Macroecology: the division of food and space among species on continents.

Analyses of statistical distributions of body mass, population density, and size and shape of geographic range offer insights into the empirical patterns and causal mechanisms that characterize the allocation of food and space among the diverse species in continental biotas. These analyses also provide evidence of the processes that couple ecological phenomena that occur on disparate spatial and temporal scales-from the activities of individual organisms within local populations to the dynamics of continent-wide speciation, colonization, and extinction events.

Scaling of biological community structure: a systems approach to community complexity.

Local community dynamics are determined by the interaction of environmental variation and the biotic properties of communities. This interaction occurs on many spatial and temporal scales, hence the expectation is that community dynamics will be complex. Previous theoretical approaches to communities have assumed linear, near equilibrium dynamics. An alternative approach suggests that community dynamics are the result of the balance between energy use by the community and its tendency to move towards thermodynamic equilibrium, in this case extinction of all species in the community. Because this balance will be imprecise, community dynamics should be oscillatory. Furthermore, because energy use by a community can be broken down into a hierarchical set of processes occurring on different time scales, community dynamics should reflect multiple periodicities. The above theoretical treatment suggests that since community dynamics are scaled, a hierarchical observational approach should help resolve important aspects of community structure. This approach of scaling community observations provides a technique for evaluation of community responses to environmental change, including human induced perturbations. A thermodynamic approach to community dynamics can also provide the basis for new theoretical and empricial discoveries about biological communities.

Genetic analysis of 23 RhL-A histocompatibility antigens of the rhesus monkey.

The lymphocytotoxicity of 116 rhesus monkey alloantisera was evaluated in 92 unrelated rhesus monkeys and in 33 pedigreed rhesus families. The study was conducted using a standard complement-dependent microcytotoxocity assay. A computer-assisted chi2 analysis of the reactivity of these sera in unrelated monkeys generated 23 groups of highly correlated antisera. The two-locus model of the mammalian major histocompatibility complex was assumed for the monkey, and genetic criteria for RhL-A antigens were determined before study. Seventeen groups of antisera which had met these predetermined criteria in a previous study using a different random population of monkeys were confirmed in the present analysis. The remaining six groups also met these predetermined criteria, although the genetic data for two were incomplete. Of the 23 antigens defined, 12 appeared to be products of the A locus and 11 of the B locus. Nineteen were similar or identical to antigens previously described by us or by Balner and coworkers in The Netherlands. Two groups have not been previously described. A frequency analysis indicated that these 23 antigens represented approximately 75% of the total expression of the RhL-A-A and RhL-A-B loci.

Definition of two LD antigens in rhesus monkeys.

Two rhesus (Macaca mulatta) monkey lymphocyte-defined (LD) antigens have been identified using two typing cells as stiumlators in a one-way mixed leukocyte culture (MLC) assay. An analysis of the genetic behavior of these LD antigens in six rhesus monkey families revealed that both antigens were linked with RhLA. One probable recombinant indicated that the LD locus lies outside the two known RhLA-SD loci and the locus which controls the serum protein, properdin B(Bf). These two antigens, LD1 and LD2, had observed gene frequencies of 0.07 and 0.25, respectively. Neither of these two new LD antigens was significantly associated with any serologically defined (SD) antigen.

Conditions for generating and assaying human leukocyte inhibitory factor (LIF) induced by purified protein derivative (PPD).

This report examines a variety of experimental conditions for the production of human leukocyte inhibitory factor (LIF). The data indicate that the production of LIF as measured in the indirect capillary-tube migration inhibition assay using human polymorphonuclear indicator cells accurately reflects delayed hypersensitivity to purified protein derivative (PPD) as detected by skin-test reactivity. Mononuclear cells and semipurified lymphocytes separated from whole blood by sedimentation in Ficoll-Hypaque were able to generate LIF in response to PPD. The quantity of cells responsible for LIF production were standardized and as little as 1 x 10(6) mononuclear cells were required for detectable LIF production. LIF produced by mononuclear cells required only temporary exposure to PPD, thus eliminating the necessity for a control to which antigen was added at the end of culture to antigen-free supernatants. In addition, the removal of antigen after a brief exposure helps to avoid the possible toxic effect of some antigens on the migrating polymorphonuclear leukocytes (PMNL) population. LIF production did not require extraneous serum protein (i.e., fetal bovine serum). Further, kinetic studies indicated that LIF was detected as early as 8 hr following a 2 hr-exposure to PPD and that even a 1 hr-exposure was sufficient to generate measurable detectable quantities of LIF. After 48 hr of culture, supernatants were found to contain considerable amounts of LIF, with reactivity at dilutions as high as 1:40.

