Painful unfused separate ossification center of the ulnar styloid: a case report.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
J Ishikawa
Publications and source records attributed to J Ishikawa.
Strong-field effects in coherent saturation spectroscopy of atomic beams.
Explore the source record for details and available documents.
Journal Article↗
Involvement of apamin-sensitive K+ channels in antigen-induced spasm of guinea-pig isolated trachea.
1. In order to examine whether K+ channels play a role in antigen-induced airway responses, the effect of K+ channel blockers on antigen-induced airway smooth muscle contraction and mediator release was examined in vitro in guinea-pigs actively sensitized with ovalbumin (OA). 2. Tracheal strips from sensitized animals were suspended in organ baths under a resting tension of 1 g and isometric tension was continuously measured. Cumulative concentration-response curves to OA (0.1-1000 ng ml-1) or histamine (10 nM-1 mM) were obtained in the presence and absence of K+ channel blockers. 3. OA (10, 100 or 1000 ng ml-1) was incubated with minced lung tissues from the same animals for 15 min in the presence and absence of K+ channel blockers, and released histamine and leukotriene C4 (LTC4) in the incubating medium were measured. 4. Apamin, a small conductance Ca(2+)-activated K+ channel (PK,Ca) blocker, (0.1, 0.3 and 1 microM) significantly inhibited OA-induced smooth muscle contraction, while charybdotoxin (ChTX, 10 nM), an intermediate and large conductance PK,Ca blocker, and iberiotoxin (IbTX, 3 nM), a large conductance PK,Ca blocker, were without effect. Apamin (0.3 microM) had no effect on exogenously administered histamine-induced airway smooth muscle contraction, suggesting that the inhibition of OA-induced contraction by apamin did not occur at the smooth muscle level. 5. The inhibition of OA-induced contraction by apamin (0.3 microM) was not significantly affected by pretreatment with a leukotriene antagonist, ONO-1078 (10 microM), but was abolished by pretreatment with a histamine H1-receptor blocker, pyrilamine (1 microM). 6. Apamin by itself (up to 0.1 MicroM) had no effect on spontaneous histamine release from minced lung tissues. Histamine release induced by low and intermediate concentrations of OA (10 and 100 ng ml-1)was significantly suppressed by apamin pretreatment (P<0.05 and P<0.001), whereas LTC4 release was not affected. ChTX (0.1 MicroM) and IbTX (10 nM) had no significant effect on either spontaneous or OA (100 ng ml-1)-induced histamine release.7. These results suggest that apamin partially but substantially inhibits antigen-induced smooth muscle contraction, presumably by inhibiting antigen-induced histamine release from airway mast cells through small conductance PKca closure.
Animals↗
Antigen-induced airway responses are inhibited by a potassium channel opener.
We have investigated the effect of a potassium channel opener, BRL 38227, on antigen-induced bronchoconstriction and airway microvascular leakage in sensitized guinea pigs by simultaneously measuring pulmonary resistance (Rl) and extravasation of Evans blue dye. Guinea pigs were sensitized 3 wk before experimentation with ovalbumin (OA) and aluminum hydroxide. The trachea was cannulated, and lungs were mechanically ventilated. All animals were pretreated 30 min before experimentation with atropine (1 mg/kg intravenously) and propranolol 1 mg/kg to block muscarinic and beta-adrenergic responses, respectively. BRL 38227 (200 micrograms/kg) was administered intravenously 1 min before intravenous dye injection (30 mg/kg); OA (3 mg/ml) was inhaled using an ultrasonic nebulizer (for 30 s) 1 min after dye injection. BRL 38227 significantly inhibited OA-induced bronchoconstrictor response (p < 0.01) and plasma leakage in trachea (p < 0.05) and main bronchi (p < 0.05). BRL 38227 also had an inhibitory effect on exogenous histamine- and leukotriene-induced bronchoconstriction and microvascular leakage. However, BRL 38227 did not affect OA-induced histamine release from minced lung tissues in sensitized guinea pigs. We conclude that the allergic bronchoconstrictor response and airway plasma leakage are inhibited by a potassium channel opener, possibly as a result of its effect on the airway smooth muscle and the postcapillary venule level.
Administration, Inhalation↗
Potassium channel opener, YM 934, inhibits neurogenic plasma leakage in guinea pig airways.
