[Prognosis of thalamic hemorrhage with special reference to CT findings].
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Aged↗
Biomedical subjects
J Hamada
Publications and source records attributed to J Hamada.
[Effects of intravitreal injection of endothelin on the visual system].
Endothelin, a novel, potent, and long-acting vasoconstrictor peptide, is thought to regulate retinal circulation and its autoregulation. A disturbance in the regulation of endothelin production might contribute to the pathogenesis of retinochoroidal or optic nerve diseases. We examined the effects of endothelin on the retina and the optic nerve using the electroretinogram (ERG) and visual evoked potential (VEP). Six male albino rabbits underwent intravitreal injection of 0.1 ml (10(-5) mol/l) endothelin-1 in the right eye. Six other male albino rabbits, which were injected intravitreally with 0.1 ml of Opeguard-MA in the right eye, were used as controls. Endothelin-1 caused marked constriction of retinal vessels and pallor of the optic nerve head. These findings persisted for 10 days after endothelin-1 injection. The amplitude of the b-wave and the latency of the oscillatory potential in the ERG were not significantly different from those in controls. On the other hand, prolongation of the VEP-N1 latency was observed for 14 days after the injection. These results indicate that endothelin acts on the circulation of the optic nerve head rather than that of the retina, and that effects persist for a relatively long period.
Animals↗
[Effect of endothelin-1 on ocular circulation].
Endothelin (ET)-1, a potent vasoconstrictor which was discovered recently, might be involved in the regulation of ocular circulation. In this paper, we studied the effects of ET-1 on capillary blood flow of the optic nerve head and choroid in rabbits, using a hydrogen gas clearance flowmeter. Intravitreal injection of 0.1 ml of ET-1 at 10(-5) M and 10(-6) M caused a significant decrease in blood flow, which in the optic nerve head continued more than 3 hours, but in the choroid recovered at 3 hours after the injection (maximum decrease occurred at 75 minutes and at 30-60 minutes, respectively). Intraocular pressure was reduced as the time passed. Intravenous administration of 10(-10) mol/kg of ET-1 induced a reduction in blood flow, which in the optic nerve head continued more than 3 hours, but in the choroid recovered at 90 minutes after the administration. Intraocular pressure was reduced during 3 hours' observation. The decrease in blood flow in the optic nerve head was inhibited by previous administration of calcium antagonist (nicardipine), so the calcium channel was thought to be involved in this reaction.
Animals↗
[Enhanced malignancy of tumor cells by the interaction with host cells reactive to foreign body].
We examined factors promoting malignant progression using a weakly malignant variant cell line, ER-1, derived from c-SST-2, a rat mammary carcinoma. ER-1 cells were converted to a highly malignant phenotype (highly tumorigenic, metastatic, invasive in vitro) by the in vitro/in vivo interaction with host cells reactive to foreign body. Epidermal growth factor (EGF) and transforming growth factor-beta (TGF-beta) produced by host reactive cells, transiently enhanced the tumorigenicity and in vitro invasiveness of ER-1 cells into an endothelial cell monolayer. The host reactive cells also produced oxygen radicals and induced mutations in ER-1 cells. It is speculated that mutations induced by host reactive cells cause cellular diversification, including the emergence of highly malignant variant cells whose growth is selectively promoted by growth factors such as EGF and TGF-beta.
Animals↗
Separable growth and migration factors for large-cell lymphoma cells secreted by microvascular endothelial cells derived from target organs for metastasis.
Metastatic variant sublines of the murine large-cell lymphoma cell line RAW117 were tested for their growth and migration properties in vitro in medium conditioned by soluble factors released from syngeneic mouse liver-, lung-, and brain-derived microvessel endothelial cells. Medium conditioned with hepatic sinusoidal endothelial cells stimulated the growth of highly liver-colonising (RAW117-H10) and highly liver- and lung-colonising (RAW117-L17) sublines at higher rates than the poorly metastatic parental line (RAW117-P) (H10 greater than L17 greater than P). Medium conditioned with lung microvessel endothelial cells selectively stimulated the growth of the lung-colonising RAW117-L17 subline. Medium conditioned with brain microvessel endothelial cells showed no growth selectivity, and equivalently stimulated the growth of various RAW117 cell sublines. Medium conditioned with hepatic sinusoidal endothelial cells preferentially promoted the migration of the liver-colonising H10 and L17 sublines, and medium conditioned with lung endothelial cells differentially stimulated the migration of the lung-colonising L17 subline; whereas medium conditioned with brain endothelial cells only slightly stimulated the migration of L17, but not H10 or P cells. Fractionation of medium conditioned with hepatic sinusoidal endothelial cells by DEAE Sephacel anion exchange chromatography revealed that the growth-stimulating activities were clearly separable from migration-stimulating activities. The growth- and migration-stimulating activities released from organ microvessel endothelial cells may be important in determining the ability of RAW117 cells to selectively form metastatic colonies in particular organs.
