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O Honda

Publications and source records attributed to O Honda.

At least 55 records · Page 3Linked to original sources
PubMed1998

Differentiation of benign from malignant nodules by accumulation of Tc-99m pertechnetate using TI-201 delayed scans.

Thyroid carcinoma usually is characterized by a nonfunctioning or "cold" nodule depicted on the Tc-99m scan. Twelve patients with functioning "hot" thyroid nodules underwent thyroidectomy (nine hemithyroidectomies, two nodulectomies, and one subtotal thyroidectomy). Histologic examination revealed that five patients (42%) had malignant nodules (papillary carcinoma in two and follicular carcinoma in three). Of the seven patients with benign nodules, five had follicular adenoma and two had adenomatous hyperplasia. TI-201 scanning (early and delayed) was performed at the same time as Tc-99m scanning. Only one of the seven benign nodules showed accumulation on the delayed TI-201 scan, whereas all five malignant nodules showed accumulation. The delayed TI-201 scan is useful for the differentiation of benign from malignant nodules that show accumulation of Tc-99m pertechnetate.

Diagnosis, Differential↗
PubMed1998

Intrathoracic multicentric Castleman disease: CT findings in 12 patients.

PURPOSE: To assess the computed tomographic (CT) findings of intrathoracic involvement in multicentric Castleman disease. MATERIALS AND METHODS: The study comprised 12 patients with lymph node biopsy-proved Castleman disease and multicentric involvement. The patients were aged 23-58 years (mean age, 42.9 years; five men, seven women). Seven patients underwent open lung biopsy (n = 3) or transbronchial lung biopsy (n = 4), which demonstrated lymphocytic interstitial pneumonitis. RESULTS: All patients had systemic symptoms, polyclonal hypergammaglobulinemia, and bilateral hilar and mediastinal lymph node enlargement. The nodes showed mild to moderate enhancement after intravenous administration of contrast material. At thin-section CT, all 12 patients showed poorly defined centrilobular nodules. Thin-walled cysts were present in 10 patients, thickening of the bronchovascular bundles in 10, and interlobular septal thickening in nine. Less common findings were subpleural nodules, ground-glass attenuation, air-space consolidation, and bronchiectasis. CONCLUSION: Multicentric Castleman disease is characterized by the presence of systemic symptoms, bilateral hilar and mediastinal lymphadenopathy, and centrilobular nodular opacities. The pulmonary parenchymal findings are due to the associated lymphocytic interstitial pneumonitis.

Adult↗
PubMed1997

Detached retina affects morphologic and biochemical changes in the retina adjacent to bullous retinal detachment in rabbits.

PURPOSE: Long-term results, more than 10 years after successful retinal detachment surgery, have shown gradually decreasing visual acuity in some cases. It is unclear if reduced functional recovery postoperatively is caused by anatomic changes or biochemical disorders. To determine the etiology of the reduced visual acuity, we cytochemically examined the changes in the cellular responses of the edges of retinal detachments. METHODS: We histochemically studied the glucose-6-phosphatase (G6P) and 5'-nucleotidase (5'-Nase) activity in the rabbit retina. Experimental rhegmatogenous retinal detachment was produced in a rabbit model after partial vitrectomy, followed by retinal tear formation. RESULTS: Although 5'-Nase activity gradually decreased during the period of detachment, activity was still detectable after 24 weeks. G6P activity increased in the region of the detached neural retina. Around the border of the detached retina, the decrease in 5'-Nase activity extended approximately 140 micrometers into the adjacent attached retina at 2 weeks after detachment and 270 micrometers at 24 weeks. CONCLUSIONS: These observations suggest that some anatomical and biochemical damages may occur in the retina adjacent to bullous retinal detachment and may explain the reduction in postoperative vision in some clinical cases.

5'-Nucleotidase↗
PubMed1997

Analysis of localization of adult T-cell leukemia-derived factor in the transient ischemic rat retina after treatment with OP-1206 alpha-CD, a prostaglandin E1 analogue.

