal slices were measured for assessing cellular calcium homeostasis using fura-2 fluorescent imaging technique. The levels of [Ca2+]i were estimated by the fluorescence ratio (R340/380). Twenty-four hours after CLP, spontaneous movement was reduced and plasma lactate was increased in the septic rats in comparison with the sham-operated rats in which laparotomy was performed without CLP. Basal level of R340/380 in the CA4 ara (.72 +/- .07) was significantly higher (p < .001) in the septic group than that in the sham-operated group (.55 +/- (.06). The fluorescence ratio of septic vs. sham-operated in other hippocampal regions were .55 +/- .09 vs. .48 +/- .06 in CA1 (not significant) and .65 +/- .10 vs. .59 +/- .08 (not significant) in CA3, respectively. Increase in [Ca2+]i due to oxygen-glucose deprivation was significant in CA1 and CA3 of the septic group and in all hippocampal regions of sham-operated group. However, it was not significantly increased in CA4 of the septic group. These results suggest that regional deregulation of cellular calcium occurs in the CNS following CLP. Cellular calcium deregulation may be one of the pathogeneses occurred in clinically observed septic encephalopathy.

Animals↗
PubMed1996

Pain-related somatosensory evoked potentials can quantitatively evaluate hypalgesia in Wallenberg's syndrome.

In 6 patients with Wallenberg's syndrome who showed a dissociated loss of pain sense, we recorded pain-related somatosensory evoked potentials following CO2 laser stimulation of the hand dorsum (pain SEPs). Two components, N2 and P2, were recorded by stimulation of the unaffected hand, whereas on the affected side they were absent or decreased in proportion to the severity of hypalgesia which was evaluated by both needle test and CO2 laser stimulation. Latency of either component, if appeared, was longer in the affected hand stimulation than that in the unaffected one. In contrast, N20 of the conventional electrically-stimulated SEPs (electric SEPs) showed no difference between the two sides. It is concluded that, unlike other electrophysiological methods, pain SEPs following CO2 laser stimulation can quantitatively evaluate functional impairment of the spinothalamic tract in Wallenberg's syndrome.

Adult↗
PubMed1996

Cerebral vasospastic vessels: histologic changes after percutaneous transluminal angioplasty.

PURPOSE: To investigate histologic changes before and after percutaneous transluminal angioplasty (PTA) in experimental cerebral vasospasm in comparison with normal vessels. MATERIALS AND METHODS: In seven monkeys, vasospasm was induced in the subarachnoid space. After 7 days, PTA was performed. Microscopic studies were performed in vasospastic vessels. In two animals, vasospasm was induced but angioplasty was not performed. The controls were two animals without vasospasm who underwent only contralateral angioplasty. RESULTS: Angiography after vasospasm revealed marked narrowing but dilatation after PTA, without changes in distal spastic vessels. Specimens after PTA showed platelets that covered denuded endothelium, stretching, and focal dehiscence of internal elastic lamina and altered myocytes in media. Myocytes were deformed and arranged irregularly. These changes were not uniform. CONCLUSION: The prolonged effect of PTA may be caused by mechanical damage of myocytes and the nonuniformity of histologic changes in vascular walls.

Angioplasty, Balloon↗
PubMed1995

Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man.

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO2 laser stimulation of the hand dorsum could not clarify whether the early cortical component N1 was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO2 laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of N1-N2 between foot and hand stimulation. It is therefore concluded that N1 of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N1 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.

Adult↗
PubMed1995

Relationship between tissue ischemia and venous endothelin-1 during abdominal aortic aneurysm surgery.

OBJECTIVES: Several substances may be released from ischemic tissues with the declamping shock that occurs during abdominal aortic aneurysm surgery. To clarify the relationship between tissue ischemia and venous endothelin-1 (ET-1) level in humans, plasma ET-1 and oxygen content in the iliac vein were measured before anesthesia, after the induction of anesthesia, after the release of the proximal and first distal clamps, after the release of the second distal clamp, and 1 hour after the second clamping. DESIGN: Prospective study. SETTING: A University hospital. PARTICIPANTS: Seven patients who underwent abdominal aneurysmectomy and replacement with bifurcated graft. INTERVENTIONS: A 20G catheter was inserted into the radial artery for the direct measurement of blood pressure and for collecting arterial blood. An 18G, 20-cm catheter was inserted into the femoral vein for collecting venous blood from the lower extremities. MEASUREMENTS AND MAIN RESULTS: The arterial and venous ET-1 levels did not change after the induction of anesthesia. Immediately after the initial release of the proximal and distal clamps, venous oxygen content dramatically decreased from 11.3 to 3.6 mL/dL (vol%) with significant increases in venous ET-1 concentration from 2.3 to 4.9 pg/mL. Concomitant with the decrease in venous oxygen content, venous plasma pH and base excess decreased with increase in PCO2, suggesting that ischemic changes in tissues distal to the cross-clamp may occur during aortic clamping. Venous ET-1 levels were significantly correlated with venous oxygen content, pH, PO2, oxygen saturation, base excess, blood sodium concentration, and potassium concentration. One hour after the second declamping, the venous ET-1 level remained high in comparison with the preanesthetic level, whereas the venous oxygen content returned to the preanesthetic level. There was no correlation between venous plasma ET-1 and venous plasma norepinephrine or epinephrine concentration. CONCLUSIONS: Tissue ischemia may increase venous ET-1 levels in humans. Factor(s) other than tissue ischemia may provoke the increase in venous ET-1 that occurs after the release of the second distal clamp.

Aged↗