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Biomedical subjects

T Yamane

Publications and source records attributed to T Yamane.

At least 433 records · Page 24Linked to original sources

[A case of recurrent sigmoid colon cancer successfully treated with 5-FU and UFT].

A 57-year-old female patient with recurrent sigmoid colon cancer was successfully treated with 5-FU and UFT for 8 years. The patient, with cancer recurrence in the para-aortic lymph nodes, which were palpated in the abdomen, was given oral 5-FU at a daily dose of 200 mg. During the second week of administration, the mass showed a remarkable decrease in size, and complete disappearance was achieved within one month. However, 5 years and 2 months after discontinuation of 5-FU administration, recurrence in the supra-clavicular lymph nodes and para-aortic lymph nodes was recognized. After administration of UFT at a daily dose of 600 mg, complete disappearance of para-aortic lymph node recurrence was observed. At present, the patient is under observation as an outpatient at our hospital. This case suggests the effectiveness of 5-FU and UFT for lymph node metastases of sigmoid colon cancer.

Adenocarcinoma↗

Fundamental tumor perfusion analysis with nuclear magnetic resonance imaging using gadolinium-diethylene triamine pentaacetic acid.

The measurement of blood perfusion is an important factor for both the diagnosis and follow-up of tumor lesions. However, noninvasive detection of this local blood flow factor is very difficult. To accomplish this, we tried to calculate tissue blood perfusion indexes with nuclear magnetic resonance imaging using gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA). We experimentally applied this method to C3H mouse's tumor NFSa (fibrosarcoma) and its recurrence tumor R1137, whose experimental hypoxic cell fraction is different; that is, R1137 is more oxic than NFSa. Imaging pulse sequence was T1 (TR = 1,000 ms, TI = 300 ms), and longitudinal relaxation rate (R1 = 1/T1) values were calculated. Injected dose of Gd-DTPA was 0.1 mmol/kg. The T1 images produced are from both the preinjection period from every 5 min postinjection for 30 min. Using two-exponential analysis and compartment analysis we calculated two fundamental parameters: uptake index and flow index as blood perfusion factors. We found that this method has the possibility of differentiating the tissue's hypoxic cell fraction and is effective both for follow-up study after radiation therapy and for tissue characterization.

Animals↗

[A case of leiomyosarcoma of the duodenum--histologic diagnostic criteria of borderline malignancy].

A case of a leiomyosarcoma of the duodenum is reported. A 52-year-old man with a duodenal submucosal tumor underwent a pancreatico-duodenectomy. Histologically, the resected tumor revealed moderate cellular atypism and moderate pleomorphism, but revealed no mitotic figures. The histological diagnosis was leiomyoma. Nine years after operation, the tumor showed a recurrence and metastasis in the liver. Thus, the patient underwent a lobectomy of the liver. The resected liver tumor showed similar histological features seen in the primary duodenal tumor but with high mitotic activity. Histologically, the patient was diagnosed as having a metastatic leiomyosarcoma. This history suggests that a smooth muscle tumor of potential malignancy, as seen in this case, should be followed continuously, even though mitoses may not be recognized.

Diagnosis, Differential↗

Immunochemical study of role of chargerin II, a product of URFA6L of mitochondrial DNA in energy transduction of rat liver mitochondria.

Antibody against chargerin II [product of the unidentified reading frame A6L (URFA6L) of mitochondrial DNA] inhibited the ATP-Pi exchange reaction and reversed electron flow from succinate to NAD in mitoplasts (inner membrane plus matrix). The antibody against chargerin II caused greater inhibition on incubation with mitoplasts in the energized than the nonenergized state, suggesting that redox reactions are coupled with a conformational change of chargerin II. The present findings showed that chargerin II, the URFA6L product, may have a key role in energy transduction of mitochondrial oxidative phosphorylation.

Adenosine Triphosphate↗

Aminergic and peptidergic amplification of intracellular cyclic AMP levels in a molluscan neural network.

1. Serotonin (5-hydroxytryptamine; 5-HT), dopamine (DA), and small cardioactive peptide B (SCPB) can activate adenylate cyclase and increase the intracellular cyclic AMP (cAMP) levels in the Limax procerebrum (PC), with differing time courses and to differing extents. 5-HT and SCPB are potent stimulators of adenylate cyclase, and when both were applied simultaneously, an additive effect was observed. 2. In contrast, DA shows a great variability in the time course of cAMP synthesis and is a weak stimulator. Ergonovine, a DA antagonist, failed to inhibit cyclase activation, indicating that ergonovine-sensitive receptors are absent or ergonovine-sensitive DA receptors are not coupled to adenylate cyclase. 3. 5-HT and SCPB cause a rapid synthesis of cAMP, reaching the maximum 20- to 30-fold increase within a minute. DA's effect is slow in onset and very prolonged, reaching a maximum of only a two- to three-fold increase in the cAMP level. Reasons for variability in DA action are discussed.

