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Biomedical subjects

T Mima

Publications and source records attributed to T Mima.

At least 91 records · Page 5Linked to original sources
PubMed1995

[Clinical and histological effect of induction chemotherapy with peplomycin, vincristine, mitomycin C and cis-platinum on oral squamous cell carcinomas].

Twenty one patients with resectable oral cancer received two courses of induction chemotherapy with peplomycin (PEP), vincristine (VCR), mitomycin C (MMC) and cisplatin (CDDP). Five patients had a complete response to the therapy and 9 had a partial response. Histological evaluation by Ohboshi-Shimozato classification indicated that Grade IV was obtained in 7 cases, Grade III was in 4 cases. Moreover, the study suggested that this regimen was less effective for metastatic lymph lesions than that for the primary tumors.

Adult↗
PubMed1994

Cortical reflex negative myoclonus.

Three patients with progressive myoclonic epilepsy (PME), two of them clinically manifesting only negative myoclonus and the other manifesting both positive and negative myoclonus, were electrophysiologically investigated, and compared with two other patients with PME presenting with only positive myoclonus. Electric stimulation of the median nerve during sustained active wrist extension in the three patients with negative myoclonus often elicited a short lapse of the posture in the stimulated hand associated with a silent period in the muscle discharge with or without being preceded by an abrupt increase in the muscle discharge (C reflex). The occurrence of the stimulus-induced silent period was significantly correlated with that of the giant somatosensory evoked potentials (SEPs), and in two patients the silent period was elicited also in the opposite (non-stimulated) hand when the giant SEP was recorded at the hemisphere ipsilateral to the stimulus as well. In one patient, the duration of the silent period was positively correlated with the amplitude of the cortical SEP. Furthermore, the duration of the induced silent period was closely related to the recovery function of SEP in each individual case. In contrast, in the two patients manifesting only positive myoclonus, the silent period was not elicited by the peripheral stimulation, and the somatosensory cortex was hyperexcitable immediately after the peripheral stimulus. Thus, this stimulus-sensitive negative myoclonus is mediated by a transcortical reflex mechanism, and corresponds to the negative form of the cortical reflex myoclonus ('cortical reflex negative myoclonus').

Adult↗
PubMed1994

[Anesthetic management of patients with dilated cardiomyopathy].

Anesthetic management of patients with dilated cardiomyopathy (DCM) was analyzed. From January 1991 to June 1993, we had 7 patients with DCM; 5 patients received general anesthesia and 2 patients received spinal anesthesia. General anesthesia was induced and maintained generally with diazepam and fentanyl. There were two patients who suffered from intraoperative arrhythmia. One patient who received spinal anesthesia suffered from ventricular fibrillation suddenly before the operation and we performed cardiopulmonary resuscitation successfully but the operation was cancelled. One patient who underwent emergency operation for gastric perforation suffered supraventricular tachycardia during the operation, and we were required to use antiarrhythmic agent that was thought to be deleterious to cardiac function. There was no patient who died perioperatively. There was one patient in the group IV of classification of Inoh which predicts the highest risk of dying from cardiac failure. In conclusion, it is important to control arrhythmia during the management of patients with DCM under anesthesia.

Adult↗
PubMed1994

[General anesthesia for patients with hypertrophic cardiomyopathy].

General anesthesia was given to six surgical patients with hypertrophic cardiomyopathy on eight occasions from 1990 to 1992. Anesthetic courses were uneventful in five patients diagnosed previously as hypertrophic cardiomyopathy. However, a patient without a diagnosis of hypertrophic cardiomyopathy had intractable cardiac arrest. A slight hypotension caused by epidural anesthesia had a devastating effect on the patient. The above experiences stress the importance of early diagnosis and careful observation in perioperative period.

Aged↗
PubMed1993

Effects of inosine on adenosine-induced coronary vasodilation in the open chest dog.

The effects of inosine (CAS 58-63-9) on adenosine-induced coronary vasodilation were studied in open-chest dogs. Inosine and hypoxanthine were infused into the coronary artery at a rate to obtain respective calculated coronary plasma concentrations of 10(-5) mol/l, and the dose-coronary flow response of adenosine was recorded with and without inosine or hypoxanthine infusion. When the maximum coronary dilation was obtained, 10 ml of 2 x 10(-3) mol/l 8-phenyltheophylline (8-PT) solution was injected into the femoral vein. Additionally, adenosine deaminase activity was measured in vitro in the presence of various concentrations of either inosine or hypoxanthine. It was found that inosine, but not hypoxanthine, intensified the coronary vasodilatory effect of adenosine, which was abolished by 8-PT injection: EC50 of adenosine was reduced from 10(-5.43) mol/l to 10(-5.90) mol/l by inosine. Inosine and hypoxanthine did not affect adenosine deaminase activity at concentrations of 10(-4) mol/l or less. These findings indicate that inosine intensifies the coronary vasoactivity of adenosine, independent of inhibition of adenosine deaminase activity.

