Biomedical subjects
K Katoh
Publications and source records attributed to K Katoh.
[Effects of dopamine and synthetic atrial natriuretic polypeptide on the release of norepinephrine and epinephrine from the adrenal medulla of rats].
We evaluated the effects of dopamine (DA) and synthetic atrial natriuretic polypeptide (ANP) on the release of catecholamines (CA) from the adrenal medulla. Adrenal glands of male Wistar rats were superfused with Ringer's solution saturated with 95%, O2, 5% CO2 by the use of a continuous flow incubation system, and norepinephrine (NE) and epinephrine (E) concentrations in the perfusate were continuously measured by high pressure liquid chromatography with fluorescent reaction. And the effects of DA and ANP on the CA release were evaluated. Next the effects of metoclopramide (MC), dopamine (D2) antagonist, and glucagon were added in the Ringer's solution, and the changes of NE and E in the perfusate were determined. Basal secretion of NE and E were 0.02-0.04 ng/mg.wet weight/min and 0.05-0.1 ng/mg.wet weight/min, respectively. DA remarkably decreased both NE and E release, and the suppressive effect was dependent on DA concentration in the perfusate. MC clearly raised NE and E release as well as glucagon. The increasing effect of MC was perfectly suppressed by 10(-4) M of DA. But the effect of glucagon was not blocked by the same dose of DA. Alpha rANP (10(-5)M) slightly decreased the releases of NE and E from adrenal medulla, and the magnitude of the effect of rANP was smaller than that of DA. MC significantly increased NE and E release even when the adrenal gland was superfused with Ringer's solution containing 10(-5)M of rANP. These data suggest that the release of CA from adrenal medulla may be regulated by DA, and that the receptors specifically binding to DA may exist in adrenal medulla as well as sympathetic presynaps. We concluded that DA (but not ANP) may play an important role in controlling (suppressing) the activity of sympathoadrenomedullary system.
Specific expression of the chicken delta-crystallin gene in the lens and the pyramidal neurons of the piriform cortex in transgenic mice.
Two transgenic mice, 5-8 and 7-5, carrying the chicken delta-crystallin gene were produced by microinjecting cloned genes into male pronuclei. The mice were analyzed at 8 weeks of age with respect to gene integration and expression by means of blotting techniques and immunohistochemistry. Southern blot analysis indicated that both mice carried, on average, 50 copies of intact delta-crystallin gene per cell. Histological analysis of the mice using DNA-DNA in situ hybridization indicated that mouse 5-8 carried the delta-crystallin gene in every cell while mouse 7-5 was mosaic, with 20-40% of the cells of various tissues carrying the gene. Western blot analysis indicated that in both mice delta-crystallin is expressed in the lens and the cerebrum, but not in any other tissue examined. Immunohistological analysis revealed that, in the cerebrum of the mice, delta-crystallin was expressed specifically in pyramidal neurons located in layer IIb of the anterior piriform cortex. Thus, our results with transgenic mice not only demonstrate the primary specificity of delta-crystallin gene expression in authentic lens tissue, but reveal the unexpected specificity of this chicken gene in the central nervous system of the mouse.
Effects of intravenous injection of butyrate on the exocrine pancreatic secretion in guinea pigs.
1. The stimulus-secretion coupling in the pancreatic exocrine responses to i.v. injection of sodium butyrate was investigated in guinea pigs in vivo and in vitro. 2. Intravenous single injection of sodium butyrate (12.5-100 mumol/100 g body wt) caused an increase in fluid and amylase secretion in a dose-dependent manner. The responses evoked by sodium butyrate (100 mumol/100 g body wt) were not affected by prior injection of atropine (0.14 mumol/100 g body wt) or hexamethonium (4 mumol/100 g body wt). 3. The chloride concentration in secreted fluid increased slightly with an increase in flow rate in response to sodium butyrate, but decreased in response to secretin. 4. The amylase release from the pancreatic segments evoked by sodium butyrate (10(-6)-10(-2) M) increased dose-dependently. The responses were potentiated in the presence of secretin (1 C.H.R.u./ml), but were suppressed in the presence of acetylcholine (10(-6) M) or in a Ca-free solution containing EGTA (10(-4) M). 5. These results suggest that the secretory effects in response to i.v. injection of sodium butyrate probably arise from direct action on the acinar cells, and that an increase in cellular calcium concentration might be an important step in the secretion process, in guinea pig exocrine pancreas.
Improved mammalian vectors for high expression of G418 resistance.
Cell lines, such as those of teratocarcinoma and embryonic stem cells, fail to support high G418 resistance after transfection of neo vectors. To alleviate this, we modified pSV2-neo in two steps, first with tandem promoters of SV40 early genes and HSVtk, then by removing an improper met codon located immediately upstream of the authentic initiator codon in the mRNA sequence. In the final product, pSTneoB, the neo transcription unit has XhoI sites at both ends. pSTneoB yields G418-resistant transformants of teratocarcinoma cells at dramatically higher efficiencies than pSV2-neo. This vector extends the application of G418 selection in gene transfer to a wider range of cell types.