The effect of a potassium channel opener, YM 934, on neurogenic airway plasma leakage was examined in anesthetized guinea pigs. Airway plasma leakage was evoked by stimulation of both vagal nerves in the presence of atropine (1 mg/kg, intravenous) and propranolol (1 mg/kg, intravenous), and was measured by extravasation of Evans blue dye (30 mg/kg, intravenous) in trachea (Tr), main bronchi (MB), and central (cIPA) and peripheral intrapulmonary airways (pIPA). Vagal stimulation significantly increased the dye leakage in all portions of the airway. YM 934 (10, 30, and 100 micrograms/kg, intravenous) inhibited vagally-induced plasma leakage in Tr, MB, cIPA, and pIPA, and this inhibitory effect of YM 934 was reduced by the ATP-sensitive potassium channel blocker, glibenclamide (25 mg/kg, intravenous). By contrast, YM 934 (100 micrograms/kg, intravenous) had no inhibitory effect on exogenous substance P (0.5 and 1 micrograms/kg, intravenous)-induced plasma leakage in any parts of the airway. These results indicate that YM 934 inhibits airway neurogenic inflammation by modulating the release of neuropeptides from the sensory nerve endings, and that the inhibitory effect can be attributed to the potassium channel opening activity of this compound.
Animals↗
[Blood volume determination in female SPF rats of Wistar--Imamichi strain by an extrapolation method with radioiodinated rat serum albumin].
The total blood volume of SPF female rats of Wistar-Imamichi strain, a strain that shows a 4-day estrous cycle at very high rates and is widely used in the study of reproductive biology in Japan, was estimated from blood radioactivity after the intravenous administration of 125I-rat serum albumin. The radioactivity of blood showed a rapid decrease until 10 min after injection and a slow decay thereafter. Radioactivity at time zero was estimated by extrapolation from this slow decay curve, and the blood volume was calculated. From 30 rats weighing 150-300 g we obtained the following equation between blood volume (BLV) and body weight (BW), and a high correlation coefficient (r): BLV = 8,4007 + 0.0430 x BW, r2 = 0.92. The blood volume per body weight decreased linearly with increasing body weight, and we obtained the following equation: BLD/100 g BW = 12.25-0.0174 x BW at r2 = 0.92.
Animals↗
[Evaluation of the effects of vibro-acoustic stimulation test on the fetus during labor under epidural analgesia and evidence of its safety by way of auditory brainstem response].
This study was undertaken to elucidate the effects of epidural analgesia on vibro-acoustic stimulation test (VAST) during normal labor and auditory brainstem response (ABR) in fifty full term parturients without any complication. The safety of VAST in relation to the ABR of neonates was also studied. The results were as follows, 1) There were some changes in CTG monitoring in five cases (10%) in the 10 minutes after epidural analgesia. However, these changes were not ominous signs but all related to the coiling of the cord, as previously reported. 2) The ABR latency-intensity curve (audio-function of the newborn infants) revealed no hazardous change in VAST-loaded infants or in the controls. The response threshold was 10dB in this study. The application of VAST to the parturients under epidural analgesia was therefore not only harmless to the fetuses but also a useful way to evaluate fetal well-being.
Acoustic Stimulation↗
Cloning of a canine gene homologous to the human interleukin-8-encoding gene.
We cloned a 2.3-kb sequence homologous to the gene (hIL8) encoding human interleukin-8 (hIL-8) from the canine genome. The sequence may encode an 11.3-kDa protein consisting of 101 amino acids, sharing 75, 80 or 85% identity with the human, rabbit or porcine IL-8 proteins, respectively. Southern and Northern blot analyses indicated that the cloned sequence appeared to exist as a single copy in the canine genome, and that its expression was inducible with lipopolysaccharide in canine mononuclear cells, respectively. Thus, it seems very likely that the cloned gene is a canine homologue of hIL8.
Amino Acid Sequence↗
Neuropeptide Y inhibits neurogenic inflammation in guinea pig airways.
