[Development of a DNA probe specific for Bacteroides fragilis: use of the cloned neuraminidase gene].
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Bacteroides Infections↗
Biomedical subjects
T Ono
Publications and source records attributed to T Ono.
[Lumbago as a presentation of B-cell lymphoma invading psoas muscle].
A 73-year-old male had severe lumbago and right inguinal lymphadenopathy. A CT scanning of his abdomen showed marked enlargement of right psoas and erector spinae muscles. The biopsies of the lymph node and the muscles revealed non-Hodgkin's lymphoma of follicular mixed type with muscle invasion. THP-COPE therapy was begun. The swelling of the muscles diminished and the lumbago resolved rapidly. It was reported that clinically prominent infiltration of of lymphoma in skeletal muscle was rarely and psoas muscle was for the most part. We have to consider that psoas muscle invasion of lymphoma cause hard to cure lumbago.
Aged↗
[Effects of mesocortical dopaminergic lesions on stress-induced changes in monoamine metabolism in the discrete brain regions of rats].
This study assessed the possible influence of the mesocortical dopamine (DA) system on the reactivity of subcortical monoamine systems to stress. Rats were either sham-operated or subjected to DA-depleting lesions of the medial prefrontal cortex (mPFC) with 6-hydroxydopamine. Fourteen days after surgery, the rats were exposed to 30 or 60 min immobilization stress, and levels of noradrenaline, 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG). DA, 3-4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin, and 5-hydroxyindoleacetic acid were measured in nine brain regions. The stress caused a significant increase in the levels of DA metabolites, DOPAC or HVA, in the mPFC of sham-operated, but not of lesioned animals. HVA concentrations in the nucleus accumbens, olfactory tubercle, and ventral tegmental area were significantly increased in both sham-operated and lesioned rats, but the effect of stress on the subcortical DA systems was unaffected by the lesion. The stress also significantly elevated MHPG levels in the amygdala and hypothalamus of both groups of animals, and these results were similar in the amygdala of rats with or without lesions. In the hypothalamus, however, 60 min stress caused a more marked increase in MHPG concentrations in lesioned rats than in sham-operated rats (lesion-group, 143%; sham-group, 122%), while 30 min stress produced a similar elevation in both groups of animals (lesion-group, 149%; sham-group, 142%). These results suggest that the mesocortical DA system may modulate the sensitivity of the noradrenergic system in the hypothalamus to stress.
Animals↗
Common phenotypic expression of gangliosides GM3 and GD3 in normal human tissues and neoplastic skin lesions.
The expression of gangliosides in non-malignant tissues (epidermis and pigmented nevus) and neoplastic lesions (melanoma, squamous cell carcinoma [SCC] and basal cell carcinoma [BCS]) of the human skin was analyzed immunohistochemically and biochemically to characterize the features associated with malignancy. Immunohistochemical staining with an anti-II3NeuAc-LacCer (GM3) monoclonal antibody (M2590 mAb) and an anti-II3(NeuAc)2-LacCer (GD3) mAb (R24) showed the expression of the gangliosides GM3 and GD3 to vary among the different tissues. M2590 clearly stained epidermal keratinocytes and the tumor cells of BCC and SCC, and strongly stained melanocytes and melanoma cells. In contrast, R24 did not stain epidermal keratinocytes and only faintly stained SCC cells, while it clearly stained BCC cells, and intensely stained melanocytes and melanoma cells. GM3 showed a similar level of staining among the tissue specimens, while the level of GD3 staining was quite variable among the tumor specimens. Biochemical analysis by thin-layer chromatography (TLC) with resorcinol staining and TLC immunostaining with either M2590 or R24 showed both GM3 and GD3 to be commonly expressed by both the normal and malignant skin tissues, including SCC. There was no close correlation between the intensity of immunohistochemical staining and the biochemically detected amounts of these gangliosides. This may have been partly due to the so-called cryptic expression of cell membrane gangliosides. Our results thus suggest that analysis of the tumor-associated expression of gangliosides requires several methods, since the sensitivity of the methods used may have a considerable effect on the diagnostic value of gangliosides as skin cancer markers.
Biomarkers, Tumor↗
Post-irradiation protective effect of irsogladine maleate on intestinal crypt stem cells in mice.
