Biomedical subjects
Publications and source records attributed to M Oka.
Explore the source record for details and available documents.
A case report of a woman with spinal angiolipoma is presented, and it is stressed that spinal angiolipoma and spinal lipoma are two different clinicopathological entities which should be clearly distinguished.
Interactions between dopamine and responses to noradrenaline as modulated by prostaglandins (PGs) were studied in the perfused rat mesenteric vascular bed. When perfused alone dopamine up to a concentration of 10(-7)M neither changed baseline pressure nor modified the pressor response to noradrenaline. Dopamine at 10(-9) to 10(-7)M significantly inhibited responses to noradrenaline which had been enhanced by the presence of 10(-10) to 10(-8) M PGE1. In preparations in which vascular responses to noradrenaline had been abolished by indomethacin and restored by adding PGE1, 10(-9) to 10(-7)M dopamine significantly inhibited the restored responses. Dopamine also attenuated the inhibitory effects of prostacyclin on pressor responses to noradrenaline but it did not change the actions of either PGE2 or PGF2 alpha. Pimozide, a mainly centrally acting dopamine antagonist, did not interfere with these peripheral actions of dopamine. The dopamine effects were blocked by another dopamine antagonist, metoclopramide. Dopamine can inhibit the effects of PGE1 and prostacyclin in the rat mesenteric vascular bed, possibly by interacting with specific dopamine receptors.
Effects of aldosterone and spironolactone on the vascular responses to noradrenaline and potassium were studied in the perfused rat mesenteric vascular bed. Aldosterone did not modify the response to either vascular agent. Spironolactone inhibited the vascular response to both pressor agents in a dose-dependent manner. The inhibitory effect of spironolactone was not altered by various concentrations of aldosterone and ouabain. However it was not apparent in preparations in which endogenous prostaglandin synthesis had been abolished in indomethacin. The observations suggest that spironolactone has actions on vascular reactivity which are not related to aldosterone or to sodium/potassium pumping. They may depend on modification of prostaglandin biosynthesis.
Explore the source record for details and available documents.
The structure of micronemata arising from the surface of the bloodstream form of Trypanosoma gambiense was studied by electron microscopy. In order to produce micronemata, trypanosomes were incubated in either 1) phosphate buffered saline supplemented with glucose (PBSG), 2) immune mouse serum or 3) PBSG after passage through a DEAE-cellulose column. Electron microscopic examination of the parasite revealed the presence of thread-like micronemata arising from the anterior end and from the flagellar pocket regardless of the incubation conditions. Negative staining revealed a distinct peripheral fringe layer with nodular protrusions covering the entire surface of the micronema. The distribution and number of intramembrane particles (IMP) on the P and E faces of the micronema were similar to those of the flagellum of T. gambiense, indicating a close relationship between the membrane structure of the micronema and the flagellum. Micronemata became fragmented and adhered to each other after incubation of the parasite in the media for 12 h. Since micronemata tend to have the characteristics of adhesiveness and fragmentation, fragments of these structures might adhere to various host organs. Dispersal of potential antigenic material might be responsible, in part, for the induction of the host immune response.
The role of the renin-angiotensin system in the control of aldosterone and other mineralocorticoids was studied in 9 hyperkalemic patients with chronic renal failure showing mild azotemia (group I) and 6 normokalemic patients with chronic renal failure showing creatinine clearance similar to that in group I (group II). In group I, the plasma renin activity (PRA) was significantly low and plasma aldosterone (PAC) and 18-hydroxycortisterone (18-OH-B) were also significantly reduced. In group II, PRA was normal or slightly increased, and PAC and 18-OH-B were also normal or slightly increased. Both the PAC and 18-OH-B in group I were stimulated by ACTH and angiotensin II, although the responses were less than those in group II. In 2 patients of group I where PRA moved into the normal range after administration of furosemide, the plasma 18-OH-B and PAC also reached the lower limit of normal. These results suggest that suppression of the renin-angiotensin system is probably related to functional disturbance in the conversion from B to 18-OH-B and/or 18-OH-B to aldosterone in most abnormally hyperkalemic patients with chronic renal failure.
The objective of our study was to determine whether the pure synthetic substance P(SP) is algesiogenic or analgesic when administered centrally or peripherally. The relationships between SP-induced analgesia and the content of morphine-like factor (MLF) in the brain were also studied. Intracarotid arterial administration of SP (20-200 microgram) produced no pseudoaffective responses to pain in six out of nine rats, but in the remaining three, there was an exhibition of these responses. Chlorpheniramine pretreatment antagonized these responses. On cantharidin blister base experiments in humans, SP (10(-3) g/ml) produced slight pain and an itchy sensation. SP given intracerebroventricularly produced an analgesia in mice in a dose of 5 ng/mouse, as determined by the acetic acid-induced writhing and hot plate methods. These SP-induced analgesia were antagonized by naloxone pretreatment. SP did not alter the content of MLF in the mouse whole brain. However, SP5-11 not only produced an analgesia but also increased the content of MLF. These results suggest that SP has a slight algesiogenic activity which might be mediated by histamine and a slight analgesic activity which might be mediated by MLF.
Explore the source record for details and available documents.