We examined the effect of neuropeptide Y (NPY) on neurogenic airway microvascular leakage. Male Dunkin-Hartley guinea pigs (250-350 g) were anesthetized with urethan (2 g/kg ip). The cervical artery and vein were cannulated for monitoring blood pressure and injecting drugs, respectively. Atropine and propranolol (each 1 mg/kg i.v.) were administered 30 min before the experiment. After pretreatment with saline (vehicle for NPY) or NPY (1-100 micrograms/kg i.v.), Evans blue dye (30 mg/kg iv) was administered. Then, bilateral vagal nerves were electrically stimulated (5 V, 7 Hz, 5-ms duration for 3 min) to induce airway plasma leakage. Airways were divided into four sections [trachea (Tr), main bronchi, central intrapulmonary airways (IPA), and peripheral IPA] and incubated in formamide (37 degrees C for 16 h). The concentration of Evans blue dye was measured by spectrophotometer. Furthermore, we examined the effect of NPY on exogenous substance P- (0.3 microgram/kg i.v.) induced plasma extravasation. Bilateral vagal stimulation significantly increased leakage of dye in Tr to peripheral IPA. NPY did not affect basal leakage but did significantly inhibit neurogenic plasma extravasation in a dose-dependent manner with maximal inhibitions of 42.3 (Tr), 67.7 (main bronchi), 38.2 (central IPA), and 26.3% (peripheral IPA) at 30 micrograms/kg. Exogenous substance P-induced plasma extravasation was not inhibited by NPY. We conclude that NPY inhibits neurogenic inflammation by prejunctional inhibition of neuropeptide release from airway sensory nerve terminals.
Adrenergic beta-Antagonists↗
[Clinical study of S-1108 fine granule in the pediatric field].
S-1108 in a fine granular form was administered in 14 children and its safety and efficacy in bacterial infections were evaluated. Among them, 2 cases of cystitis and 1 case of pneumonia were considered unevaluable for the efficacy. The results obtained are summarized as follows. 1. The overall clinical efficacy rate was 81.8% in the eleven evaluable cases treated with S-1108 fine granules including 5 cases of pharyngitis, 2 cases each of tonsillitis, pertussis and cystitis. 2. Bacteriological efficacy of 100% was achieved against pathogens identified in 5 children including 1 case each of Staphylococcus aureus, Streptococcus pyogenes and Haemophilus influenzae and 2 cases of Escherichia coli. 3. The only abnormal laboratory test results observed were eosinophilia and leukocytopenia in one case each. Diarrhea was recorded in 1 case. Judging from the above results, it appears that S-1108 in the fine granular form is an effective, useful and safe antibiotic of first choice for the treatment of infections in the pediatric field.
Administration, Oral↗
Human bone marrow stromal cell lines from myeloma and rheumatoid arthritis that can support murine pre-B cell growth.
In order to elucidate the pathologic significance of the bone marrow (BM) microenvironment in multiple myeloma (MM) and rheumatoid arthritis (RA), we established patient- or healthy donor (HD)-derived BM stromal cell lines by transfecting the plasmid for expression of SV40 large T Ag and examined their ability to support the stromal cell-dependent growth of a pre-B cell line, DW34. The means of recovered cell numbers of DW34 co-cultured with MM- and RA-derived BM stromal cell lines ranged from 6- to 10-fold more than those with HD-derived ones. Their enhanced ability to support DW34 cell growth was not caused by cytokines, including IL-6, IL-7, and c-kit ligand, although exogenous IL-7 could augment the growth-supporting ability. DW34 cell growth on the stromal cell lines was abolished by inhibiting cell-to-cell interaction with a membrane filter. FACS analysis revealed that the stromal cell lines did not express LFA-1 alpha, beta, NCAM, or ELAM-1. Both patient and HD BM stromal cell lines variably expressed ICAM-1, VCAM-1, and CD44. However, surface expression levels of these molecules did not correlate with the ability of the stromal cell lines to support DW34 cell growth. Taken together, these results suggested that BM microenvironment might play important roles in the pathogenesis of MM and RA.
Animals↗
Secondary aminoglycoside resistance in aminoglycoside-producing strains of Streptomyces.
