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Biomedical subjects

K Kojima

Publications and source records attributed to K Kojima.

At least 613 records · Page 34Linked to original sources
PubMed1986

[Experimental and clinical studies on esophageal hemodynamics in the Sugiura procedure].

Changes of esophageal hemodynamics in Sugiura procedure were studied. Fifty mongrel dogs were used for the experiment in which esophageal tissue blood flow and oxygen saturation (STO2) were measured. The above parameters showed a decrease of 56% and 10%, respectively, in the lower esophagus following the paraesophageal devascularization versus 18% and 8% after the esophageal transection. Eighty-six patients with esophageal varices were clinically studied. Significant decreasing of the STO2 level in abdominal esophagus was recognized in the group performed the paraesophago-gastric devascularization, compared with the group performed the paraesophageal devascularization. However, decreasing rate was similar at the level of the hiatus in both groups, 22% versus 21%. The STO2 level of the intrathoracic esophagus was lower in both groups as well. Thus, the paragastric devascularization appeared to have caused no effect on intrathoracic esophageal hemodynamics. A significant decrease of the STO2 level was noted in the region immediately below the site of the esophageal transection in a group performed the paraesophago-gastric devascularization. Since this was conceivably attributable to the blockage of esophageal blood flow on the oral side, it may be advisable to perform the esophageal transection a little below the level of the hiatus after the paraesophago-gastric devascularization.

Animals↗
PubMed1986

[A case report of hepatic metastasis from leiomyosarcoma of the rectum with right hepatic lobectomy].

A case of hepatic metastasis from leiomyosarcoma of the rectum submitted to right hepatic lobectomy is presented. Surgery for hepatic metastasis from intestinal leiomyosarcoma is rarely possible. The patient was a 67-year-old woman who was diagnosed as leiomyosarcoma of the rectum and underwent abdominoperineal excision of the rectum in fifteen months. Hepatic metastasis was detected by US, CT and angiography. Right hepatic lobectomy was performed, and the resected hepatic lesions were histologically identified as metastasis from leiomyosarcoma of the rectum. The patient is still alive 10 months after the second operation with no lesions of the liver.

Aged↗
PubMed1986

[Combination chemotherapy with cyclophosphamide, adriamycin, vincristine and prednisolone (VEPA) for non-Hodgkin's lymphoma].

Combination Chemotherapy with Adriamycin (VEPA) was applied to 16 patients with non-Hodgkin's lymphoma. The effects of VEPA therapy were compared with those of combination chemotherapy without Adriamycin (non-VEPA). Complete remission rate achieved with VEPA therapy was 37.5% while that with non-VEPA therapy was 27.6%. Histologically, the complete remission rate in cases of large-cell type treated with VEPA therapy was 40%, while that with non-VEPA therapy was 14.3%. No cases of stage IV showed complete remission, whereas the complete remission rate for cases of stage III was 37.5% for VEPA therapy, but 27.6% for non-VEPA therapy. From these results we concluded that VEPA therapy is more effective for non-Hodgkin's lymphoma, especially large-cell type, than non-VEPA therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1985

Action of cobra venom cardiotoxin on chick embryonal fibroblasts transformed with a temperature-sensitive mutant of Rous sarcoma virus.

The cytolytic action of cardiotoxin analogue III from the venom of the Formosan cobra on chick embryonal fibroblasts transformed with a temperature-sensitive mutant of Rous sarcoma virus was investigated. The 50% effective dose of the toxin for the cells cultured at a non-permissive temperature (41 degrees C) or for noninfected normal cells was about 8 micrograms/ml whereas the value was 2 micrograms/ml for the cells cultured at a permissive temperature (36 degrees C). This indicates that the transformed cells became more susceptible to the cytolytic action of the toxin than the non-transformed cells.

Animals↗
PubMed1985

Mechanism of inhibitory action of TMB-8 [8-(NN-diethylamino)octyl-3,4,5-trimethoxybenzoate] on aldosterone secretion in adrenal glomerulosa cells.

