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Biomedical subjects

T Oyama

Publications and source records attributed to T Oyama.

At least 163 records · Page 9Linked to original sources
PubMed1995

Malignant rhabdoid tumor of the breast: a case report.

A 66-year-old woman developed a malignant rhabdoid tumor of the breast, with a tumor doubling time of 10 days. One month after radical mastectomy, there was local recurrence, followed by multiple pulmonary metastases, and the patient died of respiratory failure 5 months after surgery. The gray-white-colored tumor measured 13 x 12 x 10 cm, and its border was well defined. The tumor was composed of diffusely growing round or polygonal cells with vesicular nuclei, prominent nucleoli, and ample cytoplasm containing eosinophilic inclusions. Lymph node involvement was widespread. Both vimentin and keratin were clearly demonstrated by immunohistochemical staining. Ultrastructural studies revealed that the MRT cells contained cytoplasmic whorls of intermediate filaments.

Aged↗
PubMed1995

The effects of imipramine, amitriptyline and clonidine administered by iontophoresis on the pain threshold.

We performed iontophoresis of aqueous solution of imipramine and amitriptyline, tricyclic antidepressant, and clonidine, an alpha 2 agonist, in a total of 30 healthy adult volunteers. Analgesic effects were compared among the 3 drugs by measurement of the pain threshold using a thermopainmeter. No significant changes in the pain threshold were observed with imipramine or amitriptyline. On the other hand, clonidine significantly increased the pain threshold, compared with the control value before iontophoresis. Although the effects of iontophoresis of clonidine were smaller than the previously reported effects of iontophoresis with other drugs, these effects seemed to be due to the action of clonidine itself not associated with electric stimulation. More marked effects may be obtained with changes in the conditions of iontophoresis.

Adrenergic alpha-Agonists↗
PubMed1995

The effect of calcium channel antagonist administered by iontophoresis on the pain threshold.

Three calcium (Ca) channel antagonists were administered to healthy adult volunteers by iontophoresis alone or in combination with lidocaine to study their effects on the pain threshold. Nicardipine, verapamil or diltiazem administered alone elevated the pain threshold to the same degree as lidocaine. When Ca channel antagonists were administered in combination with lidocaine, the pain threshold elevation was not changed, but the duration of the analgesic action was prolonged when compared with lidocaine alone. These results suggest a role of the calcium channel in the pain control mechanism and the possible clinical application of Ca channel antagonists delivered by iontophoresis in pain management.

Adult↗
PubMed1994

A truncated beta-catenin disrupts the interaction between E-cadherin and alpha-catenin: a cause of loss of intercellular adhesiveness in human cancer cell lines.

Cadherin cell adhesion molecules play an essential role in creating tight intercellular association and are considered to work as an invasion suppressor system of cancer cells. They form a molecular complex with catenins, a group of cytoplasmic proteins including alpha- and beta-catenins. While alpha-catenin has been demonstrated to be crucial for cadherin function, the role of beta-catenin is not yet fully understood. In this study, we analyzed the cadherin-catenin system in two human cell lines, HSC-39 and its putative subline HSC-40A, derived from a signet ring cell carcinoma of stomach. These cells grow as loose aggregates or single cells, suggesting that their cadherin system is not functional. In these cell lines, an identical 321-base pair in-frame mRNA deletion of beta-catenin was identified; this led to a 107-amino-acid deletion in the NH2-terminal region of the protein. Southern blot analysis disclosed a homozygous deletion in part of the beta-catenin gene. On the other hand, these cells expressed E-cadherin, alpha-catenin, and plakoglobin of normal size. Immunoprecipitation analyses showed that E-cadherin was coprecipitated with the mutated beta-catenin but not with alpha-catenin, and antibodies against beta-catenin did not copurify alpha-catenin. However, the recombinant fusion protein containing wild-type beta-catenin precipitated alpha-catenin from these cells. These results suggest that the dysfunction of E-cadherin in these cell lines is due primarily to its failure to interact with alpha-catenin, and that this defect results from the mutation in beta-catenin. Thus, it is most likely that the association between E-cadherin and alpha-catenin is mediated by beta-catenin, and that this process is blocked by NH2-terminal deletion in beta-catenin. These findings indicate that genetic abnormality of beta-catenin is one of the mechanisms responsible for loosening of cell-cell contact, and may be involved in enhancement of tumor invasion in human cancers.