The role of aminoglycoside (AG) acetyltransferases (AACs) and of the corresponding genes in resistance to foreign AGs in AG-producing strains of Streptomyces were studied. The research focussed on (i) the activation mechanism of the cryptic kanamycin(Km)-resistance-encoding gene that encodes an AAC(3) in streptomycin-producing S. griseus SS-1198, and (ii) an AAC(2') with novel activity and substrate specificity in kasugamycin-producing S. kasugaensis MB273. Activation of the cryptic kan gene in S. griseus SS-1198 is probably due to a single base substitution at the putative -10 promoter region, leading to the enhancement of transcription, resulting in resistance to AG. The coding region of the kan gene was highly homologous to that of the aacC7 gene of paromomycin-producing S. rimosus forma paromomycinus. On the other hand, resistance in S. kasugaensis MB273 was found to be due to an AAC(2') capable of acetylating astromicin group AGs at two different sites (1-NH2 with istamycin B, and 2'-NH2 with astromicin and istamycin A). These additional antibiotic resistances that are independent of a self-resistance basis may be regarded as 'secondary' resistances, so as to distinguish them from 'primary' resistances arising from a self-resistance basis.
Aminoglycosides↗
Luteinizing hormone requirements for ovulation in the rat.
Luteinizing hormone requirements for ovulation induction were studied in proestrous rats through detailed observation of the preovulatory surge, through various forms of LH injection under sodium pentobarbital blockade, and through estimation of LH uptake by the ovary. Blood LH levels in individual proestrous rats were obtained every 30 min and grouped according to their peak time (designated 0 h); mean LH levels higher than 7 and 5 ng/ml continued for 30 min and 2.5 h, respectively, the pituitary LH contents at 1400 and 2000 h on the day of proestrus were 2.1 and 0.7 micrograms, respectively, indicating that the amount of LH secreted during the surge was at least 1.4 micrograms. Single intravenous injections of 2 micrograms and 1 micrograms of pure rat LH (NIDDK-rLH-I-7; FSH and prolactin contaminations: 0.02% and less than 0.01%, respectively) to sodium pentobarbital-blocked rats induced ovulation in 4 out of 4 rats and 4 out of 6 rats, respectively, while 500 ng failed to induce ovulation in any (out of 7) rats. Two injections of 300 ng each with an interval of 20 min induced ovulation in 3 out of 8 rats, but if the interval was prolonged to between 30 and 120 min, 100% ovulation was obtained. Blood LH levels in these experiments indicated that a lower long-lasting LH level (about 5 ng/ml blood) is more important than a short, high level for ovulation induction. It was also shown that this level of LH could be given in separate doses if the interval was 30-120 min.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Recurrent intracranial germinoma refractory to conventional irradiation: effective chemotherapy consisting of cisplatin and etoposide--case report.
Recurrent intracranial germinoma with multiple spinal metastases occurred in a 16-year-old male presenting with persistent headache and visual disturbances. Computed tomography revealed enhanced lesions in the pineal region, anterior horn, and infundibulum. Conventional irradiation achieved remission, but local recurrences requiring further irradiation occurred after 23 months. Magnetic resonance imaging showed multiple spinal metastases 11 months later. Partial removal of the spinal lesions gave a histological diagnosis of typical germinoma. Postoperatively, intracranial recurrences were again detected. Chemotherapy consisting of intravenous cisplatin and etoposide achieved remission and no recurrence has occurred for 12 months.
Adolescent↗
[Adjuvant chemotherapy with MVP-CAB (methotrexate, vincristine, cisplatinum, cyclophosphamide, adriamycin and bleomycin) for epithelial tumors of the upper urinary tract].
Surgery plus adjuvant chemotherapy using MVP-CAB (Day 1; methotrexate 20 mg/m2, vincristine 0.6 mg/m2, cyclophosphamide 500 mg/m2, adriamycin 20 mg/m2, and bleomycin 30 mg, Day 2; cisplatinum 50 mg/m2) was conducted in 12 patients with epithelial tumors of the upper urinary tract who had unfavorable prognostic factors (progressive disease which was pT2 or more, or transitional cell carcinoma of grade 2 and 3). The MVP-CAB regimen was as follows: A total of 3 cycles were given either before or after surgery. MVP-CAB was given at 3- to 4-week intervals before surgery, or after surgery if the patient had macroscopic residual lesions. For the patients with micrometastases detected after radical surgery, MVP-CAB was given every 1 to 2 months. The median survival period of the 10 patients who underwent radical surgery was 17 months (5-59 months). The three-year survival rate of these 10 patients (Kaplan-Meier method) was 100% in grade 2 (5 patients), 100% in progressive cancer greater than pT3 (6), and 80% in grade 3 (5). In two patients, residual macroscopic lesions after surgery were confirmed. One of them initially responded to MVP-CAB but died of cancer 21 months later, while the other one did not respond and died of cancer 8 months later. Two renal pelvis cancer patients for whom radical surgery was considered impossible due to distant metastases showed remarkable tumor reduction after MVP-CAB administration (one showed CR for liver metastases and the other showed PR for lymph node metastases).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Nucleotide sequence and transcriptional start point of the kan gene encoding an aminoglycoside 3-N-acetyltransferase from Streptomyces griseus SS-1198PR.
