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Biomedical subjects

T Kubo

Publications and source records attributed to T Kubo.

At least 865 records · Page 48Linked to original sources
PubMed1985

Stress-induced proteins in chondrocytes from patients with osteoarthritis.

Recent studies have shown that a specific set of proteins is produced by a variety of cells after the application of some forms of stress, including heat shock. Human chondrocytes isolated from cartilage with moderate to severe osteoarthritis synthesize at least 1 of these stress proteins (Mr 70,000) at physiologic temperature (37 degrees C), whereas chondrocytes isolated from non-pathologic cartilage synthesize this protein only in response to incubation at temperatures above 39 degrees C. The active synthesis of this protein (SP-70) at 37 degrees C is positively correlated with the severity of osteoarthritis and can be a characteristic indicator of this degenerative disease. We identified the active synthesis of stress proteins after incubating the cartilage tissue in medium containing 35S-methionine and separating the cell-associated proteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The radioactive proteins were visualized by autoradiography. Analysis of the longevity of cell-associated proteins was determined by pulsing the tissue with 35S-methionine, and after different periods of chase in medium, the proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Specific proteins bands were then excised, and the radioactivity was determined by liquid scintillation counting.

Autoradiography↗
PubMed1985

Effects of asymmetric vertebral blood flow upon the vestibulo-ocular reflex of the rabbit.

Per-rotational nystagmus was recorded in rabbits with unilaterally narrowed vertebral arteries or following unilateral cervical sympathectomies. Asymmetry of per-rotational nystagmus could not be observed when the animal's systemic arterial blood pressure was within the normal range (about 90-120 mm Hg). However, directional preponderance of nystagmus occurred when blood pressure either increased or decreased beyond this level. The reason for the occurrence of directional preponderance can be interpreted as a failure of autoregulation of cerebral and/or inner ear blood flow.

Animals↗
PubMed1985

Involvement of central catecholamines in mediation of pressor responses of the rat to carotid occlusion.

Carotid occlusion evoked a pressor response in rats after transection of the spinal cord. Intraventricular pretreatment with 6-hydroxydopamine inhibited the pressor response. The pressor response to occlusion was also diminished by the intraventricular but not by the intravenous injection of guanethidine. Intravenous atropine or mecamylamine, or intraventricular captopril did not affect the pressor response. Thus, it appears that central catecholaminergic mechanisms are involved in the mediation of the pressor response to carotid occlusion.

Animals↗
PubMed1985

Caudal ventrolateral medulla. A region responsible for the mediation of vasopressin-induced pressor responses.

We localized glutamate-sensitive sites in the ventrolateral medulla of the rat with the spinal cord cut at C. When unilaterally injected into a circumscribed region of the caudal ventrolateral medulla, L-glutamate (30-300 ng) elicited a dose-dependent increase in arterial pressure. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral microinjections of kainic acid (50 ng) into the ventrolateral glutamate-sensitive area markedly reduced a vasopressin-induced pressor response to kainic acid (30 ng), injected bilaterally into the nucleus tractus solitarii. It is concluded that the glutamate-sensitive neurons in the caudal ventrolateral medulla are involved in mediation of the vasopressin-induced pressor response arising from the nucleus tractus solitarii.

Animals↗
PubMed1985

Involvement of the ventrolateral medulla in the mediation of pressor responses of the rat to afferent vagal stimulation.

Electrical stimulation of afferent vagal fibres evoked a pressor response in rats after transection of the spinal cord. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral electrolytic lesions at the sites of the caudal ventrolateral medulla markedly reduced the pressor response to afferent vagal stimulation but not that to carotid occlusion. It is concluded that the area of the caudal ventrolateral medulla is involved in mediation of the vasopressin-induced pressor response to afferent vagal stimulation.

Animals↗
PubMed1985

[Brain nicotinic acetylcholine receptors and their functions in special reference to central cardiovascular regulation].

The nicotinic acetylcholine receptors present in the mammalian brain have received less attention than those in other areas of the nervous system. However, recent studies have reported the pharmacological character and regional distribution of a high-affinity binding of [3H]acetylcholine or [3H]nicotine. In this review, the pharmacological characters and physiological functions of the brain nicotinic receptors were discussed with special reference to central cardiovascular regulation.

Acetylcholine↗
PubMed1985

[Therapeutic effect of Robaveron tablet (KN-7) on urinary disturbance by benign prostatic hypertrophy].