Dextran sulfate 500 and carrageenan, sulfated polysaccharides, have been considered as macrophage-toxic giving profound effects on the immune response. This work deals with agglutination antibody responses to T. gambiense homogenate in mice treated with dextran sulfate 500 and carrageenan. Antibody responses to the first immunization were suppressed in mice treated with the agents before the first immunization but reverse was the case with the response to the second immunization. These suppression and enhancement appeared to be dependent on the timing of treatment in regard to the time of the first immunization. The enhanced antibody response was abolished by either treating the mice with anti-thymocyte serum or transferring of spleen cells treated with anti-thymocyte serum into mice. Thus, the enhancement of antibody response is seemingly attributable for the most part to potent memory T cells induced by treatment with the agents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Effect of 3-sulfamoylmethyl-1,2-benzisoxazole (AD-810) on kindled seizures in the neocortex, hippocampus and amygdala was studied in comparison with that of clinically proved antiepileptics, and the differences in kindled seizure development in the three areas were also studied. The amygdala more rapidly developed a generalized seizure (kindled seizure) than the hippocampus and the neocortex. Although more days of stimulation were needed, the neocortex also developed a kindled seizure similar to limbic kindled seizures. Phenobarbital, carbamazepine, dipropylacetate and diazepam showed a depressant effect on the neocortical kindled seizures. Phenytoin showed a depressant effect only when it was administered intravenously. Phenobarbital and carbamazepine depressed the hippocampal kindled seizures, while phenytoin and diazepam had little effect. Phenobarbital and diazepam caused marked depression on the amygdaloid kindled seizures, but the effect of phenytoin, carbamazepine and dipropylacetate on them was weak or negligible. AD-810 showed a depressant effect on neocortical and hippocampal kindled seizures, but not on amygdaloid ones. The profile of AD-810 is similar to that seen with carbamazepine.
Heated whole fish meal, produced from mackerel, was proved to induce gizzard erosion in broiler chicks by feeding for 6 days. The constituents of the water-soluble fraction of fish meal were suspected to be the cause of this lesion. Of them, histidine, histamine and nucleotides were examined. When added to milk casein and heated, histidine appeared to be the most toxic. It seemed, however, that histamine and IMP (inosine 5'-monophosphate) might be less toxic even when treated in the same way a histidine. Feeding of a large amount of histamine alone resulted in giving rise to a much disturbed profile of body weight gain, while a low incidence of gizzard erosion was observed in this case. Both heated fish meal and a heated mixture of casein and histidine were easily reduced in toxicity by acid hydrolysis. The latter was more sensitive to this treatment. On the contrary, papain had an action to diminish the toxicity of heated fish meal at all. Even after treated with papain, the heated casein-histidine mixture was still effective to induce gizzard erosion. These results might have come from different structural changes caused by heating of the two samples.
The mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome was studied in 10 patients with primary aldosteronism and in 3 patients with Cushing's syndrome in in vivo and in vitro experiments. In all of the 10 patients with primary aldosteronism, ACTH stimulated aldosterone secretion from the adenomas more significantly than did angiotensin II and III. DOC and cortisol which were contained in the adenomas were also stimulated more significantly by ACTH than by angiotensin II and III. Responses of the adenomas of Cushing's syndrome to various stimulations were less than those of primary aldosteronism. Secretion of cortisol and aldosterone from the adenomas of Cushing's syndrome was stimulated by ACTH and angiotensin II to a similar degree. From these studies, it seems that secretion of adrenal steroid hormones from adenomas of primary aldosteronism is more sensitive to extradrenal stimulations than that of Cushing's syndrome, and ACTH is the main factor in the control of the secretion of adrenal steroid hormones from the adenomas.
10(-6) and 10(-5) M spironolactone decreased the total conversion of 14C-arachidonic acid to 6-keto-prostaglandin (PG) F1 alpha, PGE2 and PGF2 alpha in rat aortic and mesenteric artery rings by 29 and 55% respectively. Same concentrations of spironolactone decreased the total conversion of 14C-arachidonic acid to thromboxane (TX) B2, PGE2 and PGF2 alpha in human platelets by 3 and 21% respectively. These findings provide a possible basis for the significant inhibition by spironolactone of vascular reactivity to norepinephrine. Spironolactone seemed to act in both vascular tissue and platelets to suppress PG synthesis at the prostaglandin endoperoxide synthetase level. This direct action of spironolactone could contribute to its vascular and other effects.
Intubation in patients for oral surgery will often prove very difficult. The advantages of using a modified, guided, blind nasotracheal intubation in such patients are discussed.
Mutants of Klebsiella aerogenes with three types of mutations affecting regulation of tyramine oxidase were isolated by a simple selection method. In the first type, the mutation (tynP) was closely linked to the structural gene for tyramine oxidase tynA). The order of mutation sites was atsA-tynP-tynA. In the second type, the mutation that relieves catabolite repression of the syntheses of several catabolite repression-sensitive enzymes are not linked to the tyn gene by P1 transduction. These strains contained high levels of cyclic adenosine 5'-monophosphate when grown on glucose. The third type of mutation, in which tyramine oxidase was synthesized constitutively, was shown by genetic analysis to involve mutations of tynP and tynR. The tynR gene was not linked to tynA. Results using the constitutive mutants showed that the constitutive expression of the tynA gene resulted in depression of arylsulfatase synthesis in the absence of tyramine.