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T Imada

Publications and source records attributed to T Imada.

At least 163 records · Page 9Linked to original sources
PubMed1984

Specific desensitization of actin polymerization of bovine platelets.

Polymerization of actin induced by activation of platelets was investigated using deoxyribonuclease I inhibition assay. When platelets were activated with ADP or 5-hydroxytryptamine, actin was polymerized quickly followed by rapid depolymerization to the initial level. Reactivation with the same agonist, however, did not cause the polymerization of actin, though with different agonists actin polymerized quite normally. The mechanism for this agonist-specific desensitization of actin polymerization was investigated by the use of a calcium ionophore A23187. It was suggested that the cause for the desensitization is the inability of platelets to mobilize Ca2+ in response to specific agonist.

Actins↗
PubMed1984

Development of second generation merozoites of Leucocytozoon caulleryi in vitro.

Sporozoites of Leucocytozoon caulleryi were inoculated into specific-pathogen-free (SPF) chickens intravenously. Fourteen days after inoculation, the infected blood, parasitized with second generation merozoites, was collected from the chickens. The blood was then suspended in SPF chicken serum or RPMI-1640 culture medium supplemented with 20% SPF chicken serum in petri dishes, which were cultured at 37 degrees C or 41 degrees C in a humidified atmosphere of 5% CO2. Second generation merozoites in parasitized, immature erythrocytes developed continuously through several substages and finally became micro- and macro-gametocytes after 6 days of incubation.

Animals↗
PubMed1984

Rapid modulation of platelet aggregation in plasma by oxygenated sterols.

The effect of oxygenated sterols on platelet aggregation induced by thrombin and ADP has been studied. All oxygenated sterols tested with a hydroxyl group on the side chain enhanced thrombin-induced aggregation at 25 microM. In the case of ADP-induced aggregation, however, only 22S-hydroxycholesterol[(22S)-5-cholestene-3 beta,22-diol] enhanced the aggregation, and 22R-hydroxycholesterol[(22R)-5-cholestene-3 beta,22-diol], 24S-hydroxycholesterol[(24S)-5-cholestene-3 beta,24-diol], and 25-hydroxycholesterol[5-cholestene-3 beta,25-diol] inhibited it. These effects were observed within 10 min after the addition of oxygenated sterols to platelet suspensions in plasma.

Adenosine Diphosphate↗
PubMed1983

Coupling between fatty acid binding and sulfhydryl oxidation in bovine serum albumin.

Albumin with and without a free sulfhydryl group (mercapt-albumin and nonmercapt-albumin) has low and high amounts of fatty acids, respectively. It was found that this difference was brought about by the following two mechanisms: (a) the binding of fatty acids increases the rate of oxidation of the sulfhydryl group, (b) the oxidation of the sulfhydryl group of the protein enhances the binding of fatty acids. The incubation of the protein with fatty acids enhanced reversibly the reaction rate of the free sulfhydryl group with 5,5'-dithiobis(2-nitrobenzoic acid). This effect of fatty acids depends on the kind of fatty acid added. Among saturated long-chain fatty acids tested, the shortest fatty acid, lauric (dodecanoic) acid, had the strongest effect. Oleic (cis-9-octadecenoic) acid, which has a long chain but also one cis-double bond, however, was as effective as lauric acid in enhancing the reactivity of the sulfhydryl group on the protein. Analyses with palmityl-Sepharose and equilibrium partitioning of palmitic acid between heptane and aqueous protein solutions have shown that nonmercapt-albumin has higher affinity to the fatty acid than mercapt-albumin. These results imply that the binding of fatty acids and the oxidation of sulfhydryl groups of the protein are intimately coupled.

Animals↗
PubMed1983

Agonist-specific refractory states of bovine platelets-disappearance of synergism in aggregation.

The specificity of refractory state of bovine platelets developed by various agonists was examined. When bovine unwashed platelets were preincubated with 5-hydroxytryptamine (5HT) (or ADP), they became non responding to that agonist (refractory) but they responded quite normally to collagen, thrombin and ADP (or 5HT). When platelets became refractory to 5HT, the synergistic aggregation normally obtained with this agonist plus ADP was lost, but that with ADP plus thrombin was not changed. Platelets made refractory to ADP (or 5HT) after the aggregation and disaggregation cycle by the agonist responded normally to 5HT (or ADP). These results strongly indicate that platelets become refractory to one agonist without impairing the sensitivity to any other agonists.

Adenosine Diphosphate↗
PubMed1983

Pathogenicity and distribution of avian nephritis virus (G-4260 strain) in inoculated laying hens.

