232 research outputs found
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šæ§äºæž¬ã«å¯äžããä»åŸã®ç 究éçºã«è²¢ç®ãããã®ã§ãããDisease-related molecules that have been discovered through genomic research can be targeted therapeutically by antibodies. Thanks to the advance of antibody and genetic engineering techniques, research and development of therapeutic antibodies has progressed, and over 30 therapeutic monoclonal antibodies are now on the market in the United States, Europe, and Japan. These monoclonal antibodies exert efficacy as anticancer agents on many kinds of molecules through various natural functions, namely, neutralization to block the physiological function of the target antigens, complement-dependent cytotoxicity (CDC), antibody-dependent cell-mediated cytotoxicity (ADCC), or by acting as drug delivery carriers. These recent scientific advances and the shared experience of preclinical safety evaluation of biotechnology-derived pharmaceuticals have been incorporated in a guideline by the International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use (the ICH S6 R1 guideline), and compliance to this guideline is required for preclinical safety testing. One requirement of the guideline is that, because tissue injury induced by antibody treatment is thought to be consistent with antigen distribution, the binding of therapeutic monoclonal antibodies to antigens within tissues be evaluated in tissue cross-reactivity (TCR) studies using a panel of human tissues. This TCR study with a panel of human tissues can predict target organs of toxicity prior to the initial clinical dosing of these products and is a recommended component of the safety assessment package. On the other hand, because some reports show that the tissue distribution or expression level of the antigen is not consistent with tissue injury, the issue remains of how to exactly predict efficacy and toxicity when developing therapeutic antibodies, and a model suited for studying the factors that predict the biological response of therapeutic antibodies is necessary to address these matters. The anti-Thy-1.1 antibody-treated rat (rat anti-Thy-1 model) is known as an animal model for the involvement of antibody-mediated CDC in the induction of tissue injury. In the present study, we examine how the antigen and membrane complement regulatory proteins (mCRPs) are distributed, what effect an antibody has on the biological response and the factors that predict that effect, and we present novel information on, and methods for predicting, efficacy and toxicity of a therapeutic antibody.In Chapter 1, we examined the distribution of Thy-1.1 antigen in normal rats and the tissue injury induced by CDC in the rat anti-Thy-1 model to evaluate and confirm that the model would be suited for investigating what other factors than antigen expression can predict the activation of CDC. We demonstrated that Thy-1.1 antigen is broadly distributed across several organs and cells, including lymphocytes of the thymus and spleen, mesangial cells of the kidney, medullary cells of the adrenal gland, and stromal cells in several organs. We expected that injecting anti-Thy-1.1 antibody would result in tissue injury in all these Thy-1.1-expressing cells, but when the rat anti-Thy-1 model was histopathologically evaluated in detail, cell death induced by the anti-Thy-1.1 antibody was observed only in mesangial cells. Morphologically, at 0.5 and 1 hour after treatment karyolysis in the mesangial cells and infiltration of neutrophils were found; at 8 hours after injection, the number of mesangial cells had decreased and the capillaries of the glomerulus were dilated; and at 24 and 48 hours after injection, the mesangial area had decreased. Deposition of C3, the key molecule of the CDC cascade, was detected by immunohistochemistry only in the mesangial area from 0.5 hours after treatment. Judging from these results of the histopathological examination and C3 deposition, cell death of mesangial cells was induced by CDC mechanisms, as previously reported, but the other organs and tissues that express Thy-1.1 did not show cell death in this model. This result indicates that the antigen distribution data was not consistent with the organs in which antibody-mediated CDC was induced. This chapter concludes that the rat anti-Thy-1 model is thought to be a suitable model for analyzing the factors other than the expression levels of the target antigen that predict the induction of CDC, based on the following reasons: 1) mesangial cell death due to CDC was induced by external administration of the antibody, 2) although Thy-1.1 antigen was distributed broadly, it was not consistent with cell death induced by treatment with anti-Thy-1.1 antibody. In Chapter 2, to clarify the reason why the Thy-1.1 antigen distribution was not consistent with cell death we next considered two possible causes: 1) the injected antibody was not distributed in organs and tissues expressing Thy-1.1 and 2) mCRPs inhibited complement activation in the CDC reaction after the antigen bound to the antibody. Thus to elucidate the probable cause, the distribution of injected anti-Thy-1 antibody in the rat anti-Thy-1 model and the expression of Crry and CD55 in normal rats were evaluated. The injected anti-Thy-1.1 antibody was distributed in the mesangial cells of the kidney, in the lymphocytes in the perivascular areas of the cortex in the thymus and the red pulp of the spleen, and in medullary cells in the cortico-medullary junction of the adrenal gland. These results indicate that the injected anti-Thy-1.1 antibody did not bind to all of the cells that expressed the antigen but only to those cells that expressed more than a certain level of antigen. The expression of mCRPs was found in glomerular cells of the kidney, lymphocytes of