Animals↗
PubMed1994

c-erbB-2 gene product associates with catenins in human cancer cells.

Phosphorylation of beta-catenin, an intracytoplasmic cadherin-binding protein, causes disruption of the cadherin-mediated cell adhesion system in cancer cells. A 185-kDa phosphorylated protein, identified as the c-erbB-2 gene product, was co-immunoprecipitated with the E-cadherin-catenin complex. Association of the c-erbB-2 gene product with the cadherin-catenin complex was proven to be mediated through beta-catenin and plakoglobin using an in vitro protein-protein precipitation system. These results indicate that the c-erbB-2 gene product associates with catenins and may regulate the cell adhesion and invasive growth of cancer.

Cadherins↗
PubMed1994

E-cadherin gene mutations in human gastric carcinoma cell lines.

Reduced expression of E-cadherin has been regarded as one of the main molecular events involved in dysfunction of the cell-cell adhesion system, triggering cancer invasion and metastasis. However, even with a sufficient amount of E-cadherin, cell-cell adhesion is sometimes lost in "diffusely invasive" human carcinomas. Ten human cancer cell lines, showing growth characterized morphologically by loose cell-cell adhesion, were analyzed for possible structural abnormalities of their expressed E-cadherin. Four of the cell lines showed strong mRNA and protein expression with no nucleotide sequence abnormalities, and mRNA was absent in four other cell lines. mRNA sequence was abnormal in the remaining two gastric carcinoma cell lines. In MKN45 (poorly differentiated adenocarcinoma), this involved a 12-bp in-frame deletion with strong expression of mRNA and protein. In KATO-III (signet ring cell carcinoma), there were four mRNA species with insertions of different sizes, among which the major transcripts (with a 7-bp insertion) caused a frameshift, and expression of both mRNA and protein was markedly reduced. In these two cell lines, DNA mutations were detected around exon-intron junctions, revealing that aberrant RNA splicing was the cause of the mRNA abnormalities. In addition, the wild-type allele of the E-cadherin locus was lost, suggesting that the E-cadherin gene had been inactivated by two hits (mutation and allele loss), similar to the mechanism for inactivation of tumor suppressor genes.

Amino Acid Sequence↗
PubMed1994

A case of Pick's disease with unusual neuronal inclusions.

An autopsy case of unusual Pick's disease in a 61-year-old male is described. Findings included severe atrophy of the frontal and temporal lobes, pyramidal tracts and basal ganglia accompanied by numerous intraneuronal argyrophilic hyaline inclusions. His neurological symptoms were constantly progressive during the 12-year course, characterized by akinesia and emotional incontinence. The inclusions were round, well-demarcated, slightly eosinophilic and intensely argyrophilic bodies in the perikarya, and distributed mainly in the subiculum and Sommer's sector of the hippocampus, amygdala and affected gyri. Immunocytochemically, they contain antigenic determinants of both phosphorylated and nonphosphorylated neurofilaments, but were negative for ubiquitin. Ultrastructurally, they were composed primarily of skeins of neurofilaments intermingled with cell organelles. Tubular profiles studded with granular substances, previously reported as a feature of the generalized variant of Pick's disease, and Hirano body-like lattice structures were occasionally observed in the inclusions. This case represents a slowly progressive neurodegenerative disorder characterized by fronto-temporal lobar atrophy and might by categorized as a variant of Pick's disease. However, some unusual properties of neuronal inclusions may suggest a different pathogenesis from that in classical Pick's disease.

Dementia↗
PubMed1994

Elevated immunoreactivity for glutamic acid decarboxylase in the rat cerebral cortex following transient middle cerebral artery occlusion.

We investigated the expression of glutamic acid decarboxylase (molecular weight 67,000; GAD67) immunohistochemically in the rat cerebral cortex following transient middle cerebral artery occlusion (MCAO) capable of producing slowly progressive neuronal damage. An increase in GAD67 immunoreactivity was observed in the cerebral cortex ipsilateral to the ischemic insult, most prominent in lamina IV, 3 to 14 days after MCAO. At this stage, light microscopy showed GAD67-positive puncta to be larger and more strongly immunoreactive in the ipsilateral cortex than those in the contralateral side. The elevated expression of GAD67 in the insulted cortex may reflect part of the adaptive functional changes in GABA transmission with slowly progressive cortical ischemic damage.

