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Biomedical subjects

T Nakane

Publications and source records attributed to T Nakane.

At least 73 records · Page 4Linked to original sources
PubMed1990

Development of monoclonal antibodies against human gastrointestinal cancer.

We have evaluated approximately 10,000 monoclonal antibodies resulting from 14 hybridization of spleen cells from mice immunized with established cancer cell lines. They were screened by binding assays using cancer cell lines or normal fibroblast cells, followed by immunohistochemical study on tissue sections. Ninety-one monoclonal antibodies were obtained by above binding assays. One of them, named KM10 was further investigated. Isotype of KM10 was IgG1 with kappa-light chain. It was shown that KM10 has strong reactivity with tumors of colon, stomach, papilla Vater, and pancreas, while the limited reactivity displayed with normal tissues. The electron microscopic observation revealed that the antigen recognized by KM10 is expressed on the surface of cancer cells. KM10 could mediate ADCC. These results indicate that KM10 is a good candidate for a probe of diagnosis and therapy of cancer.

Antibodies, Monoclonal↗
PubMed1990

Pro-opiomelanocortin gene expression in silent corticotroph-cell adenoma and Cushing's disease.

The silent corticotroph-cell adenoma (SCCA) is characterized by the presence of immunoreactive adrenocorticotropic hormone (ACTH) in the tumor tissue in patients without symptoms of Cushing's disease. To elucidate the pathophysiology of SCCA, the expression of pro-opiomelanocortin (a ACTH precursor) genes was studied in a patient with SCCA and in three patients with Cushing's disease. Pro-opiomelanocortin messenger ribonucleic acid (mRNA) was found in the SCCA tissue to a greater degree than in the adenomas of the patients with Cushing's disease. Northern blot analysis revealed that the size of pro-opiomelanocortin mRNA present in the SCCA tissue was indistinguishable from that in the adenomas associated with Cushing's disease. A ribonuclease mapping study indicated that there were no point mutations in the coding sequence of pro-opiomelanocortin mRNA present in the SCCA tissue. Because of the presence of pro-opiomelanocortin mRNA and immunoreactive ACTH in the adenoma tissue, it is proposed that translation of the mRNA and subsequent accumulation of ACTH precursor occurred in the SCCA. Thus, the absence of Cushing's disease symptoms in this SCCA could not be caused by abnormality in the coding sequence of the pro-opiomelanocortin gene or in ribonucleic acid processing. The occurrence of abnormality at or after the translational steps was strongly suggested.

Adenoma↗
PubMed1988

[Changes of growth hormone-releasing factor (GRF) in rat peripheral blood--effect of hypophysectomy].

Accumulating evidence has emerged indicating that growth hormone-releasing factor (GRF) is present not only in the hypothalamus but in other tissues as well. Using highly specific and sensitive radioimmunoassays and immunoaffinity chromatography, we found low but clearly measurable GRF-like immunoreactivity (GRF-LI) levels in rat peripheral plasma. In order to verify the immunological findings, the peripheral plasma GRF-LI was characterized using fast protein liquid chromatography. The immunological peak was eluted at the position of synthetic rat GRF standard. These findings demonstrate that rat peripheral plasma GRF is immunologically and chromatographically indistinguishable from authentic rat GRF. Moreover, we performed studies with hypophysectomy to assess whether peripheral plasma GRF-LI changes in physiological status. At 4 weeks after hypophysectomy, there was a significant (p less than 0.05) increment in the rat plasma GRF-LI [12.4 +/- 0.5 (+/- SEM) pg/ml in hypophysectomized rats as opposed to 5.8 +/- 0.4 pg/ml in sham-operated control rars]. On the other hand, hypothalamic GRF-LI fell significantly as compared that of controls (36.1 +/- 1.0 vs. 78.3 +/- 3.0 pg/mg wet weight tissue). A similar pattern of changes in GRF-LI at 10 weeks after hypophysectomy was also revealed. The source of rat peripheral plasma GRF has not yet been elucidated. Our results, however, may suggest that GRF levels are modulated by negative feedback at the level of the hypothalamus by a pituitary factor, presumably growth hormone (GH) and that hypothalamic GRF release exceeds its synthesis in hypophysectomized rats.

Animals↗
PubMed1988

Constrictor responses of isolated and perfused monkey coronary arteries to pindolol.

We studied the mechanisms of pindolol-induced vasoconstrictions in isolated and perfused monkey coronary arteries. Phentolamine marginally reduced the vasoconstrictions, but bunazosin and DG 5128 did not. Diltiazem and methysergide significantly inhibited them, but atropine, diphenhydramine and cimetidine did not. Diltiazem significantly suppressed KCl-induced vasoconstrictions, but methysergide did not. These results suggest that pindolol-induced vasoconstrictions of monkey coronary arteries are mediated, at least partly, through 5-hydroxytryptamine receptors, but not through alpha-adrenoceptors, and that these vasoconstrictions appear to be associated with an increase of Ca2+ entry into the smooth muscle cell.