Radioprotective effect of irsogladine maleate, an anti-ulcer drug, on the intestinal crypt stem cell survival was studied in mice using a crypt microcolony assay. Irsogladine maleate was injected intraperitoneally immediately after irradiation and then, daily for three days. A successive administration of the drug following 10 Gy of irradiation increased the survival of intestinal stem cells with a clear dose-related trend. In order to estimate the D0, survival curves were determined for X-ray plus placebo and X-ray plus 10 mg/kg of irsogladine maleate. The D0, for X-ray plus the drug was 2.2 Gy while it was 1.9 Gy for X-ray plus placebo. These findings suggest that isogladine maleate can be applied for the alleviation of intestinal damages in heavily irradiated people by radiation accidents.
Animals↗
All-or-none response of isolated smooth muscle cells from guinea-pig taenia caecum to acetylcholine.
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Acetylcholine↗
[Comparative study of the efficacy of hepatic arterial and portal venous infusion of adriamycin for prevention of liver metastases in rabbit VX2].
To compare the efficacy of hepatic arterial (HA) and portal venous infusion (PV) anticancer drugs in the prevention of the liver metastasis of cancer, the following experimental study was performed. VX2 tumor cells (1 x 10(7) cells) floating in physiological saline were injected into the portal vein of Japanese white rabbit. Adriamycin (ADR) was administered to the liver via HA or PV at 3, 5, 7 (1 mg/kg) days, and immediately, 2, 4 days after tumor inoculation, respectively. The rabbits were sacrificed 3 weeks after tumor inoculation and the total number of liver metastases was counted. Results were as follows: 1) The numbers of metastatic VX2 tumor nodules in HA group were significantly smaller than in PV group (p = 0.05). 2) Starting ADR injection immediately after tumor inoculation enhanced the inhibition of tumor growth. These results suggest that immediate hepatic arterial infusion of anticancer drugs after resection of primary gastrointestinal cancer is most useful to prevent liver metastases.
Animals↗
[Evaluation of repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy of unresectable primary or secondary cancer of the liver].
Repeated hepatic dearterialization combined with intra-arterial infusion chemotherapy was performed in 29 patients with unresectable primary or secondary cancer of the liver. Partial Response (PR) was obtained in 4 cases (1 hepatocellular carcinoma and 3 gastric secondaries), when evaluated by measuring the regression rate radiologically. The most remarkable effect was found in those with metastases from gastric cancer. A satisfactory result was not obtained for hepatocellular carcinoma with liver cirrhosis because of frequent associated complications. A strategy to modulate the resistance of tumors to ischemia and anticancer drugs should be considered in order to obtain a better clinical result by this method.
Catheterization↗
[Two operated cases of mitral stenosis (MS) associated with left atrial ball thrombus].
Mitral stenosis associated with left atrial ball thrombus is rare. Removal of left atrial ball thrombus and mitral valve replacement was performed in two patients successfully. The rate of thromboembolism was high in patient who has left atrial ball thrombus. Also, sudden death was reported in these cases due to incarceration of ball thrombus in the mitral orifice (hole-in-one thrombus). We concluded that we should operate the MS associated with left atrial ball thrombus as soon as possible.
Female↗
[A case of esophageal cyst with high level of tumor marker in the cystic fluid].
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Adult↗
Striatal N-methyl-D-aspartate receptors in haloperidol-induced catalepsy.
Bilateral ablation of the frontal cortex of rats markedly reduced the catalepsy induced by haloperidol (1 mg/kg i.p.). Similarly, the selective antagonist of N-methyl-D-aspartate (NMDA) receptors, D(-)-2-amino-5-phosphonopentanoic acid (10 micrograms/side), injected bilaterally into the rostral part of the caudate-putamen (CP) reduced haloperidol-induced catalepsy whereas its injection into the intermediate part of the CP was ineffective. The quisqualate receptor antagonist, L-glutamic acid diethyl ester (100 micrograms/side), did not affect haloperidol-induced catalepsy when injected into the rostral part of the CP. On the other hand, NMDA (1 micrograms/side) injected bilaterally into the rostral part of the CP was able to restore haloperidol-induced catalepsy in frontally decorticated rats without any notable cataleptic effect of its own. These findings suggest that a certain degree of tonic stimulatory effect of corticostriatal glutamatergic pathways on NMDA receptors within the rostral part of the CP is a prerequisite for the expression of the cataleptogenic action of haloperidol.
Animals↗
Structural and functional modifications of the manganese cluster in Ca(2+)-depleted S1 and S2 states: electron paramagnetic resonance and X-ray absorption spectroscopy studies.
