Biomedical subjects

M Sasa

Publications and source records attributed to M Sasa.

At least 91 records · Page 5Linked to original sources

PubMed1995

A Comparison of Mass Screening for Breast Cancer Using Mammography and Physical Examination Alone in Japan.

To compare the sensivity of breast cancer screening methods by conventional physical examination and film mammography, a trial of mass screening for breast cancer using mammography was principally carried out in asymptomatic women over 50 years of age in Tokushima Prefecture. In this trial craniocaudal and mediolateral oblique imagings of the breast using two-view film mammography and physical examination, using inspection and palpation of the breasts were performed independently. Breast cancer was detected in 8 of a total of 950 examinees by mammography alone, and no cases of breast cancer were detected by physical examination. The detection rate of breast cancer was 0.84%, that is 7 times higher than that(0.12%) obtained by conventional mass screening using physical examination alone. The detection rate of increased especially in the sixth and seventh decades of life. The stage of the detected breast cancer was stage 0 (Tis) in 5 cases and stage T, with a tumor size of 1.0 cm or less, in 3 cases. All 8 cases were in the early stage, and they underwent breast conservation therapy. Based on these results, it is recommended to employ mammography in breast cancer screening for asymptomatic women aged over 50 years. We consider mammography alone may be sufficient for mass screening for breast cancer in these subjects.

Journal Article↗

PubMed1995

A Malignant Phyllodes Tumor of the Breast in a 6-Year Old Girl.

We recently encountered a 6-year-old girl with a malignant phyllodes tumor of the breast. The patient's mother noticed a tumor on the right breast of her first doughter at 8 months after from her birth. The baby was brought to the Second Depertment of Surgery, University of Tokushima, at age 20 months. We recommended removal of the 3.5 x 2.9 cm tumor in the right breast, but it was not done. Next, she visited our department at 6 years of age because the tumor had gradually enlarged, reaching a size of 4.3 &timus; 4.0 cm. She underwent excisional resection of the tumor, and the tumor was diagnosed as a malignant phyllodes tumor of the breast coexisting with a borderline phyllodes tumor. To our knowledge, this is the youngest reported case of a malignant phyllodes tumor of the breast. Moreover, the malignant lesion was positive for estrogen receptor (ER) and showed strong proliferating cell nuclear antigen (PCNA) staining. On the other hand, the borderline part was negative for ER and showed weak PCNA staining. Thus, in the present case, the expression of ER, the exposure to estrogen (for example, the mother's estrogen during gestation) and increase in the proliferation rate may have played important roles in the mechanism of the transformation of the phyllodes tumor.

Journal Article↗

PubMed1995

Prednisolone excitation of medial vestibular nucleus neurons in cats.

An electrophysiological study was performed to determine whether prednisolone hydrochloride directly influenced neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats. Single neuronal activities of MVN were recorded extracellularly with a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. Each barrel was filled with prednisolone, glutamate, glutamic acid diethylester (GDEE) or CoCl2. Except for prednisolone, which was administered both intravenously and microiontophoretically, other chemicals were applied microiontophoretically to the immediate vicinity of the target neurons. These MVN neurons were classified as type I and II neurons according to their responses to horizontal and sinusoidal rotations. Intravenous prednisolone (up to 5 mg/kg) enhanced spontaneous and rotation-induced neuronal firings of both type I and II neurons in a dose-dependent manner. In a similar tendency, microiontophoretically applied prednisolone (50-200 nA) dose-dependently increased spontaneous and rotation-induced firings of both type I and II neurons. Microiontophoretic GDEE, a non-selective glutamate receptor antagonist, inhibited glutamate- and rotation-induced neuronal discharges without affecting prednisolone-induced increases in neuronal responses of MVN. In addition, iontophoretically applied CoCl2, a Ca2+ channel blocker, did not affect prednisolone-, glutamate- and rotation-induced neuronal findings of MVN. These results suggest that prednisolone induces excitation of type I and II neurons, probably by acting directly on the membrane of MVN neurons. Thus, glucocorticoids such as prednisolone may be effective for the treatment of vertigo resulting from hypofunction of vestibular nucleus neurons.

Animals↗

PubMed1995

Difference in thymidylate synthetase activity in involved nodes compared with primary tumor in breast cancer patients.

