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Biomedical subjects

K Okada

Publications and source records attributed to K Okada.

At least 1,027 records · Page 57Linked to original sources
PubMed1991

Thoracic myelopathy caused by ossification of the ligamentum flavum. Clinicopathologic study and surgical treatment.

The authors reviewed 14 patients with thoracic myelopathy caused by ossification of the ligamentum flavum (OLF). The predominant locality of symptomatic OLF was at the thoracolumbar junction, particularly at T10-11 followed by T11-12. At the level of the thickest OLF in each patient, there were three types of OLF from computed tomography and operative findings: a lateral type in 3 patients, diffuse in 8, and thickened nodular in 3. The diagnosis of OLF-related thoracic spinal canal stenosis was best made by enhanced computed tomography. Histologic study revealed that the developmental mode of OLF was mainly endochondral ossification. Numerous fibrocartilaginous cells were found in the increased and swollen collagen fibers forming the hypertrophic ligamentum flavum (HLF). Ossification extended along the superficial layer of HLF. The size or extension of OLF was relevant to the corresponding diathesis of spinalhyperostosis. Results of laminectomy for OLF were poor because of the high occurrence of complications early on or later deterioration. Therefore, laminoplasty is recommended as a successful procedure for OLF-related thoracic myelopathy, avoiding further local mechanical stress due to tensile force.

Female↗
PubMed1991

Os odontoideum with posterior atlantoaxial instability.

Nine patients who had os odontoideum with posterior atlantoaxial instability are reviewed. Three parameters were measured on the lateral radiographs: the distance from the os odontoideum to the spinous process of the axis in extension (Dext), the distance from the os odontoideum to the posterior arch of the atlas (Datl), and the degree of instability (Inst). Patients were classified into four groups: Group I, local symptoms (N = 3); Group II, transient myelopathy (N = 0); Group III, progressive myelopathy (N = 6); and Group IV, cerebral symptoms (N = 0). The development of cervical myelopathy was not related to degree of instability but to distance from the os to the spinous process of the axis (Dext). Dext was more than 16 mm in Group I and less than or equal to 16 mm in Group III. Five of six patients in Group III underwent myelography. Based on myelographic findings, Group III was further subdivided into two groups, Group IIIA (N = 2) and Group IIIB (N = 3), according to the following characteristics: In Group IIIA, the distance from the os to the posterior arch of the atlas was more than 13 mm, and the spinal cord was impinged between the os odontoideum and the lamina of the axis in extension and reduced in flexion. In Group IIIB, Datl was less than or equal to 13 mm, and the spinal cord was compressed at the level of the atlas during flexion and extension. Stenotic Datl of 13 mm or less specifically defined severe cervical myelopathy. Surgical treatment for cervical myelopathy in os odontoideum with posterior instability is suggested as follows: in the absence of canal stenosis of the atlas (Group IIIA), atlantoaxial fusion in a reduced position is indicated; when associated with canal stenosis of the atlas (Group IIIB), laminectomy of the atlas followed by occiput-to-C2 arthrodesis is indispensable.

Adolescent↗
PubMed1991

Protective immunity against bovine leukaemia virus (BLV) induced in carrier sheep by inoculation with a vaccinia virus-BLV env recombinant: association with cell-mediated immunity.

The effects of vaccination of sheep with a recombinant vaccinia virus (rVV) expressing the bovine leukaemia virus (BLV) envelope glycoprotein (gp60) were studied by determining BLV titres in peripheral blood leukocytes after vaccination and challenge. The proliferation of BLV was suppressed markedly, not only when rVV was inoculated prior to challenge with BLV, but also when it was inoculated after challenge. These results indicate that vaccination with rVV induces protective immunity that can suppress the growth of BLV in carrier animals. Since rVV induced a strong anti-BLV delayed-type hypersensitivity response without producing detectable levels of binding or neutralizing antibodies, and there was no apparent correlation between the humoral immune response and BLV proliferation, a cell-mediated immune response was assumed to play a major role in protective immunity.

Animals↗
PubMed1991

Potentiation by aldosterone of vasopressin-induced calcium kinetics in vascular smooth muscle cells.

