Hominoid evolution based on the structures of immunoglobulin epsilon and alpha genes.
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Biomedical subjects
Publications and source records attributed to S Ueda.
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The present study defines assay systems for vaccinia virus-reactive Lyt-1+2- T cells mediating various functions and investigates the positivity of L3T4 antigen on these Lyt-1+2- T cells as well as the role of L3T4 antigen in the activation of these T cells with respect to their functions. C3H/He mice were immunized against vaccinia virus by inoculating viable virus intraperitoneally (i.p.). Anti-vaccinia virus reactivity in lymphoid cells from these immunized mice was assessed by proliferative response, helper T cell activities involved in cytotoxic T lymphocyte (CTL) and B cell (antibody) responses, delayed type-hypersensitivity (DTH) response, and production of lymphokines such as interleukin 2 (IL2) and macrophage-activating factor (MAF). The results demonstrate that all of the above anti-vaccinia virus responses were mediated by Lyt-1+2- T cells and that these Lyt-1+2- T cells expressed L3T4 antigens on their cell surfaces. Moreover, such anti-vaccinia Lyt-1+2- T cell responses were inhibited in the presence of anti-L3T4 antigen antibody. These results indicate that there is a reciprocal relationship between Lyt-2 and L3T4 markers, and that L3T4 antigen is closely related to the activation of various functions of anti-vaccinia virus Lyt-1+2- T cells.
MTV antigens in the resting mammary glands of GRS/A, SHN, C3H, and Balb/c virgin mice were detected by immunoperoxidase techniques using antiserum against MTV whole virion, gp 52 or p 25 to differentiate the expression between endogenous and exogenous MTV. Balb/c mice were crossed to infect MTV into each reciprocal hybrid or fosternursed inbred. Immunohistochemical stainings of gp 52 in the formol-fixed sections were almost the same as those of the whole MTV virion, and the results on various cases were as follows: In the mice with endogenous GR-MTV, positivity was first observed at the age of 14 days, while the first expression of exogenous GR-MTV was delayed to the age of 140 days. The mice with endogenous and/or exogenous SHN-MTV showed the first antigen appearance at the age of 65 days, and those with exogenous C3H-MTV did at the age of 80 days. The virgins with only endogenous C3H-MTV came to express the antigen after the age of 200 days. Staining of p 25 in Carnoy-fixed sections of MTV-positive mammary glands was found in the supranuclear cytoplasm and apical surface of the glandular cells and the lumen, all of which are the site of A and B particles. By means of preembedding method for gp 52, the reaction products were ultrastructurally detected not only on the MTV-budding apical surface, together with the intraluminal B particles, but also on the MTV-free apical cell membrane of the glandular cells in the mammary gland of the GR virgins.
In rabbit aorta, pretreatment with 2-aminoisoquinoline, 1.3 (2H.4H)-dione (AQ, 10(-5) M and 10(-4) M) shifted the concentration-response relationship to noradrenaline (NA, 10(-9) M to 10(-4) M) in a parallel manner whereas the agent (10(-4) M) failed to affect the response to potassium and only slightly depressed Ca2+-induced contractions in a Ca2+-free medium in the presence of K+ (40 mM). Ca2+-entry blockers such as nifedipine and diltiazem (10(-6) M and 10(-5) M) had very weak or no apparent effects on the response to NA but markedly attenuated or abolished the K+- and Ca2+-induced contractions. Following incubation of tissues for 15 min in a Ca2+-free medium with low EGTA (0.01 mM) and methoxyverapamil (D600, 10(-5) M), NA (3 X 10(-7) M) caused a phasic (transient) contraction and the subsequent application of Ca2+ (2mM) resulted in a tonic contraction. This NA-induced, Ca2+-dependent, D600-insensitive contraction was inhibited by AQ (10(-5) M and 10(-4) M) in a concentration-dependent manner. This suggests that the inhibitory action of AQ may be related to Ca2+ entry through specific receptor activated pathways. Following incubation of tissues for 30 min in a Ca2+-free medium with high EGTA (2.0 mM), NA (10(-5) M) caused a contraction of rabbit aorta which is dependent upon release of intracellular Ca2+, but the response was 50% to 60% less than that in a normal medium. This contraction was inhibited by AQ (10(-5) M and 10(-4) M) and nitroglycerin (10(-5) M) but not by nifedipine or diltiazem. The inhibitory action of combined treatment with AQ and nitroglycerin (10-5 M) on the response to NA was not different from that of either agent alone. 5 These results suggest that AQ may have inhibitory actions on the release of intracellular Ca2+ and also on Ca2+-entry through D600-insensitive, receptor-activated Ca2+ pathways in rabbit aorta.
