Search PubMed⌕ Search

Biomedical subjects

K Okada

Publications and source records attributed to K Okada.

At least 631 records · Page 35Linked to original sources

Early disease progression after intravesical bacillus Calmette-Guérin (BCG) therapy for superficial bladder cancer.

BACKGROUND: Disease progression after Bacillus Calmette-Guérin (BCG) instillation therapy for bladder cancer is not rare. The purpose of this study was to evaluate the outcome of patients treated with BCG for superficial bladder cancer, focusing on the patients who developed invasive disease during follow-up. The possible mechanism and risk factors for early progression after BCG therapy are discussed. METHODS: A total of 25 patients with superficial bladder cancer (pTa, pT1 and/or pTis) were treated with intravesical BCG instillation (80 mg in 80 ml saline) once a week for eight weeks. Four of the 25 patients received maintenance therapy with BCG (once a month for 3 to 10 months). Patients were followed every three months and underwent cystoscopy, biopsy, and urinary cytology at these intervals. Disease progression was defined as invasion to muscle or prostate, or development of metastatic disease. Clinicopathological features of the patients, especially those with progression, were analyzed. RESULTS: Progression was observed in six of the 25 patients, (including four of 19 patients with carcinoma in situ and two of five patients treated prophylactically with BCG). The average time to progression was 8.7 months. Four patients died of cancer despite intensive treatment. Two patients are alive: one without evidence of disease after cystectomy and the other with metastatic disease. CONCLUSIONS: Proper patient selection, careful follow-up, and immediate aggressive therapy in case of progression were considered to be important factors to obtain satisfactory results with BCG therapy for bladder cancer.

Adult↗

Vitamin K prophylaxis to prevent neonatal vitamin K deficient intracranial haemorrhage in Shizuoka prefecture.

OBJECTIVE: To compare three methods of vitamin K prophylaxis for neonatal vitamin K deficient intracranial haemorrhage. DESIGN: We designed three strategies for vitamin K prophylaxis: 1. therapeutic administration of vitamin K in a mass screening system using the hepaplastin test; 2. routine oral administration of vitamin K to newborn infants; and 3. administration of vitamin K to lactating mothers during the late neonatal period in addition to the routine method. We evaluated the efficacy of these methods by determining hepaplastin test values at the first month of age. POPULATION: 66,076 full term healthy newborn infants without any complications. RESULTS: Of 55,513 infants in the mass screening system, 3068 infants received vitamin K therapeutically. At the first month of age, in the group where vitamin K was administered therapeutically, 56 infants (1.83%) exhibited low hepaplastin test values (< 40%) despite vitamin K administration. But extremely low values (< 20%), indicating a very high risk of neonatal intracranial haemorrhage, were observed in 34 (0.06%) of 52,445 infants who did not receive vitamin K. In the routine administration system, oral administration of vitamin K twice within the first week of life showed a lower incidence (0.19%) of low level cases than a single administration (1.56%). An additional administration of vitamin K to lactating mothers throughout the late neonatal period showed an effective result.

Administration, Oral↗

Ubiquinone systems of the genus Cladosporium and morphologically similar taxa.

The ubiquinone (coenzyme Q) systems of 14 species of Cladosporium were determined. The genus was divided into two groups based on the distribution of the major ubiquinones, Q-10 and Q-10(H2). The group containing Q-10 consisted of six species, four of which were human pathogens, whereas the group containing Q-10(H2) consisted of eight plant pathogenic and/or saprophytic species. The results presented here agree with phylogenetic and physiological studies which have shown that the human-pathogenic species of Cladosporium represent a homogeneous, cohesive group.

Cladosporium↗

Characterization of spirochetes isolated from ticks (Ixodes tanuki, Ixodes turdus, and Ixodes columnae) and comparison of the sequences with those of Borrelia burgdorferi sensu lato strains.

Ixodes persulcatus serves as a tick vector for Borrelia garinii and Borrelia afzelii in Japan; however, unidentified spirochetes have been isolated from other species of ticks. In this study, 13 isolates from ticks (6 from Ixodes tanuki, 6 from Ixodes turdus, and 1 from Ixodes columnae) and 3 isolates from voles (Clethrionomys rufocanus) were characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, rRNA gene restriction fragment length polymorphism, partial sequencing of the outer surface protein C (OspC) gene, whole DNA-DNA hybridization, and 16S rRNA gene sequence comparison. All of the results revealed that these Borrelia strains clearly represent at least two new species. A third is also likely, although additional strains have to be isolated and characterized before a separate species is designated. We designated all isolates of I. tanuki and C. rufocanus as group Hk501 and all isolates of I. turdus as group Ya501. Phylogenetic analysis based on 16S rRNA gene sequences distinguished these Borrelia strains from those belonging to hitherto known Borrelia species. Furthermore, the genomic groups, each with its own tick vectors with enzootic cycles, were quite different from each other and also from those of Lyme disease Borrelia species known to occur in Japan. The results of 16S rRNA gene sequence comparison suggest that the strain Am501 from I. columnae is related to group Hk501, although its level of DNA relatedness is less than 70%.

