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Biomedical subjects

T Kaji

Publications and source records attributed to T Kaji.

At least 73 records · Page 4Linked to original sources
PubMed1996

Interaction between cadmium and zinc in the production and sulfation of glycosaminoglycans in cultured bovine vascular endothelial cells.

Previously, we showed that cadmium stimulates the production of glycosaminoglycans (GAGs) but inhibits their sulfation in cultured bovine aortic endothelial cells. The effect of zinc on such alterations of GAGs induced by cadmium was investigated in the present study. The incorporation of [3H]glucosamine and [35S]sulfate into GAGs was determined by the cetylpyridinium chloride precipitation method as a marker of GAG production and GAG sulfation, respectively. The incorporation of both [3H]glucosamine and [35S]sulfate was not changed in GAGs accumulated in the endothelial cell layer and the conditioned medium after exposure to zinc at 20 micrometers or less alone. A simultaneous exposure of the endothelial cell layer to zinc at 20 micrometers or less and cadmium at 2 micrometers resulted in prevention of the cadmium-induced decrease in [35S]sulfate incorporation; however, the cadmium-induced increase in [3H]glucosamine incorporation was not affected by zinc. Characterization of GAGs in the cell layer revealed that such an interaction between zinc and cadmium occurred in both heparan sulfate and the other GAGs. Zinc significantly prevented the inhibition of either [3H]thymidine or [3H]leucine incorporation caused by cadmium with less accumulation of intracellular cadmium suggesting that zinc decreased intracellular cadmium and protected endothelial cells from cadmium-induced inhibition of DNA and protein synthesis. The present data showed that a simultaneous exposure to cadmium and zinc resulted in an increase in heparan sulfate without a reduction of sulfation in the endothelial cell layer. The alteration may potentiate the antihrombogenic property of vascular endothelium.

Animals↗
PubMed1996

Effects of cadmium on the release of tissue plasminogen activator and plasminogen activator inhibitor type 1 from cultured human vascular smooth muscle cells and fibroblasts.

To evaluate the toxicity of cadmium on the blood fibrinolytic system during hemostasis, human vascular smooth muscle cells and human fibroblasts were cultured in the presence of cadmium chloride. It was found that cadmium markedly decreased the release of both tissue plasminogen activator antigen (t-PA:Ag) and plasminogen activator inhibitor type-1 antigen (PAI-1:Ag) from vascular smooth muscle cells. Other heavy metals including lead, manganese, mercury and nickel also decreased the t-PA:Ag and PAI-1:Ag release, however, cadmium was the most potent inhibitor. On the other hand, the release of t-PA:Ag was significantly increased whereas that of PAI-1:Ag was unaffected in fibroblasts after exposure to cadmium. Of the tested heavy metals, only cadmium increased the t-PA:Ag release from the cells. Electrophoretic enzymography revealed that cadmium reduced the activity of plasminogen activators in the conditioned medium of both vascular smooth muscle cells and fibroblasts. Cadmium markedly decreased the incorporation of [3H]leucine accompanied with a significant increase in the leakage of lactate dehydrogenase in vascular smooth muscle cells; however, the metal did not change these markers in fibroblasts. These results suggest that the regulation of fibrinolysis mediated by vascular smooth muscle cells and fibroblasts during hemostasis may be disturbed by cadmium.

Cadmium↗
PubMed1996

Fatal subarachnoid hemorrhage from an inflammatory cavernous carotid artery aneurysm: failure of conservative treatment after early diagnosis--case report.

Inflammatory carotid artery aneurysm is a rare complication of acute paranasal sinusitis. A 50-year-old female presented with a ruptured giant carotid artery aneurysm secondary to infection of the sphenoid sinus and cavernous sinus. She had been healthy until 5 days before admission, when she developed orbital phlegmon and meningitis. She received antibiotic therapy for 10 days. Computed tomography (CT) of the brain 2 days after admission showed no abnormality. However, repeat CT on day 6 showed a round isodense mass in the suprasellar cistern suggesting a cerebral aneurysm. Twelve days after admission, she suffered a fatal subarachnoid hemorrhage. Cerebral angiography revealed a giant left cavernous carotid artery aneurysm with a very irregular shape. Autopsy found sphenoid sinusitis and osteomyelitis extending into the cavernous sinuses. Diagnosis of bacterial inflammatory aneurysms before rupture is very important. Appropriate surgical intervention should be considered if there is enlargement of the original aneurysm or appearance of a new aneurysm indicating a potentially dangerous situation.

Anti-Bacterial Agents↗
PubMed1996

Does bone SPECT actually have lower sensitivity for detecting vertebral metastasis than MRI?

