Extrinsic reinnervation of the intestine after small bowel autotransplantation in dogs.
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Analysis of Variance↗
Biomedical subjects
M Tsuboi
Publications and source records attributed to M Tsuboi.
[Pulmonary blastoma--long-term survival of a patient with metastases].
We report a rare case of pulmonary blastoma. This 59-year-old woman has been apparently well with recurrent and metastatic tumors in her left lung for 9 years after the initial operation. On May 28, 1984, she underwent a thoracotomy of left upper lobectomy and lymph nodes dissection. The histologic diagnosis of resected specimen was pulmonary blastoma. In August 1986 (27 months after the initial surgery), chest X-ray revealed some nodules in the lungs. Then, the patient had two thoracotomies for the excision of 4 tumors and one chest wall resection of the tumor. In addition, she received systemic chemotherapy 28 times, directly intrapulmonary drug injection 3 times and radiation therapy once for recurrent and metastatic disease. Following some cycles of our combination chemotherapy consisting of cis-platinum and vindesine, some lesions had decreased in size and others previously seen on chest X-ray were no longer evident. She achieved an objective response with receiving two-drug chemotherapy. Our observation suggest that this intensive combination chemotherapy is effective in recurrent and metastatic disease of pulmonary blastoma as a surgical adjuvant.
Antineoplastic Combined Chemotherapy Protocols↗
[A case of superficial hemosiderosis of the central nervous system with normal CSF findings and unknown source of bleeding].
A 65-year-old woman had suffered from slowly progressive hearing loss for one year. She had neither repeated episodes of headache or vomiting nor a past history of neurosurgical operation. Neurologic examination revealed moderate diminution in hearing, pyramidal tract sign and cerebellar ataxia without dementia. CSF was under normal pressure, clear and colorless, with total protein 35 mg/dl, glucose 59 mg/dl and a cell count of 2 WBC/mm3. T2-weighted images (TR200/TE80) of high-field MRI demonstrated marginal hypointensity of the brainstem, the Sylvian fissures and the entire spinal cord. Angiography of the cerebral vessels failed to identify the source of bleeding. To our knowledge, this is the first report of superficial hemosiderosis of the central nervous system with normal CSF findings and an unknown source of bleeding confirmed by MRI.
Aged↗
Depolarization of Raman scattering from some nucleotides of RNA and DNA.
Depolarization ratios of Raman bands, excited at 488.0 nm, of guanosine-5'-monophosphoric acid, cytidine-5'-monophosphoric acid, adenosine-5'-monophosphoric acid, thymidine-5'-monophosphoric acid, and uridine-5'-monophosphoric acid have been measured in their H2O and D2O solutions in the spectral region from 300 to 1800 cm-1. For comparison, the disodium salt of 2'-deoxyadenosine-5'-monophosphoric acid was also subjected to the depolarization measurement in its H2O solution. The results have been correlated with possible orientations of the principal axes of the Raman scattering tensors as well as with the relative magnitudes of the tensor components. Results should be useful for future polarized Raman studies of synthetic and natural DNA.
DNA↗
In vivo adaptative regulation of muscarinic receptors and muscarinic stimulation-induced Ca2+ mobilization during short-term heat exposure in rat parotid glands.
1. Adaptation of muscarinic receptors (MR)--muscarinic stimulation--induced intracellular Ca2+ mobilization during short-heat exposure (33 degrees C). 2. Heat-exposure for 48 hr decreased the carbachol (CCh)-stimulated cytosolic Ca2+ concentration increase. 3. The number of MR on cell surface increased transiently at 24 hr with a subsequent decrease at 48 hr. 4. CCh-stimulated inositol triphosphate (IP3) formation decreased at 48 hr. 5. In saponin-permeabilized cells, 1,4,5-IP3-induced 45Ca2+ release decreased at 24 hr. 6. The data suggest that the adaptation for increased muscarinic stimulation occurs at IP3 generating sites as well as at intracellular IP3 receptor sites during heat exposure.