Adenosine↗
PubMed1993

[The classification of myoclonus].

The term "myoclonus" was originally used to indicate brief jerky involuntary movements. But, nowadays the meaning of myoclonus has expanded so much that its definition and classification have been considerably obscured. In this view, the definition of myoclonus is described and the characteristic clinical features are discussed. The classification of myoclonus is presented based on the pathophysiological observations. Myoclonus is divided into two large groups, cortical myoclonus directly associated with the activity of the motor cortex, and subcortical myoclonus which comprises various types of myoclonus (including spinal myoclonus). Furthermore, the electrophysiological aspects of myoclonus and its pathogenesis are briefly discussed.

Diagnosis, Differential↗
PubMed1992

Transfer of multiple sclerosis into severe combined immunodeficiency mice by mononuclear cells from cerebrospinal fluid of the patients.

To investigate the mode of the pathogenesis of multiple sclerosis (MS), we transferred cerebrospinal fluid (CSF) cells, predominantly mononuclear cells, from MS patients at both exacerbation and remission stages of the disease into severe combined immunodeficiency mice by intracisternal injection. As controls, (i) CSF cells from patients with cervical spondylosis and (ii) peripheral blood mononuclear cells from normal individuals were transferred. Four to 6 weeks after transfer, most mice transferred with CSF cells from MS patients at the exacerbation stage of the disease developed paralysis and ataxia. The histopathological examination on the sacrificed mice revealed multiple scattered, discrete lesions localized in the white matter of the brainstems and spinal cords. These lesions were characterized by various degrees of tissue necrosis, involving inflammatory-cell infiltration. Most infiltrating cells were macrophages, although a smaller number of granulocytes appeared in several foci. Reactive astrocytic gliosis was also seen around the necrotic foci. Furthermore, these lesions exhibited demyelination. These histopathological changes are similar to those seen in MS. In contrast, none of the severe combined immunodeficiency mice transferred with CSF cells from MS patients at the remission stage of the disease, or with CSF cells from the patients with cervical spondylosis, or with peripheral blood mononuclear cells from normal individuals showed any such histopathological changes. These observations provide convincing direct evidence of encephalitogenicity of mononuclear cells in CSF from MS patients at the exacerbation stage of the disease.

Animals↗
PubMed1992

Establishment of human squamous carcinoma cell lines highly and minimally sensitive to bleomycin and analysis of factors involved in the sensitivity.

Human squamous carcinoma cell lines that were highly and minimally sensitive to bleomycin were established from clinical specimens and designated as SCCKN and SCCTF, respectively. Although these cell lines showed a similar growth doubling time in vitro, SCCTF was approximately ten times less sensitive to bleomycin than SCCKN. The bleomycin high and low sensitivities were stable even at the 70-cell passage level in vitro. In addition, nude mouse tumors produced by SCCTF were less sensitive to bleomycin that those produced by SCCKN, and the ratio of the mean tumor weight in bleomycin-treated mice to that in control mice was 89.2% in SCCTF and 18.8% in SCCKN. As compared with SCCKN, SCCTF also was less sensitive to peplomycin (5-fold), mitomycin C (2.3-fold), cis-diamine dichloroplatinum (2.5-fold), and vincristine (6.5-fold). Analyses of low bleomycin sensitivity showed that SCCTF had an approximately 20% decreased cellular accumulation and retention of bleomycin, 1.2-fold increase of bleomycin hydrolase activity, elevated DNA repair activity, and increased poly(adenosine diphosphate-ribose) polymerase activity as compared with SCCKN.

Animals↗
PubMed1992

Carbon dioxide reactivity during prostaglandin E1 induced hypotension for cerebral aneurysm surgery.

The cerebral vasomotor reactivity to carbon dioxide was studied, using a thermal gradient blood flow meter in 43 patients with intracranial cerebral aneurysm under deliberate hypotension induced by prostaglandin E1 (PGE1) infusion. The patients were divided into three groups according to the neurological status. Patients in Groups A and B had subarachnoid haemorrhage due to ruptured cerebral aneurysms. Group A consisted of 23 patients with a neurological grade of I-II and Group B consisted of 11 patients with a grade of III-V. Nine patients with non-ruptured cerebral aneurysm served as controls (Group C). After the dura was opened, local cerebral blood flow (LCBF) was measured. The PGE1 was started with an initial dose of 0.1 microgram.-kg-1.min-1 and the dose was adjusted to maintain MAP at about 70 mmHg. The LCBF and carbon dioxide (CO2) reactivity were estimated during and after PGE1 administration. The LCBF did not change among groups throughout the study period. Carbon dioxide reactivity was estimated as follows: absolute; delta LCBF/delta PaCO2, and relative; % delta LCBF/delta PaCO2 after changing PaCO2 by increasing minute ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Serum dipeptidyl peptidase (DPP) IV activity in hamster buccal pouch carcinogenesis with 9,10-dimethyl-1,2-benzanthracene.