the thymus, and medullary cells of the adrenal gland. In the kidney, weak expression of Crry and no expression of CD55 were observed in the mesangial cell. In the thymus, moderate, diffuse expression of Crry and no expression of CD55 were seen in the lymphocytes. In the adrenal gland, weak expression of Crry and strong expression of CD55 were observed in medullary cells. Thus, Crry or CD55, which inhibit C3 activation, are more than moderately expressed in cells that have a level of antigen-antibody binding that does not induce C3 deposition and cell death. Through our results concerning antigen expression, antibody distribution, and cell death, the relationship between antigen-antibody binding and CDC activation was categorized into the following three types: A) antigen-antibody binding that causes cell death (mesangial cells of the kidney); B) antigen-antibody binding that does not induce cell death (lymphocytes of the thymus and medullary cells in the adrenal gland); C) no antigen-antibody binding and no cell death (the other antigen-expressing cells). There were definite differences in C3 deposition between type A and type B cells. In other words, C3 deposition was observed in mesangial cells, which showed cell death, but was not seen in lymphocytes of the thymus and medullary cells in the adrenal gland, which did not show cell death. These results suggest that mCRPs are related to CDC induction. As a conclusion of this chapter, the factors regulating CDC reaction in the rat anti-Thy-1 model were not only the distribution of antigen but also 1) distribution of the injected antibody and 2) expression of mCRPs that inhibit complement activation after antigen-antibody binding.In Chapters 1 and 2, distribution of the Thy-1.1 antigen was not consistent with cell death induced by treating the rat anti-Thy-1 model with anti-Thy-1.1 antibody; thus, the antigen distribution data alone is not sufficient to predict the induction of antibody-mediated CDC. This conclusion was supported by the following two findings: 1) regulation through the distribution of the injected antibody and 2) inhibition of complement activation after antigen-antibody binding by the expression of mCRPs. Having analyzed the distribution of the injected antibody in Chapter 2, in Chapter 3 the distributions of mCRPs (Crry and CD55) in normal rat were examined and we considered the possibility that mCRPs could be used to predict CDC reaction. Because there were 2 factors other than distribution of antigen that were related to CDC induction, we analyzed the distribution of the injected antibody and expression of mCRPs and discussed how analyzing these factors would contribute to better prediction of the biological reaction induced by treatment with a CDC-type antibody. Crry and CD55 were detected widely in rat organs and tissues. The complement system can be effective in destroying external pathogens but unintended activation of complements can cause unnecessary injury. Thus the distribution of mCRPs may be involved in tight regulation of nonspecific activation in these tissues. Crry and CD55 were co-expressed in the same organs but they were expressed distinctly differently between cells. The two molecules have a common function in inhibiting C3 deposition, but the present results show that they have a separate expression pattern, a fact that indicates specific roles in CDC regulation.We predicted the occurrence of lesion caused by a Thy-1.1 antibody injection according to 3 approaches, in which different tissues were selected as potential targets of biological reaction and were compared with the tissues that actually were affected in the rat anti-Thy-1 model: tissues in which antigen was expressed (Approach 1), tissues in which both the antigen and the injected antibody were distributed (Approach 2), and tissues in which both the antigen and the injected antibody were distributed and which had less than moderate expression of mCRPs (Approach 3). As a result, Approach 3, the approach that considers the distribution of antigen, the distribution of the injected antibody, and the expression of mCRPs, was consistent with the tissues that were actually affected, namely, the mesangial cell in the kidney. In conclusion, combining the analysis of antigen distribution, distribution of the injected antibody and the expression of mCRPs enabled us to predict the efficacy and toxicity of a CDC-type antibody more precisely.The results of TCR studies designated in the Guideline predict the target organs of therapeutic antibodies in human to a certain extent but are not necessarily consistent with the biological response caused by therapeutic antibodies in target organs, because it is difficult to predict efficacy and toxicity of therapeutic antibody in human only from the distribution of the antigen. The main achievement of this study was the discovery that analyzing the distribution of antigen, the distribution of the injected antibody, and the expression of mCRPs makes it possible to predict the efficacy and toxicity of a CDC-type antibody more precisely. These results will contribute to greatly improved prediction of efficacy and toxicity of therapeutic antibodies and will also contribute to the enhanced research and development of novel therapeutic antibodies.å士(ç£å»åŠ)麻åžå€§
Variable Stars in the Magellanic Clouds: Results from OGLE and SIRIUS
We have performed a cross-identification between OGLE-II data and
single-epoch SIRIUS JHK survey data in the LMC and SMC. After eliminating
obvious spurious variables, we determined the pulsation periods for 9,681 and
2,927 variables in the LMC and SMC, respectively. Based on these homogeneous
data, we studied the pulsation properties and metallicity effects on period-K
magnitude (PK) relations by comparing the variable stars in the LMC and SMC.