Animals↗
Progression of weakly malignant clone cells derived from rat mammary carcinoma by host cells reactive to plastic plates.
Tumor progression is the process by which tumor cells acquire more malignant properties, such as invasiveness and metastasis, during tumor development. To elucidate mechanisms of tumor progression, we examined the role of interactions between the tumor and its host by using a cloned cell line, ER-1, which was derived from a rat mammary carcinoma. ER-1 is weakly tumorigenic and non-metastatic when s.c. injected into syngeneic hosts in single cell suspension. However, ER-1 cells show a high incidence of lethal growth when s.c. implanted (5 x 10(2) cells), being attached to a 10 x 5 x 1 mm polystyrene plate. Tumor cell lines (PLT) obtained from tumors which had arisen from the plate-attached ER-1 cells no longer required plates for their growth in normal hosts, and had acquired metastatic ability to the lungs. The malignant phenotypes of PLT were stable under a usual culture condition for at least 6 months. Furthermore, the incidence of tumor development increased when small numbers of ER-1 cells were injected onto plates (or at their periphery) which had previously been implanted s.c. without tumor cells. The tumorigenicity of ER-1 cells increased after they were cocultivated for more than 30 days with host reactive cells obtained from the tissues surrounding the plates. These results suggest that host cells reactive to the foreign body (plastic plate) may not only promote the local growth of ER-1 cells but also convert them into much more malignant tumors.
Animals↗
Effect of radiation therapy against intracranial hemangiopericytoma.
Seven cases of intracranial hemangiopericytoma were studied retrospectively to investigate the efficacy of radiation therapy. Tumor response evaluated by computed tomography and magnetic resonance imaging was obvious after 20-30 Gy irradiation. The total reduction rate was 80-90% and continued as long as 5-7 months after treatment. In five patients receiving radiation therapy before radical removal, the tumors were easily removed without massive hemorrhage. Histological inspection of specimens after irradiation showed a significant disappearance of tumor cells. Pyknosis frequently occurred in endothelial cells, and proliferating vessels with hyalinoid degeneration were also seen. Reticulin fibers between tumor cells were fewer, split, or absent. Preoperative radiation therapy is useful in the treatment of hemangiopericytoma involving considerable surgical risk. Postoperative radiation therapy should be given even if removal is complete.
Adolescent↗
Dynamic magnetic resonance appearance of the vertebral dissecting aneurysm--case report.
A dissecting aneurysm of the vertebral artery occurred in a 38-year-old male presenting with ischemic attacks. Vertebral angiography revealed irregular narrowing and dilatation of the right vertebral artery, and retention of the contrast medium. Routine T1-weighted magnetic resonance (MR) imaging demonstrated signal voids compatible with a patent but narrowed vertebral lumen surrounded by three intensity components at the abnormality location identified on the vertebral angiograms. Dynamic MR imaging demonstrated strong enhancement of these components on the early images. These findings were consistent with the false lumen of the dissecting aneurysm. The different signal intensities were thought to reflect the blood flow rate.
Adult↗
Preferential growth stimulation of metastatic rat mammary adenocarcinoma cells by organ-derived syngeneic fibroblasts in vitro.
To determine whether organ-derived fibroblasts differentially affect the growth of cells from tumors that preferentially metastasize to specific organs, we investigated the effect of medium conditioned with primary cultured rat fibroblasts from various organs on the in vitro growth of metastatic cell lines and clones of the rat 13762NF mammary adenocarcinoma. The conditioned medium from fibroblasts derived from rat mammary fat pad differentially stimulated tumor cell growth in monolayer culture and clonogenic growth in soft agarose of the highly metastatic clone MTLn3 in a dose-dependent manner. Conditioned medium from fibroblasts derived from the lung and liver also stimulated the growth of clone MTLn3 cells but to a lesser extent than did mammary fat pad fibroblasts. In contrast, poorly metastatic cell clones (MTC, MTPa) did not respond to the growth stimulatory factor(s) from the fibroblast-conditioned medium. The factor(s) responsible for the growth stimulation were inactivated by heat and trypsin treatment and inhibited by low pH and cycloheximide. The result suggest that fibroblasts in different organs have different effects on tumor cell growth, and they may determine, in part, the organ specificity of tumor development and metastasis.