Animals↗
PubMed1988

Effects of DN-9693, a selective inhibitor of cyclic AMP phosphodiesterase, in isolated and perfused canine large coronary arteries.

In isolated canine epicardial coronary arteries perfused with Krebs-Henseleit solution at 37 degrees C, DN-9693, a newly synthesized selective cyclic AMP phosphodiesterase inhibitor, induced vasodilation in a dose-related manner. The threshold dose for inducing vasodilation to DN-9693 was very small, but the maximum vasodilation was not great. The order of potency for ED20 (20% dilatation) was DN-9693 greater than IBMX greater than aminophylline, but that for ED70 was IBMX greater than aminophylline greater than DN-9693, suggesting that these three PDE inhibitors have different properties.

1-Methyl-3-isobutylxanthine↗
PubMed1988

A serrated suction tip for tumor removal. Technical note.

A serrated suction tip with a variety of diameters and serrations has been developed for the microsurgical removal of tumors. These tips can dissect and aspirate tumor tissue, cerebrospinal fluid, or blood simultaneously, and the degree of suction can be controlled by the pressure of the tip against the tumor.

Equipment Design↗
PubMed1988

Detection of mRNA of prolactin and ACTH in clinically nonfunctioning pituitary adenomas.

Clinically nonfunctioning pituitary adenomas have been thought to synthesize some pituitary hormones as shown by studies involving cell culture, immunocytochemistry, or measurement of hormone levels in tumor homogenates. Nevertheless, they are not associated with hypersecretion of pituitary hormones. To further clarify hormone synthesis in such pituitary adenomas, the presence of messenger ribonucleic acid (mRNA) of prolactin (PRL) growth hormone, and adrenocorticotropic hormone (ACTH) in the cytoplasm of 16 nonfunctioning adenomas was determined by means of a hybridization technique, and compared to the immunocytochemical findings. In three adenomas (19%) PRL mRNA was detected and in one case (6%) ACTH mRNA was detected. The hybridization technique appears to be more sensitive than immunohistochemistry for detection of specific mRNA's in assigning the hormone synthesis potential to clinically nonfunctioning tumors. The results suggest that PRL and ACTH are synthesized in some cases of clinically nonfunctioning pituitary adenomas and that hybridization techniques are useful to investigate hormone synthesis in pituitary adenomas. The ability to demonstrate PRL mRNA in tumor tissues allowed differentiation between hyperprolactinemia caused by synthesis of PRL in the tumor and that due to hypersecretion from the adjacent normal pituitary.

Adenoma↗
PubMed1988

Beta adrenoceptors in the canine large coronary arteries: beta-1 adrenoceptors predominate in vasodilation.

Beta adrenoceptors of the canine large coronary artery were characterized by observing the effects of the subtype selective antagonists, metoprolol (beta-1) and ICI 118,551 (beta-2), on the vasodilator responses of isolated and perfused preparations to beta adrenoceptor agonists and in the radioligand binding assay. The integrity of the endothelium was checked by acetylcholine-induced vasodilations. Without any precontraction, isoproterenol, norepinephrine, epinephrine and procaterol (selective beta-2 agonist) dilated the canine large coronary artery pretreated with phentolamine (10(-5) M). The rank order of agonist potency was isoproterenol greater than norepinephrine greater than epinephrine greater than procaterol. The pA2 values for metoprolol and ICI 118,551 were determined by the antagonisms of the vasodilator responses to isoproterenol and procaterol. The slopes of Schild plots for metoprolol and ICI 118,551 against isoproterenol and the value for ICI 118,551 against procaterol were not significantly different from unity, but the value for metoprolol against procaterol was significantly less than unity. The pA2 value for metoprolol against isoproterenol was 7.48 and those values for ICI 118,551 against isoproterenol and procaterol was 7.19 and 7.25, respectively. These pA2 values are typical for beta-1 adrenoceptors. The beta adrenoceptors of the canine large coronary artery were examined further using an antagonist [125I]iodocyanopindolol as a ligand for the binding of beta adrenoceptors. The [125I]iodocyanopindolol binding to the canine coronary artery smooth muscle membrane was saturable with a KD of 63.7 pM and a total number of radioligand binding sites of 44 fmol/mg of protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1987

Growth hormone-releasing factor releases ACTH from an AtT-20 mouse pituitary tumor cell line but not from normal pituitary cells.