The sample analyzed here is much larger, and we found the following new
features: (1) variable red giants in the SMC form parallel sequences on the PK
plane, just like those found by Wood (2000) in the LMC; (2) both of the
sequences A and B of Wood (2000) have discontinuities, and they occur at the
K-band luminosity of the TRGB; (3) the sequence B of Wood (2000) separates into
three independent sequences B+- and C'; (4) comparison between the theoretical
pulsation models (Wood et al. 1996) and observational data suggests that the
variable red giants on sequences C and newly discovered C' are pulsating in the
fundamental and first overtone mode, respectively; (5) the theory can not
explain the pulsation mode of sequences A+- and B+-, and they are unlikely to
be the sequences for the first and second overtone pulsators, as was previously
suggested; (6) the zero points of PK relations of Cepheids in the metal
deficient SMC are fainter than those of LMC ones by ~0.1 mag but those of SMC
Miras are brighter than those of LMC ones by ~0.13 mag, which are probably due
to metallicity effects.Comment: 9 pages, 10 figures, accepted for publication in MNRAS. High
resolution version is available at:
http://www.ioa.s.u-tokyo.ac.jp/~yita/scr/astro/papers/RefereedPaper/yitaMD250
.pd
Development of an active tritium sampler for discriminating chemical forms without the use of combustion gases in a fusion test facility
A new type of active tritium sampler that can discriminate between chemical forms in a fusion test facility without the use of combustion gases was developed. The proposed tritium sampler was operated using water vapour instead of combustion gases. To test the operation and performance of the device when water vapour is used, we evaluated the catalytic oxidation properties, and the evaporation and collection of water vapour under actual sampling conditions. The properties of the added water mass and the operation temperature of catalysts in the proposed sampling system were then determined. Thereafter, we carried out air sampling for tritium monitoring. The levels of tritium concentration measured by the proposed tritium sampling system were similar to the values measured by the conventional sampling system. Our findings show that the proposed tritium sampling system without combustion gases is a good replacement for the conventional tritium sampling system in a fusion test facility
Interstellar Extinction Law in the J, H, and Ks Bands toward the Galactic Center
We have determined the ratios of total to selective extinction in the
near-infrared bands (J, H, Ks) toward the Galactic center from the observations
of the region |l| < 2.0deg and 0.5deg < |b| < 1.0deg with the IRSF telescope
and the SIRIUS camera. Using the positions of red clump stars in
color-magnitude diagrams as a tracer of the extinction and reddening, we
determine the average of the ratios of total to selective extinction to be
A(Ks)/E(H-Ks) = 1.44+-0.01, A(Ks)/E(J-Ks) = 0.494+-0.006, and A(H)/E(J-H) =
1.42+-0.02, which are significantly smaller than those obtained in previous
studies. From these ratios, we estimate that A(J) : A(H) : A(Ks) = 1 :
0.573+-0.009 : 0.331+-0.004 and E(J-H)/E(H-Ks) = 1.72+-0.04, and we find that
the power law A(lambda) \propto lambda^{-1.99+-0.02} is a good approximation
over these wavelengths. Moreover, we find a small variation in A(Ks)/E(H-Ks)
across our survey. This suggests that the infrared extinction law changes from
one line of sight to another, and the so-called ``universality'' does not
necessarily hold in the infrared wavelengths.Comment: 18 pages, 9 figures, Accepted for publication in the Ap
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