Thymidylate synthetase (TS) is a key enzyme as a methyl donor in the methylation reaction from dUMP to dTMP. TS activity was assessed in various tissue of mammary disorders. The descending order of TS activity was as follows: cancer-positive nodes, primary cancers, cancer-negative nodes, benign lesions, and normal parenchyma. Significant differences in TS activity were found between the positive nodes and each of the other tissues (p < 0.01). In node-positive cases, a significant correlation in TS activity was found between the primary cancers and positive nodes (r = 0.616, p = 0.033). There was no correlation between the nodal status and the TS activity in primary cancers. In 11 of 12 cases, the TS activity of positive nodes was higher than the 'calculated' TS activity of the primary cancer, which was defined as the TS activity per unit weight of cancer cells. A significant correlation was found between the calculated TS activity and the mitotic frequency in primary cancers (r = 0.697, p = 0.0001). On the other hand, a significant correlation could not be found between the TS activity and the mitotic frequency in positive nodes (r = 0.364, p = 0.244).

Breast↗

PubMed1995

Action of intravenously administered talipexole on the rat striatal neurons receiving excitatory input from nigral dopamine neurons.

Electrophysiological studies using rats anesthetized with chloral hydrate were performed to elucidate whether or not intravenously injected talipexole acted as a D2 receptor agonist on the striatal neurons in comparison with the action of bromocriptine. The activities of the striatal neurons were extracellularly recorded using a glass microelectrode attached along a seven-barreled micropipette, each barrel of which was filled with talipexole, bromocriptine, SCH23390 (D1 antagonist), domperidone (D2 antagonist), glutamate or 2 M NaCl. These drugs were iontophoretically applied to the immediate vicinity of the target neuron being recorded. The effects of talipexole and bromocriptine were examined on the neurons, whose spikes (induced by the stimulation of the substantia nigra pars compacta) were inhibited by the iontophoretic application of domperidone. Iontophoretic application of talipexole or bromocriptine increased spontaneous firing of these neurons and this increase in firing was also inhibited by iontophoretically applied domperidone. In the same neurons, intravenously administered talipexole (0.01, 0.02 and 0.04 mg/kg) dose-dependently increased firing, and this increase was inhibited by microiontophoretically applied domperidone, but not by SCH23390. On the other hand, the intravenous injection of bromocriptine (0.1, 0.2 and 0.4 mg/kg) also increased the firing rate. However, the increase was not dose-dependent and fluctuated; the firing transiently decreased during the increase in firing with intravenously administered bromocriptine. However, the bromocriptine-induced increase in firing was also suppressed by domperidone, and decrease in firing was inhibited by SCH23390. These findings suggest that talipexole acts as a D2 agonist on the striatal neurons receiving input from substantia nigra pars compacta and increases firing when intravenously applied.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Altered brain contents of neuropeptides in spontaneously epileptic rats (SER) and tremor rats with absence seizures.

Immunoreactive- (IR-) somatostatin (SRIF), neuropeptide Y (NPY) and corticotropin-releasing factor (CRF) contents were investigated in the brain of tremor rats with absence-like seizure and spontaneously epileptic rats (SER), which is a genetically defined double-mutant (zi/zi, tm/tm) obtained by mating zitter homozygote (zi/zi) with tremor heterozygote (tm/+) and shows both absence-like seizure and tonic convulsions. Increased levels of IR-NPY and IR-CRF were observed in several regions including the amygdala and hippocampus in homozygous SER compared to heterozygous SER (zi/zi, tm/+ or +/+). Homozygous tremor rats (tm/tm) showed lower levels of IR-NPY and IR-CRF contents mainly in the hippocampus and mesolimbic system (entorhinal and pyriform cortex and nucleus accumbens) than heterozygous tremor rats. IR-SRIF contents of homozygous SER were higher in frontal cortex than heterozygous SER and in amygdala than homozygous tremor rats. No change of IR-SRIF between groups was noted in the hippocampus among brain structures underlying epileptogenicity. The results suggest that the change of neuropeptide levels, most conspicuous in NPY among three peptides tested, may be involved in the phenotypical manifestation of seizures in SER and tremor rats, and that the development of tonic convulsion and absence seizures may be differently associated with the change of brain neuropeptide levels.

Animals↗

PubMed1995

Nitroxidergic vasodilator nerve in the canine nasal mucosa.