Prostaglandin E1 (PGE1) is commonly used in therapy for obstructive diseases, including ischemic retinopathy, in which pathogenetic reactive oxygen intermediates are responsible. However, the mechanism(s) of PGE1 in reducing tissue damage is still unclear. Adult T-cell leukemia-derived factor/human thioredoxin (ADF) is induced by oxidative stresses and has protective activity against oxidative cellular injury. To evaluate the possible involvement of ADF in the tissue-protective effect of PGE1, we analyzed ADF expression immunohistochemically using a rat transient retinal ischemia model. Rats were treated orally with 300 micrograms/kg/day OP-1206 alpha-cyclodextrin clathrate (OP-1206), a stable PGE1 analogue, for 14 days after photodynamic retinal vascular thrombosis by rose Bengal. Rats without any OP-1206 treatment were used as controls. In the OP-1206-treated rats, minimal retinal atrophy due to ischemia/reperfusion was observed histologically up to 14 days, whereas in the non-treated rats the inner layer of the retina became markedly atrophic. In parallel with the histological change, after 14 days following thrombosis ADF immunoreactivity was preserved on retinal pigment epithelial cells in the OP-1206-treated rats, whereas it was diminished in the non-treated rats. These findings suggest an important role for ADF in the OP-1206-dependent suppression of retinal tissue damage caused by oxidative insult.

Alprostadil↗
PubMed1997

Effect of 15-hydroperoxyeicosatetraenoic acid on the fibrinolytic factor release and the antithrombin binding of vascular endothelial cells.

15-Hydroperoxyeicosatetraenoic acid (15-HPETE), an arachidonate lipoxygenase product, is reported to induce severe endothelial injury. In this study, we examined the effect of 15-HPETE on the release of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) from cultured human umbilical vein endothelial cells (HUVEC). The addition of 15-HPETE to the serum-free medium reduced the release of t-PA antigen from HUVEC, while the release of PAI-1 antigen was significantly enhanced. However, treatment of the cultured HUVEC with alpha-tocopherol or nordihydroguaiaretic acid completely suppressed the 15-HPETE-induced change in t-PA and PAI-1 antigen release. 15-Hydroxyeicosatetraenoic acid (15-HETE) had no effect on the release of either antigen from cultured HUVEC. The HUVEC surfaces exposed to 15-HPETE decreased the potency for binding antithrombin III. In a reconstituted system with heparin and phosphatidylcholine, 15-HPETE decreased the ability of heparin to inactivate thrombin activity. These results suggest that the fibrinolytic factor release and the antithrombin binding of vascular endothelial cells are impaired by the attack of 15-HPETE, and that the presence of antioxidants prevents the injurious action of lipid hydroperoxide.

Antioxidants↗
PubMed1996

Vascular endothelial cell monolayer formed on membrane filter potentiates the defense against tumor cell invasion by treatment with brefeldin A.

We constructed vascular endothelial cell monolayer on a fibronectin-coated filter in a Boyden chamber and assessed the ability of 3 LL cells to penetrate through the artificial blood vessel wall. The defense of endothelial cell monolayers against the tumor cell invasion was greatly potentiated by their pretreatment with 5 or 10 micrograms/ml of brefeldin A (BFA) for 1 h (52% or 28% of control invasion). Treatment of the endothelial cell monolayers with BFA resulted in an increase in the release of inhibitory material(s) against urokinase-type plasminogen activator (u-PA) activity of 3 LL cells. Parallel experiments with the cultured endothelial cells and BFA indicated that the fungal metabolite enhanced a rate of accumulation of plasminogen activator inhibitor-1 (PAI-1) antigen, but not of tissue-type plasminogen activator antigen in the medium. The BFA-induced enhancement of PAI-1 antigen release was accompanied with the increased accumulation of the extracellular (membrane/matrix-bound) and intracellular PAI-1 antigen (219% of control at 24 h). These results suggest that BFA can strengthen the defense of vascular endothelium against tumor-cell invasion by enhancing the release and accumulation of PAI-1, which plays a critical role in the regulation of the u-PA-plasmin-collagenase activation cascade.

Brefeldin A↗
PubMed1996

Pathogenesis of hyponatremia following subarachnoid hemorrhage due to ruptured cerebral aneurysm.

BACKGROUND: Hyponatremia following subarachnoid hemorrhage (SAH) occurs due to the inappropriate secretion of antidiuretic hormone (SIADH). However, this condition is also sometimes associated with certain dehydration states. METHODS: To clarify the pathogenesis, daily values of urine volume, water balance, and sodium balance (Na Bal) were correlated with plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in 31 cases of SAH. RESULTS: Na Bal was markedly negative on days 2 and 3. Cumulative Na Bal showed continuous negative values until day 10 following SAH. ANP values showed a consistent elevation, while ADH showed only an initial surge. PRA, as the gross indicator of circulatory volume, showed a lack of suppression, indicating no increase in the circulatory volume. CONCLUSION: Hyponatremia following SAH therefore appears to be the result of increased natriuresis, due to the inappropriate elevation of ANP rather than SIADH. In this situation, water restriction should not be recommended, since the circulatory volume is decreased.