UNLABELLED: We compared the ability of bone SPECT and MRI to detect vertebral metastasis. METHODS: Skeletal scintigraphy, including planar and SPECT imaging, and spinal MRI examinations, were performed in 22 cancer patients in whom a total of 88 metastatic foci and 12 degenerative joint disease lesions were detected. Metastatic foci were defined as lesions that suggested metastasis on MRI and/or bone destruction on radiographs or CT and/or aggravation of increased tracer uptakes on serial bone scans. Image reconstruction of axial, coronal and sagittal sections was processed in a 128 X 128 matrix. MRI studies were performed with a 1.5 tesla signal scanner using fast spin-echo sequences. T1- and T2-weighted images were obtained in the sagittal plane. RESULTS: Twenty patients had at least one vertebral metastasis. MRI diagnosed 86 of the 88 (97.7%) metastatic foci; bone SPECT correctly diagnosed 81 of 88 (92.0%); and planar imaging detected 62 of 88 (70.4%). The two vertebrae with metastasis not detected by MRI were clearly seen by bone SPECT. Extra-vertebral body metastases (e.g. in the pedicle, lamina, transverse and spinous processes) were, however, most often detected by SPECT, followed by MRI and planar imaging (40 versus 32 versus 4). CONCLUSION: Vertebral SPECT, using high-resolution SPECT equipment, produced excellent results that were comparable to and complementary with MRI in detecting vertebral metastasis. Our data suggest that vertebral SPECT is superior to MRI in detecting extra-vertebral body metastasis.

Adolescent↗
PubMed1995

Stimulatory effect of lead on the proliferation of cultured vascular smooth-muscle cells.

The effect of lead nitrate on the DNA synthesis of cultured bovine aortic smooth-muscle cells has been studied. Lead at 0.5-10 microM stimulated the incorporation of [3H]thymidine into the acid-insoluble fraction of the cells in a dose-dependent manner. However, other heavy metals including zinc, copper, manganese and nickel did not show such a stimulatory effect. Stimulation of [3H]thymidine incorporation by basic fibroblast growth factor was additive to that by lead. However, stimulation by either platelet-derived growth factor or acidic fibroblast growth factor was reduced by the metal. The leakage of lactate dehydrogenase into the medium from smooth-muscle cells, a marker of cell death, was not changed by the metal. Calcium ionophore A23187 inhibited [3H]thymidine incorporation in vascular endothelial cells but stimulated it in vascular smooth-muscle cells. These results suggest that lead may stimulate the proliferation of cultured vascular smooth-muscle cells probably via a calcium-dependent pathway; the metal may mimic calcium within the cells.

Animals↗
PubMed1995

Inhibitory effect of lead on the proliferation of cultured vascular endothelial cells.

We investigated the effect of lead nitrate (0.5, 1.0, 2.0 or 5.0 microM) on the proliferation of cultured bovine aortic endothelial cells. After exposure to lead, the number of cells and the incorporation of [3H]thymidine into the acid-insoluble fraction of the cells were reduced in parallel in a concentration-dependent manner. Histologically, lead treatment resulted in a decrease in the cell number accompanied by a change in the cell shape from polygonal to spindle; however, no degenerative change was observed except in 5.0 microM lead-treated cells. Furthermore, stimulation of [3H]thymidine incorporation by either basic or acidic fibroblast growth factor was significantly reduced by lead. However, the leakage of lactate dehydrogenase into the medium from the cells, a marker of nonspecific cell damage, was not changed by lead. From these results, it was revealed that lead inhibits the proliferation of cultured vascular endothelial cells without nonspecific cell damage. Although lead does not destroy the monolayer of endothelial cells, the metal may exhibit its noxious effect in the repair process of the vascular endothelium.

Animals↗
PubMed1995

Regulation by basic fibroblast growth factor of glycosaminoglycan biosynthesis in cultured vascular endothelial cells.

The alteration of glycosaminoglycans (GAGs) in cultured bovine aortic endothelial cells after exposure to basic fibroblast growth factor (bFGF) was investigated. It was found that the incorporation of [3H]glucosamine into GAGs was markedly increased by bFGF in both the cell layer and the conditioned medium; however, that of [35S]sulfate was not changed by the growth factor. These results indicated that bFGF enhanced the sugar-chain formation but did not affect their sulfation in endothelial GAG production. Similar changes were observed in either bovine aortic smooth-muscle cells and human fibroblastic IMR-90 cells to greater and lesser degrees, respectively. Characterization of GAGs in the endothelial cell layer and the conditioned medium revealed that bFGF enhanced both heparan sulfate and the other GAGs to a similar degree. The present data suggest that bFGF may be involved in the regulation of the blood coagulation system via altering GAGs of the vascular tissue when the endothelium was damaged.

