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Biomedical subjects

T Okajima

Publications and source records attributed to T Okajima.

At least 73 records · Page 4Linked to original sources

[Clinical study on the prognosis of complete denture wearers covering 10 years. 4. Masticatory efficiency].

The purpose of this study was to estimate masticatory efficiency of complete denture wearers. The subjects were 72 patients, treated before 5-10 years at students' clinic of Tsurumi University, School of Dental Medicine. The masticatory efficiencies with peanuts and Kamaboko were calculated. Results 1. The mean masticatory efficiency with peanuts for 63 patients was 35.8%, and with Kamaboko (steamed fishpast) for 64 patients was 94.5%, in comparison with natural dentition. 2. The mean masticatory efficiency with peanuts was 124.3%, and with Kamaboko was 99.6%, for complete denture wearers. 3. Comparing the measured value of masticatory efficiency with 5 to 10 years wearing period, there was significant difference in the masticatory efficiency between peanuts and Kamaboko. 4. There was significant difference in the masticatory efficiency with peanuts between the group needed new denture and the group not needed but there was not significant difference with Kamaboko.

Denture, Complete↗

[An autopsy case of HTLV-I associated myelopathy (HAM)].

An autopsy case of HTLV-I associated myelopathy (HAM) was reported. The patient was a 55-year-old man from Kagoshima, who had no history of blood transfusion. He was admitted to our hospital because of muscle weakness of legs and dysuria, which having since one month ago. On admission, he was able to walk with assistance, but his legs were severely spastic, and Babinski's sign was positive bilaterally. Superficial sensation was normal, but vibration sense was mildly decreased in his legs. CSF showed mild mononuclear pleocytosis with elevated protein. Myelogram and CT were normal. Serum and CSF antibodies to HTLV-I were positive at titers of X4,096 and X128, respectively by immunofluorescent assay, and specific IgG bands (p19, p24, p28 and p53 in serum and p19, p24, p53 in CSF) were detected by western blot analysis. His paraparesis continued to worsen. He became bed-ridden within 2 months. He was received corticosteroid medication. He regained the ability to walk with assistance, and continued taking corticosteroid. In July 4, 1986, macrohematuria appeared and inoperable transitional cell carcinoma of rt. kidney was found by further examination. Chemotherapy were not effective against the carcinoma and he died on July 21, 1987. Neuropathological findings were summarized as follows: cerebral hemisphere was normal except for mild cellular infiltration in the leptomeninges; lesions consisted in unilateral pyramidal tract of pons & medulla and in partial anterior, posterior and lateral columns of the spinal cord; demyelination with axonal degeneration, marked gliosis, numerous lipid-laden macrophages and mild perivascular infiltration of mononuclear cells in these areas.(ABSTRACT TRUNCATED AT 250 WORDS)

HTLV-I Antibodies↗

[A case of acute idiopathic pandysautonomia].

A 19-year-old male student who complained of orthostatic syncope and low grade fever was admitted to our hospital and diagnosed acute idiopathic pandysautonomia (AIPD). He had dysesthesia and hypalgesia of his face and the upper part of the level of Th4, slight hypalgesia of the limbs and slightly exaggerated jaw jerk and diminished deep tendon reflexes of the limbs, but his main clinical manifestations were orthostatic hypotension (OH), sweating disturbance and alternative diarrhea and constipation. Paroxysmal cough and vomiting attack, severe weight loss and slight emotional change were also observed. There were no abnormal findings in the routine laboratory examinations, but the protein in the cerebrospinal fluid was slightly elevated in the initial state. The results of autonomic function tests, such as OH on tilting, no blood pressure effects on cold pressor test and hand grip test, no overshoot in Valsalva maneuver, low norepinephrine (NE) level at resting and poor NE response on tilting, exaggerated response to a small dose of NE infusion (denervation supersensitivity), suggested that the sympathetic post-ganglionic sites were chiefly affected. The parasympathetic nervous functions were seemed to be almost intact by the results of Aschner test, Czermak test and coefficient variation of R-R intervals. Sural nerve biopsy revealed a marked loss of small myelinated and unmyelinated fibers, suggesting axonal degeneration. These findings were different from those of the Guillain-Barré syndrome (GBS), although the allergic or immunological mechanisms are suggested as the cause of both AIPD and GBS. In this case, amezinium metilsulfate, an indirect sympathomimetic agent, was most effective to OH and cough attack.

Acute Disease↗

[Lateral inferior pontine syndrome: a case report].