Dynamic change of serum DPP IV activity in carcinogenesis of hamster buccal pouch epithelium with DMBA was investigated. The serum enzyme level in hamster (21.5 +/- 3.1 IU/l serum) was decreased gradually from the 8th to the 10th wk when papillomas were induced by DMBA application (18.9 +/- 2.7 IU/l serum). The enzyme level was further decreased in the formation of carcinoma in situ or early invasive carcinoma (13.2 +/- 0.5 IU/l serum), and reached to less than half of the normal level at the time when tumors were diagnosed as squamous cell carcinoma histologically (8.1 +/- 1.3 IU/l serum). This enzyme level was increased by tumor excision and decreased again by tumor recurrence toward death. These findings suggested that the decrease of serum DPP IV activity occurred from the early stage of hamster buccal pouch carcinogenesis as a tumor-burden marker.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1991

Characterization of the effect of endothelins in canine cerebral arteries.

In a few populations of endothelial cells of dog basilar arteries, endothelin (ET)-like immunoreactivity was detected to be present. ET-1, ET-2, and ET-3 caused vasoconstrictor responses but not vasodilator responses in isolated ring preparations of dog cerebral arteries in vitro. The ED50 values for the contractions were 411 pM, 478 pM, and 26.5 nM for ET-1, ET-2, and ET-3, respectively. NiCl2 (10(-3) M) attenuated the contractions induced by ET-3 (10(-8)-3 x 10(-7) M) and those to relatively low doses (10(-9) M) but not higher doses (10(-8)-10(-7) M) of ET-1 and ET-2. The contractions in response to ET-1, ET-2, and ET-3 were greatly attenuated in Ca(2+)-free solutions, although high concentrations of ET-1 and ET-2 still evoked contractions. These results suggest that the vasoconstriction induced by ET-3 and lower doses of ET-1 and ET-2 largely depends on the influx of Ca2+ ions. Furthermore, additional distinct mechanisms may contribute to the vasoconstrictor effects of high concentrations of ET-1 and ET-2. The presence of endothelin-like immunoreactivity in endothelial cells suggests that endothelin is a potential endogenous spasmogen.

Animals↗
PubMed1991

Possible role of endothelin in the pathogenesis of cerebral vasospasm.

Since the discovery of endothelin-1 (ET-1), its involvement in cerebral vasospasm after subarachnoid hemorrhage (SAH) has been suspected. We performed various experiments, first to demonstrate the presence of ET in both patients and dogs with SAH, and second to examine the effects of ET synthesis inhibition in experimental vasospasm. Here we report that ET was present in both plasma and cerebrospinal fluid (CSF) in SAH, but did not correlate with vasospasm. However, ET was locally expressed in the vascular endothelium in vasospasm. Several therapeutic approaches causing the inhibition of ET synthesis were effective in preventing the development of vasospasm. Such approaches utilized drugs that inhibited RNA and DNA synthesis. Among them, actinomycin D treatment was most effective. We also utilized phosphoramidon, a recently found conversion inhibitor of big ET to ET. However, this product failed to ameliorate the development of vasospasm. Therefore, although we cannot yet conclude that ET is the main cause of cerebral vasospasm, it may, at least, act as one of the modifying factors in cerebral vasospasm.

Animals↗
PubMed1991

Endothelins: vasoconstrictor effects and localization in canine cerebral arteries.

1. The vascular effects of endothelin and localization of endothelin-like immunoreactivity were characterized in isolated cerebral arteries of dogs. 2. Endothelin-like immunoreactivity was detected in a few populations of endothelial cells of dog basilar artery. 3. Endothelin-1, endothelin-2 and endothelin-3 contracted isolated ring preparations of cerebral arteries in a dose-dependent manner independently of the presence of endothelium. The ED50 values (and 95% confidence intervals) for the contraction were 411 pM (242-697 pM) and 478 pM (295-776 pM) for endothelin-1 and endothelin-2, respectively. Endothelin-3 induced vascular contraction at a higher concentration (ED50 = 26.5 nM, 95% confidence interval = 15.7-45.7 nM). 4. The increases in tone induced by endothelin-1 and endothelin-2 did not return to the resting level after repeated washings, while a rinse with Krebs solution reversed the vasoconstrictor response to endothelin-3. The endothelins did not cause any vasodilator response in arteries precontracted with uridine 5'-triphosphate even in the presence of intact endothelial cells. 5. NiCl2 (1 mM) attenuated the contractions induced by endothelin-3 (10-300 nM) and those to relatively low doses (1 nM) but not higher doses (10-100 nM) of endothelin-1 and endothelin-2. The contractions in response to endothelin-1, endothelin-2 and endothelin-3 were greatly attenuated in Ca(2+)-free solutions although high concentrations of endothelin-1 and endothelin-2 still evoked contractions. 6. These results suggest that the vasoconstriction induced by endothelin-3 and lower doses of endothelin-1 and endothelin-2, largely depends on the influx of Ca2+ ions. The apparent insensitivity to Ni2+ shows that additional distinct mechanisms also operate in the vasconstrictor responses to high concentrations of endothelin-1 and endothelin-2. 7. The presence of endothelin-like immunoreactivity in endothelial cells suggests that endothelin is a potential endogenous spasmogen.