The effect of extraction of weakly bound Ca2+ by low-pH treatment on the O2-evolving apparatus was studied by use of low-temperature electron paramagnetic resonance (EPR) and X-ray absorption spectroscopy. In low-pH-treated PSII membranes, an S2 EPR multiline signal with modified line shape was induced by illumination at 0 degrees C, but its signal amplitude decreased upon lowering the excitation temperature with concomitant oxidation of cytochrome (cyt) b-559 in place of Mn. The half-inhibition temperature for formation of the modified multiline signal was found at -33 degrees C, which was much higher than that for formation of the normal S2 state in untreated control membranes. Signal IIf was normally induced down to -30 degrees C, but its dependence on excitation temperature was different from that for modified S2. This was interpreted as indicating that the low-temperature blockage of modified S2 formation is due to the incapability of electron abstraction from the Mn cluster. The Mn K-edge of X-ray absorption near-edge structure (XANES) spectrum shifted to lower energy by 0.8 eV after low-pH treatment, but the shift was reversed by addition of Ca2+. Upon illumination at 0 degrees C of treated membranes, the K-edge energy was up-shifted by 0.8 eV, but was not upon illumination at 210 K. These results were interpreted as indicating that extraction of weakly bound Ca2+ by low-pH treatment gives rise to structural and functional modulations of the Mn cluster.
Calcium↗
The effects of TFC-612, a 7-thia prostaglandin E1 derivative, on platelet function.
The anti-platelet activities of TFC-612, methyl 6-(((1R, 2S, 3R)-3-hydroxy-2-((1E, 3S, 5R)-3-hydroxy-5-methyl-1-nonenyl)-5- oxocyclopentyl) thio)hexanoate, were compared to prostaglandin E1 (PGE1). TFC-612 inhibited human, guinea-pig and rabbit platelet aggregation induced by ADP, collagen or epinephrine with potency 1-8 times that of PGE1. TFC-612 also inhibited thrombin induced (14C) serotonin release in rabbit platelets. Platelet aggregation was dose dependently inhibited 1 hr after oral administration of TFC-612 (0.32-1.0 mg/kg) and the inhibition lasted up to 6 and 24 hours at 0.32 and 1.0 mg/kg, respectively, in guinea-pigs. In contrast, PGE1 had no effect with oral administration at a dose of 3.2 mg/kg. TFC-612 (0.32-3.2 micrograms/kg, i.v.) induced platelet disaggregation of thrombi on Achilles tendon in the extracorporeal shunt model in cats. In addition, TFC-612 (1 mg/kg, po) inhibited the adhesiveness of guinea-pig platelets to a glass bead column ex vivo. TFC-612 increased cyclic AMP (cAMP) levels in rabbit platelets. Thus, the anti-platelet action of TFC-612 may be due to an increase in cAMP levels. These results indicate that TFC-612 might be an orally active anti-thrombotic drug.
Alprostadil↗
A possible role of redox-active histidine in the photoligation of manganese into a photosynthetic O2-evolving enzyme.
Our previous experiments with a histidine modifier suggest that in Mn-depleted photosystem (PS) II a histidine residue is photooxidized and charge recombination between the oxidized histidine and QA-emits the thermoluminescence AT-band [Ono, T., & Inoue, Y. (1991) FEBS Lett. 278, 183-186]. By use of the AT-band as an index for histidine oxidation, and EPR signals IIf and IIs as indexes for tyrosine oxidation, we studied the role of this putative redox-active histidine in the photoactivation of the O2-evolving enzyme in NH2OH-treated PSII. The following results have been obtained. (i) Strong-light photoinhibition of NH2OH-treated PSII quickly impaired both capabilities of photoactivation and AT-band emission with almost the same half-inhibition time of 1-2 s, while signal IIf was well retained and signal IIs was not affected at all after complete loss of photoactivation capability. (ii) The capability of exogenous Mn2+ photooxidation was relatively sensitive to strong-light photoinhibition, but DPC was relatively sensitive to strong-light photoinhibition, but DPC photooxidation was highly resistant. (iii) Weak-light photoinhibition simultaneously impaired the capabilities of photoactivation, AT-band emission, and signal IIf with the same half-inhibition time of 1 min, leaving signal IIs unaffected. (iv) It was inferred that the putative redox-active histidine is essential for the photooxidation of coordinated Mn2+, the probable initial step of photoactivation, and its photodamage results in the loss of the capabilities of photoactivation and AT-band emission. Based on these, a scheme of electron transfer on the donor side of PSII involving histidine oxidation via Z+ is proposed.
2,6-Dichloroindophenol↗
The effects of TFC-612, a 7-THIA prostaglandin E1 derivative, on platelet function.