Corticotropin-releasing factor (CRF) and both human pancreatic growth hormone-releasing factor (hp-GRF) and rat hypothalamic GRF (rh-GRF) stimulated ACTH release from neoplastic AtT-20 mouse pituitary tumor cells in a dose-dependent fashion, with CRF inducing a 10-fold increase and GRF a maximal increment of approximately one-half that of CRF. Neither rh-GRF nor hp-GRF induced ACTH release in normal anterior pituitary cells. Pretreatment with either dexamethasone or somatostatin prior to the addition of rh-GRF inhibited the increase in ACTH release. Both ovine CRF and rh-GRF stimulated adenosine 3,5-monophosphate production in AtT-20 cells. The weak but clearly discernible effect of GRF on ACTH release from AtT-20 cells may be due to an abnormality in the AtT-20 cell receptor.

Adrenocorticotropic Hormone↗
PubMed1987

Postjunctional alpha-adrenoceptor subtypes in isolated and perfused canine epicardial coronary arteries.

In isolated and perfused canine coronary arteries pretreated with propranolol (5 x 10(-6) M), effects of bunazosin (E 643, a selective alpha 1-antagonist) and DG 5128 (a selective alpha 2-antagonist) on vasoconstrictor responses to phenylephrine, xylazine, clonidine, and norepinephrine (NE) were examined. A stainless steel cannula was inserted into the coronary artery segment (1.1-2.4 mm OD, 1.5 cm long) and perfused with Krebs-Henseleit solution at a constant flow rate. The perfusion pressures were 60-110 mm Hg. Acetylcholine readily caused a vasodilation in used arterial preparations. Phenylephrine produced a strong vasoconstriction in a dose-dependent manner, but xylazine and clonidine induced slight vasoconstrictions and a vasodilation followed by a slight vasoconstriction in large doses. Phenylephrine-induced vasoconstrictions were dose-dependently attenuated by bunazosin but not by DG 5128. Neither bunazosin nor DG 5128 blocked the vascular responses to clonidine and xylazine. NE produced a slight vasoconstriction in the presence of prazosin (10(-6) M), and DG 5128 did not influence that vasoconstriction. Diltiazem significantly suppressed KCl-induced vasoconstriction, but bunazosin did not. Removal of endothelium by 1 mg of saponin significantly attenuated acetylcholine (ACh)-induced vasodilation, but did not suppress clonidine-induced vasodilation. It is suggested that only alpha 1-adrenoceptors are involved in the vasoconstrictions induced by the adrenergic agonists in canine epicardial coronary arteries and that the vascular responses to clonidine and xylazine may be direct actions.

Acetylcholine↗
PubMed1987

Long term results of transsphenoidal adenomectomy in patients with Cushing's disease.

As part of an ongoing series, 100 patients with Cushing's disease underwent transsphenoidal operations. Pituitary adenomas were confirmed in 93 patients, and initial remission was achieved in 86 (92%) of them. Hypercortisolemia was not corrected in 7 patients, and in 4 this was due to invasive adenomas. These patients were subjected to irradiation, medical treatment, or both after operation. Only 7 of the 100 patients had no pituitary adenoma found at operation, and they obtained no clinical remission even after partial or subtotal hypophysectomy. Follow-up review, with an emphasis on endocrinological studies, was performed on these patients for a mean period of 38 months. Seventy-eight patients were in long term remission after operation and had restoration of noncorticotropic hormone secretion as well as pituitary-adrenal function. Recurrence was noted in 8 patients after 19 to 82 months in remission. In all of these patients, pituitary adenomas were verified by reoperation and no case of corticotrophic cell hyperplasia was noted. We conclude that late recurrence of Cushing's disease may occur after adenoma removal and is due to the regrowth of adenoma cells left behind in the peritumoral tissue at the first operation. In view of the overall remission rate, transsphenoidal adenomectomy is considered a highly effective treatment for Cushing's disease.

Adenoma↗
PubMed1987

Characteristics of histamine receptors in the isolated and perfused canine coronary arteries.

The vascular responses of isolated and perfused canine epicardial coronary arteries to histamine, 2-pyridylethylamine (2-PEA, a selective histamine H1-receptor agonist) and dimaprit (a selective histamine H2-receptor agonist) were studied. Histamine produced only a vasodilatation at small doses (less than 0.3 microgram) and a biphasic response, i.e., vasoconstriction followed by vasodilatation at large doses. 2-PEA produced only a vasoconstriction at small doses and at large doses a slight vasodilatation following vasoconstriction. Dimaprit usually induced only a vasodilatation. The selective histamine H1-receptor antagonist chlorpheniramine shifted the dose-response curves of histamine and 2-PEA for inducing vasoconstriction to the right. Cimetidine (a selective histamine H2-receptor antagonist) caused dose-dependent shifts of the dose-response curves of histamine and dimaprit for vasodilatations to the right. Chlorpheniramine did not attenuate the vasodilatations by 2-PEA and histamine. The removal of endothelial cells by an intraluminal injection of saponin (1 mg) did not affect the vascular responses to histamine, 2-PEA and dimaprit. These results indicate that there are 2 types of histamine receptors in canine epicardial coronary arteries: (i) a H1-receptor mediating vasoconstriction and (ii) a H2-receptor, which is not endothelium-dependent, mediating vasodilatation.