Acetylcholine↗
Intralysosomal pH and release of lysosomal enzymes in the rat liver after exhaustive exercise.
The mechanism underlying exhaustive exercise-induced release of lysosomal enzymes was studied in the rat liver. Exhaustive exercise resulted in the release of beta-glucuronidase and cathepsin D, but not beta-glucosidase and acid phosphatase, into the blood and cytosol, suggesting that the release of lysosomal enzymes is not due to disruption of lysosomal membranes. The intralysosomal pH of the liver, which was approximately 5.5 at the resting level, rose significantly after exhaustive exercise to pH 6.3. In vitro, beta-glucuronidase and cathepsin D were released at an intralysosomal pH exceeding 6.2. In contrast, beta-glucosidase and acid phosphatase were not released. The elevation of intralysosomal pH reduced the aggregation of beta-glucuronidase and cathepsin D. The rate of ammonia accumulation increased markedly in the lysosome-enriched subcellular fraction after exercise. There was a positive relationship between the rate of ammonia accumulation and the elevation of intralysosomal pH in vitro. Lysosomes isolated after exhaustive exercise showed significantly increased osmotic fragility. Our findings suggest that, during exhaustive exercise, the accumulation of ammonia in lysosomes leads to the elevation of intralysosomal pH, resulting in the reduced aggregation of certain lysosomal enzymes. Thus, less aggregated lysosomal enzymes may be released into the cytosol through the lysosomal membrane, the permeability of which has been increased.
Acid Phosphatase↗
Effect of insulin on adipocyte lipolysis in exercise-trained rats.
The effect of exercise training on the antilipolytic action of insulin was studied in rat adipocytes. Exercise training enhanced lipolysis induced by norepinephrine. Insulin dose dependently inhibited norepinephrine- (1 microM) stimulated lipolysis in both groups. Its inhibition rate was significantly greater in the trained than in the control group. Thus, exercise training enhanced the antilipolytic action of insulin. In the control group, insulin (1,000 microU/ml) reduced the displacement rate of [3H]CGP-12177 binding to adipocytes by low concentrations of (-)-norepinephrine. The slope factor without insulin was 0.76, whereas that with insulin was 0.95. In the trained group, insulin did not affect the competition binding of (-)-norepinephrine for [3H]CGP-12177. The displacement rate of [3H]CGP-12177 binding from adipocytes by low concentrations of (-)-norepinephrine was significantly greater in the trained than in the control group. The number of surface beta-adrenergic receptors per adipocyte was smaller in the trained than in the control group. Cilostamide, which blocks the antilipolytic action of insulin, restored lipolysis in both groups. The recovery rate was significantly greater in the trained than in the control group. These findings suggest that the enhanced antilipolytic action by insulin in the trained group occurs at a site distal to the binding of norepinephrine to beta-adrenergic receptors and that it is due to the increased activity of particulate low-Michaelis constant phosphodiesterase.
3',5'-Cyclic-AMP Phosphodiesterases↗
Mechanism of isoprenaline-stimulated diacylglycerol formation in rat parotid acinar cells.
The kinetics and mechanism of sn-1,2-diacylglycerol (DAG) formation induced by isoprenaline were studied in rat parotid acinar cells. DAG accumulation induced by 100 microM isoprenaline reached its maximum at 1 min, rapidly decreased (about 50%) at 5 min and then remained constant for 30 min. DAG accumulation 1 min after isoprenaline treatment was dose-dependent. Either propranolol or phentolamine inhibited isoprenaline-stimulated DAG accumulation in a dose-dependent manner. Addition of a vasoactive intestinal polypeptide, forskolin, or dibutyryl cyclic AMP had no effect on DAG accumulation. Isoprenaline did not cause the release of [3H]choline or [3H]ethanolamine metabolites into the medium. Based on the kinetics of DAG formation and [32P]phosphoinositide breakdown, we conclude that isoprenaline-induced DAG formation was mainly related to the hydrolysis of [32P]phosphatidylinositol 4,5-bisphosphate ([32P]PIP2). These results suggest that the effect of isoprenaline on DAG formation is mediated by alpha 1-adrenoceptor activation, that it is not related to the increase in cyclic AMP, and that it is closely related to PIP2 hydrolysis.
