Impacts of forest insects and diseases: Significance and measurement

Forest insects and diseases are integral components of the forest ecosystem; complexes of each have coevolved with forest ecotypes and are involved in the dynamic processes of forest establishment, growth, senescence, and mortality. Insects and diseases which feed on, or use trees as substrates for their life processes, affect forest, stands, and even entire forests positively and negatively. These effects are termed impacts. The positive impacts are primarily ecological; negative impacts are those which alter values defined by forest management objectives or public perception. The former have received little attention: the latter have been of major concern since their quantification provides the justification for extensive pest management programs. Concepts of impact are examined with emphasis on those affecting the eight resource elements and four support elements defined as goals and objectives of the National Forest System in the National Forest Management Act of 1976. Positive impacts are less thoroughly reviewed, largely because of the paucity of information available. An attempt is made, however, to examine the positive role of insects and diseases in the forest ecosystem and the effects of pest management activities on them. The base line for the review is September 1972, when over 60 experts from Canada and the U.S. examined the state‐of‐the‐art within the USDA Forest Service, the largest practitioner of pest management and hence the agency most concerned with justification of such activities. Their conclusion: “The Forest Service does not have an adequate system for measuring, evaluating, and predicting insect and disease‐caused impacts on the forest resources of the Nation.” Progress on these tasks is compared with the recommendations made in 1972. Additional recommendations are suggested based on changing concepts and attitudes towards pest management. Significant progress has been made in measurement, evaluation, and prediction of negative impacts — particularly in development of forest growth and yield models, and population and damage models for insects and diseases. Less encouraging is the progress made in monitoring ecological impacts.     

Amino acid sequence versus morphological data and the interordinal relationships of mammals

To a large extent, the mutual affinities of the mammalian orders continue to puzzle systematists, even though comparative anatomy and amino acid sequencing offer a massive data base from which these relationships could potentially be adduced. In the present paper the consistency index--the number of character states less the number of characters in a data set, divided by the total number of changes in the character states on a cladogram--was used to examine the relative resolving powers of recently published morphological and molecular- sequence data. Consistency indices were calculated for previously published alpha crystallin A chain and myoglobin amino acid-sequence cladograms and for four original amino acid-sequence cladograms (alpha crystallin A, myoglobin, and alpha and beta hemoglobin); these were found to be comparable to the consistency indices of morphologically based cladograms. Qualitative comparisons between the morphologically based and molecularly based trees were also made; only moderate congruence between the two was observed. Moreover, there was a general lack of congruence between the cladograms specified by each of the four proteins. Amino acid-sequence and morphological data agreed on the placement of edentates as an early eutherian offshoot and on the grouping of hyracoids, proboscideans, and sirenians. Otherwise there was only limited congruence: morphology strongly supported the grouping of lagomorphs and rodents and the alliance of pholidotes and edentates, but sequence analyses did not. The placement of tubulidentates differed widely among proteins. Morphology indicated the close association of sirenians with proboscideans; proteins suggested a pairing of sirenians with hyracoids. Sequence data did not identify many (morphologically well-diagnosed) orders as monophyletic (e.g., Lagomorpha).(ABSTRACT TRUNCATED AT 250 WORDS)      

Use of computerized data listings and activity profiles of genetic and related effects in the review of 195 compounds

Computer-generated listings of data from short-term tests for genetic and related effects (activity profile listings) were prepared for 195 compounds that included for each compound, the test system (identified by a three-letter code word), qualitative results and the lowest effective dose (LED) or highest ineffective dose (HID) tested. A corresponding bar or line graph (activity profile) was also generated, in which test systems are displayed along the x-axis and the LED or HID values along the y-axis. The listings were reviewed and the data summarized by an IARC Working Group. The methodology used to generate these listings and plots is described, and results are given for one compound, benzene. The entire data base contains approximately 7000 entries from 4000 references.     

The genetic toxicology of Gene-Tox non-carcinogens

The Gene-Tox Program has identified 61 chemicals that have been tested in chronic rodent carcinogenesis bioassays and found to be inactive. The genetic toxicology data of these 61 non-carcinogens is reviewed and summarized. A large proportion of these chemicals have been tested to a limited extent in genetic toxicity bioassays: 32 in 2 tests or less. Of the remaining 29 chemicals, 28% have been tested in 9 or more tests which encompass a range of genetic endpoints: gene mutation, chromosomal effects, other genetic endpoints, and cell transformation. The genetic toxicity of 12 chemicals with sufficient data is discussed in detail: benzoin, caffeine caprolactam, ethanol, halothane, hycanthone methanesulfonate, malathion, maleic hydrazide, methotrexate, 1-naphthylamine, 4-nitro-o-phenylenediamine, and p-phenylenediamine. A new technique for the evaluation of multiple test data, the "genetic activity profile", has been applied to 6 of these chemicals, allowing the qualitative and quantitative information to be compared collectively. In the evaluation of the genotoxicity effects of these non-carcinogens, a number of discrepancies between the results from genetic toxicity bioassays and chronic rodent bioassays have been uncovered. These discrepancies are discussed in light of current knowledge on the strengths and weaknesses of both genetic toxicity bioassays and chronic rodent bioassays.     

