[Two-channel bronchial artery infusion of cisplatin for the treatment of primary lung cancer].
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Biomedical subjects
Publications and source records attributed to H Inoue.
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The effect of the immunosuppressant cyclosporin A on the survivability of newborn mouse cerebral cortex transplanted into the third ventricle of adult rats was investigated. Hematoxylin staining revealed that the transplanted mouse brain tissue was rejected by 4 weeks after the transplantation in the control group. In contrast, a large mass of grafted tissue was clearly detected in the third ventricle even 4 weeks after the transplantation in the cyclosporin A-treated group, and the grafted tissue was heavily stained with Thy-1.2 mouse monoclonal antibody. The results indicate that cyclosporin A is an effective immunosuppressant in neuronal transplantation as well as in transplantation of other organs.
Intracranial metastasis of Wilms' tumor is very rare. Furthermore, intracerebral hemorrhage is an unusual presentation of metastases. We report the case of a 4-year-old girl who had multiple intracranial metastatic lesions, initially presenting as an intracranial hemorrhage. Removal of the tumors and hematoma was followed by radiation therapy and chemotherapy. Thereafter, complete remission occurred. It is thought that this malignant tumor with metastases may be curable through combined therapy.
Rat brain tumor was used as a model to evaluate radiation therapy with and without misonidazole. BD-IX rats were implanted intracerebrally with an ethylnitrosourea-induced glioma. Three series of experiments were performed, with radiation given 14 days after inoculation of the glioma clone. In each series, the following radiation doses were given: 500 rads once, 1,000 rads once; and 1,000 rads twice, every time with or without two different doses of misonidazole. Radiation therapy significantly prolonged survival when compared to the longevity of the control group. The dose of 1,000 rads given twice was highly effective and the life-span of tumor-bearing rats increased from 72% to 121%. Misonidazole plus irradiation negated the prolongation of survival, achieved with radiation therapy alone.
A newly synthesized compound, cis-1-methyl-4-isohexylcyclohexane carboxylic acid (IG-10), has been reported as an inhibitor of delayed hypersensitivity reaction. In the present paper, the mechanisms regarding the inhibitory action of IG-10 was investigated on delayed hypersensitivity reactions. p-Phenylenediamine-induced contact dermatitis in guinea pigs was significantly inhibited when the drug was given in a dose of 100 mg/kg p.o. at various times after challenge with the antigen. IG-10 inhibited both contact dermatitis and monocytes or neutrophils infiltrations induced by picryl chloride in mice. A skin reaction, similar to that seen in the case of delayed hypersensitivity reaction, was induced by an intradermal injection of phytohemagglutinin-P (PHA-P) stimulated lymphocytes in guinea pigs. This reaction was a useful method for assessing the effect of drugs on the release of lymphokines, particularly skin reactive factor (SRF). IG-10 in a concentration of 10(-5) g/ml inhibited the release of SRF as well as the release of migration inhibitory factor (MIF) from guinea pig lymphocytes stimulated by PHA-P. The reduction of delta 4-3-ketone of aldosterone and/or hydrocortisone by rat liver homogenates was not affected with IG-10, unlike that seen in the case of glycyrrhizin.