DNA of the oncogenic strain BC-1 of Marek's disease virus contains three units of tandem direct repeats with 132 base pairs in the terminal repeat and internal repeat, respectively, of the long region of the Marek's disease virus genome, whereas the attenuated, nononcogenic viral DNA contains multiple units of the tandem direct repeats.
Two groups of virus-specific polypeptides were identified in the nuclei of infected cells by cross-reacting monoclonal antibodies with three serotypes of Marek's disease virus. Of these, a 135,000-molecular-weight polypeptide common to all three serotypes was found to bind to both double-stranded and single-stranded DNAs.
In vivo phosphorus-31 magnetic resonance (MR) spectra were obtained by a surface coil method from rat glioma tissue inoculated subcutaneously in CD Fisher rats, and the effects of photoradiation therapy on tumors were evaluated by sequentially observing spectral changes. In the control group, the nucleoside triphosphate (NTP) and phosphomonoester peaks were large, the phosphocreatine peak was small, and the inorganic phosphate (Pi) peak was intermediate. In all eight cases in the group in which a dose of 10 mg/kg of hematoporphyrin derivatives (HpD) was given before photoirradiation, NTP peaks decreased, and the Pi peak increased remarkably within 1 hour after the 60-minute white-light irradiation. Spectral changes were observed before histologic changes were apparent. Histologic examinations 3 days after irradiation showed extensive necrosis in the tumor tissue. With preinjection of 5 mg/kg HpD, three of the eight cases showed spectrum changes after the irradiation. No spectrum changes were observed in the group with preinjection of 2.5 mg/kg. In vivo P-31 MR spectra measurements are useful not only to investigate the energy metabolism of tumor tissue in vivo but also to evaluate the effects of photoradiation therapy on tumors.
Effects of nicorandil on contractile responses to alpha 1- and alpha 2-adrenoceptor agonists were examined in isolated rabbit aorta. Nicorandil (10(-6) or 10(-5) M) inhibited contractile responses to clonidine (CL) and BHT-920 in a concentration-dependent manner, but had no effect on the response to methoxamine (MO). Nifedipine (10(-6) and 10(-5) M) had no significant effect on responses to CL and MO, but it had a noticeable inhibitory effect on the response to BHT-920. In tissues pretreated with phenoxybenzamine, nicorandil (10(-5) M) inhibited the residual response to MO, and nifedipine (10(-5) M) inhibited responses to MO and CL. The relationship between maximum contraction and percent receptor occupancy was found to be nonlinear for MO, but was near linear for CL and BHT-920. The inhibitory effect of prazosin (pA2 of about 9) on MO and CL was much greater than that of yohimbine (pA2 of about 6). Nicorandil had no apparent or slight inhibitory effect on responses to potassium and Ca2+, and this inhibitory effect was much less than that of nifedipine. These results indicate that the responses induced by MO, CL, and BHT-920 in the rabbit aorta are due to activation of alpha 1-adrenoceptors. It is also suggested that nicorandil minimally affects voltage-dependent Ca2+ influx and that differential effects of nicorandil on the responses to alpha 1 and alpha 2 agonists may be the result of differences in the amount of receptor reserve that exist for MO, CL, and BHT-920 in this blood vessel.