The patient, a man aged 57, was admitted to our clinic on May 1, 1987, because of severe vertigo and unsteadiness in standing. Since the age of 55 he had been suffered from hypertension and atrial fibrillation. In September, 1986, he experienced vertigo but recovered soon without therapy. On April 25, 1987, while working, he noticed severe vertigo, nausea and vomiting. He was admitted to a hospital, and then transferred to our clinic. On admission, he was alert and the mentality was normal. Slight ptosis abducent nerve paresis, hypalgesia on the forehead, nose and cheek, facial paresis of peripheral type and hypacusis were detected on the left side. No anisocoria was observed. Sweating was impaired over the left side of the face. Elevation of the soft palate was limited on the left side and the tongue deviated to the left on protrusion. Dysarthria was detected. Though there was no muscular weakness in the extremities, incoordination and dysmetria were noted in the left arm and leg. He could not stand up because of vertigo and unsteadiness. There was no sensory disturbance in the trunk and extremities. Deep tendon reflexes were well elicited and no pathological reflex was observed. These clinical manifestations, except for the ipsilateral palatal and lingual disturbances, were typical of the lateral inferior pontine syndrome caused by occlusion of anterior inferior cerebellar artery, and the lesion was clearly demonstrated by horizontal and coronal MRI. The palatal and lingual disturbances might be due to the involvements of the corticobulbar tracts of the 10th and 12th nerves after the fibers had decussated.

Arterial Occlusive Diseases↗

Minamata disease demonstrated by computed tomography.

Computed tomography was studied in the patients with Minamata disease, a methylmercury poisoning caused by the ingestion of contaminated sea foods. The characteristic changes in the acquired cases were atrophy of the visual calcarine cortex and of the cerebellar vermis and/or hemisphere. Marked atrophy of the calcarine cortex produced the sac-shaped low density areas between the occipital lobes and diffuse and marked cerebellar atrophy with enlargement of the fourth ventricle and cisterns of the posterior fossa produced a shrunken image on CT. Morphometric analysis confirmed these findings. In the fetal cases, the changes on CT were slight and no definite atrophy was demonstrated in either the calcarine cortex or the cerebellum. Morphometric analysis disclosed an increase of size of the middle portions of the lateral ventricle and the third and fourth ventricles.

Adult↗

Effect of taurine on growth hormone and prolactin secretion in rats: possible interaction with opioid peptidergic system.

The effect of taurine on growth hormone (GH) and prolactin (PRL) secretion was investigated in the urethane-alpha-chloralose anesthetized rats, considering the interaction with endogenous opioid peptidergic system. Intraventricular injection of taurine (0.25 and 1.0 mumol) stimulated GH and PRL secretion in a dose-dependent manner. However, 4.0 mumol taurine failed to show these effect. The intravenous infusion of naloxone (4 mg/kg b.w.) completely inhibited both the GH and PRL secretion induced by taurine (1.0 mumol). The combined treatment of taurine (1.0 mumol) and FK33-824 (Met-enkephalin derivative, 100 micrograms/kg b.w., i.v.) significantly increased GH and PRL responses induced by taurine or FK33-824 alone. These results indicate that taurine is an effective stimulator of GH and PRL secretion in rats, and that the mechanism of this action involves the opioid peptidergic system in the hypothalamus.

Anesthesia↗

An autopsy case of human T-lymphotropic virus type I-associated myelopathy.

This report describes the first autopsy case of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM). The disease mainly affected the spinal cord, particularly the lateral and anterior columns, where loss of myelin and axon was observed. The changes were bilateral and occurred mainly along the tract. Perivascular and parenchymal infiltration with lymphocytes and macrophages, as well as astrocytosis, were observed in the white and grey matters of the spinal cord. Blood vessels in the spinal cord and in the subarachnoid space of the spinal cord showed hyalinoid thickening of media and adventitia associated with infiltration of lymphocytes. These findings are similar to those of tropical spastic paraparesis (TSP).

Autopsy↗

Suppressions of ischemic paw oedema in mice, rats and guinea pigs by superoxide dismutases from different sources.

Various sources of superoxide dismutases (SOD) suppressed ischaemic paw oedemata (tourniquet poditis) of mice, rats and guinea pigs with different potencies. Intravenous (i.v.) dosing of mouse Cu,Zn-SOD had no effect on mouse ischaemic oedema, yet rat and guinea pig Cu,Zn-SOD suppressed ischaemic oedemata of rats and guinea pigs. Homologous SOD was anti-inflammatory at least in these two models. Guinea pig SOD was one of the most potent in all models, but showed a very narrow range of effective dose. This bell-shape suppressive pattern was ameliorated by concomitant catalase injection. Bovine and human Cu,Zn-SOD had a rather broad range of effective dose. Bacterial Mn-SODs were suppressive in mice, as well as the oxygen radical scavenger MK-447 and cytochrome c. Dexamethasone was effective only when administered more than 3 hrs in advance. As ischaemic paw oedema of mice was not sensitive to cyclooxygenase and lipoxygenase inhibitors, this model could serve for screening new types of anti-inflammatory or anti-ischaemic drugs.