Therapeutic effect of Robaveron tablet (KN-7) was studied on 101 patients with urinary disturbance accompanied by benign prostatic hypertrophy. Robaveron tablet, which contains 20 mg of a swine prostatic extract per tablet, was administered 6 tablets daily for 3 weeks in principle. Evaluation of drug efficacy was based on residual urine, cystometric findings, urethral pressure profile, uroflowmetry and subjective symptoms. Remarkable decrease of residual urine was observed at all stages of Guyon classification, in parallel with increases of cystometric pressure amplitude and average flow rate. Rate of residual urine reduction rose in proportion to the higher stage or bulkier volume of residual urine. Improvements of subjective symptoms were also obtained. The overall effectiveness, rated slightly improved or better was 76.8%. Side effects were seen at a low rate of 3.9%, and there were no abnormal changes directly due to the drug in clinical laboratory tests. These results indicate that Robaveron tablets act on the detrusor muscle and contribute to improve the depressed voiding efficiency and incidental symptoms of the subjects.

Aged↗
PubMed1985

Hyperthyroidism after primary hypothyroidism. Follow-up with serial thyroid biopsies.

Hyperthyroidism occurred following primary hypothyroidism in a 46-year-old man with serologically and histologically proved chronic lymphocytic thyroiditis. Repeated thyroid biopsy specimens revealed that histologic features compatible with chronic lymphocytic thyroiditis seen at the initial hypothyroid state subsequently underwent a remarkable resolution, with titers of circulating antithyroid antibodies being reduced in correspondence with the histologic improvement. This case shows that primary hypothyroidism in adults can spontaneously evolve into a hyperthyroid state, as has been suggested previously, and that the histologic abnormalities in chronic lymphocytic thyroiditis may not necessarily be irreversible.

Antibodies↗
PubMed1985

Autoregulation of endogenous epinephrine release via presynaptic adrenoceptors in the rat hypothalamic slice.

High-K+ (30 mM)-evoked release of endogenous epinephrine in hypothalamic slices from three rats in the presence of tetrodotoxin, 3 X 10(-7) M, was measured by high-performance liquid chromatography with an electrochemical detector. Spontaneous and evoked release of epinephrine was markedly reduced, when rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p., before decapitation. The amount of epinephrine released during the resting state was lower by a factor of approximately 2 orders than that of norepinephrine and dopamine but was consistently higher than the limit of the sensitivity of this assay system, 0.1 to 0.3 pmol. The evoked release of epinephrine was Ca++ dependent. Isoproterenol, 10(-8) M to 10(-7) M, dose dependently increased this parameter. I-Propranolol, 3 X 10(-8) M, shifted the dose-effect curve of isoproterenol to the right. Atenolol, 10(-6) M, and butoxamine, 3 X 10(-8) M, beta-1 and beta-2 antagonists, respectively, antagonized the action of isoproterenol, 3 X 10(-8) M. Tazolol, 3 X 10(-7) and 10(-6) M, a beta-1 agonist, and salbutamol, 10(-8) and 3 X 10(-8) M, a beta-2 agonist, dose dependently increased the evoked release of epinephrine. I-Propranolol, 3 X 10(-7) M and 3 X 10(-6) M alone, dose dependently decreased this parameter, but the d-isomer produced no effect. Clonidine, 10(-8) and 10(-7) M, an alpha-2 agonist, dose dependently decreased the parameter, and this decrease was antagonized by yohimbine, 10(-6) M, an alpha-2 antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1985

Involvement of epinephrine in the presynaptic beta adrenoceptor mechanism of norepinephrine release from rat hypothalamic slices.

Using high-performance liquid chromatography with electro-chemical detector, we measured field impulse (5 or 2 Hz)- and high K+ (20 mM)-evoked release of endogenous norepinephrine from rat hypothalamic slices. Release by impulses at 5 Hz was tetrodotoxin-sensitive and both types of release were Ca++-dependent. Isoproterenol (10(-10) to 10(-8) M) dose-dependently facilitated impulse-evoked release and l-propranolol (10(-8) M) shifted dose-effect curve of isoproterenol to the right. Atenolol (10(-8) to 10(-6) M) or butoxamine (10(-9) to 10(-8) M), beta-1 and beta-2-antagonist, respectively, dose-dependently antagonized the facilitatory effect of isoproterenol (10(-8) M). Tazolol (10(-8) to 10(-7) M), beta-1-agonist, and salbutamol (10(-10) to 10(-8) M), beta-2-agonist, dose-dependently increased impulse-evoked release. Epinephrine (10(-9) M) also facilitated impulse-evoked release and the action was antagonized by l-propranolol (10(-8) M). Isoproterenol (10(-8) M) also facilitated high K+-evoked release in the presence of tetrodotoxin (3 X 10(-7) M) to exclude possible involvement of axonal conduction or neuronal loops. This facilitatory effect was antagonized by l-propranolol (10(-8) M). l-Propranolol (3 X 10(-7) M) alone decreased release by impulses at 2 Hz, but the d-isomer produced no effect. When rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p. before decapitation, the l-propranolol-induced decrease was abolished completely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Presynaptic inhibitory dopamine receptors on noradrenergic nerve terminals: analysis of biphasic actions of dopamine and apomorphine on the release of endogenous norepinephrine in rat hypothalamic slices.