The canine nasal mucosa was studied by in vitro bioassay. Non-adrenergic, non-cholinergic (NANC) vasodilator response to transmural electrical stimulation was observed in the presence of guanethidine and atropine. This vasodilator response was abolished by NG-nitro-L-arginine (L-NA) which is an inhibitor of nitric oxide (NO) formation but not by NG-nitro-D-arginine. The inhibitory effect of L-NA was partially reversed by treatment with L-arginine but not with D-arginine. The vasodilator response was significantly suppressed by tetrodotoxin. The present results indicate that NO may mediate neurogenic vasodilation in the canine nasal mucosa.

Animals↗

PubMed1995

Antagonizing effects of a novel antipsychotic quinolinone derivative (OPC-14597) on dopaminergic inhibition of neuronal activities in the nucleus accumbens.

1. The effects of a newly synthesized quinolinone derivative, 7-(4-[4-(2,3-dichlorophenlyl)-1-piperazinyl]butyloxy)-3,4-di hydro-2-(1H)- quinolinone (OPC-14597), an antipsychotic drug, on neuronal activities of the nucleus accumbens (Acc) were investigated in rats anesthetized with chloral hydrate using a microiontophoretic method. 2. Spikes elicited by stimulation of the parafascicular nucleus (Pf) of the thalamus were extracellularly recorded in the Acc neuron of chloral hydrate-anesthetized adult Wistar rats using a glass microelectrode attached along a seven-barreled micropipette, each of which was filled with dopamine, OPC-14597, SKF 38393 (D1 receptor agonist), quinpirole (D2 receptor agonist) and 2M NaCl. The drugs were microiontophoretically applied to the target neurons recorded. 3. Effects of the drugs on the Acc neurons activated monosynaptically by stimulation of the Pf were examined. Spikes elicited by Pf stimulation were inhibited by iontophoretic application of dopamine, SKF 38393 and quinpirole in a dose-dependent manner. 4. Microiontophoretic application of OPC-14597 alone affected the spikes elicited by the Pf stimulation in none of 26 neurons tested. However, the dopamine-, SKF 38393- and quinpirole-induced inhibition of the spike generation in the Acc neurons was antagonized during simultaneous application of OPC-14597. 5. The firing induced by iontophoretically applied glutamate was inhibited by dopamine, SKF 38393 and quinpirole, but not by OPC-14597. However, the dopamine-, SKF 38393- and quinpirole-induced inhibition of the glutamate-induced firing was also antagonized during simultaneous application of OPC-14597 in a dose-dependent manner in all neurons tested. 6. These findings suggest that OPC-14597 blocks dopaminergic inhibition of the Acc neurons receiving input from the Pf by acting on both D1 and D2 receptors located on the neurons.

Animals↗

PubMed1995

High positive rate of pS2 expression in forefront intraductal cancerous area in breast cancer.

Multiple sections of 40 consecutive cases with invasive ductal carcinoma of the breast, all of which bad wide intraductal cancerous extension, were examined by immunohistochemical analysis for evaluation of hormone dependency in several areas of breast cancer tissues. In this study, we examined the expression of pS2 protein in the central invasive area (CIV), central intraductal cancerous area (CDC) and forefront intraductal cancerous area (FDC). pS2 staining was positive in 52.5% (21/40) of CIV and a significant correlation was found between pS2 expression in CIV and the estrogen receptor status (ER). pS2 staining was positive in 77.5% of CDC and 85.0% of FDC, respectively. A majority (68.4%) of the cases that were negative pS2 in CIV were positive for pS2 in FDC. Moreover, the cases with noncomedo intraductal carcinoma in premenopausal status showed a higher positivity of pS2 expression in FDC than the cases with comedo-carcinoma, though the number of cases of comedo-carcinoma was limited. These findings suggest that endocrine therapy may be useful after breast conserving treatment regardless of the ER status of the primary tumor.

Breast Neoplasms↗

PubMed1995

Effect of antiepileptic drugs on absence-like seizures in the tremor rat.

We examined the effects of conventional antiepileptic drugs (AEDs) on absence-like seizures in homozygous tremor rats (tm/tm) to determine if they corresponded pharmacologically to human absence seizures and absence-like seizures in spontaneously epileptic rats (SER: zi/zi, tm/tm) with both tonic convulsive and absence-like seizures. Cortical and hippocampal EEG activity was recorded with chronically implanted electrodes. The effects of AEDS on seizures of the tremor rat showed profiles similar to those observed in human absence seizures and also in absence-like seizures of SER. The absence-like seizures, associated with paroxysmal bursts of 5-7-Hz spike-wave complexes, were inhibited by trimethadione (TMO 200 mg/kg intraperitoneally, i.p.), ethosuximide (ESM 100 and 200 mg/kg, i.p.), valproate (VPA 100 mg/kg, i.p.), and phenobarbital (PB 10 and 20 mg/kg, i.p.). Phenytoin (PHT 20 mg/kg, i.p.) was ineffective. These results are consistent with the conclusion that the tremor rat is a useful model for evaluating new AEDS for human absence seizures.