Alkaloids↗
Mechanism of carbachol-stimulated diacylglycerol formation in rat parotid acinar cells.
We studied the relationship between phosphoinositide hydrolysis, phosphatidylcholine hydrolysis, and sn-1,2-diacylglycerol (DAG) formation in response to carbachol stimulation in rat parotid acinar cells. Previously, we demonstrated that DAG formation stimulated with 1 microM carbachol was biphasic: the first peak occurred at 5 min and the second one at 20 min. It was also demonstrated that the second peak was regulated in part by a calmodulin/protein kinase C-dependent mechanism. Based on the kinetic analysis of DAG formation and [32P]phosphoinositide breakdown, the first peak of carbachol (1 microM)-stimulated DAG accumulation was found to be related to the breakdown of [32P]phosphatidylinositol 4-monophosphate ([32P]PIP) and [32P]phosphatidylinositol 4,5-bisphosphate ([32P]PIP2). The second peak was found to be related to [32P]PIP2 breakdown. Carbachol stimulated the release of [3H]phosphocholine into the medium, indicating that the predominant pathway for phosphatidylcholine hydrolysis was via phospholipase C. Moreover, carbachol stimulated the release of [3H]choline metabolites in a time- and dose-dependent manner. This agonist slightly stimulated the release of [3H]ethanolamine metabolites. A calmodulin/protein kinase C-dependent mechanism was also studied and was found to be involved in carbachol-stimulated phosphatidylcholine hydrolysis; W-7, a calmodulin inhibitor and staurosporine, a protein kinase C inhibitor, inhibited the carbachol (1-microM)-induced release of [3H]choline metabolites at 20 min in a dose-dependent manner, but did not have inhibitory effects at 5 min. These results suggest that the first peak of DAG accumulation induced by carbachol is predominantly associated with the breakdown [32P]PIP and of [32P]PIP2 and that the second peak is predominantly associated with [32P]PIP2 breakdown and phosphatidylcholine hydrolysis.
Alkaloids↗
Ca2+ potentiates corticotropin-induced, but not isoproterenol-induced, [3H]guanosine diphosphate release in rat adipocyte membranes.
EGTA abolished corticotropin (ACTH)-stimulated adenylate cyclase in rat adipocyte membranes. In contrast, the potency of guanosine triphosphate (GTP) stimulation of adenylate cyclase activated with ACTH was greater in the presence of Ca2+ (1 mmol/L). EGTA (1 mmol/L) powerfully inhibited ACTH-stimulated [3H]guanosine diphosphate (GDP) release from membranes prelabeled with [3H]GTP in the presence of isoproterenol (ISO) or ACTH, whereas Ca2+ significantly increased it. In contrast, neither EGTA nor Ca2+ affected ISO-stimulated [3H]GDP release. These data clearly show that Ca2+ is necessary for the binding of ACTH to its receptor, and that Ca2+ stimulates the interaction of the ACTH-occupied receptor with GTP-binding proteins.
Adenylyl Cyclases↗
Effect of mammalian lignans on fMLP-induced oxidative bursts in human polymorphonuclear leucocytes.