To investigate the role of renal prostaglandin E2 (PGE2) in renovascular hypertension, urinary PGE2 was measured in rabbits with hypertension produced by left renal artery constriction. In the acute phase of renovascular hypertension (1 week after the constriction), urinary excretions of PGE2 and sodium were significantly increased without correlations with changes in the systemic blood pressure (delta BP). In this phase, delta BP was directly proportional to plasma renin activity and plasma aldosterone concentration (p less than 0.001). In the intermediate phase (5 weeks), delta BP lost significant correlations with plasma renin activity and plasma aldosterone concentration and had a inverse correlation with urinary sodium excretion (p less than 0.01). In the maintenance phase (10 weeks), delta BP showed inverse correlations (p less than 0.01) with both PGE2 and sodium excretions, although their excretions decreased to normal levels. In the clipped kidney, only urinary PGE2 excretion in the acute phase was significantly elevated (p less than 0.02), and both sodium and PGE2 excretions were significantly decreased (p less than 0.01) in the maintenance phase. In the nonclipped kidney, urinary PGE2 and sodium excretions were elevated in the acute and intermediate phases, but decreased to the control levels in the maintenance phase. In this phase, delta BP showed inverse correlation (p less than 0.01) with both PGE2 and sodium excretions from the nonclipped kidney. The infusion of saralasin, an angiotensin II analogue, dose dependently reduced the blood pressure in the acute phase, but showed no effect in the intermediate and maintenance phases.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of prostaglandins (PGE1, PGE2, PGF2 alpha, and PGI2) on the isolated human minor calyceal strips were isometrically investigated in vitro. PGE2 and PGF2 alpha, 10(-7) to 10(-6) g/ml, increased the basal tone of spontaneous contractions. PGE1 and PGI2 did not affect the contractions of the isolated human minor calyceal strips. The increases on the basal tone induced by PGE2 and PGF2 alpha were not affected by the pretreatment with atropine, hexamethonium, and phentolamine. Following incubation in a Ca2+-free medium, spontaneous contractions and the responses to PGE2 and PGF2 alpha were abolished. The results suggest that the contractile effects of PGE2 and PGF2 alpha may not be mediated by activation of muscarinic, nicotinic, or alpha-adrenergic receptors and result from a consequent increase of the transmembrane Ca2+ influx.
To determine the presence and distribution of cardiac myosin isozymes in the human conduction system, we performed an immunohistochemical study using monoclonal antibodies CMA19 and HMC14, which are specific for myosin heavy chains of human atrial type (alpha-type) and ventricular type (beta-type), respectively. Serial frozen sections of human hearts were obtained from autopsy samples and examined by indirect immunofluorescence. Alpha-type was found in all myofibers of sinus node and atrio-ventricular node, and in 55.2 +/- 10.2% (mean +/- SD, n = 5) of the myofibers of ventricular conduction tissue, which consists of the bundle of His, bundle branches, and the Purkinje network. In contrast, beta-type was found in all myofibers of the atrio-ventricular node and ventricular conduction tissue, whereas almost all myofibers of the sinus node were unlabeled by HMC14. Although the number of ventricular myofibers labeled by CMA19 was small, the labeled myofibers were more numerous in the subepicardial region than in the subendocardial region. These findings show that the gene coding for alpha-type is expressed predominantly in specialized myocardium compared with the adjacent ordinary working myocardium.
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An abnormal hemoglobin, Hb Owari [alpha 121 (H 4) Val----Met], was discovered in seven Japanese. This variant was isoelectrofocused to the site between the Hb A and Hb F bands and amounted to 12.7-19.0% of the total hemoglobin in the hemolysate. This hemoglobin showed normal functional properties.
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We previously reported that DNA of the oncogenic strain BC-1 of Marek's disease virus serotype 1 (MDV1) contains three units of tandem direct repeats with 132 base pair (bp) repeats within the inverted repeats of the long regions of the MDV1 genome, whereas the attenuated, nononcogenic viral DNA contains multiple units of tandem direct repeats (Maotani et al., 1986). In the present study, the difference in the copy numbers of 132 bp repeats of oncogenic and nononcogenic MDV1 DNAs in other strains of MDV1 was investigated by Southern blot hybridization. The main copy numbers in different oncogenic MDV1 strains differed: those of BC-1, JM and highly oncogenic Md5 were 3, 5 to 12 and 2, respectively. The viral DNA population with two units of repeats was small, but detectable, in cells infected with either the oncogenic BC-1 or JM strain. The MDV1 DNA in various MD cell lines contained either two units or both two and three units of repeats. The significance of the copy number of repeats in oncogenicity of MDV1 is discussed.
Prostaglandin (PG) D2 was examined for its effect on the growth of a mouse brain tumor cell line in vitro and in vivo. In this study, we used 203 glioma which had been originally induced by methylcholanthrene in C57BL mice and proved to be subcutaneously transplantable and also maintainable in a cell culture system in vitro. Marked inhibition of cell growth was observed in a PGD2-treated group in vitro at a concentration of 5 micrograms/ml. In the in vivo experiment, intraperitoneal or intratumoral administration of PGD2 (0.5 mg/kg) every day for four weeks was started after subcutaneous transplantation. In a control group, the same amount of ethanol without PGD2 was administered. Inhibition of tumor growth was seen with intratumoral administration, although no inhibition was seen with intraperitoneal administration. Histological examination revealed no remarkable change after PGD2 administration. However, on the DNA histogram, an increment of the G0G1 phase and a decrement of the G2M phase occurred after intratumoral administration of PGD2. It was suggested that local administration of PGD2 might be effective through the inhibition of DNA synthesis.