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Biomedical subjects

Y Ishiyama

Publications and source records attributed to Y Ishiyama.

At least 19 recordsLinked to original sources
PubMed1992

Cross-resistance pattern in brain tumour cells resistant to antitumour chloroethylnitrosoureas.

We tested acquired resistance and cross-resistance of brain tumour cells after repeated treatments of antitumour agents including chloroethylnitrosoureas (CENUs) in clinical use for brain tumour chemotherapy. Within ten repeated 2-day incubation periods with either 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) or methyl-6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyr anoside (MCNU), brain tumour cells (9L) developed high degrees of resistance to these drugs, as evidenced by about 3- and 6-fold increases, respectively, at the 10% survival dose (SD10). The resistance has unchanged with time after termination of challenging treatments. Repeated challenges with bleomycin (BLM), cis-diaminedichloroplatinum (II) (CDDP), and methotrexate (MTX) did not develop a significant resistance. ACNU-resistant (9L/ACNU) cells showed complete cross-resistance to MCNU, and MCNU-resistant (9L/MCNU) cells to ACNU. Drug sensitivity to other DNA-damaging agents (BLM, NCS, CDDP, etoposide) than CENUs fluctuated to a lesser extent among 9L parent, 9L/ACNU, and 9L/MCNU cells. These data suggest clinical disadvantage of prolonged adjuvant CENU chemotherapy and advantage of combined CENU chemotherapy with other agents than CENUs in brain tumours.

Animals↗
PubMed1992

Development of resistance to antitumor chloroethylnitrosoureas in vitro in brain tumor cells.

Rat brain tumor cell lines (9L, C6-1, C6-2), human brain tumor cells (T98G), and HeLa S3 cells were studied to assess their acquired resistance to the chloroethylnitrosoureas (CENUs), 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and methyl-6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyr anosid e (MCNU), after 10 repeated exposures of a panel of different drug concentrations. Assay end-point was colony-forming ability after 24-h drug exposure. Intrinsic resistance was tested at the 10% survival dose (SD10) and C6-1, T98G, and HeLa S3 cell lines were 3 to 16 times more resistant to ACNU than 9L and C6-2 cell lines. After repeated exposures to ACNU, 9L and C6-2 cells acquired 2- and 5-fold resistance to ACNU respectively, whereas C6-1 and T98G cells retained a resistance almost equivalent to the respective parent cells. HeLa S3 cells also acquired resistance to ACNU, as evidenced by a 3.5-fold increase. The SD10 of the cells to MCNU ranged from 4.3 microM (C6-2 cells) to 151.7 microM (T98G cells). After long-term exposure to MCNU, all five cell lines became significantly resistant compared to their respective parent cells. The easily obtained acquired resistance to CENUs suggests a clinical disadvantage of continual and repeated adjuvant monochemotherapy with these agents.

Animals↗
PubMed1987

Studies of prevalence of Japanese cedar pollinosis among the residents in a densely cultivated area.

Prevalence studies of Japanese cedar pollinosis in densely planted areas were performed using pollen counts, patient studies, and population surveys with questionnaires. The incidence of pollinosis was increased and appeared to be related to dispersed pollen, which resulted in high immunologic responses. Onset of symptoms was influenced by hereditary factors as well as pollution from automobile exhausts.

Age Factors↗
PubMed1987

[Trigeminal somatosensory evoked potentials: II. Some clinical experiences].

Compared to other somatosensory evoked potentials (SEP), little information has been published so far on trigeminal somatosensory evoked potentials (TSEP) in the various kind of disorders. This may be due to few recording technique suitable for clinical practice. We previously reported a new recording method and showed the normal pattern of TSEP. The purpose of this report is to examine its reliability for clinical use. Sixty patients, with either a complaint of facial numbness or an organic lesion supposed to involve facial sensory pathway, were investigated. Their age ranged from 13 to 74 years old (mean 47.0). They consisted of 34 organic lesions (30 brain tumors and 4 cerebrovascular diseases) and 26 non-organic lesions (16 hemifacial spasms, 6 trigeminal neuralgias and other miscellaneous disorders). TSEP was recorded by the stimulation of the half of the contralateral upper or lower lip with the clip-shaped electrode. C'5 or C'6 (midpoint between Cz and the external auditory porus) was used as an active electrode and Fz as a reference. Two hundred or four hundred responses were averaged by a Nicolet Pathfinder II. All recordings were repeated at least twice to confirm the reproducibility. (1) Among 21 patients with a complaint of facial numbness except for neuralgia, the abnormality rate of TSEP was significantly different (p less than 0.02) between organic and non-organic lesions. The former was 87.5% (14 out of 16 cases) and the latter was 20% (1 out of 5 cases).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[Trigeminal somatosensory evoked potentials: I. Recording technic and normal responses].