We examined the effects of mammalian lignans, enterolactone, prestegane B and 2,3-dibenzylbutane-1,4-diol (DBB) on superoxide production and luminol-dependent chemiluminescence (LCL) response in human polymorphonuclear leucocytes (PMNs). The three lignans had no direct effect on the responses of human PMNs. DBB and prestegane B enhanced the superoxide production and LCL response induced by formylmethionyl-leucyl-phenylalanine (fMLP), but enterolactone inhibited fMLP-induced effects. The effects of DBB were stronger than those of prestegane B and the effects of DBB were inhibited by bromophenacyl bromide, mepacrine, N-(6-aminophenyl)-5-chloro-1-naphthalene, sulphonamide and trifluoroperazine, but not by gossypol, nordihydroguaretic acid, indomethacin, staurosporine, 1-(5-isoquinolinesulphonyl)-2-methylpiperazine dihydrochloride or (R,S)-2-methoxy-3-(octadecyl-carbamoyloxy)-propyl-2-(2-thiazoli o)-ethylphosphate. These results suggest that DBB primes the responses of human PMNs, and the priming effect is caused by the activation of phospholipase A2--and Ca(2+)-calmodulin-pathways, but not by the activation of lipoxygenase, cyclo-oxygenase and protein kinase C or by the release of platelet activating factor.
Humans↗
Influence of melatonin on reproductive behavior in male rats.
The influence of melatonin on reproductive behavior was examined by administering it to pinealectomized male rats for 30 consecutive days. After the 30-d administration of melatonin or vehicle, each male rat was introduced into a female rat's cage on the day of proestrus and allowed to mate overnight. All rats administered the vehicle and the pinealectomized rats copulated; five of the twelve melatonin (8.0 mg/kg)-treated rats did not copulate. These findings suggest that melatonin inhibits the reproductive behavior of male rats.
Animals↗
[Strain differences of mice in learning of swimming behavior and effect of hemicholinium and vasopressin. Observation by a simple water maze apparatus].
In order to determine the strain differences in learning of swimming behavior and to study the influence of vasopressin or its derivatives on hemicholinium-3-induced impairment of water maze learning in mice, we designed a new apparatus using water maze which has three panels in small fish breeding water bath (L60 x W30 x H36 cm). In the first swimming, six strains of adult male mice, ICR, ddY, ddN, C3H/He, BALB/C and C57BL were subjected to learn swimming behavior twice a day for 6 d in a straight course. Only ICR, ddN, C57BL and BALB/C strain mice were chosen for the next experiment. In the second swimming, mice (ICR, ddN, C57BL, BALB/C) were swum in the water maze apparatus. Scopolamine-induced impairment of water maze learning was produced only in ICR, BALB/C mice, but not in C57BL and ddN strain, which was recovered by physostigmine. Amnesia was not obtained by intracerebroventricular injection (i.c.v.) of cycloheximide and AlCl3 in mice (ICR). Hemicholinium-induced amnesia was improved by vasopressin and desmopressin. Lysine-vasopressin and oxytocin were without affecting hemicholinium-induced amnesia. Pretreatment with a vasopressin antagonist, ([1-(beta-mercapto-beta,beta-cyclopenta-methylene propionic acid), 2-(o-methyl)tyrosine arginine]-vasopressin) resulted in a reversible effect on the improvement of hemicholinium-induced amnesia by vasopressin. Of four different strain mice, ICR mice were the most preferable to the presently used test. They were also more responsive to hemicholinium and vasopressin than the other strains. These results suggest that the simple water maze apparatus may be useful for a pre-examination of nootropics or a study of learning of swimming behavior in mice.
Animals↗
Ca2+ ionophore and phorbol ester stimulate diacylglycerol formation and phosphatidylcholine hydrolysis in rat parotid acinar cells.
We investigated the effects of A23187 and phorbol 12,13-dibutyrate (PDBu) on sn-1,2-diacylglycerol (DAG) accumulation and phosphatidylcholine (PC) hydrolysis in rat parotid acinar cells. Both A23187 and PDBu, in concentration ranges of 0.001-0.1 microM, stimulated DAG accumulation and PC hydrolysis in a time- and concentration-dependent manner. Treatment with A23187 and PDBu stimulated the release of [3H]choline and [3H]phosphocholine into the medium, indicating [3H]PC hydrolysis is due to the activation of phospholipases C and D; however, [3H]phosphatidylethanolamine hydrolysis was not indicated. These releases were unaffected by the addition of glucose 6-phosphate, a phosphatase inhibitor. Staurosporine, a protein kinase C inhibitor, significantly inhibited the DAG accumulation and the PC hydrolysis stimulated by these agents. Combinations of A23187 and PDBu potentiated the stimulatory effect which each of these agents alone had on DAG accumulation and PC hydrolysis. This mode of action was additive but not synergistic. These results suggest that DAG accumulation induced by A23187 and PDBu is related to the PC hydrolysis mediated via the activation of phospholipases C and D, and that it is not related to phosphatidylethanolamine hydrolysis.