Animals↗
PubMed1995

Severe damage of cultured vascular endothelial cell monolayer after simultaneous exposure to cadmium and lead.

This study evaluates the toxicity of lead in the presence or absence of cadmium on the maintenance of a monolayer of cultured bovine aortic endothelial cells. It was histologically shown that lead at 50 microM or less induced a slight formation of de-endothelialized areas on the monolayer after a 24-h incubation. Although lead accumulated in endothelial cells in a dose-dependent manner, the cytotoxicity (evaluated by the [3H]adenine release assay) was not detected. However, cadmium (1.0 or 2.0 microM)-induced de-endothelialized areas on the monolayer was considerably larger in the presence of lead at 10 microM; the cytotoxicity of cadmium was significantly enhanced by lead. It was concluded that vascular endothelial cell monolayer is severely destroyed by a greater cytotoxicity of combination of cadmium with lead.

Animals↗
PubMed1995

A comparison of hard and soft copies processed with linear conversion and nonlinear conversion of skeletal fractures--a preliminary study.

To compare hard copies and soft copies processed with linear and nonlinear conversion of skeletal fractures, we performed a receiver-operating characteristics study of 25 digital radiographs. There was no statistical difference between hard copies with linear and nonlinear conversion. However, it may be difficult to detect small fractures on images processed by nonlinear conversion. No significant difference was seen between CRT diagnosis and that on a hard copy processed with linear conversion and frequency enhancement.

Adolescent↗
PubMed1995

Zinc-induced tolerance to cadmium cytotoxicity without metallothionein induction in cultured bovine aortic endothelial cells.

We investigated the cytotoxicity of cadmium in cultured vascular endothelial cells from bovine aorta pretreated with zinc. The cytotoxicity was evaluated by the [3H]adenine release assay. It was shown that the increase in the [3H]adenine release after challenge with cadmium was significantly prevented by pretreatment with zinc. It was histologically observed that cadmium-induced occurrence of the de-endothelialized areas was reduced in zinc-pretreated cell layer. Intracellular accumulation of cadmium was significantly less but that of zinc was more in zinc-pretreated cells. The content of cadmium in both the particulate and the cytosol fraction was decreased by zinc pretreatment; however, metallothionein content after challenge with cadmium was not changed. It was therefore concluded that zinc is capable of inducing a tolerance to cadmium cytotoxicity in cultured vascular endothelial cells; this tolerance is postulated to be due to a decrease in the intracellular cadmium accumulation rather than a metallothionein induction.

Adenine↗
PubMed1995

Intraarterial infusion of dibutyryl cyclic adenosine monophosphate plus mitomycin C for unresectable hepatocellular carcinoma: long-term survival and response to tumor growth inhibition.

RATIONALE AND OBJECTIVES: Dibutyryl cyclic adenosine 3',5'-monophosphate (dBcAMP) has the capacity to promote morphologic differentiation and to inhibit tumor growth in vitro, but it has not been well researched in the clinical setting. In this study we examined the effects of intraarterial infusion of dBcAMP plus mitomycin C (MMC) on long-term survival and growth inhibition of tumors. METHODS: Thirty-one previously untreated patients with unresectable hepatocellular carcinoma (HCC) received intraarterial infusion of dBcAMP plus MMC. According to the International Union Against Cancer staging system, three patients had stage T3, eight had stage T4a, and 20 had stage T4b cancer. Growth inhibition was defined as no computed tomography (CT) scan evidence of increase in tumor diameter for at least 6 months after treatment. RESULTS: In all 31 patients with HCC, the cumulative survival rate was 34% at 1 year, 14% at 3 years, and 9% at 5 years. The median survival was 5.0 months, with the longest survival period being 92 months. Among 21 patients in whom a tumor response could be evaluated on the basis of follow-up CT studies, two had complete regression of their primary tumors. Overall, the response rate was 43% (9 of 21). Among the 12 stage T4b patients who had HCC that included the main trunk and its major branches of the portal vein, portal thrombi had disappeared in four (33%). Among eight patients who survived more than 1 year and were evaluated for tumor response using follow-up CT scan studies, six (75%) had growth inhibition of tumor. CONCLUSION: Chemotherapy combined with dBcAMP and MMC showed a favorable response in approximately one third of 31 patients who had unresectable HCC. Because of our results, combined therapy should be strongly considered in the treatment of patients with HCC including occlusion of the main portal vein.

Antibiotics, Antineoplastic↗
PubMed1995

Stimulation of cultured vascular smooth muscle cell proliferation by thrombospondin is potentiated by zinc.