The anti-platelet activities of TFC-612, methyl 6-(( 1R,2S,3R)-3-hydroxy-2-((1E,3S,5R)-3-hydroxy-5-methyl-1-nonenyl)-5- oxocyclopentyl) thio)hexanoate, were compared to prostaglandin E1 (PGE1). TFC-612 inhibited human, guinea-pig and rabbit platelet aggregation induced by ADP, collagen or epinephrine with potency 1-8 times that of PGE1. TFC-612 also inhibited thrombin induced (14C) serotonin release in rabbit platelets. Platelet aggregation was dose dependently inhibited 1 hr after oral administration of TFC-612 (0.32-1.0 mg/kg) and the inhibition lasted up to 6 and 24 hours at 0.32 and 1.0 mg/kg, respectively, in guinea-pigs. In contrast, PGE1 had no effect with oral administration at a dose of 3.2 mg/kg. TFC-612 (0.32-3.2 micrograms/kg, iv) induced platelet disaggregation of thrombi on Achilles tendon in the extracorporeal shunt model in cats. In addition, TFC-612 (1 mg/kg, po) inhibited the adhesiveness of guinea-pig platelets to a glass bead column ex vivo. TFC-612 increased cyclic AMP (cAMP) levels in rabbit platelets. Thus, the anti-platelet action of TFC-612 may be due to an increase in cAMP levels. These results indicate that TFC-612 might be an orally active anti-thrombotic drug.
Administration, Oral↗
Triggering of the vascular permeability reaction by activation of the Hageman factor-prekallikrein system by house dust mite proteinase.
A 30-kilodalton (kDa) proteinase from the house dust mite Dermatophagoides farinae (Df-proteinase) was recently purified (Takahashi et al. (1990) Int. Arch. Allergy Appl. Immunol. 91, 80-85). In this paper we detailed the biological activities of the Df-proteinase. The activation of the kinin cascade by Df-proteinase was examined in vitro by using purified guinea pig Hageman factor (HF), prekallikrein (PK) and high-molecular-weight kininogen (HMWK) and the effect of this proteinase on endogenous human plasma proteinase inhibitors (serpins) and alpha 2-macroglobulin was tested. In addition, enhancement of the vascular permeability reaction in guinea pig skin by Df-proteinase was examined in vivo. These experiments showed that Df-proteinase could activate all the steps of the kinin-generating cascade, i.e., HF, PK and HMWK, and that Df-proteinase retained proteolytic activity even in the presence of an excess amount of endogenous proteinase inhibitors in plasma. We also found that the marked enhancement of the vascular permeability reaction was induced by Df-proteinase via the activation of the kinin-generating cascade without the release of histamine. From these results, we conclude that the proteinase of the house dust mite, Df-proteinase, has the potential to generate bradykinin and that the presence of this proteinase in biological systems would exacerbate inflammatory reactions in some pathological conditions.
Animals↗
Cloning of the cDNA encoding human skeletal-muscle fatty-acid-binding protein, its peptide sequence and chromosomal localization.
A cDNA clone for the human skeletal-muscle fatty-acid-binding protein (FABP) was isolated by screening of a human adult muscle lambda gt11 expression library with an anti-(muscle FABP) serum. The identify of the clone was confirmed by transcription/translation in vitro in plasmid pSP6.5, followed by immunoprecipitation. The nucleotide sequence of the 551 bp cDNA insert showed an open reading frame of 399 nucleotides, coding for a protein of 133 amino acid residues with a calculated molecular mass of 14858 Da and a pI of 4.94. Only one cysteine residue was found, at position 125. Peptide sequence analyses of human skeletal-muscle and heart FABP, after carbamoylmethylation and lysyl endopeptidase digestion followed by automatic Edman degradation, showed that both proteins are identical. No evidence was found for the existence of isoproteins in muscle. The chromosomal localization of the human muscle FABP gene was determined by analysing 31 human x rodent somatic-cell hybrid lines. The human muscle FABP gene could be assigned to chromosome 1pter-q31.
Adult↗
Stimulation of biosynthesis of nerve growth factor by acidic fibroblast growth factor in cultured mouse astrocytes.
Bovine acidic and basic fibroblast growth factors (aFGF and bFGF) dose-dependently stimulated the release of nerve growth factor (NGF) in a culture medium of mouse astrocytes. The NGF concentration in the medium started to increase compared to that of the control cultures 4 h later and was further sustained for 24 h when aFGF was contained. The content of NGF mRNA in the astrocytes treated with aFGF peaked at eightfold over the control level after 4 h. The astrocytes did not proliferate until after 72 h when treated with FGFs under the conditions employed. These results indicate that aFGF stimulates the biosynthesis of NGF in cultured astrocytes without promoting cell proliferation.
Animals↗