Amino Acid Sequence↗

A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism.

A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism, presenting severe hyponatremia, is described. A 57-year-old man complaining of nausea, vomiting and fatigability was admitted to our hospital because of hyponatremia (114 mEq/I). The low levels of serum cortisol and urinary 17-OHCS suggested glucocorticoid deficiency, and that the glucocorticoid deficiency was due to isolated ACTH deficiency was confirmed by a continuous ACTH loading test and pituitary gland stimulation tests. Although the low level of serum sodium was normalized after the administration of cortisone acetate (50 mg/day) combined with an increase in oral salt intake, urinary sodium loss persisted by the results of hypertonic saline infusion test. Treatment led to improvement of impairment of water diuresis due to hypersecretion of ADH. Hyporeninemic hypoaldosteronism persisted after treatment. We have shown that severe hyponatremia that occurs with combined deficiency of glucocorticoids and mineralocorticoids can be corrected with high salt intake and glucocorticoid replacement without correcting mineralocorticoid deficiency.

Adrenocorticotropic Hormone↗

Effect of FK 506 administered topically versus intramuscularly on suppression of the corneal immune reaction in rats.

The immunosuppressive effect of FK 506 on penetrating keratoplasty in rats was evaluated following intramuscular and topical administration. Implanted corneal grafts were inspected weekly by clinical evaluation for 3 weeks. Cytotoxic T lymphocyte (CTL) activity was measured in the spleen on postoperative day 21, and the grafts were examined histologically. A dose of FK 506, 0.1 mg/kg given intramuscularly, only moderately suppressed CTL activity and the graft failed. In contrast, doses of either 0.024 mg/day topically or 0.3 mg/kg intramuscularly suppressed CTL activity and the grafts remained intact. Results suggest that FK 506 administered topically would be effective in preventing failure of human corneal grafts.

Administration, Topical↗

Improvement of atherosclerosis and stiffness of the thoracic descending aorta with cholesterol-lowering therapies in familial hypercholesterolemia.

The thoracic aorta is frequently involved in atherosclerotic lesions associated with familial hypercholesterolemia (FH). Transesophageal echocardiography (TEE) allows quantitative evaluation of the wall properties of the thoracic aorta. Using TEE, we tested whether atherosclerosis of the thoracic aorta in FH could be improved by cholesterol-lowering therapies. The subjects investigated were 22 FH patients and 22 age-matched normal subjects. The descending aorta (DA) was divided into four longitudinal portions of equal length. Atheromatous lesions of each portion of the DA were scored by character and extension of lesions by biplane two-dimensional TEE. The scores of atheromatous lesions from all four portions of the DA were added together to give the total atheromatous score (TAS). We also measured instantaneous dimensional changes of the DA in a cardiac cycle by M-mode TEE and blood pressure by a cuff method and calculated the stiffness parameter beta (In[SBP/DBP]/[Dmax-Dmin]/Dmin), where SBP is the systolic arterial blood pressure, DBP is the diastolic arterial blood pressure, Dmax is the maximum aortic dimension during the ejection period, and Dmin is the minimum aortic dimension during the preejection period. TAS was higher in FH (3.70 +/- 1.32) than normal (0.62 +/- 0.54, P < .0001) subjects. Beta in FH (10.35 +/- 4.87) was greater than in normal (5.10 +/- 1.25, P < .0001) subjects, but there were no significant differences of DA dimensions between the groups. In both normal subjects and FH patients, beta correlated with age (r = .52, P < .02 and r = .59, P < .005, respectively). In FH patients, beta and TAS correlated well with pretreatment total cholesterol levels (r = .43, P < .05 and r = .60, P < .005, respectively). In 12 of 22 FH patients, strict cholesterol-lowering therapies with diet and cholesterol-lowering drugs (pravastatin and probucol) were undertaken for 13 months. Cholesterol levels were significantly decreased from 333 +/- 45 to 219 +/- 39 mg/dL (P < .0001); this was associated with significant decreases in beta and TAS (from 9.88 +/- 5.03 to 7.88 +/- 3.92, P < .005, and from 3.61 +/- 1.50 to 2.94 +/- 1.22, P < .0005, respectively). In FH patients, the incidence and severity of morphological and physiological atherosclerosis of the DA were significantly higher than in age-matched normal subjects. A significant regression of atherosclerosis was achieved by strict cholesterol-lowering therapies in relatively young FH patients.