The mechanism of 8-(NN-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) action was evaluated in isolated adrenal glomerulosa cells. TMB-8 inhibits both angiotensin II- and K+-stimulated aldosterone secretion in a dose-dependent manner. The ID50 for angiotensin II- and K+-stimulated aldosterone secretion is 46 and 28 microM, respectively. In spite of the fact that 100 microM-TMB-8 inhibits angiotensin II-stimulated aldosterone secretion almost completely, TMB-8 (100 microM) does not inhibit angiotensin II-induced 45Ca2+ efflux from prelabelled cells nor does it affect inositol 1,4,5-trisphosphate-induced calcium release from non-mitochondrial pool(s) in saponin-permeabilized cells. TMB-8 has no inhibitory effect on A23187-induced aldosterone secretion, but 12-O-tetradecanoylphorbol 13-acetate-induced aldosterone secretion is completely abolished. TMB-8 effectively inhibits both angiotensin II- and K+-induced increases in calcium influx but has no effect on A23187-induced calcium influx. TMB-8 inhibits the activity of protein kinase C dose-dependently. These results indicate that TMB-8 inhibits aldosterone secretion without inhibiting mobilization of calcium from an intracellular pool. The inhibitory effect of TMB-8 is due largely to an inhibition of plasma membrane calcium influx, but this drug also inhibits the activity of protein kinase C directly.

Adrenal Glands↗
PubMed1985

Simple purification of aromatic L-amino acid decarboxylase from human pheochromocytoma using high-performance liquid chromatography.

We purified aromatic L-amino acid decarboxylase (AADC) homogeneously and rapidly from human pheochromocytoma using high-performance liquid chromatography. HPLC with gel permeation and hydrophobic columns was highly effective, and the entire purification could be finished within 3 days. Purified AADC showed a single band with an Mr of 50,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and decarboxylated L-3,4-dihydroxyphenylalanine, L-5-hydroxytryptophan, and L-threo-3,4-dihydroxyphenylserine (a synthetic precursor of natural norepinephrine). Amino acid analysis of purified AADC was performed.

Adrenal Gland Neoplasms↗
PubMed1985

Molecular and physiological properties of tyrosine hydroxylase induced by reserpine in rat adrenal gland.

Newly synthesized tyrosine hydroxylase (TH) induced by reserpine was compared with the enzyme in control rats in terms of the molecular and physiological properties. When repeated doses of reserpine were given at daily intervals for three days, the enzyme activity measured in homogenates of the adrenal glands was increased 3-fold. Furthermore, when TH in the adrenal glands from both control and reserpine-treated rats was purified, both total activity of the enzyme and the enzyme protein content purified from reserpine-treated rats were also about 3-fold higher than those of the control rats. The two purified enzymes revealed similar properties; a single subunit with a Mr of 60,000 was observed by SDS polyacrylamide gel electrophoresis, and the Km value for a pterin cofactor, 6-methyl-tetrahydropterin was about 300 microM. In contrast, in situ TH activity measured under physiological conditions at pH 7.2 in adrenal tissue slices was elevated 6-fold by reserpine pretreatment for 3 days, and was stimulated by carbachol (0.1 mM) and elevated K+ (52 mM) in a roughly proportional rather than additive way relative to slices from untreated rats. These results indicate that newly synthesized TH induced by reserpine in rat adrenal gland had similar properties as the enzyme in control rats and that reserpine increased not only the amount of TH molecules but also the in situ activity of TH. Since reserpine also increases the biosynthesis of tetrahydrobiopterin as demonstrated by Viveros and co-workers, this 6-fold increase in in situ TH activity may depend both upon the 3-fold increase in the amount of enzyme molecules and upon the increase of the physiologically available tetrahydrobiopterin in the adrenal gland.

Adrenal Glands↗
PubMed1985

One-step sandwich enzyme-linked immunosorbent assay of human tissue plasminogen activator using monoclonal antibodies.

Five monoclonal antibodies to human tissue plasminogen activator (t-PA) were obtained. Three of them recognized a determinant designated alpha, and other two, another determinant named beta. A t-PA molecule was found to bear one each of determinants alpha and beta arranged in such a manner that the binding of alpha with one of its corresponding antibodies did not interfere with the binding of beta with one of its corresponding antibodies and vice versa. This allowed the development of a one-step sandwich enzyme-linked immunosorbent assay (ELISA) in which the antibody to beta was immobilized on wells of a microtiter plate and the bound t-PA was detected with the enzyme-conjugated antibody to alpha. The ELISA detected both one- and two-chain t-PA with a high sensitivity. We also discuss the determinants, alpha and beta.

