Biomedical subjects

Yutaka Masuda

Publications and source records attributed to Yutaka Masuda.

27 records · Page 2Linked to original sources

PubMed2002

Endoscopic thoracic sympathectomy attenuates reflex tachycardia during head-up tilt in lightly anesthetized patients with essential plamar hyperhidrosis.

PURPOSE: Our purpose was to examine perioperative alterations in hemodynamic changes with head-up tilt (HUT) in patients undergoing endoscopic thoracic sympathectomy (ETS). METHODS: The subjects were 11 patients with essential hyperhidrosis scheduled to undergo ETS (ETS group) and 9 age-matched volunteers undergoing minor surgery (control group). HUT was performed (40 degrees; 5 min) before and after the surgery, under nitrous oxide anesthesia. Orthostatic hypertension and hypotension in response to HUT were defined as changes of 10% or greater in systolic blood pressure. RESULTS: The increase in heart rate in response to HUT was significantly reduced after surgery in the ETS group (from 34 +/- 18 to 14 +/- 11 beats.min(-1); P < 0.001), but not in the control group (from 23 +/- 18 to 22 +/- 12 beats.min(-1); P = 0.911). Orthostatic hypertension disappeared completely after ETS (from 5 of 11 to none of 11 patients; P = 0.035), whereas the prevalence of orthostatic hypotension increased significantly after ETS (from 3 of 11 to 9 of 11 patients; P = 0.030). In the control group, the prevalence of neither orthostatic hypertension nor orthostatic hypotension changed after surgery. CONCLUSIONS: ETS attenuates autonomic circulatory response under nitrous oxide anesthesia.

Journal Article↗

PubMed2002

Fragment of human beta-fibrinogen induces a behavioral effect on mouse forced swimming.

We detected a peptide having a behavioral activity on mouse forced swimming from sera of healthy volunteers without affective and psychotic diseases. The amino acid sequence was GVNDNEEGF, which was found in the sequence of human beta-fibrinogen. The synthesized peptide also showed the behavioral activity dose-dependently, but human fibrinopeptide B (QGVDNEEGFFSAR) did not. The activity was decreased by dopamine 1 antagonist SCH-23390, but not by dopamine 2 antagonist sulpiride. These findings strongly suggest that metabolism of human beta-fibrinogen induces the fragment affecting the mouse behavior via the dopamine1 neuronal activity.

Amino Acid Sequence↗

PubMed2002

An investigation of monoamine receptors involved in antinociceptive effects of antidepressants.

UNLABELLED: We attempted to determine which monoamine receptor subtypes are predominantly involved in antidepressant-induced antinociception. Antinociceptive effects were evaluated by using formalin tests with rats. Antidepressants acting as potent inhibitors of norepinephrine reuptake (nisoxetine, nortriptyline, and maprotiline) or inhibiting reuptake of both norepinephrine and serotonin (5-HT) (imipramine and milnacipran) induced dose-dependent antinociception. Simultaneous intraperitoneal administration of antidepressants and either prazosin (alpha(1) antagonist) or ketanserin (5-HT(2) antagonist) significantly antagonized antinociceptive effects. Fluvoxamine (selective serotonin reuptake inhibitor) induced antinociception less potently than other antidepressants and was significantly antagonized by ketanserin, but not prazosin. Ondansetron (5-HT(3) antagonist) significantly antagonized antinociception by 10 mg/kg of imipramine. In contrast, SDZ-205,557 (5-HT(4) antagonist) markedly enhanced antinociception by small-dose (2.5 mg/kg) imipramine. Imipramine-induced antinociception was significantly antagonized by intracerebroventricular administration of prazosin or ketanserin, but not by yohimbine (alpha(2) antagonist) or ondansetron, and was significantly enhanced by intracerebroventricularly administered SDZ-205,557. These findings suggest that alpha(1) adrenoceptors and 5-HT(2) receptors in the brain are involved in antidepressant-induced antinociception. In addition, the results suggested functional interactions between noradrenergic and serotonergic neurons as mechanisms for antidepressant-induced antinociception. IMPLICATIONS: Formalin tests of rats treated with antidepressants and antagonists of monoamine receptors indicate that alpha(1) adrenoceptors, serotonin (5-HT)(2) receptors, and 5-HT(3) receptors are involved in antidepressant-induced antinociception, suggesting functional interactions between noradrenergic and serotonergic neurons as mechanisms of antidepressant-induced antinociception.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2002

Costunolide triggers apoptosis in human leukemia U937 cells by depleting intracellular thiols.

We have previously demonstrated that costunolide, a biologically active compound that was isolated from the stem bark of Magnolia sieboldii, induced apoptosis in human cancer cells. In the present study, we investigated the underlying mechanisms and suggest that costunolide induces apoptosis in human promonocytic leukemia U937 cells by depleting the intracellular thiols. Costunolide treatment rapidly depleted the intracellular reduced glutathione (GSH) and protein thiols, and this preceded the occurrence of apoptosis. Pretreatment with sulfhydryl compounds such as GSH, N-acetyl-L-cysteine, dithiothreitol and 2-mercaptoethanol almost completely blocked the costunolide-induced apoptosis, highlighting the significance of the intracellular thiol level in the process. Furthermore, overexpression of Bcl-2 also significantly attenuated the effects of costunolide. The apoptosis-inducing activity of costunolide is likely to depend on the exomethylene moiety because derivatives in which this group was reduced, such as dihydrocostunolide and saussurea lactone, did not deplete the cellular thiols and showed no apoptotic activity. Taken together, the present study demonstrates that the costunolide-induced apoptosis depends on intracellular thiols contents, which are modulated by Bcl-2.