1. The present study was undertaken to examine the effect of aldosterone on arginine vasopressin (AVP)-induced Ca2+ kinetics in cultured rat vascular smooth muscle cells (VSMC). The pre-incubation of cells with 1 x 10(-6) mol/L aldosterone for 24 h did not affect the basal cytosolic free Ca2+ [( Ca2+]i) but enhanced the AVP-induced mobilization of [Ca2+]i (1 x 10(-8) mol/L AVP; 287 vs 401, 1 x 10(-6) mol/L AVP; 430 vs 714 nmol/L). 2. The pre-incubation of cells with 1 x 10(-7) mol/L aldosterone for 24 h did not show this enhancing effect on the AVP-induced mobilization of [Ca2+]i. Without the preincubation, aldosterone did not change the basal [Ca2+]i or the AVP-induced mobilization of [Ca2+]i. This enhancement was still observed in the Ca2+-free solution containing 0.1 mmol/L EGTA (1 x 10(-8) mol/L AVP; 169 vs 341 nmol/L). 3. The enhancement by aldosterone of the AVP-mobilized [Ca2+]i was completely blocked by the simultaneous administration of 1 x 10(-4) mol/L spironolactone (1 x 10(-8) mol/L AVP; 258 vs 265 nmol/L). The treatment with aldosterone also stimulated the AVP-produced [45Ca2+] efflux during a 3 min period (1 x 10(-8) mol/L AVP; 32 vs 49, 1 x 10(-6) mol/L AVP; 50 vs 58% released from the resting intracellular [45Ca2+]-contents). 4. The present results indicate that aldosterone enhances the vascular action of AVP mediated through the stimulation of Ca2+ kinetics which may be dependent on the changes in the cellular signal transduction systems.

Aldosterone↗
PubMed1991

Giant hydroureteronephrosis associated with primary obstructed megaureter.

The case is presented of a four year old boy with a large left abdominal mass. The patient was diagnosed as having a left giant hydroureteronephrosis due to a primary obstructed megaureter, based on the findings of ultrasonography, micturating cystourethrography, excretion urography, computed tomography and percutaneous antegrade pyeloureterography. Diuretic renography showed that the obstruction was partial. Since a static renal scintigram indicated that renal function on the affected side was moderately well preserved, ureteroplasty is planned.

Child, Preschool↗
PubMed1991

[Ofloxacin in the treatment of infection caused by Salmonella paratyphi A].

We reported a case of salmonellosis treated with ofloxacin (OFLX) which showed excellent clinical and bacteriological effect in a 22 year-old Japanese male with Salmonellosis paratyphi A. He had stayed in India from Sept. 6, 1990 to Oct. 13, 1990. On Oct. 25, 1990, he complained of a high fever and headache. On Oct. 29, he was admitted to our hospital and was diagnosed as Salmonellosis paratyphi A by the blood culture. He was treated with 2.0 g/day of chloramphenicol (CP) for 7 days, but the clinical efficacy was not sufficient. Therefore, we added 900 mg/day of OFLX for 10 days. He was treated successfully with them, the temperature became on the 2nd day. No side effect and no changes of laboratory data were observed and no recurrence was observed clinically and bacteriologically for three months after his discharge.

Adult↗
PubMed1991

[A case of Plasmodium vivax malaria with findings of DIC].

We reported a rare case of Plasmodium vivax malaria who showed findings of disseminated intravascular coagulation (DIC). A 50-year-old Japanese male was sent to our hospital with the diagnosis of Plasmodium vivax malaria on the 26th of April, 1990. He had stayed in the Solomon Islands from Oct. 1987 to Dec. 1989, and had febrile episodes during his stay in the island. On April 18, 1990, he complained of a high fever with chills, and showed the same episodes on the 20th, 22th and was diagnosed as malaria. He was treated successfully with the sulfadoxine 500 mg and pyrimethamine 25mg (Fansidar), following the normal temperature on the 4th day and disappearance of malarial parasites in the peripheral blood smear on the 6th day. Interestingly, he had thrombocytopenia and a high titer serum level of fibrin degradation product (FDP) supporting the questionable diagnosis of DIC. Even on the 12th day after improved thrombocytopenia by treatment with Gabexate (FOY), the serum level of FDP, D-dimer and thrombin-nati-thrombin (TAT)III complex still remained at high titer levels. One month later he was readmitted for a relapse of Plasmodium vivax malaria, when he showed thrombocytopenia but the serum level of FDP, D-dimer, TAT III complex and PM.alpha 2 PI complex were normal levels. We concluded that the thrombocytopenia and the high titer of FDP at his first admission was a manifestation of DIC.

Animals↗
PubMed1991

Effects of extra- and intracellular pH on vascular action of arginine vasopressin.

Compared with control studies performed at an extra-cellular pH (pHe) of 7.4, when vascular smooth muscle cells (VSMC) were preincubated in an acid extracellular medium (pHe 7.0) for 60 min the maximal arginine vasopressin (AVP)-induced sustained cellular contraction was reduced, whereas preincubation in an alkaline extracellular medium (pHe 7.8) enhanced the vascular action of AVP. These changes in VSMC contraction were accompanied by a parallel decrease in AVP receptor affinity and cytosolic free calcium ([Ca2+]i) mobilization in the acid medium, increased AVP receptor affinity, and [Ca2+]i mobilization in alkaline medium. Because the changes in pHe were parallelled by changes in pHi, studies were performed in which only pHi was altered by administering the proton ionophore, carbonyl cyanide m-chlorophenylhydrazone (CCCP) (10(-6) M for 10 min). CCCP inhibited VSMC contraction in the absence of changes in AVP receptor binding and AVP-induced [Ca2+]i mobilization but abolished the AVP-induced cellular alkalinization. The results therefore indicate that in a nonbicarbonate buffer alterations in pHe may modulate the vascular responses to AVP by altering hormone receptor affinity, [Ca2+]i mobilization, and pHi.