Animals↗
PubMed1985

Characteristics of angiotensin II-, K+- and ACTH-induced calcium influx in adrenal glomerulosa cells. Evidence that angiotensin II, K+, and ACTH may open a common calcium channel.

The characteristics of angiotensin II-, K+-, and adrenocorticotropin (ACTH)-induced calcium influx were studied in isolated adrenal glomerulosa cells. Basal calcium influx rate is 0.64 +/- 0.09 nmol/min/mg of protein. Addition of angiotensin II (1 nM) causes a rapid 230% increase in calcium influx rate. This angiotensin II-induced calcium influx is sustained and is rapidly reversed by angiotensin II antagonist, [Sar1,Ala8]angiotensin II. Addition of either K+ or ACTH (1 nM) causes a 340 or 160% increase, respectively, in the rate of calcium influx. The effect of either angiotensin II, K+, or ACTH on calcium influx is dependent on extracellular calcium. The apparent Km for calcium is 0.46, 0.35, and 0.32 mM, respectively. When the extracellular concentration of K+ is 2 mM, neither angiotensin II nor ACTH stimulates calcium influx. Conversely, when extracellular K+ is increased to 6 mM, both angiotensin II and ACTH cause a greater stimulation of calcium influx than at 4 mM K+. When extracellular K+ is increased to 10 mM, calcium influx is 360% of the basal influx seen at 4 mM K+, and neither angiotensin II nor ACTH further stimulates the influx rate. Nitrendipine (1 microM) blocks both angiotensin II- and K+-induced calcium influx completely. In contrast, 10 microM nitrendipine does not completely block ACTH-induced calcium influx. The calcium channel agonist, BAY K 8644, also stimulates calcium influx; 10 nM BAY K 8644 leads to a rate of calcium influx which is 185% of basal. This BAY K 8644-induced increase in calcium influx and that caused by either angiotensin II or ACTH are additive. In contrast, BAY K 8644 has more than an additive effect on the calcium influx when paired with 6 mM K+. These results suggest that angiotensin II, K+, and ACTH stimulate calcium influx via a common calcium channel but act by different mechanisms to alter its function.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

Role of calcium fluxes in the sustained phase of angiotensin II-mediated aldosterone secretion from adrenal glomerulosa cells.

When angiotensin II stimulates aldosterone secretion, it causes a rapid but transient mobilization of calcium from an intracellular pool and a sustained increase in the influx of calcium in adrenal glomerulosa cells. The present studies were undertaken to determine the respective roles of the two angiotensin II-induced changes in cellular calcium metabolism in modulating events during the sustained phase of cellular response which is thought to be mediated by the C-kinase branch of the calcium messenger system. The sustained response to angiotensin II is only 50% of maximal in cells pretreated with dantrolene in a concentration sufficient to inhibit the angiotensin II-induced mobilization of intracellular calcium. Also, if A23187 is added to cells simultaneously with 1-oleoyl-2-acetylglycerol (OAG), the aldosterone secretory response is similar to that seen after angiotensin II. However, if A23187 is added first and the transient aldosterone secretory response allowed to decay, and OAG then added, the sustained aldosterone secretory response is only 45-50% of maximal. Addition of the calcium channel agonist, BAY K 8644, with OAG leads to an aldosterone secretory response which is only 50% of maximal, but if upon addition of OAG and BAY K 8644 the cells are also exposed for 5 min to media containing 8 mM K+, then the sustained secretory response is maximal. These data imply that the initial transient rise in the [Ca2+] of the cell cytosol plays a role in determining the extent to which C-kinase is shifted from its calcium-insensitive to its calcium-sensitive form. The second group of experiments examined the relationship between the sustained angiotensin II-induced increase in plasma membrane calcium influx and the sustained aldosterone secretory response. The results show that in the presence of 1 microM nitrendipine or 2 mM extracellular K+, angiotensin II causes no increase in calcium influx and only a transient rather than a sustained increase in the rate of aldosterone secretion indicating that the sustained phase of the response is dependent upon a continued high rate of Ca2+ influx which regulates the rate of turnover of the activated C-kinase.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