Characterization of the fine specificity and antigen markers associated with the receptor of autoreactive T-cell hybridomas

In this study we attempted to define the determinants on Ia molecules recognized by autoreactive hybridomas obtained from (C57BL/6 X BALB/c)F1 mice. The epitopes recognized by the T cells were characterized (a) using stimulating cells from various congenic and H-2 recombinant inbred strains and (b) by inhibition of activation with anti-Ia antibodies. Our hybridomas were strictly autoreactive and did not exhibit any alloreactivity, as is often observed for such cells. Our results show that more epitopes than previously believed are recognized by autoreactive T cells. One T-cell hybridoma (QW27.1) is unique in that it recognizes a hybrid F1 Ia determinant. Antigenic markers associated with the receptor of the T-cell hybridomas were studied with monoclonal antibodies (mAbs) specific for L3T4 and a V beta "idiotype". The results indicate that all Lyt 1.2 autoreactive T cells express L3T4 antigen in association with their receptor. One clone (QW64.14) expresses the V beta idiotype recognized by F23.1 monoclonal antibody. Moreover, this clone is activated by F23.1, linked to Sepharose 4B beads, which was believed previously to activate only Lyt 2+, L3T4 T cells. The supernatant of one clone (QW17.5) helps B cells to differentiate into antibody-producing cells without requiring direct contact with the autoreactive clone.     

Challenge of chimpanzees (Pan troglodytes) immunized with human immunodeficiency virus envelope glycoprotein gp120.

The human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome, infects humans and chimpanzees. To determine the efficacy of immunization for preventing infection, chimpanzees were immunized with gp120 purified from human T-cell lymphotrophic virus type IIIB (HTLV-IIIB)-infected cell membranes and challenged with the homologous virus, HTLV-IIIB. A challenge stock of HTLV-IIIB was prepared by using unconcentrated HTLV-IIIB produced in H9 cells. The titer of the virus from this stock on human and chimpanzee peripheral blood mononuclear cells and in human lymphoid cell lines was determined; a cell culture infectivity of 10(4) was assigned. All chimpanzees inoculated intravenously with 40 cell culture infectious units or more became infected, as demonstrated by virus isolation and seroconversion. One of two chimpanzees inoculated with 4 cell culture infectious units became infected. Chimpanzees immunized with gp120 formulated in alum developed antibodies which precipitated gp120 and neutralized HTLV-IIIB. Peripheral blood mononuclear cells from gp120-vaccinated and HIV-infected animals showed a significantly greater response in proliferation assays with HIV proteins than did peripheral blood mononuclear cells from nonvaccinated and non-HIV-infected chimpanzees. Two of the gp120-alum-immunized chimpanzees were challenged with virus from the HTLV-IIIB stock. One animal received 400 cell culture infectious units, and one received 40 infectious units. Both animals became infected with HIV, indicating that the immune response elicited by immunization with gp120 formulated in alum was not effective in preventing infection with HIV-1.     

The genetic toxicology of benzoin and caprolactam

A summary is presented of the published literature on the genetic toxicology of the two rodent non-carcinogens benzoin and caprolactam.     

Contextual organismality: Beyond pattern to process in the emergence of organisms

Biologists have taken the concept of organism largely for granted. However, advances in the study of chimerism, symbiosis, bacterial‐eukaryote associations, and microbial behavior have prompted a redefinition of organisms as biological entities exhibiting low conflict and high cooperation among their parts. This expanded view identifies organisms in evolutionary time. However, the ecological processes, mechanisms, and traits that drive the formation of organisms remain poorly understood. Recognizing that organismality can be context dependent, we advocate elucidating the ecological contexts under which entities do or do not act as organisms. Here we develop a “contextual organismality” framework and provide examples of entities, such as honey bee colonies, tumors, and bacterial swarms, that can act as organisms under specific life history, resource, or other ecological circumstances. We suggest that context dependence may be a stepping stone to the development of increased organismal unification, as the most integrated biological entities generally show little context dependence. Recognizing that organismality is contextual can identify common patterns and testable hypotheses across different entities. The contextual organismality framework can illuminate timeless as well as pressing issues in biology, including topics as disparate as cancer emergence, genomic conflict, evolution of symbiosis, and the role of the microbiota in impacting host phenotype.