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This paper is an integrated analysis of newspaper coverage, epidemiological rates, and recent social history of six prominent diseases.Newspaper coverage of a disease has three developmental stages (emergence, maturation, and declinedeath). Trends in newspaper coverage of a disease reflect trends in its mortality, prevalence, and incidence. Magnitudes of newspaper coverage of diseases reflect their differential mortality rates.Using the LEXIS-NEXIS news archive for major U.S. newspapers, we retrieve articles about cancer, heart disease, AIDS, diabetes, Alzheimer disease, and arthritis for the period 1977-1997. We also obtain mortality, prevalence, and incidence trends for the six diseases.During the two decades, newspaper coverage emerges for AIDS and Alzheimer disease and is in the mature stage for the other diseases; declines begin for heart disease and AIDS. Trends in news coverage closely parallel mortality trends, and less consistently prevalence and incidence trends. Sharp downturns and upturns in mortality are mirrored in news volume. High-mortality diseases prompt both the most news coverage and the largest proportions of articles with death topics.Newspaper coverage of diseases is responsive to their mortality levels and trends.

Fructose diphosphate aldolase has been crystallized from a Novikoff ascites hepatoma and its properties compared with those of aldolases of normal rat liver and muscle. The identity of the tumor enzyme with the normal muscle enzyme was established on the basis of amino acid composition and tryptic fingerprints, as well as the sensitivity to inactivation by L -glyceraldehyde 3-phosphate.

Fructose diphosphate aldolases have been isolated as crystalline proteins from rat liver, muscle and the Novikoff hepatoma. All three enzymes exhibit identical properties in sedimentation velocity and sedimentation equilibrium ultracentrifugation, corresponding to a molecular weight of 158,000. Dissociation in guanidinium chloride yields subunits of molecular weight approximately 40,000 in each case. Tumor and muscle aldolases exhibit identical electrophoretic properties on cellulose acetate or disc gel which are markedly different from those of liver aldolase. The tumor and muscle enzymes are 50 times more active with fructose-1,6-P2 than with fructose-1-P and treatment of these enzymes with carboxypeptidase A to remove the COOH-terminal tyrosine residues decreases the rate of cleavage of fructose-1,6-p2 so that it becomes equal to the rate of cleavage of fructose-1-P. Native rat liver aldolase, on the other hand, cleaves both substrates at equal rates and digestion with carboxypeptidase, while also liberating tyrosine from the COOH-terminus, does not affect the substrate specificity. The amino acid compositions of muscle and heppatoma aldolases were found to be identical and to differ significantly from that of the rat liver aldolase. Tryptic fingerprints of muscle and tumor aldolases are identical and differ significantly from that of liver aldolase. However, a number of peptides, including the active site peptide, are similar or identical in all three aldolases. The results provide support for the conclusion that the liver aldolase is replaced by muscle aldolase during the development of the Novikoff hepatoma.

A general feature of all aging populations is the progressively impaired ability to adapt to changes in the surrounding environment. Biochemical expressions of adaptive response include modifications in the rates of enzyme synthesis and degradation, as well as alterations in physiological activity. Therefore, the effects of aging on enzyme adaptation were surveyed in an attempt to explore fundamental biochemical mechanisms in the deterioration of responsiveness. The ability to stimulate adaptive increases in the activity of a large number of enzymes is impared during aging in a variety of tissues from several different species. The impaired capability for liver enzyme adaptation in a rigorously controlled colony of aging male Sprague-Dawley rats probably reflects alterations in hormonal control mechanisms. The present article reviews and evaluates our interest in understanding the effects of aging on regulation of liver enzyme activity by the hormones, insulin and corticosterone. Specific areas currently under investigation include: (1) the regulation of their concentrations in blood; (2) the integrity of their receptor systems in liver; and (3) effectiveness of the endogenous hormone pools fromthe viewpoints fothe availability of physiological antagonists and the potential for alterations in molecular structure.

Factors contributing to modifications in the capability for enzyme adaptation as an expression of aging are reviewed. Specific examples of altered enzyme adaptations during aging include the responses of hepatic glucokinase activity to glucose and hepatic tyrosine aminotransferase activity to starvation in Sprague-Dawley rats. These impaired enzyme adaptations apparently are not the consequence of alterations in hepatic function during aging. Instead, they reflect disturbances in extrahepatic hormonal regulatory mechanisms. Specific examples include modifications in the control of circulating levels of insulin glucagon, corticosteroids, and thyroid hormones. Age-dependent changes in the regulation of circulating levels of insulin probably originate within the impaired ability of pancreatic islets of Langerhans to secrete the hormone in response to glucose. The rationale for exploiting this experimental approach as a means to understand biological aging is discussed.

The selection of rats for aging research and the interpretation of experimental results require knowledge of spontaneous age-associated lesions in specific stocks and strains. We have compared selected age-associated pathological changes, as determined by postmortem examination of 113 outbred Crl:CD(SD)BR male retired breeder rats 12--39 months old, with those reported by others in a group of 122 virgin male 12- to 33-month-old F344 rats, an inbred strain from the same commercial source as the outbred rats. Numerous degenerative, inflammatory, and neoplastic lesions occurred in both groups. The wide prevalence and severity of many of the lesions suggest that they could be the source of significant variability in the results of specific aging studies, by their direct and indirect effect(s) on target organs. The prevalence of spontaneous lesions should be defined for each stock or strain intended for use in aging research by postmortem examination of representative groups of animals at various ages. Antemortem diagnostic screening of old rats may also be useful in culling animals bearing lesions that could add to the variability of experimental results, or in selecting for specific lesions that are of research interest themselves.