Adult↗

Effect of the 21-aminosteroid U-74006F on antigen-induced bronchoconstriction and bronchoalveolar eosinophilia in allergic sheep.

U-74006F, a non-glucocorticoid 21-aminosteroid, has been developed as an inhibitor of iron-dependent lipid peroxidation. This class of compounds has been shown to prevent antigen-induced eosinophil accumulation in the lungs. In this study, Ascaris-sensitive, "dual-respondent" sheep (showing both immediate (IAR) and late (LAR) asthmatic response) (n = 6) were used to assess the effect of U-74006F on antigen-induced bronchoconstriction and airway inflammation and reactivity 8 h after antigen challenge. Antigen provocation induced dual-phase bronchoconstriction, bronchoalveolar eosinophilia and airway hyperreactivity (AHR) to methacholine. Throughout the experiment, intravenous administration of the drug significantly reduced the IAR and inhibited the LAR along with the inhibition of eosinophil influx, but did not inhibit the increase in airway reactivity observed 8 h after antigen challenge. Post-antigen challenge treatment with U-74006 from 3 h after antigen challenge also significantly reduced the LAR and bronchoalveolar eosinophilia, although the degree of inhibitory effect was milder. The development of the LAR appeared to be dependent on eosinophil recruitment into the lungs. These findings suggest that lipid peroxidation is involved in antigen-induced bronchoconstriction and eosinophil recruitment into the lungs, and that the inhibitor U-74006F may be an effective drug for the treatment of bronchoconstriction and airway inflammation characterized by eosinophil infiltration in asthmatics.

Allergens↗

Intracerebroventricular administration of the growth hormone-releasing peptide KP-102 increases food intake in free-feeding rats.

Recent evidence suggests that growth hormone-releasing peptides (GHRPs) mimic an unidentified native GH-releasing hormone (GHRH)-amplifying hormone. GHRH has been shown to stimulate food intake acting on the central nervous system. The present studies were conducted to test the hypothesis that GHRPs may also potentiate the central effect of GHRH on feeding in free-feeding rats. Intracerebroventricular (ICV) administration of picomole doses of a newly developed GHRP, KP-102, or human GHRH stimulated feeding, but the phenomenon was not reproduced by systemic injection. A prior ICV injection of a GHRH antagonist completely prevented the increase of food intake evoked by GHRH, but this pretreatment did not influence the increase in food intake induced by KP-102. When maximally effective doses of GHRH and KP-102 were co-administered ICV, the amount of food intake increased significantly compared with after ICV injection of a maximum dose of either peptide alone. These findings suggest that GHRPs stimulate food intake via a specific receptor for GHRPs in the central nervous system and amplify the central effect of GHRH on feeding.

Animals↗

Isolation and identification of styrene-degrading Corynebacterium strains, and their styrene metabolism.

By supplying styrene in the gas phase as the sole carbon and energy source, styrene-degrading aerobic microorganisms were readily isolated from soil samples. They were identified as Corynebacterium pseudodiphtheriticum and similar species, or Pseudomonas sp. Growth experiments on some aromatic compounds, resting-cell reactions with them, and the measurement of degrading enzyme activities suggest that Corynebacterium sp. AC-5 and St-5 strains metabolize styrene through styrene oxidation into styrene oxide, then convert it into phenylacetaldehyde by a reaction using styrene oxide isomerase, and phenylacetaldehyde is reduced to 2-phenylethanol. The Corynebacterium sp. ST-10 strain did not have styrene oxide isomerase, and metabolized styrene oxide by an unknown enzymatic reaction. Possible metabolism of styrene was proposed for the Corynebacterium strains.

Biodegradation, Environmental↗

Inhibition by adrenomedullin of arginine vasopressin-activated mitogen-activated protein kinase in rat glomerular mesangial cells via cAMP production.