Animals↗

PubMed1995

Selective blockade of P-type calcium channels by lead in cultured hippocampal neurons.

The effects of lead ions (Pb2+) on neuronal calcium channels were examined in cultured hippocampal neurons. Pb2+ blocked calcium channels in a concentration-dependent manner. The current-voltage relationship of the inhibition suggested a selective blockade of high-threshold calcium channels by Pb2+ up to a concentration of 3 microM. Pb2+ (3 microM) preferentially suppressed the omega-agatoxin IVA-sensitive components of the calcium channels. These findings suggest that Pb2+ mainly affects the P-type calcium channels at low concentrations.

Animals↗

PubMed1995

Potentiation of GABA-induced inhibition by 20-hydroxyecdysone, a neurosteroid, in cultured rat cortical neurons.

Effects of 20-hydroxyecdysone (20-HE), a neurosteroid, on cultured rat cortical neurons were examined using the whole cell recording technique. Under the voltage and current clamp conditions, brief application (5 sec) of 20-HE alone did not produce current changes nor any changes in the membrane potential. However, the chemical dose-dependently potentiated the GABA-induced current and hyperpolarization, which were blocked by bicuculline. These results suggest that 20-HE acts on the modulatory site of the GABAA receptor and potentiates GABAergic inhibition in rat cortical neurons.

Animals↗

PubMed1995

Role of glucocorticoid in vestibular compensation in relation to activation of vestibular nucleus neurons.

It is still not established whether or not glucocorticoids are effective in the treatment of vestibular disorders such as dizziness and imbalance, although these drugs in combination with several others are used to treat dizziness and imbalance in some diseases. This study was undertaken to investigate the effects of a glucocorticoid, dexamethasone, on vestibular disorder following unilateral labyrinthectomy in pigmented rabbits. Neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats were also investigated. Systemic injection of dexamethasone decreased the frequency of nystagmus and head deviation dose-dependently following hemilabyrinthectomy, and the rate of decrease was faster than that obtained by saline. In contrast, RU38486 (a glucocorticoid receptor antagonist) delayed the reduction of nystagmus and head deviation. Micro-iontophoretic application of dexamethasone rapidly enhanced the spontaneous firing of MVN neurons in a dose-dependent manner. These increases were blocked by RU38486, but not by GDEE (a glutamate receptor antagonist) or Co2+ (a Ca2+ channel blocker). These results suggest that dexamethasone directly activates the MVN neurons, thereby accelerating vestibular compensation.

Adaptation, Physiological↗

PubMed1995

Release of glutamate from the vestibular nerve in the medial vestibular nucleus as a neurotransmitter: in vivo microdialysis study.

Histochemical and electrophysiological studies suggest that glutamate is the primary afferent neurotransmitter from the vestibular nerve to vestibular nucleus. To further examine this possibility, a microdialysis study using alpha-chloralose-anesthetised cats was performed to elucidate whether glutamate is released from the vestibular nerve terminal in the medial vestibular nucleus (MVN). A microdialysis probe (CMA/10.2 mm) was inserted into the MVN and perfused with Ringer solution at 2 microliters/min. Samples were collected at 10-min intervals. Endogeneous glutamate was measured using the HPLC-ECD method. When electrical repetitive stimuli (200 microseconds duration, 0.5 mA, and 5 Hz) were given to the vestibular nerve for 10 min, an increase in the release of glutamate was observed in the MVN but not in the spinal trigeminal nucleus. These findings indicate that glutamate is the afferent neurotransmitter from the vestibular nerve to the MVN neurons.

Afferent Pathways↗

PubMed1995

Protective action of zinc against glutamate neurotoxicity in cultured retinal neurons.

PURPOSE: To examine the effects of Zn2+ on glutamate-induced neurotoxicity in cultured retinal neurons. METHODS: Primary cultures obtained from fetal rat retinas (16 to 19 days gestation) were used. The neurotoxic effects of excitatory amino acids were quantitatively assessed using the trypan blue exclusion method. RESULTS: A brief exposure of retinal cultures to glutamate or N-methyl-D-aspartate (NMDA) induced delayed cell death. Zn2+ at concentrations of 3 to 30 microM ameliorated glutamate- and NMDA-induced neurotoxicity in a dose-dependent manner. By contrast, neurotoxicity induced by a 1-hour exposure to kainate was not affected by Zn2+. CONCLUSIONS: These findings demonstrate that Zn2+ protects retinal neurons from NMDA receptor-mediated glutamate neurotoxicity.