Antineoplastic Agents, Phytogenic↗

PubMed2002

Beta-hydroxyisovalerylshikonin is a novel and potent inhibitor of protein tyrosine kinases.

Beta-hydroxyisovalerylshikonin (beta-HIVS), a compound isolated from Lithospermium radix, most efficiently induced cell-death in two lines of lung cancer cells, namely, NCI-H522 and DMS114, whereas shikonin was effective against a wide variety of tumor cell lines. During our studies of the mechanism of action of beta-HIVS on tumor cells, we found that this compound inhibited protein tyrosine kinase (PTK) activity. The tyrosine kinase activities of a receptor for EGF (EGFR) and v-Src were strongly inhibited and that of KDR/Flk-1 was weakly inhibited by beta-HIVS. The inhibition by beta-HIVS of the activities of EGFR and v-Src was much stronger than that by shikonin. The IC50 values of beta-HIVS for EGFR and v-Src were approximately 0.7 microM and 1 microM, respectively. Moreover, the inhibition of v-Src by beta-HIVS was non-competitive with respect to ATP. These results strongly suggest that the action of beta-HIVS, as well as that of shikonin, involves the inhibition of PTK, and they also suggest the possibility of producing a novel group of PTK inhibitors based on shikonin as the parent compound.

3T3 Cells↗

PubMed2002

Humoral GalNAc alpha1-3GalNAc-lipid reactivity of humans in hypomanic state.

A glycolipid having GalNAc alpha1-3GalNAc in the terminal increases a behavior climbing in a depression model, mouse forced swimming. Antidepressants, which sometimes induce hypomanic state in patients, increase the glycolipid and an anti-manic substance lithium decreases the glycolipid in mice. We detected the humoral GalNAc alpha1-3GalNAc-lipid reactivity of humans in different affective states. Although the reactivity was also showed in serums of the depression patients and the volunteers without affective disorders, the reactivity was remarkably increased in serums of hypomania patients. These strongly suggest that the humoral glycolipid increased the activities of the hypomania patients, but did not relate to the decrease of the activities in the depression patients.

Adult↗

PubMed2002

[Severe low back pain and muscular weakness in the thigh following urological surgery in the hyperlordotic position].

A 57-year-old male with prostatic cancer was scheduled for a radical prostatectomy under general anesthesia combined with epidural anesthesia. An epidural catheter was introduced at the L 1-2 interspace without problem. The patient was placed in a hyperlordotic supine position with a bolster under his lower back for the seven and a half hour operation. Upon emergence from anesthesia, he complained of severe low back pain in addition to incisional pain. On the second postoperative day, the epidural catheter was removed. After residural analgesic effects had fully disappeared, he experienced muscular weakness in the left thigh and could not walk. Regional sensory loss and edema were also observed where pressure had been applied by the bolster, although spinal cord magnetic resonance imaging studies were almost normal. It took him seven weeks to walk without the support of a brace after surgery. Hyperextension of the lumbar spine could increase the pressure on the inferior vena cava which is transmitted to the intraspinal vein, and could lead to the disci intervertebrales compression and the stress on the facet joint. We believe that the primary cause of the presented symptoms was related to this position. Prolonged and/or excessive hyperlordosis during surgery should be avoided.

Humans↗

PubMed2002

[The development of methicillin-resistant Staphylococcus aureus sepsis in a patient with herpes zoster during treatment with continuous epidural infusion].

A 79-year-old man with herpes zoster was referred to our hospital for pain control. He was a survivor of the atomic bombing of Hiroshima, and had a history of cerebral infarction and hypertension. A cervical epidural catheter was placed for continuous analgesic infusion. After 20 days of catheterization, he gradually developed a high fever and confusion, and complained of nausea and headaches. An urgent blood examination revealed a white blood cell count of 15,200 mm-3 and a C-reactive protein of 32.4 mg.dl-1. The catheter was removed and antibiotic therapy was started. Repeated magnetic resonance imaging could not confirm epidural abscess formation. The bacterial culture of the cerebrospinal fluid was negative, but the cultures of the blood, the catheter tip, and the nasal cavity swab were positive for methicillin-resistant Staphylococcus aureus. Although intravenous vancomycin was administered, systemic inflammation persisted. The patient consecutively suffered varied disorders such as acute renal failure, disseminated intravascular coagulation, and gastrointestinal bleeding. Although symptomatic treatment had been prolonging his life, 58 days after the catheter removal, the patient suddenly developed cerebellopontine infarction, which made mechanical ventilation necessary. He remained unconscious until his death 117 days after the catheter removal. We discussed the possible pathogenetic mechanisms of the present case.

Aged↗

PubMedDate not supplied

Mandibular nerve block treatment for trismus associated with hypoxic-ischemic encephalopathy.

BACKGROUND AND OBJECTIVES: We describe the use of mandibular nerve block for the management of bilateral trismus associated with hypoxic-ischemic encephalopathy. CASE REPORT: The patient was a 65-year-old man with bilateral trismus due to hypoxic-ischemic encephalopathy. Despite his impaired consciousness, we performed fluoroscopically guided bilateral mandibular nerve block. The bilateral symptoms were sufficiently improved, without obvious side effects, by injecting a local anesthetic near the right mandibular nerve and a neurolytic near the left mandibular nerve. CONCLUSIONS: Mandibular nerve block may be an effective treatment for patients with bilateral trismus due to ischemic-encephalopathy, even when consciousness is impaired.

Aged↗