The present study was undertaken to determine whether adrenomedullin modulates the arginine vasopressin (AVP)-activated mitogen-activated protein (MAP) kinase in cultured rat glomerular mesangial cells. AVP dose-dependently increased cellular free calcium, and this increase was unaffected by adrenomedullin. Adrenomedullin increased cellular cAMP production in a dose-dependent manner and AVP activated MAP kinase in a dose-dependent manner. When cells were preincubated for 15 min with adrenomedullin at concentrations of 1 X 10(-8) M or higher, the AVP-activated MAP kinase was significantly reduced. In addition, the activation of MAP kinase by phorbol-12-myristate-13-acetate (PMA) was significantly inhibited by adrenomedullin. Similarly, forskolin also diminished the activation of MAP kinase by AVP and PMA. The inhibition by adrenomedullin or forskolin of AVP-activated MAP kinase disappeared when cells were preexposed to H-89, an inhibitor of protein kinase A. These results indicate that adrenomedullin inhibits the AVP activation of MAP kinase mediated through cAMP in glomerular mesangial cells and that the site of action of adrenomedullin is behind the site of activation of protein kinase C.

Adrenomedullin↗

Inhibitory effect of BQ-123 on endothelin-1-stimulated mitogen-activated protein kinase and cell growth of rat vascular smooth muscle cells.

Studies have suggested that endothelin-1 (ET-1) activates cellular contraction and proliferation in rat vascular smooth muscle cells (VSMC). We examined whether an ET(A) receptor antagonist, BQ-123, inhibits the following cellular actions of ET-1 in rat VSMC: cytosolic free calcium ([Ca2+]i) mobilization, cellular contraction, mitogen-activated protein (MAP) kinase activation, [3H]thymidine incorporation, and MTT reduction. [Ca2+]i was measured by the fluorescent method. MAP kinase activity was measured by the phosphorylation of a synthetic peptide of a specific substrate for MAP kinase. The specificity of BQ-123 for ET-1-activated MAP kinase was checked by Western blotting analysis. [3H]thymidine incorporation and MTT reduction studies were performed using the cells incubated for 12 h with serum-free medium containing effectors. BQ-123 inhibited ET-1 receptor binding and blocked [Ca2+]i mobilization, cellular contraction, MAP kinase activation, [3H]thymidine incorporation, and MTT reduction in response to ET-1. BQ-123 did not affect the arginine vasopressin (AVP)- and angiotensin II (Ang II)-induced increases in [Ca2+]i mobilization or in MAP kinase activity. Preincubation with BQ-123 did not enhance its inhibitory effects but these effects of BQ-123 were diminished by washing after preincubation. Receptor studies revealed that the washing procedure decreased the inhibitory effect of BQ-123 on ET-1 binding to receptors. These results indicate that BQ-123 is a potent and specific ET(A) receptor antagonist that blocks the ET-1-induced cellular contraction and proliferation in rat VSMC.

Angiotensin II↗

The proto-oncogene c-myb is expressed in sporadic bovine lymphoma, but not in enzootic bovine leukosis.

We examined bovine c-myb gene expression in six samples of sporadic bovine lymphomas (two calf, three thymic and one intermediate) and five of enzootic bovine leukosis. Tumor cells of the sporadic bovine lymphomas were of immature cell lineage (one B lymphoma and five T lymphomas). The c-myb mRNA was expressed in almost all the sporadic bovine lymphomas (except for one thymic form) including a BoCD8 single positive T lymphoma. On the contrary, c-myb was not expressed in mature B lymphomas of enzootic bovine leukosis. The results suggest that c-myb expression is closely associated with tumor cell differentiation of bovine lymphomas.

Animals↗

Immunohistological evaluation on respiratory lesions of pigs intranasally inoculated with Actinobacillus pleuropneumoniae serotype 1.

