Review of states' practices on the use of psychotropic medication.

Concerns involved with prescription of psychotropic medication to persons with developmental disabilities to ameliorate maladaptive behavior were described. Responses to a national survey of state agencies regarding statutes, regulations, and operating procedures for initiating and monitoring psychotropic drug regimens were examined. The survey showed that most states had more rules and regulations for persons in institutions than in community settings.

Characterization of the spontaneous autoimmune (anti-erythrocyte) response in NZB mice using a pathogenic monoclonal autoantibody and its anti-idiotype.

A monoclonal anti-mouse RBC antibody (G-8) has been prepared that appears to represent a pathogenic autoantibody related to those that arise spontaneously in aging NZB mice and which cause autoimmune haemolytic disease (AIHD). When G-8-producing hybridoma cells were grown as tumours in BALB/c mice, the mice developed AIHD characterized by a decrease in the number of erythrocytes (haematocrit) and the development of Coombs-positivity. An anti-idiotypic antibody (E8) was prepared against G-8 and was found to recognize an idiotypic determinant present on most autoantibody-forming cells derived from old (Coombs-positive) NZB mice.

Development of self-tolerance in normal mice. Appearance of suppressor cells that maintain adult self-tolerance follows the neonatal autoantibody response.

T cell populations from BALB/c mice at different ages were analyzed to determine when in development Ts cells specific for the anti-mouse RBC (MRBC) autoantibody response become activated. Previous studies have shown that adult CD8+ T cells actively suppress this autoimmune response and adult spleen cells depleted of CD8+ cells can generate an anti-MRBC response in culture with MRBC. The present results demonstrate that T cells from mice less than 1 wk of age do not suppress the in vitro anti-MRBC response of adult spleen cell populations depleted of CD8+ Ts cells.

Suppressor T cells and self-tolerance. Active suppression required for normal regulation of anti-erythrocyte autoantibody responses in spleen cells from nonautoimmune mice.

Spleen cells from young, nonautoimmune strains of mice cultured with syngeneic E do not develop a significant anti-mouse E response in vitro, consistent with a state of self-tolerance to this Ag. In order to study the role of active suppression in regulating mouse RBC-(MRBC) specific cells in nonautoimmune cell populations, the effect of depleting T cell subsets on the generation of anti-MRBC autoantibodies by nonautoimmune spleen cells was determined. Spleen cells from young BALB/c and C57BL/6 mice were found to generate significant numbers of IgM and IgG anti-MRBC autoantibody-forming cells in culture with MRBC after depletion of Ly-2+ cells by anti-Ly-2 and C treatment.

Active role of T cells in promoting an in vitro autoantibody response to self erythrocytes in NZB mice.

The in vitro anti-self erythrocyte antibody response of NZB spleen cells appears to be influenced directly by T cells. Thy-1+, L3T4+ helper T cells are required for: (i) the generation in vitro of MRBC-specific IgM and IgG AFC by spleen cells from 'autoimmune' (9-12-month old) NZB mice and (ii) the generation in vitro of MRBC-specific IgM and IgG AFC by spleen cells depleted of suppressor cells from pre-autoimmune (2-3-months-old) NZB mice which show no clinical signs of an anti-MRBC response. It is evident from the present and previous studies that the anti-MRBC autoantibody response is regulated in pre-autoimmune spleen cell populations by Ly2+ T cells.

Effect of antigen priming on T-cell suppression. I. Activity of Ly 1+2+ feedback suppressor T-cell precursors after isolation from competing Ly 2-T cells.

Previous experiments have demonstrated that feedback suppression of murine antibody responses occurs in vitro after exposure of unprimed T-cell subsets to suppression-inducing signals from primed cells, resulting in suppression of primary and secondary IgM as well as IgG anti-SRBC responses. However, following priming with antigen when cells appear which are capable of inducing feedback suppression, the ability of unfractionated splenic T-cell populations to mediate detectable feedback suppression in vitro rapidly disappears, suggesting that priming alters the expression of feedback suppression at the same time as providing for its induction. In the present study, we have succeeded in isolating active feedback suppressor T-cell precursors (preTs) in the Ly 1+2+ and L3T4- T-cell populations from SRBC-primed as well as from unprimed mice, demonstrating that preTs are not lost after priming.

The implementation of postgraduate training programs through state and local resources.

A profile of implementation strategies for funding postgraduate training programs using local or state resources is described. The need for those implementation strategies as well as basic principles for successful implementation is documented. Two programs are briefly described--a University Affiliated Program (UAP) in western New York and a UAP in Missouri--as the basis for generating implementation strategies.

The effects of rate change in body weight on tissue development and meat quality of youthful bulls.

Forty-eight Angus bulls about 13 mo of age were used to study the effects of rate of change in live weight on muscle fiber, collagen and sensory characteristics of meat. Bulls were fed a finishing diet before treatment, and assigned to three treatments: negative, zero or positive weight gain for 30 or 60 d prior to slaughter. Treatments were imposed by adjusting feed intake.

Modulation in vivo of Lyt 2 antigen expression on T cells by anti-Lyt 2 antibody: effects on Con A-induced unresponsiveness.

After a series of intraperitoneal injections of rat monoclonal anti-Lyt 2 antibody supernatant, BDF1 mice showed a loss of cells bearing Lyt 2 surface antigens but no reduction in the numbers of T cells in the spleen. With overnight culture in vitro, splenic T cells from anti-Lyt 2-treated mice regenerated surface Lyt 2, with the proportion of Lyt 2+ cells returning to control levels. Anti-rat IgG antibody was found in the serum of mice that had received the anti-Lyt 2 treatments.

