[A case of metastatic leiomyosarcoma of the heart originating in the uterus].
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Biomedical subjects
Publications and source records attributed to T Azuma.
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A plasma prealbumin variant with a methionine-for-valine substitution at position 30 is closely associated with familial amyloidotic polyneuropathy (FAP) type I. Secondary ion mass spectrometry of the tryptic digest of a carrier's prealbumin could easily detect an abnormal peptide containing the substitution besides the normal peptide. This is a sensitive and reliable method for the diagnosis of FAP.
Immunocytochemical identification of cellular origins of different forms of gastrin in canine and human antral mucosa has been carried out using region specific monoclonal antibodies. Three types of gastrin cells were identified. The first type of cell was stained with both the C-terminal specific antibody of G17 and the N-terminal specific antibody of G17. The second type of cell was stained only with the C-terminal specific antibody of G17 but not with the N-terminal specific antibody of G17. The third type of cell was stained only with the N-terminal specific antibody of G17. From these findings we propose that the first type of cell contains gastrins with the amidated C-terminus of G17 such as component 1, G34, G17, or G14 as well as the free N-terminus of G17 such as G17, or C-terminal extended gastrins, the second type of cell contains gastrins only with the C-terminus of G17 but not with the N-terminus of G17 such as G34, or component 1, and the third type of cell contains C-terminal extended gastrins with intact N-terminus G17.
Effects of exogenous and endogenous bombesin on gastrin secretion were examined using rat antral mucosa in tissue culture. Gastrin secretion was significantly stimulated by exogenous bombesin at a dose of 10(-8) M. Atropine 10(-6) M, which abolished the action of the cholinergic agent carbachol to stimulate gastrin secretion, had no effect on bombesin-stimulated gastrin secretion. In addition, gastrin secretion was significantly inhibited by anti-bombesin antiserum used to block the effect of endogenous bombesin by immunoneutralization. These findings suggest that the stimulation of gastrin secretion by bombesin does not involve cholinergic neural pathways and that endogenous bombesin exerts a continuous stimulation on gastrin secretion in the basal state.
Gastrin release was significantly stimulated by the cholinergic agent carbachol at doses of 10(-4) M, 10(-5) M, and 10(-6) M. Peak stimulation was observed at 10(-5) M. Gastrin release was also significantly stimulated by bombesin at a dose of 10(-8) M, and 10(-6) M atropine which abolished the effect of carbachol in stimulating gastrin release had no effect on the bombesin-stimulated gastrin release. In addition, anti-somatostatin antiserum significantly stimulated gastrin release. These findings suggest that gastrin release is regulated by cholinergic and noncholinergic neurons the latter being thought to be a bombesin-containing neuron, and that antral somatostatin exerts a continuous restraint on gastrin release by the paracrine mechanism.
We studied isolated bovine mesenteric lymphatics to elucidate the pharmacological characteristics of pre- and postjunctional alpha-adrenoceptors at the sympathetic neuroeffector junction. Cylindrical strips were incubated with [3H]-noradrenaline and mounted for superfusion. Electrical stimulation (2 Hz, 0.5 msec, 50 V) augmented the fractional release of labeled noradrenaline. Exogenous noradrenaline and clonidine caused a depression of the evoked tracer release. Phenoxybenzamine and yohimbine markedly enhanced the evoked overflow of adrenergic transmitter. Rings of lymphatic vessels were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer bicarbonate solution. The vessels contracted when exposed to phenylephrine and clonidine. The ED50 of clonidine was significantly lower than that of phenylephrine. Prazosin caused a parallel shift to the right of the dose-response curve to phenylephrine. The antagonist, however, suppressed the magnitude of the maximum response to clonidine. Yohimbine caused parallel shift to the right of the dose-response curves to phenylephrine and clonidine, respectively. The Schild plots for yohimbine demonstrated that the drug was a competitive antagonist to phenylephrine and clonidine. The pA2 value of yohimbine to clonidine (7.6 +/- 0.4) was larger than that to phenylephrine (6.2 +/- 0.4). The pA2 value of prazosin to phenylephrine was 7.2 +/- 0.3. These results suggest that prejunctional alpha-adrenoceptors are involved in the negative feedback mechanism for autoregulation of noradrenaline release during postganglionic sympathetic nerve stimulation, and that both alpha 1- and alpha 2-like adrenoceptors do exist on lymphatic smooth muscle cells.
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The delayed-type hypersensitivity (DTH) response in BALB/c mice to the idiotype of M315 (alpha,lambda 2), a BALB/c myeloma protein, can be suppressed by a single i.v. injection of soluble M315. This suppression involves the generation of suppressor T cells. Mice tolerized by M315 produce subcellular factors that suppress the M315-DTH response. Such suppressor factors can be obtained by mechanical disruption of spleen cells or thymocytes from mice treated i.v. with M315. The fine specificity of the factor was studied using various immunoadsorbents such as L315 and germline V lambda 2 chain-Sepharose beads with known amino acid sequences. The results indicated that the specificity of the factor depended on three contiguous somatically mutated amino acid residues, Phe94, Arg95 and Asn96, in the third hypervariable region of the V domain of the L chain of M315.
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We recently encountered a tracheal schwannoma presenting as a polypoid mass. Computed tomography (CT) was very effective in evaluation of the size, shape and site of this rare tumour. Furthermore, CT images in the prone position made it easy to exclude tumour extension into the mediastinum.
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