Animals↗
PubMed1991

Interaction between adenosine and beta-adrenoceptors.

Interaction between adenosine and isoproterenol (ISP) on myocardial inotropic action was studied in open-chest dog hearts. The local myocardial force and the left ventricular (LV) dP/dt were measured as indices of myocardial contractility. Isoproterenol [ISP, 9.47 microM (2 micrograms/ml)] was infused into the left circumflex coronary artery at rates of 0.05 ml/min (low dose ISP) or 0.2 ml/min (high dose ISP). Two mM adenosine or 0.5 mM N6-phenylisopropyl-adenosine (PIA) were infused into the coronary artery at rates of 0.2 (4 x 10(-7) mol/min), 0.5 (1 x 10(-6) mol/min) and 10 ml/min (2 x 10(-5) mol/min) in the presence of either a low or a high dose of ISP. Adenosine infusion at a rate of 0.2 ml/min did not modify myocardial contractility in the presence of the both doses of ISP. The larger doses of adenosine, 0.5 ml/min and 10 ml/min, decreased myocardial-developed tension and LVmax dP/dt dose-dependently. However, the dose of adenosine which affected myocardial contractility was inphysiologically high in comparison with the concentration in the ischemic myocardium. PIA, a potent agonist of adenosine A1-receptor, attenuated an increase in myocardial contractility in a dose-dependent manner which was caused by intracoronary ISP infusion. This indicates that A1-adenosine receptors exist, but a functional adenosine-catecholamine antagonism does not play a significant role in the canine left ventricle.

Adenosine↗
PubMed1991

Prevention of cerebral vasospasm by actinomycin D.

The role of endothelin, a newly found vasoconstrictor peptide, is examined in the pathogenesis of cerebral vasospasm after experimental subarachnoid hemorrhage (SAH) in the dog. Endothelin immunoreactivity was overexpressed in the endothelium of the vasospastic basilar artery. Because endothelin synthesis is regulated at the messenger ribonucleic acid transcription level, the effect of actinomycin D, a ribonucleic acid synthesis inhibitor, was studied as a means of preventing vasospasm. It was found that treatment with intravenous actinomycin D for 5 days beginning on the day of SAH completely inhibited the development of vasospasm. This novel experimental therapy may lead not only to the elucidation of the pathogenesis of cerebral vasospasm but also to the availability of a prophylactic adjuvant therapy for patients with SAH.

Animals↗
PubMed1991

Amelioration of delayed neuronal death in the hippocampus by nerve growth factor.

Selective neuronal death in the CA1 sector of the hippocampus [delayed neuronal death (DND)] develops several days after transient global cerebral ischemia in rodents. Because NGF plays a potential role in neuronal survival, it was decided to study its effect in DND. We report here that intraventricular injection of NGF either before or after 5 min forebrain ischemia in the Mongolian gerbil significantly reduced the occurrence of DND. The tissue content of NGF in the hippocampus was decreased 2 d after ischemia and recovered to the preischemic level by 1 week. By the Golgi staining technique, changes first began in the dendrites of affected neurons as early as 3 hr. Such changes could be ameliorated by NGF treatment. Although previous knowledge of NGF is limited to the survival of cholinergic neurons in the CNS, it is assumed that other mechanisms must be operating in the hippocampus, for example, postsynaptic modification at dendrites or aberrant expression of NGF receptors possibly at the initial excitation period by glutamate. Furthermore, because previous work has shown that inhibition of protein synthesis reduces the occurrence of DND, a program leading to cell death might also be operating via de novo synthesis of certain protein(s), collectively termed "killer protein," because of a lack of NGF.

Animals↗
PubMed1990

Reduction of delayed neuronal death by inhibition of protein synthesis.

Brief forebrain ischemia in rodents causes delayed neuronal death selectively in the CA1 pyramidal cells of hippocampus. Treatment with a reversible protein synthesis inhibitor, anisomycin, significantly reduced the occurrence of delayed neuronal death in the Mongolian gerbil. This result indicates that de novo synthesis of certain protein(s), collectively termed 'killer protein' is required, possibly due to deprivation of nerve growth factor or other trophic factors.

Animals↗