Animals↗
PubMed1994

In vivo induction of the growth associated protein GAP43/B-50 in rat astrocytes following transient middle cerebral artery occlusion.

Immunohistochemistry was used to investigate the induction of growth-associated protein GAP43/B-50 in the astrocytes of rat cerebrum in vivo following ischemic injury produced by 30 min of transient middle cerebral artery occlusion. Three days after operation, GAP43 immunoreactivity first appeared in some astrocytic populations surrounding the infarcted lesion. Induction of GAP43 in those astrocytes persisted for up to 14 days and disappeared at 30 days postoperation. Double-immunofluorescence staining confirmed that the GAP43-immunoreactive astrocytes examined were all positive for glial fibrillary acidic protein. Our present data suggest that certain astrocytes could be induced to synthesize GAP43 in vivo in response to an ischemic insult in adult rats.

Animals↗
PubMed1994

Efficiency of serum copper/zinc ratio for differential diagnosis of patients with and without lung cancer.

We examined serum copper (Cu), serum zinc (Zn), and the serum copper/zinc ratio (Cu/Zn) in 162 patients. All of them were seen to have an abnormal shadow in the chest X-ray films, that is, 109 patients with lung cancer (LC) and 53 patients with no lung cancer (NLC). The mean Cu and Cu/Zn in LC patients were significantly higher than those in NLC patients (p < 0.05). In LC patients, Cu and Cu/Zn were higher and Zn was lower in advanced tumors than early ones. There was a significantly clear relation between Cu or Cu/Zn and the tumor (T) stages. When the relative risk (RR) of LC was estimated, it was seen that the higher Cu and Cu/Zn became, the higher RR became. Furthermore, we showed the sensitivity of the receiver operator characteristic of the test (ROC) curve for Cu, Cu/Zn, and carcinoembryonic antigen (CEA) to diagnose LC, as explained in a paragraph of methods. The determinations of Cu, Zn, and Cu/Zn are simple and inexpensive. They also appear to have a great diagnostic value in determining the local invasion of LC and as a screening test in the high-risk patients for LC.

Adult↗
PubMed1994

A comparative study of flow cytometry and histopathologic findings in thyroid follicular carcinomas and adenomas.

As a possible diagnostic aid in the often difficult histopathologic distinction of thyroid follicular carcinomas from adenomas based on invasion most flow cytometry studies have indicated a higher aneuploidy incidence in carcinomas. However, these reports often are difficult to analyze mainly due to nonuniformity of pathologic diagnostic criteria. The present study compares the flow cytometry results of 65 follicular tumors with pathologic findings based on the World Health Organization's specific diagnostic and staging criteria. Aneuploidy was significantly higher in the 28 cancers than in the 27 hypercellular (fetal and embryonal) adenomas (57% v 22%; P = .02). There was a high percentage of aneuploidy (75%; nine of 12 cases) in the widely invasive follicular carcinomas, compared with 40% (six of 15 cases) in the minimally invasive carcinomas, 22% (six of 27 cases) in the hypercellular adenomas, and 10% (one of 10 cases) in the normofollicular or macrofollicular adenomas. However, aneuploidy was not significantly different between the most difficult differential histopathologic diagnoses of minimally invasive follicular carcinoma (40%; six of 15 cases) and hypercellular adenoma (22%; six of 27 cases) (P = .12). Other data included relatively high frequencies of aneuploidy in hypercellular adenomas (29%; six of 21 cases) and diploid status of carcinomas (36%; 12 of 33 cases). In summary, although the overall findings show a trend toward increasing aneuploidy from well-differentiated and hypercellular adenomas to minimally and widely invasive follicular carcinomas, the aneuploidy data are inconsistent and indicative of its nonspecificity and limited diagnostic usefulness.

Adenocarcinoma, Follicular↗
PubMed1994

Cellular localization of type II Ca2+/calmodulin-dependent protein kinase in the rat basal ganglia and intrastriatal grafts derived from fetal striatal primordia, in comparison with that of Ca2+/calmodulin-regulated protein phosphatase, calcineurin.