Nine-week-old pigs were inoculated intranasally with 6.10 X 10(3) (group 10(3)), 10(5) (group 10(5)) and 10(7) (group 10(7)) colony-forming unit of Actinobacillus pleuropneumoniae (App) serotype 1 designated HA-337 strain, respectively. One pig in group 10(5) and 2 pigs in group 10(7) died with dispnea and hemorrhagic pleuropneumonia within 20 to 48 hr post inoculation (PI). All pigs necropsied on 7 days in groups 10(5) and 10(7) had focal fibrous pleuropneumonia. Histologically, pulmonary lesions were classified into three stages; peracute, acute and subacute. Fatal cases in group 10(7) had peracute lesion composed of severe edema, hemorrhage and necrobiosis of alveoli, with mononuclear cells infiltration in the dilated interlobulus. The fatal case in group 10(5) had acute pulmonary lesion composed of focal or linear infiltration of round and fusiform cells that frequently showed swirling pattern in alveoli. The surviving cases in group 10(5) and 10(7) had subacute lesion composed of multifocal pulmonary necrosis surrounded by fibrous tissue. The swirling pattern was clearly seen in demarcation zone. Immunohistochemically, App antigens scattered as intact bacteria in alveoli, dilated interlobular septa and pleura, and lymph vessels in peracute and acute lesions. Areas of necrosis were also stained weakly. Although no antigen was detected in cytoplasm of macrophages and infiltrated cells in peracute lesions, App antigen was detected as positively stained mass in cytoplasm of some macrophages in acute lesions. In subacute lesions, App antigens were recognized as intact bacteria in necrotic areas and among the swirling pattern cells of demarcation zone. Macrophages had App antigens as a large mass of pigment in the cytoplasm in area of fibrosis.

Actinobacillus Infections↗

Inhibition of collagen-induced platelet aggregation in Japanese black cattle with inherited platelet disorder, Chediak-Higashi syndrome.

Aggregation properties of platelets were examined in Japanese Black cattle with Chediak-Higashi syndrome (CHS) and normal control cattle. Platelet aggregation induced by collagen was decreased in platelets of the cattle with CHS, but not ADP (10-20 microM), thrombin (0.5-1.0 U/ml) and phorbol-12-myristate 13-acetate (PMA, 3.2 microM). The aggregation response induced by collagen in CHS platelets lacks the change in shape which usually occurs in normal platelets. Simultaneous stimulation by collagen (10 micrograms/ml) + ADP (10 microM) is effective in restoring collagen-induced aggregating response in CHS platelet, although pretreatment of ADP (10 microM) could not restore the collagen (10 micrograms/ml)-induced aggregating response, suggesting that there is a certain threshold of stimulation intensity above which collagen-induced aggregation of CHS platelet can begin. Control normal platelets, previously exposed to ADP (10 microM) and collagen (10 micrograms/ml), showed no further response to exposure to a third aggregating agent (arachidonic acid, 5 mM). On the other hand, the final agent was able to elicit aggregating responses in CHS platelets, suggesting that the arachidonate aggregating system may be suppressed in CHS cattle, but fully activated in control animals. Furthermore, normal platelets showed a significant decrease in aggregating response to collagen when pretreated with a cyclooxygenase inhibitor, indomethacin (10(-5) M), whereas CHS platelet was insensitive to indomethacin. This indomethacin-treated normal platelet mimicked the CHS collagen-induced aggregation pattern. These data suggest that a signal transduction process from receptor-operated events to arachidonate metabolism is suppressed in collagen-induced CHS platelet aggregation.

Adenosine Diphosphate↗

Involvement of arginine vasopressin and renal sodium handling in pathogenesis of hyponatremia in elderly patients.

The present study was undertaken to determine the pathophysiological role of arginine vasopressin (AVP) in elderly patients with hyponatremia, and the efficacy of fludrocortisone acetate in treating their hyponatremia. Eleven hospitalized patients aged 65 years or older whose serum sodium levels were less than 130 mEq/l were examined. The hyponatremic patients included two groups of patients: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and central salt-wasting syndrome. And 24 healthy, young subjects aged 20 to 34 years, and 24 healthy, elderly subjects age 65 to 80 years were recruited by community announcement. The elderly subjects had decreased urinary concentrating ability and exaggerated response of AVP secretion to osmotic and nonosmotic stimuli, as compared to the young subjects. All the patients had hyponatremia, with the exaggerated urinary loss of Na. Plasma AVP levels were elevated despite hypoosmolality in all the 2 groups of hyponatremic, elderly patients. Plasma renin activity and plasma aldosterone concentrations were low in the patients with SIADH and central salt-wasting syndrome. Fludrocortisone acetate therapy was effective in the patients with central salt-wasting syndrome and 3 patients with SIADH whose hyponatremia remained unchanged after water restriction. Water restriction therapy normalized serum Na levels in only 3 patients with SIADH. These results indicate that AVP is involved in the mechanism for hyponatremia in the elderly patients with SIADH and central salt-wasting syndrome. Severe hyponatremia associated with SIADH and central salt-wasting syndrome responds well to mineralocorticoid therapy. Both the secretion of AVP and renal sodium handling may be involved in the mechanism of action of the disorders. The diagnostic criteria for SIADH in the elderly patients may have to be reevaluated and should be considered to indicate fludrocortisone acetate therapy.

Adult↗