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Biomedical subjects

Y Furuta

Publications and source records attributed to Y Furuta.

At least 145 records · Page 8Linked to original sources
PubMed1989

[Appropriate lymph node dissection in thyroid adenocarcinoma].

Thirty-four patients underwent thyroid surgery for papillary and follicular adenocarcinomas in the period from 1985 to 1989. Fourteen patients were treated with local neck dissection and 20 patients, with modified or radical neck dissection. Cervical lymph node metastasis was found in 25 patients (74%). Our recent policy for lymph node dissection is as follows: When deep cervical lymph node metastasis is clinically demonstrated, radical or modified neck dissection is performed. In patients without clinically demonstrated metastasis, local neck dissection and sampling of the internal jugular chain are performed. When microscopic metastasis is found in frozen sections, modified neck dissection is added. Thus we could select patients for modified neck dissection and choose appropriate neck dissection for more complete cancer clearance without losing postoperative functions.

Adenocarcinoma↗
PubMed1988

Prostaglandin production by murine tumors as a predictor for therapeutic response to indomethacin.

We investigated whether there is a relationship between the production of eicosanoids by murine solid tumors and their response to the prostaglandin H (PGH) synthase inhibitor indomethacin. Three sarcomas, designated FSA, NFSA, and SA-NH, and two carcinomas, designated MCA-K and HCA-I, syngeneic to C3Hf/Kam mice were used. In general, FSA and NFSA produced more PGH synthase products than lipoxygenase products, whereas HCA-I produced both types of metabolites in large quantities. All three tumors responded well to indomethacin treatment by slowing their growth. In contrast, MCA-K and SA-NH tumors produced insignificant quantities of PGH synthase products, but substantial amounts of lipoxygenase products. Their growth was not affected by treatment with indomethacin. Indomethacin did not influence tumor cell survival either in vitro or in vivo, but it reduced the proportion of S-phase cells in the tumors. The antitumor effect of indomethacin was not reduced by immunosuppression of the tumor host and was independent of tumor immunogenicity, implying that indomethacin acted through nonimmunological mechanisms. Thus, the effectiveness of indomethacin was directly related to the ability of tumors to produce PGs. Consequently, the eicosanoid profile of tumors could serve as a valuable way to select patients likely to respond to indomethacin and other PGH synthase inhibiting agents.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Increase in radioresponse of murine tumors by treatment with indomethacin.

Indomethacin, an inhibitor of prostaglandin (PG) synthesis, was investigated for its ability to increase radioresponse of two fibrosarcomas, FSA and NFSA, in C3Hf/Kam mice. In addition, the effect of indomethacin on radioresponse of hematopoietic tissue, jejunum, hair follicles, and tissues involved in the development of radiation-induced leg contractures was determined. Indomethacin greatly increased radioresponse of 8-mm tumors, as assessed by both tumor growth delay and TCD50 assays. Enhancement factors for tumor growth delay and tumor radiocurability (TCD50) were 1.55 and 1.39, respectively, for FSA, and 1.4 and 1.26, respectively, for NFSA tumors. Of four normal tissues assessed, two (hair follicles and tissues responsible for development of leg contractures) showed no change in radioresponse after treatment with indomethacin, one (hematopoietic tissue) exhibited radioprotection, and one (jejunum) exhibited slight radiosensitization (enhancement factor, 1.12). Therefore, indomethacin significantly augmented tumor radiocurability but had minimal effect on radioresponse of some normal tissues.

Animals↗
PubMed1988

The role of chloride in the sympathetic nervous system in DOCA-salt hypertension.

Elevation in blood pressure in the deoxycorticosterone acetate (DOCA)-treated rat with a high-sodium, normal-chloride diet was less than that in the DOCA-salt rat not on such a diet. Compared with the DOCA-salt rat, there were greater sodium concentration in the carcass, and less norepinephrine turnover rates in the heart and the spleen than in the DOCA treated rat given a high sodium normal chloride diet. Extracellular fluid volumes were similar. These results suggest that not only water and sodium retention by sodium loading but also that activation in sympathetic nervous system by the combined effect of chloride and sodium are responsible for the development of DOCA-salt hypertension.

Animals↗
PubMed1988

[Treatment of malignant gliomas with high-dose ACNU and autologous bone marrow transplantation].

Two patients with malignant gliomas located in the frontal lobe were treated by supraophthalmic intracarotid infusion of high-dose ACNU 15 mg/kg (ca. 600 mg/m2) combined with a total 60 Gy of irradiation after surgery. Irradiation therapy was started 13 days (case 1) and 10 days (case 2) after surgery, and single chemotherapy with ACNU 1,020 mg (case 1) and 1,100 mg (case 2) was performed when 36 Gy of whole brain irradiation was done. Chemotherapy was followed by autologous bone marrow transplantation containing 6.8 X 10(9) and 8.9 X 10(8) nucleated cells, respectively. Nadirs of white cell counts on 9 days in case 1 and 14 days in case 2 after chemotherapy were 280 cells and 240 cells/mm3, respectively, and the white cell counts less than 1,000/mm3 continued for 7 and 12 days, respectively. Local irradiation was started again when the number of white cells became more than 1,000/mm3 and 24 Gy was completed in each case. CT scanning carried out on discharge demonstrated no apparent abnormal high density area by contrast medium in both cases. These two patients did not show severe side effects at 10 months in case 1 and at 3 months in case 2 after high dose ACNU therapy, and remained progression-free at that time. Dose 15 mg/kg of ACNU may be the maximum tolerable dose patients can recover from severe myelosuppression, caused by high dose ACNU therapy combined with irradiation therapy, by marrow rescue.

Antineoplastic Agents↗
PubMed1988

[Hypertrophic cardiomyopathy with left ventricular dilatation].