[Effect of the organophosphorus compounds leptophos and TOCP on creatine kinase activity in hens].
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Effect of diltiazem on acute myocardial ischemia. Study of the relationship between regional myocardial blood flow and myocardial energy metabolism.
To examine the effects of diltiazem on myocardial ischemia, 200 micrograms/kg of diltiazem were injected intravenously into anesthetized open-chest mongrel dogs 10 min after coronary ligation. This was followed by a continuous infusion of diltiazem at 10 micrograms/kg/min for 50 min. Regional myocardial blood flow (MBF) was measured by the hydrogen gas clearance method. Sixty minutes after ligation, myocardial specimens were taken from the areas where MBF was measured, and the ATP and CP contents were determined by the bioluminescence method. Simultaneously, mitochondria were isolated from the ischemic and nonischemic areas, and both the respiratory control index (RCI) and the rate of oxygen consumption in state III (QO2 III) were calculated. The aortic systolic pressure and heart rate of diltiazem treated and untreated dogs were not significantly different, and diltiazem did not increase the MBF in the area with a MBF below 40 ml/min/100 g. When MBF was 10 to 30 ml/min/100 g, the ATP content in the diltiazem treated hearts was significantly higher than that in the untreated dogs, whereas the CP content was not significantly changed. Thus, diltiazem administered after ischemia preserved ATP content in the ischemic myocardium with a MBF of 10 to 30 ml/min/100 g without significantly affecting the hemodynamics or MBF. This suggests that diltiazem exerts a cardioprotective effect by acting directly on the ischemic myocardium if it has an MBF above a certain level, even when the drug is administered after the onset of ischemia.
[Sensitivity of antineoplastic agents in squamous cell carcinoma of the uterine cervix xenografted into nude mice].
Antitumor efficacies of five antineoplastic agents, cisplatin, mitomycin, doxorubicin, 5-fluorouracil and bleomycin were tested against the human carcinoma of the uterine cervix xenografted into nude mice in order to search for effective combination chemotherapy. Antineoplastic agent was administered i.p. 6 times once a week to nude mice with tumor growing to 8-10 mm in diameter. The effect in each group was evaluated by Battelle Columbus Laboratories' method, measuring at 6th week the tumor growth rate in the treatment group (Tn/T0) and in the control group (Cn/C0) where the comparative tumor growth ratio (Tn/T0/Cn/C0) was taken as the index. As the result, the response rates of cisplatin and mitomycin on the tumor growth were high as 83.3% and 66.7% respectively. It is concluded that combination chemotherapy including cisplatin and mitomycin is recommendable for the treatment of squamous cell carcinoma of the uterine cervix.
[Statistical review on surgeries with difficult intubation in the first Department of Oral Surgery, Josai Dental University Hospital].
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Prevalence of hepatitis B surface antigen and antibody in the Cook Islands with reference to difference in rates between islands.
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[Influence of the introduction of percutaneous transluminal coronary angioplasty on coronary artery bypass surgery].
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Establishment of monoclonal antibodies which possess the same characteristics as the naturally occurring thymocytotoxic autoantibodies (NTA).
Autoantibody-secreting hybrid cell lines were obtained by fusion of spleen cells from unimmunized (NZB X NZW) F1 mice with the HAT-sensitive mouse myeloma cell line SP2/0-Ag14. Eight hybridoma cell lines producing autoantibodies to mouse thymocytes were cloned and the resultant antibodies were partially characterized. All eight monoclonal antibodies lysed mouse thymocytes in the presence of rabbit complement. The anti-thymocyte cytotoxic antibody activities were absorbed with thymocytes, lymph node cells, unfractionated spleen cells, and splenic T cells; but not with bone marrow cells, splenic B cells, or homogenates of mouse kidney, liver, or striated muscle cells. In addition, the cytotoxic activities of culture supernatants from seven of the eight hybrid clones were absorbed with mouse brain tissue homogenates. Isotyping of the monoclonal antibodies revealed that five were IgM and three were IgG2a. Mouse thymocytes sensitized with each of the eight monoclonal antibodies in vitro became highly susceptible to phagocytosis by syngeneic macrophages. The monoclonal antithymocyte antibodies, thus, appear to be similar to the naturally occurring, (NZB X NZW) F1 thymocytotoxic autoantibodies (NTA) described by Shirai et al.
Effects of adrenergic neurotransmitter on K transport in superfused segments of rat submaxillary gland.
The effect of the adrenergic neurotransmitter on K transport in the segments isolated from the rat submaxillary gland was investigated, employing the technique of electrical field stimulation (FS) and applying tyramine, a releasing drug for the catecholaminergic neurotransmitter. FS (16 Hz, 2 ms and 80 V for 1 min) caused a K release (peak value, 1.0 mumol/g/min) followed by a K uptake (peak value, 0.4 mumol/g/min) in the absence of any autonomic antagonist. Both FS-induced K release and uptake were blocked by the addition of tetrodotoxin (10(-7) g/ml). In the presence of atropine (1.4 X 10(-6) M), FS caused only a transient K uptake, which was abolished by the superimposed addition of propranolol (5 X 10(-6) M). Application of tyramine (6 X 10(-6)-6 X 10(-4) M) always only caused K uptake (peak value, 0.96 mumol/g/min), which was abolished by the addition of propranolol. The K uptake evoked either by FS or by tyramine application in the presence of atropine was not seen in the segments from rats pretreated (i.p.) with 6-hydroxydopamine. These results suggest that the adrenergic neurotransmitter activates mainly a beta-adrenergic receptor and evokes K uptake through receptor activation.