Animals↗

Functional compartmentalization of arginine-vasopressin-activated cyclic AMP in anterior pituitary gland: the presence of a compartment activated by prostaglandin E2.

AVP(10(-8)-10(-6)M) increased ACTH as well as PGE2 release from rat anterior pituitary quarters in vitro in a concentration dependent manner. IBMX (0.1 mM), a phosphodiesterase inhibitor, increased the ACTH response to AVP. The cAMP content in pituitary tissue was increased by AVP. Cyclooxygenase inhibition by indomethacin(1.4 X 10(-5) M) or diclofenac (1.8 X 10(-5)M) led to a potentiation of AVP-evoked ACTH secretion and to a decrease in AVP-stimulated cAMP formation. PGE2(10(-6)M) significantly increased pituitary cAMP content and indomethacin did not affect cAMP levels activated by PGE2. PGE2 attenuated the AVP-induced ACTH release. These results indicate that at least two functional compartments of AVP-activated cAMP responses are involved in the AVP-induced ACTH release. One compartment is directly activated by AVP and participates in the propagation of AVP-induced ACTH release. The second compartment is activated by PGE2. The contribution of the second compartment to the regulation of ACTH secretion is not well understood since PGE2 shows an inhibitory effect on AVP-induced ACTH secretion.

Adrenocorticotropic Hormone↗

The possible involvement of cytochrome P-450 monooxygenase in AVP-induced ACTH secretion.

AVP (10(-7) M) induced ACTH as well as PGE2 release from rat anterior pituitary quarters. Inhibitors of P-450 monooxygenase, metyrapone (10 mM) and piperonyl butoxide (1 mM and 10 mM) attenuated the ACTH and PGE2 response to AVP. 7,8-benzoflavon (10 mM) which inhibits 3-methylchloranthrene inducible form of P-450 isoenzymes showed no inhibition of AVP-induced ACTH secretion. The decrease in ACTH response to AVP was still observed following the inhibition of prostaglandin synthesis by indomethacin. These results suggest that cytochrome P-450 monoocygenase systems are involved in the process of AVP-induced ACTH secretion, 3-methylchloranthrene inducible form of P-450 isoenzymes do not seem to be involved in this process.

Adrenocorticotropic Hormone↗

Delta-sleep-inducing peptide (DSIP) inhibited CRF-induced ACTH secretion from rat anterior pituitary gland in vitro.

Delta-sleep-inducing peptide (DSIP, 10(-9) - 10(-7) M) significantly inhibited the CRF-induced ACTH release from rat anterior pituitary quarters in vitro. 10(-8) M DSIP showed the most prominent inhibition. DSIP (10(-8) M) also inhibited the CRF-activated cAMP levels in anterior pituitary tissue. DSIP did not influence basal ACTH or cAMP levels. Prostaglandin E2 (PGE2)-release from anterior pituitary quarters was not changed by DSIP. From these results, we conclude that DSIP inhibits CRF-induced ACTH release at the pituitary level through the inhibition of the cAMP system in corticotrophs. The involvement of PGE2 in this phenomenon is unlikely.

Adrenocorticotropic Hormone↗

Bradykinin-induced ACTH release from rat pituitary tissue in vitro.

Bradykinin (10(-6) and 10(-5) M) stimulated ACTH-IR release from rat anterior pituitary tissue in vitro concentration-dependently. The onset of this effect was delayed in comparison to that of AVP or CRF. The combined treatment of bradykinin with AVP or CRF produced additive effects of ACTH-IR release. Bradykinin may represent another candidate involved in the regulation of ACTH release. In contrast to AVP, bradykinin did not stimulate prostaglandin E2 synthesis in the pituitary tissue. Bradykinin-induced ACTH-IR release remained unchanged following cyclooxygenase inhibition by indomethacin. It can be concluded that prostaglandins are not involved in the action of bradykinin on the anterior pituitary. Bradykinin did stimulate cyclic AMP accumulation in pituitary tissue. Inhibition of phosphodiesterase by 3-isobutyl-l-methylxanthine (IBMX) potentiated the ACTH-IR release evoked by bradykinin. From the results obtained, we concluded that cyclic AMP appears to be involved as a second messenger in the bradykinin-evoked ACTH-IR release.

1-Methyl-3-isobutylxanthine↗