Animals↗

PubMed1995

[Improvement of recurrent lung metastasis of breast cancer by Zoladex and cyclophosphamide].

The patient was a 38-year-old woman who was diagnosed as having right breast cancer (T1aN1bM0, stage II) at the age of 36 when she underwent right mastectomy. Postoperative adjuvant therapy was performed using UFT and tamoxifen. After 2 years and 4 months, pulmonary metastasis was diagnosed from elevated tumor markers and chest X-P. After the relapse, treatment with goserelin acetate (Zoladex) and CPA was started. After 2 months of this treatment, the tumor in the lung had shrunk in size, and after 5 months partial remission (PR) was evaluated from improvements in chest X-P and normalization of tumor markers, This PR condition continues at present. A case report is presented of a patient with premenopausal recurrent breast cancer in whom good results were obtained by concomitant administration of Zoladex and CPA.

Adenocarcinoma↗

PubMed1994

Locus coeruleus noradrenergic neurons as a micturition center.

The micturition reflex arch is composed of an afferent pathway from the urinary bladder to the pontine micturition center via the pelvic nerve and spinal cord. The efferent pathway projects from the center to the bladder through the sacral parasympathetic center of intermediolateral column cells. The pontine micturition center is thought to be noradrenergic (NA) neurons in the locus coeruleus (LC) due to the following observations: (1) LC stimulation induces bladder contraction in cats, and this response is blocked by intrathecal application of alpha 1-adrenergic antagonist (prazosin), but not the alpha 2- nor beta-adrenergic antagonist. Although this contraction is not observed after NA depletion with reserpine, with subsequent i.v. injection of L-dopa a NA precursor induces recurrence of the response. (2) The micturition reflex induced by bladder distention is similarly reversed with alpha 1-adrenergic antagonist and chemical destruction of NA cells by injecting 6-hydroxydopamine in the LC. However, subsequently applied alpha 1-adrenergic agonist induces the contraction due to bladder distention. (3) LC stimulation elicits spike generation of sacral intermediolateral cells. Microiontophoretically applied alpha 1-adrenergic antagonist inhibits the LC stimulation-induced spikes of the neuron, which is not antidromically activated by pelvic nerve stimulation. However, spikes in neurons activated antidromically were not affected by the drug. This indicates that the former and latter neurons are interneuron and parasympathetic projecting neurons, respectively. The existence of NA terminals from the LC and alpha 1-adrenergic receptors in the intermediolateral column cells supports the concept that NA cells in the LC are units constituting the micturition center.

Animals↗

PubMed1994

Dopamine-induced protection of striatal neurons against kainate receptor-mediated glutamate cytotoxicity in vitro.

The effects of dopamine on glutamate-induced cytotoxicity were examined using the primary cultures of rat striatal neurons. Cell viability was significantly reduced by exposure of cultures to glutamate or kainate for 24 h. In contrast, similar application of N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) did not induce cytotoxicity. Kainate-induced cytotoxicity was significantly inhibited by kynurenate but not by MK-801. Dopamine at concentrations of 1-100 microM dose-dependently reduced kainate-induced cytotoxicity. Forskolin also significantly reduced kainate cytotoxicity. The neuroprotective effect of dopamine was antagonized by SCH 23390, a D1 receptor antagonist, but not by domperidone, a D2 receptor antagonist. Moreover, kainate-induced cytotoxicity was prevented by SKF 38393, a D1 receptor agonist, or forskolin but not by quinpirole, a D2 receptor agonist. The patch clamp study revealed that the same striatal neurons responded to both kainate and NMDA. During voltage clamp recording, neither kainate-induced currents nor NMDA-induced currents were affected by dopamine. Moreover, dopamine did not affect glutamate- or kainate-induced Ca2+ influx measured with fura-2. These findings indicate that dopamine prevents kainate receptor-mediated cytotoxicity without affecting the kainate receptor activities and intracellular Ca2+ movement. Dopamine-induced neuroprotection may be mediated by an increased intracellular cAMP formed following activation of D1 receptors.

Animals↗