We investigated immunohistochemically the cellular localization of multifunctional type II Ca2+/calmodulin-dependent protein kinase in the rat basal ganglia and intrastriatal grafts derived from fetal striatal primordia, in comparison with that of calcineurin, a reliable marker for striatal medium-sized spinous neurons. The type II Ca2+/calmodulin-dependent protein kinase-positive neurons were of medium size, with a mean diameter of 16.1 +/- microns (average +/- S.D., n = 72, range 13.6-18.3 microns) and comprised approximately 70% of the total neuronal population in the striatum. Light microscopy showed that the type II Ca2+/calmodulin-dependent protein kinase-positive cells had round, triangular or polygonal cell bodies with relatively little cytoplasm. Analysis of serial sections showed that type II Ca2+/calmodulin-dependent protein kinase and calcineurin immunoreactivities were co-localized in the striatal neurons examined with a similar distribution pattern. Type II Ca2+/calmodulin-dependent protein kinase-positive cells were always immunoreactive for calcineurin and cells negative for type II Ca2+/calmodulin-dependent protein kinase showed no apparent calcineurin immunoreactivity. Type II Ca2+/calmodulin-dependent protein kinase-positive nerve fibers in the globus pallidus and substantia nigra almost disappeared following striatal ischemic injury produced by transient middle cerebral artery occlusion and cerebral hemitransection, respectively, suggesting that these immunopositive fibers were striatal projections. Thus, most type II Ca2+/calmodulin-dependent protein kinase-positive neurons in the rat striatum are considered to be of the medium-sized spinous type. Type II Ca2+/calmodulin-dependent protein kinase or calcineurin immunoreactivity was also observed in a large number of neurons in transplants derived from fetal striatal primordia grafted into striatal ischemic lesions. In addition, type II Ca2+/calmodulin-dependent protein kinase- or calcineurin-immunoreactive nerve fibers appeared in the deafferented globus pallidus of the host rats, suggesting that the striatopallidal pathway was reformed by striatal projection neurons of the transplants. This finding may also indicate that Ca2+/calmodulin-regulated enzymes are useful for tracing striatal projection fibers as endogenous marker proteins.

Animals↗
PubMed1994

A clinicopathological evaluation of nucleolar organizer region proteins in human breast carcinoma.

The number of nucleolar organizer region proteins (NORs) identified by silver staining (Ag) was studied in 106 primary breast carcinomas. The AgNOR score (mean +/- SD) in tumours smaller than 2 cm was significantly lower than that in tumours larger than 2 cm (P < 0.05). However, there was no significant difference according to other clinicopathological characteristics. According to postoperative distant recurrence, the AgNOR count was significantly higher in the group with recurrence than in the group without recurrence (P < 0.05). Further, the survival rate was significantly lower in the high AgNOR score (> or = 3) group than in the low score (< 3) group (P < 0.01). The present study indicates that the AgNOR score in human breast cancer cells is useful for evaluating cell proliferative activity and may help predict postoperative distant recurrence and, ultimately, the postoperative prognosis of patients.

Adult↗
PubMed1994

Inhibition of gastric cancer cell proliferation by antisense oligonucleotides targeting the messenger RNA encoding proliferating cell nuclear antigen.

Proliferating cell nuclear antigen (PCNA) is a nuclear protein that regulates DNA synthesis by DNA polymerase delta, and is essential for DNA replication. PCNA expression level is related to the malignancy of gastric cancer cells. Seven different gastric cancer cell lines and two kinds of control cell lines were treated with antisense oligonucleotides complementary to the messenger RNA of PCNA. Treatment of each gastric cancer cell line with antisense oligonucleotides at concentration of 10-40 microM inhibited the cell growth, colony formation and PCNA protein production in a dose-dependent manner, but only affected normal cells slightly. A random sequence oligomer showed no effect. These results show that PCNA is essential for gastric cancer cell proliferation and that the use of synthetic oligonucleotides is an effective way of producing antisense-mediated changes in the behaviour of human gastric cancers.

Base Sequence↗
PubMed1994

Antinociceptive mechanism of the aconitine alkaloids mesaconitine and benzoylmesaconine.

We explored the possible role of the specific regions in the brain stem on the antinociceptive actions of mesaconitine (MA) and benzoylmesaconine (BM) by the microinjection of MA and BM into nucleus reticularis paragigantocellularis (NRPG), nucleus raphe magnus (NRM), and periaqueductal gray (PAG). MA microinjected into NRPG, NRM, or PAG elicited a dose-dependent antinociceptive action, whereas BM injected into NRM or PAG elicited a dose-dependent antinociceptive action but not in NRPG. The NRM appeared to be the most sensitive region among the three tested locations.

Aconitine↗