We determined the nucleotide sequence of a 1794-bp BglII-BamHI fragment containing the kan gene (KmR) which encodes a novel aminoglycoside 3-N-acetyltransferase of Streptomyces griseus SS-1198PR. The sequence was found to contain four open reading frames (ORF) in the direction of transcription determined by low resolution S1 nuclease mapping. Except for the largest one, these ORF are unlikely to be the coding sequence of kan, because of their inability to confer kanamycin resistance. The largest ORF could encode a 30.8-kDa protein consisting of 284 amino acids (aa) with 93.3 mol% G + C in the third position of codons, and is preceded by potential ribosome-binding sites. Thus, the largest ORF was likely to represent the kan gene. The transcription start point of kan was located 84 bp upstream from the start codon. The -10 region showed similarity to the Escherichia coli consensus promoter motif, while no sequence similarity was found in the -35 region. The deduced aa sequence of kan showed 85% similarity with that of the aacC7 gene of Streptomyces rimosus forma paromomycinus [Lopez-Cabrera et al., J. Bacteriol. 171 (1989) 321-328] suggesting that these genes are derived from a common ancestral gene.
Acetyltransferases↗
Proliferation of human myeloid leukemia cell line associated with the tyrosine-phosphorylation and activation of the proto-oncogene c-kit product.
We investigated the expression, degree of phosphorylation, and activation of the proto-oncogene c-kit product before and after stimulation with the c-kit ligand in a human factor-dependent myeloid leukemia cell line, MO7E. The culture supernatant of the BALB/3T3 fibroblast cell line, which contains the ligand for the murine c-kit product, was found to stimulate proliferation of the MO7E cell line in a dose-dependent manner. The proliferation was significantly inhibited by a tyrosine kinase inhibitor, genistein. An immunoblot technique with a monoclonal antibody specific for phosphotyrosine, showed that there was rapid, dose-dependent tyrosine-phosphorylation of the c-kit product in response to murine c-kit ligand. Furthermore, the murine c-kit ligand increased autokinase activity of the c-kit product in vitro. Similar results were obtained with human stem cell factor (SCF), a recombinant human ligand for the c-kit product. These results suggest that the phosphorylation and activation of the c-kit product are involved in proliferative signals of some human leukemia cells, as well as of normal hematopoietic cells.
Blotting, Northern↗
Expression and functional role of the proto-oncogene c-kit in acute myeloblastic leukemia cells.
The c-kit proto-oncogene encodes a receptor tyrosine kinase that is thought to play an important role in hematopoiesis. In a series of human acute myeloblastic leukemia (AML), the expression of the c-kit proto-oncogene and its product was studied by means of Northern blot and immunoblot analyses. The c-kit mRNA was expressed in 20 of 25 cases of AML, and in those cases the product of the c-kit proto-oncogene was detected by immunoblotting with anti-c-kit antibody. The expression of c-kit transcripts and protein was barely detectable in normal bone marrow cells as a control. The expression of c-kit transcript did not correlate with the French-American-British classification nor clinical manifestations. In 6 of 11 cases that expressed c-kit product, AML cells were found to proliferate in response to recombinant human stem cell factor (rhSCF), the ligand for c-kit, and the synergistic stimulation of AML cells was observed by rhSCF and granulocyte-macrophage colony-stimulating factor. Immunoblotting with anti-phosphotyrosine antibody showed that the c-kit receptor protein was detectably phosphorylated in 7 of 12 cases tested before the stimulation with rhSCF, while the rhSCF treatment resulted in an increased tyrosine phosphorylation of c-kit in AML cells. These results indicate that c-kit proto-oncogene is expressed in most cases of AML and is functional in terms of supporting proliferation.
Blotting, Northern↗