The interaction of zinc sulfate with thrombospondin (TSP) derived from bovine platelets, on the proliferation of bovine aortic smooth muscle cells was investigated using cell culture. Zinc alone has no effect but potentiates the stimulatory effect of TSP on the incorporation of [3H]thymidine into the acid-insoluble cell fraction. Other heavy metals including copper, lead, manganese and nickel did not exhibit a similar effect. In bovine aortic endothelial cells, [3H]thymidine incorporation was stimulated by zinc alone and suppressed by TSP alone; the stimulation by zinc was significantly reduced by TSP. In human fibroblastic IMR-90 cells, [3H]thymidine incorporation was stimulated by either zinc or TSP; a simultaneous treatment with zinc and TSP showed an additive effect. The present data suggest that zinc may be a unique heavy metal that potentiates the proliferation of vascular smooth muscle cells stimulated by TSP; in addition, such an interaction was observed selectively in this cell type. Since a large amount of TSP is released from alpha-granules of aggregated platelets, zinc may augment TSP activity which is involved in the physiology of vascular tissues.

Animals↗
PubMed1995

Induction of metallothionein by thrombin in cultured vascular endothelial and smooth muscle cells.

Metallothionein induction by thrombin was investigated using a culture system of vascular endothelial and smooth muscle cells. It was found that the protease induced metallothionein in endothelial cells derived from human aorta and umbilical vein as well as bovine aorta in a concentration-dependent manner. Thrombin also induced metallothionein in vascular smooth muscle cells derived from bovine aorta but not in cells derived from human, rabbit and rat aortas. In bovine aortic endothelial and smooth muscle cells, induction of metallothionein by thrombin was unaffected by the protein kinase C inhibitor staurosporine; in addition, a protein kinase C activator, phorbol 12-myristate 13-acetate, failed to induce metallothionein, suggesting that the induction by thrombin occurred through pathway(s) other than protein kinase C activation. It is suggested that metallothionein may be induced during hemostasis in the vascular tissue through protein kinase C-independent pathway(s).

Animals↗
PubMed1995

Vascular smooth muscle cells in culture are highly sensitive to cadmium cytotoxicity without species-related differences: comparison with Chang liver cells.

Human, rabbit and rat aortic smooth muscle cells (hSMC, rSMC and A10 cells, respectively) were cultured with cadmium chloride and compared with human Chang liver cells to characterize the response of vascular smooth muscle cells to the metal. It was revealed that all tested vascular smooth muscle cells were markedly more sensitive to cadmium cytotoxicity than Chang liver cells. Cadmium accumulated more markedly in vascular smooth muscle cells than in Chang liver cells. After exposure to cadmium, metallothionein was induced in a concentration-dependent manner in Chang liver cells, it was constitutively high in hSMC, sensitively induced in rSMC and was constitutively low and induced within narrow limits in A10 cells. The intracellular content of reduced glutathione was greater and significantly enhanced by cadmium only in A10 cells. The present data suggest that vascular smooth muscle cells are, in general, sensitive to cadmium cytotoxicity without any species-related differences, mainly due to a higher accumulation of the metal within cells.

Animals↗
PubMed1995

[A penetrating injury of the extracranial vertebral artery: a case report].

Penetrating injury to the vertebral artery is a very rare accident and no case except ours has been reported to date in Japan. We reported a case of successful treatment of a penetrating injury by a nail to the left vertebral artery with the use of interventional radiologic procedure. A 27-year-old man was admitted to our hospital with a complaint of penetrating injury in his neck. Left vertebral angiography revealed that a nail had penetrated into the vertebral artery at the C6 level. Considering the possibility of thrombus formation around the metallic foreign body and the risk of uncontrollable bleeding, we performed embolization of the injured vertebral artery with Interlocking Detachable Coil.

Adult↗
PubMed1995

Zinc promotes the repair of wounded monolayers of cultured vascular endothelial cells.

The effect of zinc on the repair of wounded monolayers of bovine aortic endothelial cells in a culture system was investigated. It was morphologically found that zinc promotes the appearance of the cells in the wounded area; cell number in the area was significantly increased by zinc. However, other heavy metals including copper, manganese, nickel and cobalt failed to exhibit a similar effect. The repair induced by exogenous basic fibroblast growth factor (bFGF) was potentiated by zinc but that by exogenous acidic fibroblast growth factor was unaffected by the metal. Promotion of the repair of the wounded area by zinc was completely blocked by either cycloheximide or anti-bFGF antibody. In addition, zinc-induced repair was significantly inhibited by a lipoxygenase inhibitor, nordihydroguaiaretic acid but not by a cyclooxygenase inhibitor, indomethacin. From these results, it is suggested that zinc promotes the repair process of damaged vascular endothelium through the lipoxygenase pathway that mediates the response of vascular endothelial cells to endogenous bFGF.

Animals↗