Adult↗
PubMed1995

Sphingomyelinase and cell-permeable ceramide analogs increase the release of plasminogen activator inhibitor-1 from cultured endothelial cells.

We investigated the effect of exogenous staphylococcal sphingomyelinase (SMase) on the release of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) from cultured human umbilical vein endothelial cells (HUVEC). Addition of SMase (2 units/ml) to the culture medium induced an approx. 15-fold increase in the extracellular level of PAI-1 antigen at 3 h. No significant increase in the level of t-PA antigen was detected. Treatment of HUVEC with SMASE (2 units/ml) for 3 h resulted in a significant decrease in the cellular sphingomyelin (SM) level, accompanied by a corresponding increase in the ceramide level. Cell-permeable ceramide analogs also enhanced the release of PAI-1 from cultured HUVEC in concentration- and time-dependent manners. A 6-fold increase in PAI-1 antigen level was observed after incubation for 3 h with 10 microM N-acetylsphingosine. Similar effect was noted as early as 2 h with 10 microM N-hexyanoylsphingosine. Addition of sphingosine failed to affect the release of PAI-1 from cultured HUVEC, indicating that the effects of ceramide analogs were independent of sphingosine generation. Pretreatment with cycloheximide or actinomycin D abated the response of HUVEC to N-acetylsphingosine in the increased levels of both extracellular and intracellular PAI-1. These results suggest that ceramide, generated via "SM cycle", acts as a lipid mediator of PAI-1 release from vascular endothelial cells, and may contribute to a better understanding of the pathogenesis of the PAI-1-associated thrombotic disorders.

Cell Membrane Permeability↗
PubMed1994

Aminated fucoidan promotes the invasion of 3 LL cells through reconstituted basement membrane: its possible mechanism of action.

Fucoidan is reported to have an antimetastatic activity. In the present study, we prepared an amino group-introduced derivative of fucoidan and examined its effect on the invasion of 3 LL cells through a reconstituted basement membrane (MatrigelTM). Unlike native fucoidan, the aminated derivative promoted the tumor cell invasion: maximal promotion (240% of control invasion) was obtained with 5 micrograms/ml. However, with higher concentrations (10-30 micrograms/ml) of the fucoidan derivative, the promotion was gradually reduced to 130% of control. Both native and aminated fucoidans inhibited specifically the attachment of 3 LL cells to laminin. Interestingly, aminated fucoidan, unlike the native one, promoted the tumor cell adhesion to immobilized synthetic laminin B 1 chain peptide, YIGSR, over a concentration range of 0.5-5 micrograms/ml. Higher concentrations (7-20 micrograms/ml) of the aminated derivative suppressed the adhesive ability of 3 LL cells to YIGSR. 3 LL cells secreted a 50-kDa form of urokinase-type plasminogen activator (u-PA) in the culture medium. Addition of aminated fucoidan (5 micrograms/ml) or YIGSR (10 micrograms/ml) resulted in a 1.7-fold increase in u-PA activity. This effect was enhanced up to 3.5-fold when both substances were simultaneously added. The addition of native fucoidan had no effect. The present results suggest that the 67-kDa receptor-mediated binding of 3 LL cells to laminin activates their invasiveness, especially by enhancing the extracellular u-PA levels. Aminated, but not native, fucoidan may act to enhance the laminin-receptor interaction at the limited concentration range.

Amination↗
PubMed1994

Glial-, neuronal- and photoreceptor-specific cell markers in rosettes of retinoblastoma and retinal dysplasia.

Previous studies have shown that a rosette formation represents an attempt to form embryonic retinal tissue, primarily rods and cones. To test the theories as to the origin and characteristics of retinoblastoma cells, we compared the characteristics of tumor rosettes with those of dysplastic rosettes seen in retinal dysplasia using the glial, neuronal and photoreceptor markers. Forty-four retinoblastoma and one retinal dysplasia specimens were analyzed by indirect immunohistochemistry, using specific antibodies against glial fibrillary acidic protein, S-100 protein, myelin basic protein, neuron-specific enolase, neurofilament, retinal S-antigen and retinal pigment epithelial antigen. In human retinoblastoma, all the glial, neuronal, retinal pigment epithelial, and photoreceptor cell markers, except for the neurofilament, were present in parts of rosette-forming tumor cells. However, their localization was different for each antigen and it was not clear whether each tumor cell possesses several antigens. These immuno-positive tumor cells were cytologically indistinguishable from other rosette-forming cells at the light microscopic level. In retinal dysplasia, neuron specific enolase and retinal S-antigen were diffusely expressed in the dysplastic rosettes, however, other antigen were not seen in those rosettes. The staining pattern by immunocytochemistry is totally different in tumor rosettes from dysplastic ones. We found varying localizations of different immunoreactivities within tumor rosettes. These results led us to suggest that tumor cells in the rosettes of retinoblastoma may have the ability to differentiate into neural and glial cells. To prove the theory that retinoblastoma cells may have originated from a primitive neuroectodermal cell capable of multipotentiality, further investigation is needed.