Definition of 17 Rhesus monkey histocompatibility antigens, including one new antigen.

The lymphocytotoxic activity of 144 rhesus allonantisera was evaluated in 112 unrelated rhesus monkeys and 33 pedigreed rhesus families. This study was conducted using a standard complement-dependent microcytotoxicity assay. A computer-assisted chi2 analysis of the reactivity of these sera in the unrelated monkeys generated 23 groups of highly correlated antisera. The two-locus model of the mammalian major histocompatibility complex was assumed for the monkey, and genetic criteria for RhLA antigens were determined prior to study. Seventeen groups of antisera met these predetermined criteria. Six were products of the B locus and 11 were products of the A locus. Sixteen were similar or identical to antigens previously described by us or by Balner and coworkers in The Netherlands. One has not been previously described. A frequency analysis indicated that these 17 antigens represented approximately 74% of the total expression of these two loci.

Cell-mediated immunity in mice against papain-solubilized histocompatibility and tumor-specific antigens by a macrophage migration inhibition microassay.

The cell-mediated immune status of B10.D2 (H-2d) mice immunized with spleen cells from a congenic strain, B10.A (H-2a), differing at the H-2 locus and of BALB/c mice immunized with a syngeneic simian virus 40 (SV40)-induced sarcoma (mKSA-TU5) was evaluated by an agarose microassay for migration inhibition factor. The inducing antigens in this experiment were papain-solubilized and partially purified chromatographic preparations of spleen cells from A/J mice (H-2a) and a papain-solubilized antigen extract prepared from a tissue culture-adapted cell line (TU-5), derived from the SV40-induced mKSA tumor. The assay used microliters of normal or immune peritoneal exudate cells (PEC) resuspended in a 2-mul droplet of agarose and cultured in the presence or absence of antigen. Specific migration inhibition of PEC from immunized mice was observed with concentrations of solubilized antigen preparations as low as 2.0 mug/ml (3.67 mug/chamber).

Cellular immune reactivity in vitro and tumor rejection provided by tumor-associated antigens of friend-virus-induced leukemia.

Cell-mediated immunity (CMI) and tumor rejection were studied in the Friend virus leukemia system of C57Bl/6 mice. Mice were immunized with Friend leukemia virus (FLV) or X-irradiated FBL-3 leukemic cells and studied temporally for the development of CMI reactivity by assays of 51Cr release lymphocyte cytotoxicity, lymphocyte transformation, migration inhibition, Winn tumor cell neutralization and transplantation rejection. High levels of specific lymphocyte cytotoxicity were observed by day 7 f0llowing FLV infection; this reactivity reached a peak between 17 and 21 days, and returned to background levels by day 36. Further, positive Winn assays were obtained with spleen cells from mice immunized with FLV at times when the mice resisted live FBL-3 tumor challenge. Positive lymphocyte transformation was obtained with spleen cells from mice immunized with FLV or FBL-3, but not with cells from normal mice or mice immune to a syngeneic methycholanthrene-induced tumor, when cultured with papain-soluble FBL-3 or RBL-5 tumor-cell extracts or mitomycin-C (MMC)-treated FBL-3 or RBL-5 cells. Positive reactivity in the lymphocyte transformation assay occurred after reactivity had peaked in the lymphocyte cytotoxicity test. Similar positive macrophage migration inhibition patterns were also obtained with peritoneal exudate cells (PEC) from FLV-immunized mice using papain-solubilized tumor-associated antigen (TAA) from FBL-3 cells. These data suggest that sequential development and modulation of CMI reactivity occurs as observed in different assays following immunization in this system.