Specific-pathogen-free laying hens were inoculated intravenously with the G-4260 strain of avian nephritis virus (ANV). The distribution of the virus in organs, histological changes in main organs, the condition of laying, and egg transmission of the virus were examined in them. Over an experimental period of 27 days, no clinical sings were observed. In a chronological study on the distribution of the virus in organs, the virus was recovered from liver, kidney, jejunum, and rectum for 6 days postinoculation (PI). The virus titer in organ emulsion was the highest in the jejunum of all the main organs. The virus was recovered from the kidney for 8 days PI, although it was not so high in this organ. It was not recovered from the ovary or oviduct. Fluorescent antigens were not observed at all in any material. In a pathological examination, some local inflammatory changes were observed only in the kidney. There were no significant changes in the ovary, oviduct, or any other organ. Antibody appeared 10 days PI and was detectable even 27 days PI, although it was not so high in titer. There was no significant difference in the rate of egg-production between the infected and the sham inoculated groups. No virus was isolated from 111 fertile eggs laid by infected hens over a period from 2 to 27 days PI.

Animals↗
PubMed1983

Isolation of chicken anemia agent with MDCC-MSB1 cells from chickens in the field.

An attempt was made to isolate chicken anemia agent (CAA) from chickens suffering from anemia in the field by using MDCC - MSB1 , which was an established cell line derived from Marek's disease lymphoma. When 99 chickens of 15 flocks were examined, CAA was isolated from 58 chickens of 12 flocks. The rate of CAA isolation with MDCC - MSB1 cells was almost the same as that determined by an in vivo method by chick inoculation. It was shown that CAA was more closely concerned with anemic diseases of chickens in the field than fowl adenoviruses.

Adenoviridae Infections↗
PubMed1983

Distribution of chicken anemia agent (CAA) and detection of neutralizing antibody in chicks experimentally inoculated with CAA.

When chicks were inoculated experimentally with chicken anemia agent (CAA) at 1 day of age, CAA was consistently recovered from all the organs, including the brain, up to 28 days postinoculation (PI). It was recovered from the brain and rectal contents even 49 days PI, when the experiment was finished. In chicks inoculated with CAA at 28 or 42 days of age, CAA was also proved to multiply in all the organs, except the brain. It disappeared from these chicks earlier than from the chicks inoculated at 1 day of age. Neutralizing antibody against CAA began to be detected 21 days PI in the chicks inoculated at 1 day of age, and 7 days PI in the chicks inoculated at 28 or 42 days of age.

Anemia↗
PubMed1982

Pathogenicity of avian nephritis virus for embryonating hen's eggs.

The pathogenicity of avian nephritis virus (ANV) for embryonating hen's eggs was studied by various routes of inoculation. When inoculated with ANV by the yolk sac route, 6-day-old embryos showed the highest susceptibility and all of them died 3 to 14 days postinoculation (PI). They manifested hemorrhage and edema of the whole body (3 to 6 days PI) and stunting (7 to 14 days PI). The 50% egg-infective dose of the virus by yolk sac inoculation coincided well with the virus titer expressed in plaque-forming units determined on the monolayer of chicken kidney cell cultures. The virus could be passed serially through the chorioallantoic membrane (CAM) of embryonating hen's eggs. In these eggs the CAM presented edematous thickening at the inoculation site, and the embryo stunting. when inoculated by the CAM route, high virus doses killed all embryos, but low virus doses allowed some of the infected embryos to hatch normally. When inoculated by the allantoic cavity route, the virus did not multiply in the allantoic cavity of embryonating eggs, but some of these eggs became infected. Fluorescent antigens were present only in the kidneys and CAM of embryos infected with the virus. The virus was recovered at a low rate from cloacal swabs of chicks from normally hatched eggs inoculated with the virus by the CAM route. These chicks were variable in growth, but had antibodies against the virus and developed nephritis at 36 days of age.

Animals↗
PubMed1982

Survey on antibody against egg drop syndrome-1976 virus among chicken flocks in Japan.

A survey on antibody against egg drop syndrome-1976 virus was carried out with 4,518 sera collected from 667 flocks over a period from 1971 to 1981 in Japan. Antibody-positive sera were initially detected in 1976, and the number of positive sera increased suddenly in 1979, and a total of 270 sera from 23 flocks were positive. The positive flocks consisted of 20 broiler parent flocks belonging to 9 farms and 3 layer flocks belonging to 2 farms. It seemed from the results of this survey that the prevalence of the virus might have been limited in Japan.

Adenoviridae↗
PubMed1982

Survey on antibody against hemorrhagic enteritis virus among chicken flocks in Japan.

A survey on antibody against hemorrhagic enteritis virus was conducted by the agar-gel precipitation test among chicken flocks in Japan. The positive rate of individual serum samples increased with the advance in age of chickens. Ninety-one of 181 sera (50%) and 23 of 33 flocks (79%) were positive among chickens more than 181 days old.

Adenoviridae↗