Animals↗

Compartmentalization of cyclic AMP elevation in neurons of Aplysia californica.

We have measured by radioimmunoassay the amount of total, free, and bound forms of cyclic AMP (cAMP) within the abdominal ganglion and in five identified cell bodies of neurons from Aplysia californica. In the abdominal ganglion the unbound (free) cAMP levels comprised approximately 25-30% of the total cAMP content under the unstimulated condition, i.e., bathed in high-magnesium saline. Under pharmacological conditions that blocked endogenous phosphodiesterase and activated adenylate cyclase, ganglionic free cAMP levels were elevated more than fourfold, while bound cAMP levels more than doubled. Freeze-substitution techniques were employed to facilitate isolation of individual cell bodies either before or after pharmacological manipulation of cAMP levels. The basal, free cAMP content of cells R2, LP1, R15, L11, and L2-L6 was in the range of 10-40 pmol/mg of cell protein, which accounted for approximately one-half of the total cAMP content per cell body. Determinations of individual cell volumes indicated that the basal, free cAMP concentrations ranged from 1 to 6 microM. Under the same pharmacological conditions that elevated ganglionic cAMP in levels, no changes were measured in either the free or the bound forms of cAMP in isolated cell bodies. Our results indicate that the cAMP elevation was compartmentalized within the neuropilar region of the ganglion, most likely within the processes of the nerve cells. Previous results demonstrated that cAMP injections into the same Aplysia neurons studied here induced a cAMP-activated sodium current, INa (cAMP). In this report we discuss the possibility that pharmacological elevation of cAMP within neuronal processes may reach concentrations similar to those produced by cAMP injections into somata.

Animals↗

Roles of neonatal and prepubertal testicular androgens on androgen-induced proliferative response of seminal vesicle cells in adult mice.

Male mice were castrated at 0, 10, 20, 30, 40 and 60 days of age; daily injections of testosterone propionate (TP, 4 micrograms/g b. wt) were started from day 90. On various days after starting the TP injections, the incorporation of 5-[125I]iodo-2'-deoxyuridine into the whole seminal vesicles was determined as an index for proliferation. The seminal vesicle cells in mice castrated on days 0 and 20 were characterized by low weight (0.5-1 mg) before TP injection, long duration of androgen-induced proliferation (greater than 20 days) with a low peak, and involvement of both epithelial and fibromuscular cells (neonatal castration type). The seminal vesicle cells in mice castrated on days 60 and 40 were characterized by relatively high weight (5-10 mg) before TP injection, short duration of androgen-induced proliferation (10 days) with a high peak, and involvement of only the epithelial cells (adult castration type). In mice castrated on days 0 and 20, the neonatal castration type of androgen-induced proliferation was completely changed to the adult castration type when TP pretreatment (2 micrograms/g b. wt per 12 h) had been given from day 20 to day 40. However, the TP pretreatment given from day 90 to day 110 instead of days 20-40 had no such effect in 140-day old mice castrated on day 0. The present findings suggest that testicular androgens secreted from day 20 to day 40 play an indispensable role in the induction of irreversible proliferative response of the mouse seminal vesicle. The activity of the prepubertal androgens may not be completely compensated by androgen activity at adulthood.

Androgens↗

Effect of long term androgen removal on androgen-induced proliferation of seminal vesicle cells in adult mice.

Male mice were castrated on day 60 after birth; daily injections of testosterone propionate (TP, 4 micrograms/g b.wt) were started 1.2 or 6 months after the castration. The incorporation of 5-[125I]iodo-2'-deoxyuridine [( 125I]IdUrd) into the whole seminal vesicles was determined on various days after starting the TP injections as an index for proliferation. Although the peak of [125I]IdUrd uptake was observed 3 days after starting the TP injections in both short (1-2 months) and long (6 months) term castrated mice, the peak was significantly lower and the period of proliferation was longer in the long term group than in the short term group; the weights of seminal vesicles before TP injections were 6 and 10 mg in the long and short term groups, respectively. Although TP injections induced the proliferation of only epithelial cells in the short term group, the same treatment induced the proliferation of both epithelial and fibromuscular cells in the long term group. The deficient responsiveness to androgen of the seminal vesicle cells found in the long term castrated mice was completely recovered by TP pretreatment for 2 weeks. The present findings suggest that so-called imprinted cells in the mouse seminal vesicle induced by neonatal and prepubertal testicular androgens are very slowly lost at least in part by androgen removal for long periods such as more than 6 months in adult mice and that the loss is at least in part due to the death of fibromuscular cells, which is recovered rather quickly by androgen pretreatment.

Aging↗