Effect of phenobarbital on the delayed neurotoxicity of leptophos in hens.
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Beta-thromboglobulin release within coronary circulation--a potential role of platelets in ergonovine-induced coronary vasospasm.
The role of platelets in the pathogenesis of acute myocardial ischemia is not yet agreed upon. In this study, the gradient of plasma beta-thromboglobulin concentration between coronary sinus and aorta was used as an indicator of platelet activation within the coronary circulation. Blood samples were drawn before and after injection of ergonovine maleate in patients without fixed coronary stenosis in whom significant coronary spasm was induced by ergonovine (n = 8, Group 1), patients with significant stenosis (greater than or equal to 75%) of the left anterior descending artery and positive ergonovine test (n = 7, Group 2) and patients with significant stenosis of left anterior descending coronary artery and negative ergonovine test (n = 11, Group 3). Fifteen patients with normal coronary arteries who were negative in the ergonovine test served as controls (Group 4). After the ergonovine test, all Group 1 patients revealed a significant increase of beta-thromboglobulin gradient (P less than 0.001), while those in other groups did not. Additionally, the gradient after the ergonovine test of Group 1 patients was larger than those of the other groups (P less than 0.01). All blood samples after the ergonovine test were collected before or at the onset of angina attacks. These results suggest that platelet activation within the coronary circulation has some pathogenic role, probably as an aggravating factor, in coronary artery spasm.
Risk analysis of multiple environmental factors: radiation, zinc, cadmium, and calcium.
Simultaneous effects of four risk factors, i.e., radiation exposure at a sublethal dose and excessive administration of zinc or cadmium and calcium deprivation, were examined by animal experiments. Deaths among 360 mice within 30 days after the whole body irradiation of 524-617 rad gamma rays were observed under 36 experimental conditions set by all possible combinations of varied levels of the four risk factors. A similar experiment was conducted a month later to check the reproducibility by using another 360 mice. The reproducibility of the experiment was confirmed and therefore the data from the two experiments were pooled. The analysis of data based on a multiple logistic model suggested that administration of zinc acts protectively against radiation.
Effects of cholinergic and adrenergic nerve stimulations on amylase release from superfused small segment of rat parotid gland.
The effects of the cholinergic and adrenergic nerve stimulations on amylase release from the segment isolated from the rat parotid gland were investigated, employing the combined techniques of electrical field stimulation (FS) and tyramine application with automated fluorescence method for measuring amylase. The maximum amylase release in response to FS for a short period (1 min) was attained at 16 Hz frequency, 2 ms pulse width and 8 V strength stimulation in the absence of any autonomic antagonist. Periodic short-lasting FS using these parameters at intervals of about 15 min could reproduce similar sizes of amylase release for about 2 h. Continuous long-lasting FS (3 V, 2 ms, 16 Hz) caused a transient sharp increase in amylase release followed by a sustained one. The FS-evoked amylase release was completely abolished by tetrodotoxin (TTX) (10(-7) g/ml) and markedly reduced by atropine (7 X 10(-6) M) or by propranolol (10(-5) M), while it was scarcely affected by hexamethonium (3 X 10(-4) M) and phentolamine (10(-5) M). The maximum stimulus frequency of short-lasting FS for amylase release in the presence of propranolol was similar to that (16 Hz) in the control, but it was higher (32 Hz) in the presence of atropine. Reduced response in amylase release to FS by propranolol was completely restored by the superimposed addition of dibutyryl cyclic AMP (10(-4) M). Application of tyramine (5 X 10(-4) M) evoked amylase release in the presence of atropine, which was blocked mostly by propranolol and partly by phentolamine, while tyramine was ineffective in the tissue segment from rats pretreated with 6-hydroxydopamine. From these results the following were suggested; that the intrinsic cholinergic neurotransmitter activates a muscarinic receptor of the acinar cell, while the adrenergic neurotransmitter stimulates mainly a beta-adrenergic and partly an alpha-adrenergic receptor, resulting in amylase release.
Effects of monensin and salinomycin on amylase release from the superfused parotid segments of sheep and rat.
The effects of monensin and salinomycin (ionophorous antibiotics) on amylase release in the parotid glands were investigated in the superfused segments of sheep and rat. Monensin and salinomycin as well as acetylcholine and isoprenaline caused enhanced amylase release in a dose-dependent manner. Salinomycin was significantly more effective than monensin in both animals. The enhanced amylase release evoked by these ionophores and acetylcholine was significantly reduced in a calcium-free solution containing EGTA. From these results it is concluded that monensin and salinomycin transport calcium ions into the cytosol of parotid acinar cells from the extracellular fluid, resulting in amylase release.