Animals↗
PubMed1986

Possible involvement of histamine H2-receptors in the vasodilator effect of clonidine on isolated and perfused canine coronary arteries.

The mechanism of clonidine-induced vasodilatation was investigated in the isolated and perfused canine coronary arteries. Clonidine produced a slight vasoconstriction at small doses whereas it induced a dose-related vasodilatation at large doses (more than 3 micrograms). The vasodilatation was reversed to vasoconstriction by treatment with 100 micrograms of cimetidine (a selective H2-receptor antagonist) but was not affected by 100 micrograms of chlorpheniramine (a selective H1-receptor antagonist). These results suggest that clonidine can dilate the isolated and perfused canine coronary arteries by acting on histamine H2-receptors.

Animals↗
PubMed1986

Responses of isolated and perfused dog coronary arteries to acetylcholine, norepinephrine, KCl, and diltiazem before and after removal of the endothelial cells by saponin.

The vascular responses to acetylcholine (ACh), norepinephrine (NE), KCl, and diltiazem were examined before and after removal of endothelial cells by an intraluminal bolus injection of saponin (1 mg) in isolated and perfused dog coronary arteries. Without any precontraction, ACh induced a long-lasting vasodilation in small doses (less than 1 microgram), and an initial brief vasoconstriction was occasionally accompanied in large doses. These vascular responses to ACh were not significantly affected by the pretreatment with propranolol (5 X 10(-6) mol/l). The endothelial removal by intraluminal saponin was confirmed electron microscopically. After 20-60 min of saponin treatment, the responses to drugs were observed and compared with the control. The ACh-induced vasodilation was significantly attenuated by saponin (P less than 0.01), but the ACh-induced vasoconstriction was not affected by it. The vasodilation was blocked by atropine. The NE- and KCl-induced vasoconstrictions and diltiazem-induced vasodilation were not affected by saponin treatment. It is suggested that: (1) ACh produced a vasodilation in the nonpreconstricted condition of dog coronary arteries; (2) the vasodilation caused by ACh is mostly endothelium-dependent, which is considered to be mediated by muscarinic receptors; and (3) the vascular responses to NE, KCl, and diltiazem and the vasoconstriction produced by ACh are not influenced by removal of the endothelium in a relatively large epicardial coronary artery of the dog.

Acetylcholine↗
PubMed1986

Effect of estrogen on prolactin mRNA in the rat pituitary. Analysis by in situ hybridization and immunohistochemistry.

The effect of estrogen on prolactin (PRL) synthesis at a single-cell level was studied by in situ hybridization and immunohistochemistry. Long-term estrogen treatment increased PRL-containing cells from 10-20% of total cell population to 80-90%, as revealed by immunohistochemistry. PRL mRNA containing cells also increased in a similar fashion. Moreover, cytoplasmic PRL mRNA expressed as the number of silver grains per cell increased 4- to 5-fold by estrogen. These results suggest that long-term estrogen treatment causes not only PRL cell proliferation but also an increase in PRL mRNA in a single cell.

Animals↗
PubMed1986

Comparison of vascular responses of isolated, perfused simian and canine coronary arteries to adrenergic agonists.

The vascular responses of the isolated, perfused simian left circumflex coronary arteries to adrenergic agonists were compared to those of canine coronary arteries in isolated, perfused preparations. Norepinephrine and epinephrine produced only vasoconstriction in monkey arteries in contrast to vasoconstrictor, vasodilator and biphasic responses of canine coronary arteries. Isoproterenol induced a dose-dependent vasodilatation. Salbutamol, a selective beta 2-agonist, produced either a slight vasodilatation or no response. Phenylephrine, a selective alpha 1-agonist, usually caused a marked vasoconstriction in a dose-related manner in both preparations. Xylazine and clonidine, selective alpha 2-agonists, caused a slight vasoconstriction in low doses, but these two agonists relaxed both preparations in high doses. These observations suggest that adrenoceptor subtypes may be mainly alpha-1 and beta-1 in the large coronary arteries of monkeys and dogs and that the alpha-adrenoceptor is predominant in simian large coronary arteries.

Adrenergic Agonists↗