In anaesthetised open chest dogs, 30 mg . kg-1 of quinidine sulphate was injected intravenously over 5 min to produce QT prolongation. The sinus node was crushed. Effective refractory period (ERP) was determined at eight test points of the right ventricle using extra-stimuli after every seven basic ventricular pacings. Stimuli were of 2 ms duration and 1.5 times diastolic threshold. Temporal dispersion was estimated as the difference between the maximum and the minimum ERP of eight test points. Cycle lengths of basic ventricular drive were 700, 600, 500, and 400 ms. Time course of changes in ERP and its temporal dispersion was tested in five dogs. The effect of a 2 mg . kg-1 bolus injection followed by 70 micrograms . kg-1 . min-1 drip infusion lignocaine, on quinidine-induced changes in ERP was studied in eight dogs, and that of a 0.06 microgram . kg-1 . min-1 infusion of isoprenaline, was tested in six dogs. ERP was significantly prolonged after quinidine injection (220 +/- 20 vs 258 +/- 25 ms n = 19, basic cycle length = 500 ms, p less than 0.001). Temporal dispersion was also increased after quinidine (18 +/- 9 vs 33 +/- 12 ms n = 19, basic cycle length = 500 ms, p less than 0.001). With shortening of basic cycle length (BCL), ERPs were shortened significantly. Temporal dispersion, however, did not change. Lignocaine prolonged ERP even further (250 +/- 25 vs 273 +/- 16 ms BCL = 500 ms, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
We studied effects of bretylium tosylate (6 mg X kg-1, injected intravenously over 60s) on ventricular refractoriness and its inhomogeneity, and ventricular fibrillation threshold (VFT) in canine hearts with quinidine-induced long QT interval. In 3 anaesthetised open chest dogs, 30 mg X kg-1 of quinidine sulphate was injected intravenously over 5 min to produce QT prolongation. Effective refractory period (ERP) was determined at 8 test points of the right ventricle using extrastimuli. Temporal dispersion as an expression of inhomogeneity of ventricular refractoriness was estimated as the difference between the longest and the shortest ERP. VFT was determined using a train of pulses, 4 ms in duration and at 10 ms intervals. Effects of bretylium were determined from 30 to 60 min after injection. Quinidine-induced long QT interval did not change after bretylium (358 +/- 37 vs 348 +/- 26 ms) when transiently elevated blood pressure returned to the pre-bretylium level. Bretylium shortened ERP slightly (278 +/- 16 vs 268 +/- 14 ms, p less than 0.02) but did not shorten ERP after premature depolarisation (209 +/- 14 vs 209 +/- 15). However, temporal dispersion was significantly decreased by bretylium. VFT, which was lowered by quinidine (14.5 +/- 5.0 vs 8.5 +/- 2.9 mA, p less than 0.01), was elevated significantly by bretylium (21.9 +/- 6.9, p less than 0.001). These effects of bretylium might be attributed to the combination of its direct electrophysiology and indirect adrenergic actions.
Phosphatidylinositol phosphodiesterase activity was found to be entirely absent in the head of the Drosophila visual mutant, norpA. It was also demonstrated that the enzyme activity was highly concentrated in the retinular cells of a normal head. Furthermore, the enzyme was revealed to be in a membrane bound form. In view of the present results and our previous work on the reduction of diacylglycerol kinase activity in the norpA mutant, phosphatidylinositol metabolism may play an important role in the generation of photoreceptor potentials.
We have found that arachidonic (20 : 4) acid is indetectable in phosphatidylinositol and diacyglycerol extracted from Drosophila heads. After careful examinations of the lipid extraction processes and fatty acid detection system (gas-liquid chromatography), we excluded the possibility of the oxidation of polyunsaturated fatty acids or of having overlooked a trace amount of the fatty acid. The precursors of arachidonic, dihomo gamma-linolenic (20 : 3), and gamma-linolenic (18 : 3) acid, were also indetectable in these lipids. On the basis of these results, it appears that the arachidonic acid cascade is essentially absent in Drosophila head, including the brain and compound eyes. Since arachidonic acid is considered to be a key molecule in phosphatidylinositol turnover in the brain, it is of interest that Drosophila brain and eyes do not require arachidonic acid for their functions.
Epidermal regeneration in 17 patients with deep dermal and third degree burns was studied by light and electron microscopy. At the junction between the regenerated epidermis and granulation, a fibrin network or collagen fibrils arranged in a similar form covered the regenerated epidermal cells. In the deep layer of the regenerated epidermis, squamous cells contained rich glycogen granules in the cytoplasm and the basement membrane appeared under these cells. In the ulcerated area, fibroblastic cells with rich, rough endoplasmic reticulum and granules were found in the extracellular matrix composed of collagen fibrils and amorphous substance. Regeneration of the epidermis seems to be facilitated by anchorage of the regenerating cells in the fibrillar network as well as by formation of the basement membrane, which probably is produced by the squamous and fibroblastic cells.
The effects of preillumination were investigated on ion-stimulated stomatal opening of epidermal strips isolated from Commelina communis L. leaves, which are dark-starved 24 hours or more. The rate and the extent of ion-stimulated stomatal openings were increased by preexposure of epidermal strips to light. The evidences are interpreted as indicating that the energy induced by preillumination can be conserved in guard cells for considerable time periods and then used for a delayed stomatal opening in the presence of higher concentration of potassium or sodium ions. Action spectrum showed two peaks, one in blue and one in the red light region. The ratio of the blue peak to the red peak is 1.2; which is the smallest reported value in action spectra of stomatal movements. 3-(4-chlorophenyl)-1,-1-Dimethylurea suppressed the ion-stimulated stomatal opening induced by the preillumination. We conclude that the photosynthetic electron transport system, containing photosystem II, in guard cell chloroplasts is a basic system of energy acquirement for stomatal opening.