The general wave form and time course of somatosensory evoked potentials (SEP) to the stimulation of upper and lower extremities has been well known in recent years. However, only a little information has been published so far on SEP to the trigeminal nerve stimulation (TSEP), and at present there is not always common methodology available in clinical practice. These may be due to the technical problems from the close proximity of stimulating and recording electrodes. The purpose of this report is to attempt to solve some of the difficulties of the procedure, as well as to show the morphology and time course of TSEP in a group of normal healthy subjects. Twenty healthy volunteers were investigated. Their age ranged from 22 to 61 years old (mean 29.3). Clip shaped silver-balled stimulating electrodes with 2 mm contact surface and interelectrode distance of 10 mm were applied to the inner surface of the lips. They were held in place without any support, thus minimizing muscle activity of the subject. Each half of the upper and lower lip was then stimulated in turn by an electrical rectangular pulse of 3 or 4 times sensory threshold (usually 1.5-2.0 mA) and 0.2 msec duration, at a rate of 2.3 per second. TSEP was recorded contralaterally from C'5 or C'6 (midpoint between Cz and external auditory porus). Fz was used as a reference. Four hundred responses were averaged by a Nicolet Pathfinder II, which also generated stimulation pulses. Stimulus polarity was reversed after each 100 stimuli to eliminate stimulus artifact. Analysis time was set to 50 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Elimination of EKG artifacts from EEGs recorded with balanced non-cephalic reference electrode method.

The EKG artifacts contaminating EEGs recorded by the balanced non-cephalic reference electrode system were removed from EEGs by using a device composed of a one channel averager and simple hardware. This device has the following advantages to the others which have been previously proposed: (1) it is possible by averaging of a few (i.e., 5) EKG artifacts in EEG records successfully with only one channel averaged EEG derived from an earlobe; (2) the averaged EKG pattern is able to follow rapid EKG pattern change due to altered body position; (3) the possibility of being affected by another kind of artifact was decreased, because the time of averaging process to obtain averaged EKG became shorter. A remaining problem in achieving a complete removal of EKG artifacts (maximally of 100 micro V) was beat-by-beat small changes in EKG wave forms due to the respiratory cycle. Therefore, it was felt that our method was sufficiently accurate for clinical examination of EEG.

Computers↗
PubMed1979

Bilaterally recorded brain stem auditory evoked responses. Their asymmetric abnormalities and lesions of the brain stem.

Simultaneous bilateral recordings (C3 to A1 and C4 to A2) of brain stem auditory evoked responses have been studied in 67 supratentorial lesions, nine midbrain lesions, 21 intrinsic pontine lesions, and 23 extrinsic compressions of the pons. The responses in supratentorial lesions showed completely normal records. In midbrain lesions, wave V was specifically altered. As wave 1 has been shown to be a far-field seventh nerve potential, and wave V the midbrain potential, waves II to IV can be inferred to originate in the central auditory pathway between the seventh nerve and the midbrain. Alterations of waves II to IV correlated well with localization of pontine lesions, and asymmetric alterations of the bilaterally recorded responses were associated with unilateral lesions of the brain stem auditory pathway and/or lesions of the crossed auditory projections.

Acoustic Stimulation↗
PubMed1975

Changes in contractility and calcium binding of guinea pig taenia coli by treatment with enzymes which hydrolyze sialic acid.

The effects of neuraminidase and phospholipase C on the contractility and the Ca++ -binding of guinea pig taenia coli were investigated. Potassium contracture or histamine-induced contracture of taenia coli was inhibited by treatment with neuraminidase, though acetylcholine-induced contracture was not. Treatment with phospholipase C markedly inhibited the contracture induced by isotonic potassium, histamine or acetylcholine. By treatment with neuraminidase for 4 hr, about 40 mumol/100 mg wer wt of sialic acid was released from taenia coli. This corresponded to two-fifths of total content of sialic acid. By treatment with phospholipase C for 2 hr, a similar amount of sialic acid to that produced by neuraminidase treatment was released. The Scarchard plot of Ca++-binding was a biphasic pattern indicating the presence of two types ofthe Ca++ -binding site with different affinity constants. Neuraminidase produced a 57% decrease in the amount of bound Ca++. The Scatchard plot of Ca++ -binding changed to a monophasic pattern indicating the disapperance of thel ow affinity Ca++ -binding site. Phospholipase C caused a 59% decrease of bound Ca++. The Scatchard plot also indicated the disappearance of the low affinity Ca++ -binding site. From these results, we speculated that sialicacid residue of surface membrane of the muscle cell was first site in the Ca++ -influx mechanism.

Acetylcholine↗