Adenosine Diphosphate↗
PubMed1991

Mechanisms of rapid desensitization to arginine vasopressin in vascular smooth muscle cells.

This study characterized the rapid desensitization induced by arginine vasopressin (AVP) in vascular smooth muscle cells (VSMC) in culture. The Ca2+ mobilization response and, in some experiments, the intracellular pH changes were used as a probe for the desensitization phenomenon. In VSMC, AVP desensitization was homologous, concentration dependent, and occurred in less than 30 s. The desensitization was complete with 10(-7) M AVP. Receptor occupancy was a critical factor in the maintenance of desensitization, since complete hormone washing by acid glycine buffer produced an earlier (less than 5 min) recovery of the cell response, whereas partial hormone washing with saline (pH 7.4) required 15 min to produce any significant recovery. Protein kinase C activation was a significant mechanism in AVP desensitization, because protein kinase C downregulation inhibited the desensitization phenomenon. Receptor internalization was, however, not important for the desensitization phenomenon, since it still occurred at 4 degrees C. Treatment with pertussis toxin did not affect the Ca2+ mobilization response but decreased the AVP-mediated intracellular alkalinization, therefore suggesting that a Gi or Go protein may be involved in some but not all the aspects of the AVP signal transduction and the desensitization phenomena.

Animals↗
PubMed1991

Mechanisms of vasopressin-induced increase in intracellular Na+ in vascular smooth muscle cells.

The present study was undertaken to examine the interrelationship between the arginine vasopressin (AVP)-induced dynamic changes in intracellular Ca2+ and Na+ concentrations in cultured rat aortic vascular smooth muscle cells (VSMC) by the direct measurements of intracellular Na+ concentration [( Na+]i), cytosolic free calcium [( Ca2+]i), and intracellular pH (pHi) using fluorescence dyes. AVP increased [Ca2+]i and [Na+]i in a dose-dependent manner; the rise in [Ca2+]i preceded the rise in [Na+]i. Pretreatment with the V1 antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid) 2-(O-methyl)-tyrosine] AVP [( d(CH2)5Tyr(Me)]AVP) completely blocked the effects of AVP on [Ca2+]i and [Na+]i. The V2 agonist 1-desamino-8-D-AVP, DDAVP, did not affect basal [Na+]i or the AVP-induced increase in [Na+]i. Also, Ca(2+)-free solution completely blocked the AVP-induced increase in [Na+]i. Moreover, Ca(2+)-free solution decreased the AVP-induced intracellular acidification and blunted the later AVP-induced intracellular alkalinization. These results therefore indicate that after binding to the V1 receptor AVP increases [Na+]i mediated by the activation of Na(+)-Ca2+ and Na(+)-H+ exchanges in VSMC. All of these cellular events are completely dependent on an increase in cellular Ca2+ uptake produced by AVP.

Angiotensin Receptor Antagonists↗
PubMed1991

Electrical stimulation of hypothalamic periventricular nucleus is followed by a large rebound secretion of growth hormone in unanesthetized rats.

The effect of electrical stimulation of the hypothalamic periventricular nucleus (PVN) on plasma GH profile was studied in unanesthetized female Wistar rats. A bipolar concentric electrode was implanted into the PVN, hypothalamic ventromedial nucleus (VMH), or intervening area between the PVN and VMH. Serial blood specimens were collected from an indwelling right atrial cannula. Plasma GH levels were reduced significantly during electrical stimulation of PVN, and a large rise of plasma GH levels followed after cessation of stimulation. An identical plasma GH profile was observed in response to the repeated stimulation. This rebound secretion of GH was completely inhibited by the administration of rat GRF antiserum. The effect of electrical stimulation of VMH on plasma GH levels was similar to that of PVN stimulation. However, the stimulation of hypothalamic area intervening between PVN and VMH was not followed by a surge of GH secretion. Since a continuous exposure of somatotrophs to GRF even in a concurrent presence of somatostatin (SS) is known to induce attenuation of the GH response to GRF through receptor effect, the results suggest that the release of endogenous GRF is augmented following the cessation of electrical stimulation of neurons providing hypophysiotropic SS.

Animals↗
PubMed1991

Detection of P-glycoprotein in human urogenital carcinomas and its relationship to epidermal growth factor receptor expression.

P-glycoprotein and epidermal growth factor (EGF) receptor expression were surveyed immunohistochemically in the tissue of urogenital carcinomas including 12 renal cell carcinomas, 9 bladder transitional cell carcinomas, 2 prostate adenocarcinomas and 1 penile squamous cell carcinoma. Three bladder carcinomas and the penile carcinoma were following initial chemotherapy at the time of relapse. P-glycoprotein expression was detected in 3 of 12 renal cell carcinomas and in all recurrent carcinomas. EGF receptor was not detected in any of the specimens.

ATP Binding Cassette Transporter, Subfamily B, Mem↗