Adenocarcinoma↗
Mechanisms of c-erbB2/neu oncogene-induced metastasis and repression of metastatic properties by adenovirus 5 E1A gene products.
c-erbB2/neu is a transforming oncogene that encodes a 185-kDa transmembrane glycoprotein. In many but not all studies, amplification and/or overexpression of the human c-erbB2/neu oncogene has been correlated with poor prognosis and the number of lymph node metastases in node-positive breast cancer patients. We have shown that expression of the activated rat c-erbB2/neu oncogene in mouse embryo fibroblast 3T3 cells is sufficient to induce experimental metastases in nude mice. Important steps in the metastatic event are tumor cell adhesion to endothelial cells and invasion of basement membranes. Therefore, we further examined the ability of c-erbB2/neu oncogene-transformed 3T3 cells to adhere to microvessel endothelial cells and secrete basement membrane-degradative enzymes. The c-erbB2/neu oncogene-transformed 3T3 cells were shown to be more adherent and have higher gelatinase activities. Since we had previously shown that the adenovirus 5 E1A gene product can suppress c-erbB2/neu-induced transformation of 3T3 cells, we examined the possibility that E1A can abrogate the metastatic properties of c-erbB2/neu-transformed 3T3 cells. We found that introduction of the E1A gene into c-erbB2/neu-transformed 3T3 cells reduced the formation of experimental metastatic tumors and inhibited metastasis-associated properties, such as adhesion to microvessel endothelial cells, migration through a layer of reconstituted basement membrane (Matrigel) and secretion of basement membrane-degradative enzymes. The results indicate that the mechanism by which the c-erbB2/neu gene induces higher metastatic potential is to promote adhesion and invasion steps of the metastatic cascade. The E1A gene, which functions by inhibiting these steps, is thus a suppressor gene for c-erbB2/neu-induced experimental metastasis.
Adenovirus E1A Proteins↗
Suramin. A potent inhibitor of melanoma heparanase and invasion.
Suramin, a polysulfonated naphthylurea, has anti-reverse transcriptase and anti-proliferative activities and inhibits the binding of various growth factors to their cell surface receptors. This drug is used in the treatment of acquired immunodeficiency syndrome and several types of cancers. Increased levels of circulating glycosaminoglycans have been observed in suramin-treated cancer patients, suggesting that it may inhibit glycosaminoglycan catabolism. Melanoma-derived heparanase, a heparan sulfate-specific endo-beta-D-glucuronidase that plays an important role in metastatic melanoma cell invasion through basement membranes, is inhibited by suramin in a dose-dependent manner: 100% inhibition was observed at a concentration of approximately 100 microM. Structurally related polysulfonated compounds, such as trypan blue and Evans blue, had lower heparanase inhibitory activities: the concentrations required for 50% heparanase inhibition (ID50) were 310-320 microM and six times higher than for suramin (ID50 = 46 microM). Oversulfated heparin tetrasaccharide, whose average molecular size is similar to suramin, had also much lower heparanase inhibitory activity than suramin. The inhibition constants (Ki) for suramin and oversulfated heparin tetrasaccharide were 48 and 290 microM, respectively. Suramin had a remarkable inhibitory activity against B16 melanoma cell invasion through reconstituted basement membranes (ID50 less than 10 microM). The inhibitory effects of suramin on melanoma heparanase and cell invasion appeared to be completely independent of its antiproliferative activity, because significant effects on melanoma cell growth were not observed at the concentrations of suramin used in this study. The results suggest that the antimetastatic effects of suramin may be due to its antiinvasive rather than antiproliferative activities.
Animals↗
Locus coeruleus stimulation exerts different influences on the dynamic changes of cerebral pial and intraparenchymal vessels.
The present experimental study was undertaken to investigate the effects of locus coeruleus stimulation on the dynamic changes of intraparenchymal vessels and pial vessels. Twelve cats were anaesthetized with alpha-chloralose and urethane. For stimulation of the locus coeruleus, a concentric stainless-steel needle electrode was inserted stereotaxically. During the stimulation, volumetric changes of the intraparenchymal vessels were monitored by a photoelectric method for estimating the cerebral blood volume (CBV) (6 cats), and the diameters of pial arteries were measured continuously using a video camera system (6 cats). The CBV followed a decreasing course during the stimulation of the locus coeruleus. The decrease in CBV from the control value (6.3 vol%) was 0.14 +/- 0.04 vol% at 80 s (p less than 0.05), 0.15 +/- 0.05 vol% at 100 s (p less than 0.05), and 0.15 +/- 0.03 vol% at 120 s (p less than 0.01). After cessation of the stimulation, CBV showed a gradual recovery. On the other hand, the diameters of the pial arteries did not change during or after the stimulation of the locus coeruleus. The above results suggest that the locus coeruleus has a vasoconstrictive effect on the intraparenchymal vessels, although it exerts no apparent influence on the pial arteries.