ECG measurements of consecutive 100 R-R intervals were done on depressive patients. The patient group presented lower mean values for coefficients of variation (CV) at each generation than the control group (normal subjects); the differences were significant especially for the subjects 40 to 49 years of age (P less than 0.05) and for those 60 to 69 years of age (P less than 0.01). These results can probably be regarded as a significant and objective index of autonomic disturbances in depression.
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The mechanisms governing increased central (Rc) and peripheral airway resistance (Rp) during hemodynamic edema formation were studied in anesthetized dogs. Rc and Rp were measured by forced oscillation at 1 Hz by use of a retrograde catheter to partition resistance and a pleural capsule to detect alveolar pressure. After elevation of left atrial pressure to 30 cmH2O by inflation of the left atrial balloon, Rc gradually increased an average of 60% above control in approximately 100 min. Vagotomy had a small influence on the change. On the other hand, Rp with vagus nerves intact increased triphasically: first, it increased transiently by 160% above the control value within 15-20 min before returning to near base line. It then increased gradually for approximately 40 min and finally rose sharply up to five times the control value after approximately 100 min. With vagi cut, the initial phase disappeared, but the second gradual and final rapid phases were not affected. Several sequential mechanisms of increased Rp can be proposed: 1) transient bronchoconstriction mediated by vagal reflex; 2) gradual formation of peribronchial edema; and 3) a sharp increase in airway fluid and formation of bronchial froth. In addition, narrowing of the airways by vascular engorgement may have contributed to the increase of Rp throughout all stages.
In an attempt to identify the site and nature of nonadrenergic inhibitory nervous regulation in airways, we studied the relative effectiveness of the nervous system in reversing bronchoconstriction along various generations of airways by comparing it with that seen during sympathetic (beta-adrenergic) stimulation in 9 cats. After giving atropine (3 mg/kg), airway dimensions were obtained from roentgenograms after insufflation of powdered tantalum. Baseline bronchoconstriction was then induced by an intravenous infusion of serotonin (50 to 250 micrograms/kg/min). Electrical stimulation of the sympathetic nerves inhibited constriction throughout the airways from trachea down to bronchioli less than 0.5 mm in diameter, with the maximal effect in airways 1 to 4 mm in diameter. The vagi were then stimulated after blocking the adrenergic inhibitory nervous system with propranolol (2 mg/kg). The distribution and potency of the remaining nonadrenergic inhibitory nerve's effect on airway constriction induced by serotonin was comparable to that obtained with sympathetic stimulation. We conclude that the nonadrenergic inhibitory nerves preferentially dilate the midsized airways, which essentially correspond to the sites maximally constricted by vagal stimulation without atropine. The largest (tracheal) and the peripheral airways (less than 1 mm in diameter) are only slightly affected by either inhibitory system.
We examined the secretory effects of two beta 2-adrenergic agonists, procaterole and terbutaline, on the submandibular glands of anesthetized rats. After stimulation with these agents with and without a range of antagonists (non-specific alpha- and beta-adrenergic blockers), submandibular saliva was collected. The flow rate, protein concentration, the electrophoretic patterns, and amino acid composition of saliva were examined. These parameters were compared with their counterparts in saliva stimulated with isoproterenol (IPR), with and without antagonists. Assessed by these criteria, secreted proteins were classified as the alpha- or beta-type. In addition, IPR-stimulated proteins were compared in submandibular saliva of rats chronically treated with IPR or procaterole. Both beta 2-agonists were potent secretagogues for the submandibular glands of rats. All beta-antagonists completely abolished the secretory effects elicited by both beta 2-agonists, with the exceptions of carteolol and propranolol. However, no blocking agent abolished the secretory effects of IPR (60 mg/kg). The types of proteins in all submandibular saliva samples elicited by both beta 2-agonists with and without antagonists were the beta-type. Enlargement of the submandibular glands was not observed in rats subjected to chronic administration of procaterole, nor were abnormal and additional proteins observed, as confirmed by electrophoresis and by the amino acid analyses.