Rapid loss of feedback suppressor T-cell activity after priming in vivo.

T cells from antigen-primed mice have a diminished capacity to mediate feedback suppression when compared to T cells from unprimed mice. This was demonstrated using an in vitro model of B-cell induced feedback suppression in which spleen cells from mice primed with sheep erythrocytes (SRBC) activate feedback suppressor T-cell precursors to mediate suppression of the primed spleen cell response. The addition of splenic T cells from unprimed mice to cultures of spleen cells from SRBC-primed mice resulted in suppression of the secondary IgM and IgG anti-SRBC response.

Growth, carcass and palatability traits of intact males and steers implanted with zeranol or estradiol early and throughout life.

This study was conducted to assess the impact of implanting intact beef males with protein anabolic agents at varying intervals throughout life. Ninety-six intact males were assigned to three implant treatments: 1) not implanted, 2) implanted at 9 wk of age, weaning and at 56-d intervals thereafter with a 36-mg zeranol implant or 3) estradiol implant at 9 wk of age and 68 d post-weaning. During the 118-d, post-weaning growing period, eight animals per treatment (one replication) were castrated.

In vitro regulation of the pathogenic autoantibody response of New Zealand black mice. I. Loss with age of suppressive activity in T cell populations.

An investigation of the regulation of specific anti-self responses was initiated with the development of an in vitro system in which spleen cells from NZB mice were stimulated by syngeneic mouse erythrocytes (MRBC) to produce MRBC-specific autoantibody-secreting cells. The response was measured by a modification of the focus-forming cell (FFC) assay, which enumerates cells secreting IgG, which specifically bind MRBC. Spleen cells from 9- to 12-mo-old NZB mice developed MRBC-specific FFC after 3 to 5 days in culture with MRBC.

Specific anti-erythrocyte focus formation as a measure of autoantibody secreting cells in NZB mice.

Using a modification of the antibody forming cell (AFC) focus assay, it is possible to quantitate the spontaneous anti-erythrocyte autoantibody response of New Zealand Black (NZB) mice at the level of the autoantibody secreting cell. This complement independent assay is specific for an antigen(s) present on unmodified mouse erythrocytes. A comparison with the direct Coombs' test showed that the focus assay detected autoantibody responses earlier and demonstrated a wide range of AFC levels in responding mice.

Formation of antigen specific foci as a complement independent assay for individual antibody-secreting cells.

Antibody-forming cells (AFC) could be demonstrated by the binding of antigen to secreted antibody localized around the AFC. Using sheep red blood cells (SRBC) as antigen, this antigen binding was detected as foci of erythrocytes surrounding individual lymphocytes. Focus formation was antigen specific and involved the active secretion of antibody.

Lymphocyte subsets involved in tumor-activated nonspecific feedback suppression.

Cells from the spleen, lymph nodes, and peritoneum of DBA/2 mice bearing a subcutaneous tumor mediate nonspecific suppression of an in vitro antibody response to sheep red blood cells (SRBC) when cocultured with a normal T-cell subset(s). The spleen cells from the tumor-bearing mouse required for the suppression bear the Lyt 1 and Ala 1 surface markers characteristic of "inducer" T cells and activated cells, respectively. The activity of this cell population is also sensitive to irradiation.

Interactions between primed and unprimed cells in the regulation of in vitro antibody responses. I. Role of "plasma cells" as inducers of suppression.

Specific immune suppression has been shown to be activated in culture by the interaction of primed and unprimed T cell subsets. The primed cell involved is found 8 days after immunization in spleen but not in lymph node or thymus cell populations. When the primed spleen cells were fractionated by nylon wool passage or anti-Thy-1 plus complement (C) treatment, prior to culture with unseparated unprimed cells, suppression was detectable only with primed B cells present in the co-cultures.

Evidence for interaction between T cell populations of tumor-bearing and normal mice in immune suppression.

Spleen cells of DBA/2 mice bearing subcutaneous implants of the syngeneic tumor L5178Y induce suppression of the in vitro antibody response of normal spleen cells to sheep erythrocytes (SRBC). Cells mediating suppression are detected in the spleens of tumor-bearing mice as early as 24 hr post-implantation but are no longer detected there 15 days post-implantation. These spleen cells are nylon wool nonadherent, sensitive to anti-Thy 1.

The Qa-1 antigenic system. Relation of Qa-1 phenotypes to lymphocyte sets, mitogen responses, and immune functions.

The antiserum (B6 X A-Tlab) anti-A (Tlaa) defines several TL antigens expressed exclusively on thymocytes. When reacted with peripheral lymphocytes, the same antiserum defines another antigenic system, provisionally termed Qa-1. The genotypic disparity distinguishing the recipients and donors in this immunization comprises a section of chromosome 17 extending from a crossover point between H-2D and Tla to a presently unmarked point beyond Tla.

Changes in suppressor mechanisms during postnatal development in mice.

The activity of suppressor cells from spleens of mice of varying ages was assessed by their addition to cultures of normal or SRBC immune spleen cells together with a challenge of SRBC. 1-wk and adult spleen cells were highly suppressive of the secondary in vitro antibody response to SRBC. 3-wk spleen cells were less active in suppressing this response.

Cell interactions in the suppression of in vitro antibody responses.

Normal T and immune B lymphocytes interact in a fashion that leads to suppression of the immune response. Normal spleen cells added to cultures of primed spleen cells specifically suppressed both the IgM and IgG secondary antibody response of the primed cells to less than 30% of the response of the immune cells cultured alone. Cell crowding as a possible in vitro artifact was ruled out.