Animals↗
Epidural tuberculoma of the spine: case report.
Epidural tuberculomas of the spine have been reported only rarely during the past few decades. A case of a surgically treated epidural tuberculoma of the thoracic spine in a 76-year-old women is presented.
Aged↗
Abnormal origin of bilateral ophthalmic arteries. Case report.
The case of a 64-year-old woman with multiple intracranial aneurysms and abnormal ophthalmic arteries arising from the bifurcation of the internal carotid artery is described. It is believed that this type of anomaly of the ophthalmic artery has not previously been reported. The neuroradiological and operative findings of this case are presented.
Cerebral Angiography↗
[Interaction between visual and auditory memories in repetitive learning].
A serial recall experiment under same- and cross-modality conditions was carried out according to Hebb's (1961) paradigm. Subjects memorized strings of nine digits in 18 trials, which were divided into early trials and late ones. Under the same-modality condition the strings used in the 18 trials were presented through the same modality, i.e., visual or auditory, whereas under the cross-modality condition the strings used in the early and late trials were presented through two different modalities. A repeated string and unrepeated strings were presented 3 and 6 times respectively in both early and late trials. The results showed that (1) repetitive learning in the same-modality occurred for both visual and auditory; (2) there was a non-additivity of cross-modal repetitive learning from auditory to visual, whereas there was an additivity of cross-modal repetitive learning from visual to auditory. We inferred that the visual inputs received both visual coding and auditory coding through an audio-transformation so as to be separately memorized in visual and auditory memories, whereas the auditory inputs were memorized in the auditory memory through the auditory coding alone.
Adult↗
[A case of "non specific multiple ulcers of the small intestine" with perforation as a presenting sign].
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Humans↗
Junctional communication of highly and weakly metastatic variant clones from a rat mammary carcinoma in primary and metastatic sites.
We have investigated junctional intercellular communication (JC) in primary and metastatic sites, using two highly and two weakly metastatic variant clones which had been isolated from a rat mammary carcinoma cell line, c-SST-2. After each variant had been subcutaneously inoculated into syngeneic rats, tumor cells were isolated from local tumor (primary tumor) and their metastatic foci (lung, heart and kidney). The cells were then recultured, and we measured their JC in vitro by the dye transfer method with the fluorescent dye Lucifer yellow CH, and found that the homologous (tumor cell-tumor cell) JC of highly metastatic clones were less in recultured tumor cells from primary tumors than that of weakly metastatic clones. At the same time, the heterologous (tumor cell-normal fibroblast) JC of highly metastatic clones was less than that shown by weakly metastatic clones. On the other hand, tumor cells obtained from metastatic foci showed relatively reduced JC (homologous and heterologous) when compared with those from their primary tumors in the weakly metastatic clones. These data suggest that a decrease in and/or a loss of JC may play a role in the expression of metastatic properties.
Animals↗
Ultrastructural differences in junctional intercellular communication between highly and weakly metastatic clones derived from rat mammary carcinoma.
We examined by electron microscopy the differences in junctional intercellular communications among highly metastatic clones, weakly metastatic clones, and the parent clone obtained from a spontaneously developed rat mammary carcinoma. We also investigated intercellular communications of the highly and weakly metastatic clone cells with normal fibroblasts. The results showed that ultrastructural changes of the highly metastatic clone cells, such as microvilli, microfilaments, and small organelles including endoplasmic reticulum, Golgi apparatus, and mucous particles, were more distinct than those of the weakly metastatic clone cells, and that the numbers of desmosome and gap junctions of weakly metastatic clone cells were significantly greater than those of highly metastatic clone cells. The formation of gap junctions and desmosomes was found only between weakly metastatic clone cells and normal fibroblasts. When both highly and weakly metastatic clone cells were cultured with normal fibroblasts, a tight junction was observed only in the culture of weakly metastatic clone cells and normal fibroblasts. These results suggest that ultrastructural differences are related to the proliferation and detachment of tumor cells from the primary site in the initial stage of tumor metastasis.
Animals↗