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To clarify the influence of lead on the host's defense mechanisms, antibody production in mice pretreated with lead was tested using the hemagglutination titer against SRBC (Sheep Red Blood Cells) and HRBC (Hamster Red Blood Cells) as indicator and the following results were obtained. 1. When mice were pretreated intraperitoneally with lead one day or six days before immunization and then immunized with SRBC, which is known as a strong antigen, antibody developed smoothly in the first immunization showing the same tendency as that of the control group. After the booster immunization, antibody production was markedly suppressed in the group of mice pretreated with lead six days before the immunization. When mice were immunized with HRBC, which is known as a weak antigen, antibody production was very poor in the first immunization, but after the booster immunization, the antibody titers rose rapidly in the group pretreated one day before the immunization. However, the titers of the group pretreated with lead 6 days before the immunization was considerably suppressed, showing the same tendency as that of mice immunized with SRBC. 2. When mice received intraperitoneally three or six doses of lead before immunization with SRBC or HRBC, antibody titer of these groups were somewhat lower than that of the control group. 3. When mice were pretreated intravenously with lead one day or six days before immunization with SRBC or HRBC, the antibody production ability was not remarkably damaged, showing almost the same titer as in the control group.

The antigen-dependent proliferative response of the Ia- T lymphocyte population in peritoneal exudate cells (PEC) of C3H/HeN mice immunized with horse red blood cells (HRBC) was examined by determining the uptake of tritiated thymidine ([3H]TdR) into the cells in vitro. Both the antigen and accessory cell population, which was either macrophages or B lymphocytes that had been prepared from the PEC or spleen of unimmunized mice, were necessary for the proliferative response of the Ia- T cell population and also the production of IL-2 by the Ia- T cells, but the Ia- T cell population could proliferate in the absence of antigen and accessory cells, if IL-2 was present. The IL-2-dependent proliferation of the Ia- T cells was augmented in the presence of macrophages, but not B cells. The Ia- T cells that had been treated previously with anti-IL-2 receptor (IL-2R) antibody showed no response to IL-2 in the presence or absence of B cells, but responded to IL-2 in the presence of macrophages. Direct contact of the Ia- T cells with macrophages seemed to be necessary for augmentation of the proliferative response of the Ia- T cells to IL-2 because the separation of these cell populations by a membrane filter in a Marbrook type culture vessel resulted in poor augmentation of the response. Cell-associated IL-1 did not participate in the augmentation because paraformaldehyde-treated macrophages did not help the response. When the Ia- T cells had been previously treated with complement and anti-asialo GM1 antibody, the IL-2-dependent proliferative response was not affected, but the augmentation of the response by macrophages was blocked. Previous treatment of the cells with anti-L3T4 antibody diminished the response to IL-2, but did not affect the augmentation of the response by macrophages. Pretreatment of the cells with anti-Thy-1.2-antibody reduced the response to IL-2 and the augmentation by macrophages. Therefore, we concluded that there are at least two populations, capable of responding to IL-2 in the immune Ia- T cell population; one with L3T4 surface antigen and another with asialo GM1 antigen. The response of the latter cells, but not the former, to IL-2 is augmented in the presence of macrophages.

Ten temperature-sensitive (ts) mutants derived from the Edmonston strain of measles virus were characterized by the complementation test and were shown to have four defective sites (A, B, C, and D). Five ts mutants which were confirmed to have a defective site D, induced neither cytopathic effect (CPE) nor an infectious virus. Among the other five ts mutants which produced viral proteins with CPE and showed positive HAD at 39.5 degrees C, the three ts mutants (P253-505, P333, and F2-104) were studied in detail. P253-505 had a defective site C and both P333 and F2-104 had a defective site A. P253-505 and F2-104 produced neither a cell-free nor cell-associated infectious virus and P333 produced only a low level of cell-associated infectious virus. P253-505 and P333 produced virus particles at 39.5 degrees C, while F2-104 did not. The pulse-chase experiment showed a normal pattern of synthesis and processing of viral proteins, but immunofluorescence tests using monoclonal antibodies indicated that P253-505 lacked two epitopes of the M protein at 39.5 degrees C, and both P333 and F2-104 lacked one epitope of the P protein. The lack of these viral epitopes was shown to correlate with the temperature-sensitivity of the three ts mutants.

Anatomy has accumulated a vast amount of morphological data of the body. In addition, anatomy has long an aggregate of sharply subdivided specialities. Re-organization and systematic integration of the knowledge across these subdivisions with the aim of attaining a more comprehensive approach is not an easy task because of the continued predominance of analytical principles and the deep-rooted academic inclination toward analysis. Despite these difficulties, I have endeavored to formulate a framework for unity of anatomy (Re-arranged comprehensive anatomy). A book of anatomy in a wide sense, in which macroscopic, microscopic, and developmental anatomy of the body are incorporated in one volume, would be of great convenience. Establishment of new concepts of organology as well as profound thinking over the shape and the structure is an urgent task for remodelling of anatomy into a more integrated science.

Lead added to plasma was rapidly incorporated into suspended human red blood cells at 37 degrees C. The rate of lead uptake into the cells reached a maximum of 35 micrograms (0.17 mumole)/10(10) cells/h. The rate of lead uptake with resealed ghosts was comparable to that of intact cells. These findings indicate that the transport of lead across the erythrocyte membrane is, energy-independent, carrier-mediated passive transport, which confirms the conclusion of Simons. On the other hand, little release of incorporated lead from the cells in lead-free plasma was observed. Some 98% of intracellular lead was in cytoplasm, mostly in protein-bound form, and only 2% was in the membrane fraction. When red blood cells were incubated in plasma containing lead at about 10 mg/dl concentration for 24 hours at 37 degrees C, no progressive accumulation of lead and protein in the membrane fraction was observed. Thus, lead-protein complexes in cytosol are unlikely to associate with membranes. Human haemoglobin had forty-five binding sites for lead with the dissociation constant of 0.5 x 10(-6) M. The binding of lead to oxyhaemoglobin did not show any effect on the iron atom in the heme.

On the basis of some models (bacteria and animal blood groups), it was demonstrated that monoclonal antibody-preparations obviously possess a much higher specificity against the ABO-properties of human than the usual human antisera or lectins. The behaviour of polyclonal and monoclonal reagents for ABO-determination should now be tested in comparative studies using contaminated blood stain material. The results presented in this paper suggest advantages in using monoclonal antibodies.

The epithelial neoplasms were observed on the mouth of the cultured coho salmon, Oncorhynchus kisutch. Histopathologically, the tumors were formed to be proliferative epithelial cells, but no change was observed in other organs. The virus from this tumor was isolated in RTG-2 and CHSE-214 cells and developed the cytopathic effect which characterized to be the formation of syncytia and the migration of chromatin. This virus was neutralized with anti-Oncorhynchus masou virus (OMV) rabbit serum.