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Driven by the same Ig enhancer and SV40 T promoter ras induced lung adenomatous tumors, myc induced pre-B cell lymphomas and SV40 large T gene a variety of tumors in transgenic mice.

Different types of tumors developed in transgenic mice following the introduction of the entire coding region of ras, myc or SV40 large T gene (T) linked to the same regulatory unit, consisting of a human immunoglobulin gene enhancer (Ig) and SV40 early gene promoter (Tp) with a 21-bp repeat. All the 12 transgenic mice harboring the intact T gene developed a variety of tumors including choroid plexus tumor, B cell lymphoma, histiocytic lymphoma, thymoma and others. This suggests that the Ig/Tp regulatory unit has transcriptional activity in these heterologous tissues. With this regulatory unit, myc gene induced solely pre-B cell lymphomas (five out of nine mice). Contrary to our expectation, however, the mutated ras gene induced lung adenomatous tumors in six out of eight transgenic mice over the 10-month observation period; the tumors are histologically comparable to adenocarcinomas in man. The tumors developed as early as 4 weeks after birth and the introduced ras gene was as efficiently expressed in both normal and neoplastic bronchioloalveolar epithelial cells as in normal lymphoid cells. An unidentified secondary event thus appears to be necessary for these ras-expressing cells to become neoplastic, as observed for myc (Leder et al., 1986). In a variety of tumors induced by Ig/Tp-T, on the other hand, T gene was expressed only in the tumor cells, but not in normal cells. Thus, derepression of T gene in normal cells appears to be closely related to their malignant change as observed in development of pancreatic acinar cell tumors by the T gene (Ornitz et al., 1985). These results suggest that ras and myc oncogenes penetrate differentially specific types of cells, while the SV40 T gene is tumorigenic in a variety of cell types.

Adenoma↗
PubMed1987

Splenic arteriovenous fistula formation due to angiodysplasia in a splenic aneurysm of a patient with liver cirrhosis--a report of a case.

A 53 year-old Japanese woman with liver cirrhosis manifested massive hematemesis due to ruptured esophageal varices. Celiac angiography demonstrated an aneurysm of the splenic hilus and arteriovenous fistula around the aneurysm. She underwent splenectomy, proximal gastrectomy, distal esophageal devascularization and pyloroplasty. Histological examination of the aneurysm revealed arterial dysplasia with a focal medial gap. Microscopic tissue clefts at the site of a medial gap were considered to be the source of the angiographic arteriovenous fistula.

Aneurysm↗
PubMed1987

Bilateral congenital posterolateral diaphragmatic hernia.

The 11th recorded case of bilateral congenital posterolateral diaphragmatic hernia is here presented. Left-sided diaphragmatic hernia was corrected surgically, while the baby expired because of respiratory failure on the 31st operated day. Autopsy revealed that the baby had right posterolateral diaphragmatic defect with sac. From this experience, it might be said that at surgery for left-sided hernia, right diaphragm should be examined carefully.

Hernia, Diaphragmatic↗
PubMed1987

The role of chloride on deoxycorticosterone acetate-salt hypertension.

Selective sodium loading attenuated the development of hypertension in the deoxycorticosterone acetate (DOCA) treated rat. The DOCA treated rat fed a diet equimolar in sodium to a 7% sodium chloride diet and in chloride to a standard diet, differed in various parameters from the DOCA treated rat fed a 7% sodium chloride diet: it had higher sodium concentration in both erythrocytes and muscles, a higher erythrocyte ouabain sensitive 22Na efflux rate constant (Kos), and a lower norepinephrine turnover rate in the heart and the spleen. These results suggest that the suppressed sympathetic nervous system activity and the activated cell membrane sodium pump contribute in part to the mechanism for the suppression of the development of hypertension in the DOCA-selective sodium loaded rat.

Animals↗
PubMed1987

[Hypertrophic cardiomyopathy manifesting different modes of illness: report of three cases].

Three cases of hypertrophic cardiomyopathy (HCM) which presented with different modes of appearance of left ventricular hypertrophy are reported. Case 1: A 24-year-old man had three relatives with HCM. At 13 years of age, he showed no electrocardiographic or echocardiographic abnormalities characteristic of HCM. During the ensuing 11 years, he developed asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM), with right bundle branch block and T-wave inversion. Cardiac catheterization confirmed the diagnosis of hypertrophic obstructive cardiomyopathy by demonstrating an intraventricular pressure gradient of 25 mmHg. These observations indicate that this case developed abnormal hypertrophy during adolescence on the basis of genetic predisposition of an autosomal dominant trait. Case 2: A 51-year-old woman had three proven and three possibly affected relatives. At 35 years of age, she had a normal electrocardiogram, although the echocardiogram was not available. Now, 16 years later, she had developed ASH with abnormal Q-waves and was diagnosed as having non-obstructive HCM. These suggest that ASH can be manifested as late as during middle-age, even in those with genetic predisposition. Case 3: A 47-year-old woman was diagnosed as having hypertension and her blood pressure was 190/100 mmHg at 40 years of age, though she had no abnormal electrocardiographic findings and heart murmurs. Now, at 47 years of age, she had developed T-wave inversion, ASH, SAM, and an intraventricular pressure gradient of 50 mmHg. Thus, her ASH appeared during middle-age, and was probably provoked by hypertension, though a complete family survey could not be conducted. These three patients' findings indicate that there may be various modes of appearance of left ventricular hypertrophy in HCM. In the majority of patients with genetic predisposition, abnormal hypertrophy may develop during adolescence as in Case 1. In others, it may develop in middle-age, as it did in Case 2. The disease spectrum of HCM may additionally include those who develop abnormal hypertrophy during middle-age, following provocation by hypertension, as in Case 3.

Adult↗