Biomarkers, Tumor↗
PubMed1994

Oxidative stress induces adult T cell leukemia derived factor/thioredoxin in the rat retina.

BACKGROUND: Adult T cell leukemia derived factor (ADF), originally defined as an interleukin-2 receptor inducer, is a human thioredoxin homolog. ADF/thioredoxin has several biologic functions, such as defense against cellular damage, activity to scavenge oxidative stress by hydrogen peroxide radicals and cytokine-like properties. We hypothesized that under certain conditions, ischemia followed by reperfusion and/or light exposure, ADF may be induced in the retina. EXPERIMENTAL DESIGN: To test this hypothesis, we prepared experimental animal models in which oxidative stress could be applied to the retina. In the present study, we examined ADF expression in the rat retina using temporary ischemia and reperfusion, and photodynamic retinal vascular thrombosis by immunohistochemical and Western blotting methods. RESULTS: ADF expression was strongly induced in the retinal pigment epithelial cells after 2 hours of ischemia followed by 2, 24, or 48 hours of reperfusion. ADF was also expressed in retinal pigment epithelial cells as early as 3 hours after light exposure followed by rose bengal injection, and this expression increased with time. Western blotting data showed that ADF expression increased in the retinal pigment epithelial cells in the experimental group, as compared with the control group. These results indicate that ADF is actively induced in retinal pigment epithelial cells upon oxidative stress. CONCLUSIONS: ADF induction in retinal pigment epithelial cells may be involved in the defense mechanism against cellular damage caused by active oxygen species generated during oxygen stress to the retina.

Animals↗
PubMed1994

Mitochondrial induction of adult T cell leukemia derived factor (ADF/hTx) after oxidative stresses in retinal pigment epithelial cells.

PURPOSE: Adult T cell leukemia derived factor (ADF) is a human homologue of thioredoxin (hTx), which exhibits scavenging activity with reactive oxygen intermediates. In their previous study, the authors found that after transient retinal ischemia, the expression of thioredoxin in rat retinal pigment epithelium (RPE) layer increased markedly. The present investigation is to determine intracellular ADF localization in RPE after transient ischemia and in cultured human RPE cells after oxidative insult by H2O2. METHODS: The authors employed immunoelectron microscopy to examine ADF localization in RPE. Labeling density analysis was performed to supplement the main observation in the experiment of transient retinal ischemia. 3-(4,5-dimethylthiazol-2yl)-2-5-diphenyltetrazolium bromide (MTT) assay was performed to verify the protective role of recombinant ADF (rADF) against H2O2. RESULTS: In immunogold electron microscopy, sparse ADF-positive labeling was seen in the cytosol and mitochondria in normal rat RPE and in untreated cultured RPE cells. After oxidative stress, it was concentrated in mitochondria in both groups. MTT assay proved that rADF protected cultured RPE from the toxicity of H2O2. CONCLUSIONS: This study shows the induction of ADF/hTx in mitochondria of RPE after oxidative stresses and its protective effect on cultured RPE exposed to H2O2. The data indicate the possibly important role of ADF/hTx in the protection of retinal cells from the oxidative stresses associated with retinal ischemic disease and probably with regular visual activity.

Adult↗
PubMed1994

[Technical tactics to preserve cortical venous drainage in interhemispheric approach for anterior communicating artery aneurysms].

The interhemispheric approach has been selected for clipping of the anterior communicating artery aneurysm located high above the sphenoidal plate, and in a posterior direction. However, this approach is sometimes complicated with postoperative hemorrhagic infarction due to excess brain retraction combined with damages of the cortical bridging veins. We have devised a modification in this approach to eliminate these complications. Our newly devised methods include the following; 1) Small bifrontal craniotomy performed, 2) Continuous ventricular drainage performed to minimize the effect of compression by the spatula during resection of interhemispheric fissure, 3) Bifrontal dural incision made along the frontal skull base, 4) Mobilization of the major cortical vein in the operated field, if necessary, by resection of the overlying arachnoid membrane with or without sacrificing its small tributaries, 5) Gradual dissection of the olfactory nerves according to the process of operation. We analysed the incidence of operative complications in thirteen consecutive cases with this approach. Major frontal ascending veins were carefully preserved in all cases. None showed hemorrhagic infarction, regardless of the cortical venous drainage patterns. The degree of smell preserved in 10% of the examined 11 cases was more than unilateral. In conclusion, this method is useful for the elimination of perioperative complications even in the acute stage of subarachnoid hemorrhage.