Alkaloids↗
Assignments of Raman tensors to Raman bands of nucleic acids: use of a single crystal of adenosine triphosphoric acid and DNA fibers.
A polarized laser (488.0 nm) Raman spectroscopic measurement has been made of a single crystal of adenosine triphosphoric acid trihydrate (ATP.3H2O), whose space group is P2(1)2(1)2(1), and whose dimensions are about 10 microns x 100 microns x 100 microns along the crystallographic a, b and c axes, respectively. For each Raman band in the 300-1800 cm-1 range, relative scattering intensities, Ibb and Icc, which correspond to the bb and cc components of the Raman tensor of the crystal, have been determined. In an aqueous solution of ATP, the depolarization ratio of each Raman band has also been determined. On the basis of these experimental results, some discussions are given of the shapes and orientations of the Raman scattering tensors localized in the base residue, ribose portion, and phosphodiester portions. A similar type of study has been made with a few DNA fibers.
Adenosine Triphosphate↗
Phorbol ester alters carbachol-stimulated diacylglycerol formation in parotid acinar cells through the hydrolysis of phosphoinositides and phosphatidylcholine.
Incubation of rat parotid acinar cells with phorbol 12,13-dibutyrate (PDBu) resulted in inhibition of carbachol-stimulated formation of sn-1,2-diacylglycerol (DAG). PDBu pretreatment inhibited carbachol-induced turnover of phosphoinositides; this inhibition was indicated by phosphatidylinositol 4,5-bisphosphate breakdown. This pretreatment also attenuated the effect of carbachol on inositol phosphate generation and phosphatidylcholine hydrolysis. These results show that PDBu alters carbachol-stimulated DAG formation through the hydrolysis of phosphoinositides and phosphatidylcholine.
Animals↗
[The local hyperthermochemotherapy for pleural carcinomatosis].
Local hyperthermochemotherapy was performed in 17 cases to control malignant effusion and intrathoracic disseminated lesions. Of these 15 patients, 11 cases primary lung cancer, 4 cases metastatic lung cancer had pleural carcinomatosis and 2 cases were malignant diffuse mesotheliomas. The procedure was radiofrequency hyperthermia (13.56 MHz) maintaining the peripleural temperature at 42-43 degrees C for 45-60 minutes, combined simultaneously with the intrathoracic administration of cisplatin (1-2 mg/m2, bolus) through a thoracic double lumen trocar tube. The treatment was repeated from 2 to 4 times at 7-day intervals. In 14 cases (87.5%) complete or partial response according to the criteria of the Japan Lung Cancer Society were obtained. There were 2 cases of no change and one case that was impossible to evaluate. In one lung cancer case, the disappearance of pleural disseminated lesions was confirmed by flexible thoracoscopy after the procedure. In 12 cases, there were abdominal complaints due to side effects of the hyperthermochemotherapy, such as vomiting and nausea, but these symptoms were milder than those caused by intravenous injection of anti-cancer agents, for example cisplatin, in conventional chemotherapy treatment. The median survival time and 2 years survival of the patients with the present procedure were 15 months and 41.7% respectively. Although distant metastases appeared in most cases, none had local recurrence and particularly noteworthy pleural effusion was well controlled. The above experience suggested that the local hyperthermochemotherapy is useful to control pleural effusion and can improve the quality of life of patients with pleural carcinomatosis.
Aged↗
Inhibitory effect of 2,3-dibenzylbutane-1,4-diol, a mammalian lignan, on contraction induced by norepinephrine in rat aorta.
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Animals↗