Electrical field stimulation (5 Hz)- or high K+ (20 mM)-evoked release of endogenous norepinephrine from superfused rat hypothalamic slices in the presence of cocaine (20 microM) was measured by high-performance liquid chromatography with an electrochemical detector. Apomorphine (10-1000 nM) dose-dependently facilitated the electrically evoked release. Apomorphine (1 microM)-induced facilitation was abolished by pretreatment with yohimbine (100 nM), was converted to inhibition by yohimbine (1 microM), but was not antagonized by propranolol (300 nM). Epinephrine (100 nM) decreased the electrically evoked release and the decrease was antagonized by yohimbine (100 nM) and by apomorphine (100 nM), but not by S-sulpiride (100 nM). In the presence of yohimbine (1 microM), apomorphine (10-1000 nM) dose-dependently inhibited the electrically evoked release. Furthermore, in the presence of tetrodotoxin (300 nM), apomorphine (100 nM) also decreased the high K+-evoked release and this decrease was antagonized by S-sulpiride (100 nM). Dopamine produced biphasic actions on the electrically evoked release, a dose-dependent decrease at 30 and 100 nM and an increase at 300 and 1000 nM. Dopamine (300 nM)-induced increase was antagonized by propranolol (300 nM) but not by yohimbine (100 nM). The dopamine (100 nM)-induced decrease was antagonized by S-sulpiride (1 nM), but not by the R-isomer. S-sulpiride (10 to 100 nM) alone dose-dependently increased the electrically evoked release, whereas the R-isomer had no effect. Haloperidol (100 nM) also increased the electrically evoked release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Emphysematous pyelonephritis: report of a case].

A case of emphysematous pyelonephritis is presented. A 49-year-old male with diabetes mellitus complaining of high grade fever attack and right flank pain was referred from internal medicine. KUB demonstrated that the right ureter, pelvis and calyces were filled with gas. Anti-bioticus was given intensively and the abnormal gas shadow on plain film disappeared before RP was done, but high grade fever attack persisted and right nephrectomy was undergone. After this operation, the fever was relieved and the patient was discharged at the 30th day post-operatively. A search of available literature in Japan has disclosed only 17 reported cases. Diagnostic methods, treatment, complication and etiology are discussed.

Diabetes Complications↗
PubMed1985

[Implant operation of penile inflatable prosthesis for a patient with erectile impotence due to radical cystectomy: a case report].

The hydraulically inflatable penile prosthesis consists of an inflate-deflate pump, a storage reservoir and paired cylinders and it is able to provided a more physiologically functional penis. We report our surgical experience of implant of an inflatable penile prosthesis for postoperative impotence. The patient was a 51-year-old male with impotence, who had received radical cystectomy and ilial conduit formation for transitional cell carcinoma of the bladder (G3, pT3NoMo.) 9 months earlier. There was nothing particular except for the postoperative status on physical, laboratory and X-ray examinations. He was diagnosed to have organic impotence (vasculogenic) by sexual functional tests. Auto-injection of the corpus cavernosum with papaverine HCl was attempted but an erection was not induced by the injection. So, implant operation of an inflatable penile prosthesis was performed by the lower abdominal approach. His postoperative course was uneventable and practice to deflate and inflate the cylinders was started at 2 weeks after the operation and he was able to have sexual intercourse at 5 weeks after the surgery. Now (3 months after the operation), he can have sexual intercourse with an orgasm but without ejaculation and he and his wife are both satisfied with the postoperative status.

Carcinoma, Transitional Cell↗
PubMed1985

Further studies on vasopressin-induced pressor responses to kainic acid injected into the nucleus tractus solitarii of the rat.

Kainic acid, an analogue of L-glutamate, was microinjected into the nucleus tractus solitarii of cordotomized rats. Kainic acid (30 ng) injected bilaterally into the nucleus elicited hypertension. The pressor response to kainic acid was restricted to sites in the intermediate one-third of the nucleus tractus solitarii. Plasma vasopressin levels were markedly increased during the kainic acid-induced pressor response. Intravenous injection of atropine sulphate or mecamylamine, or intraventricular injection of captopril did not affect the pressor response. It is concluded that in cordotomized rats the pressor response to kainic acid injected into the nucleus tractus solitarii is mainly mediated via increased release of vasopressin. It seems unlikely that the central cholinergic and angiotensin mechanisms are mainly responsible for the response to kainic acid.

Animals↗