Adult↗
PubMed1993

[Severe carotid artery stenosis in the neck is frequently associated with coronary heart disease].

We have reviewed 15 cases of carotid artery stenosis in the neck, consisting of 11 patients with cerebral ischemia and 4 asymptomatic patients, in relation to associated coronary heart disease. The 15 patients had systemic complications, including hypertension in 87%, diabetes mellitus in 40% and hyperlipidemia in 57%. Systemic vascular complications other than coronary heart disease were present in 27% of the patients. Three of the 15 patients had a history of ischemic heart disease and had been treated by cardiologists. One patient developed angina pectoris on the second day of a cerebral ischemic attack. Coronary angiography (CAG) and simultaneous cerebral angiography following carotid endartectomy (CEA) were performed 4 of the remaining 12 patients, who had symptoms or history of ischemic heart attacks. Three of these four patients had stenotic lesions in their coronary arteries. Another one patient among the remaining 8 developed angina pectoris one year after undergoing CEA. This patient had 3-vessel coronary artery disease. These findings suggest that a strong correlation between stenotic lesions of the carotid arteries in the neck and coronary heart disease, with or without episodes of ischemic heart disease. CAG should be strongly recommended in such patients to assess the severity of complicating ischemic heart disease and to improve the prognosis following CEA.

Adult↗
PubMed1992

Successful removal of intracavernous neurinoma originating from the oculomotor nerve--case report.

An oculomotor neurinoma was confirmed intraoperatively to be located in the lateral wall of the cavernous sinus in a 55-year-old male. By protruding into the true venous cavity, it caused obliteration of the blood flow in the cavernous sinus. The tumor was totally removed without entering the true venous cavity of the cavernous sinus. The cavernous sinus was closed by suturing the dural membrane to the thin fibrous membrane, preventing intraoperative bleeding.

Adult↗
PubMed1992

[Pathogenesis of hyponatremia observed in the treatment of acute subarachnoid hemorrhage].

The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. Although the patients received an adequate amount of fluid (more than 4080ml/day; daily average in seventeen cases) and sodium (more than 277 mEq/day; daily average in seventeen cases), eight out of the seventeen cases showed transient hyponatremia of a slight degree beginning on 8.8 days after SAH. ANP values were elevated markedly in fifteen out of the seventeen cases, remaining high during the first two weeks following SAH. ADH values were elevated remarkably in eight out of the seventeen cases. However, these values declined immediately to a normal range within two days following SAH. PRA were increased or came within the normal range, suggesting the lack of water retention. Overall sodium balance and water balance did not differ significantly between hyponatremia cases and normonatremia ones, whereas, sodium balance in acute phase was significantly negative, associated with marked natriuresis in patients with hyponatremia. These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.

Acute Disease↗
PubMed1992

[Significance of plasma atrial natriuretic peptide measurement during the management of hyponatremia in neurosurgical patients].

We have examined the total number of admitted cases to clarify the pathogenesis of hyponatremia during the management of neurosurgical patients. We experienced 32 cases of hyponatremia during the past year by measuring the sodium balance and atrial natriuretic peptide (ANP) level. According to these two factors, we divided the cases into three groups. The first group shows normal ANP levels in spite of hyponatremia. Low administration of the sodium was thought to be the cause in these cases. The second group shows the elevated ANP levels with a positive sodium balance. Elevated circulatory volume due to the inadequate level of antidiuretic hormone and mild heart and/or kidney failures cause these conditions. Water restriction and/or diuresis were effective methods in the management of the cases. The last group shows the elevated ANP levels with a negative sodium balance. There is a statistically significant negative correlation between sodium balance and the ANP level. Marked natriuresis due to the elevated ANP causes the decrement of the circulatory volume in these cases. Pathogenesis of the last group is very important in the management of neurosurgical patients in an acute state, especially in subarachnoid hemorrhage cases. The decrement of the systemic circulatory volume would jeopardize the patient's neurological condition. In this group, water restriction that has been commonly recommended is contraindicated. Satisfactory water and sodium replenishment seems to be the best recommended treatment for this group.

Adult↗