Confronting cancer on thirtysomething: audience response to health content on entertainment television

This study addresses the potential of entertainment television to educate about serious subject matter, such as health content. Through the use of open-ended, in-depth interviews of regular viewers in two metropolitan sites, this study explores audience response to a fictionalized, serialized portrayal of ovarian cancer on thirtysomething. Our questions were directed to the audience's (a) viewing process, including interpersonal contact, identification with characters, and prior experience with cancer, (b) understanding of content, especially illness imagery and coping strategies, and (c) applications to real life, including questions, insights, knowledge, and actions. The details of this exploration indicate the complexity of audience response to this kind of content and suggest guidelines for health communicators as they work with the entertainment industry to embed health-promoting messages in the media.     

Health advertising: prevention for profit.

The National Cancer Institute (NCI) estimates on the basis of current knowledge alone that, at a minimum, 30,000 lives could be saved in the year 2000 if Americans would modify their dietary habits. A recent innovative way of responding to this challenge was the Kellogg Company/NCI All-Bran advertising campaign. This paper will describe the campaign, and its impact on consumers, cereal industry sales, food industry advertising practices, health regulatory policy, and the organizational credibility of both NCI and Kellogg. For the past three years, Kellogg has included NCI's cancer prevention messages in their advertisements for All-Bran cereal and on their bran cereal boxes. This collaborative effort has stimulated considerable controversy over whether the health claims made on the cereal label are in violation of federal food labeling regulations. Meanwhile, research has demonstrated the positive impact of the campaign on consumer's knowledge and behavior regarding fiber as well as on Kellogg's profits. Other manufacturers are anxious to jump on the "branwagon"; however, many unanswered questions remain about this new approach to health advertising.     

Hierarchies in eukaryotic genome organization: Insights from polymer theory and simulations

Eukaryotic genomes possess an elaborate and dynamic higher-order structure within the limiting confines of the cell nucleus. Knowledge of the physical principles and the molecular machinery that govern the 3D organization of this structure and its regulation are key to understanding the relationship between genome structure and function. Elegant microscopy and chromosome conformation capture techniques supported by analysis based on polymer models are important steps in this direction. Here, we review results from these efforts and provide some additional insights that elucidate the relationship between structure and function at different hierarchical levels of genome organization.     

Hilfen für die Pflegenden zur Bewältigung beruflicher Belastungen

Work load and work stress are reasons for a reduction in the quality of nursing care and for nurses leaving hospitals. In parallel, there is an increase in the need for nursing because of demographic developments such as the increase in the number of chronically ill patients. Today, hospitals are understaffed in the nursing sector. This personnel problem is a challenge for the management of human resources in hospitals. In competition with other hospitals, it is not enough to focus only on economic management outcome. The concentration on human resources will be the decisive factor in being successful in the future. Qualified management of human resources will improve general work conditions, patient’ outcomes and staff satisfaction.     

Recipient humoral immunity against leukoreduced allogeneic platelets is suppressed by aminoguanidine, a selective inhibitor of inducible nitric oxide synthase

Leukoreduced allogeneic platelet transfusions have been previously shown to initially stimulate an in vitro cellular cytotoxicity and subsequently Induce the formation of immunoglobulin G (IgG) antidonor alloantibodies. To further characterize these responses and determine if they are related, recipient BALB/c H-2d mice were treated with aminoguanidine (AMG), a selective inhibitor of inducible nitric oxide synthase (iNOS), and transfused weekly with 2 x 10(8) C57BL/6 H2b platelets. In control, non-AMG-treated mice, transfusion significantly (P < .01) increased serum levels of interferon-gamma (IFN-gamma) by day 1 posttransfusion (PT). IFN-gamma returned to pretransfusion levels by day 3 PT, and its production was not affected by AMG treatment. Serum interleukin-4 (IL-4), on the other hand, was undetectable before and during the transfusion protocol. By day 3 PT, recipient spleen cells could mediate in vitro anti-P815 (auto), anti-EL4 (allo), and anti-R1.1 (third-party MHC) cytotoxicity, and these responses were maximal by day 7 PT. Concurrently, a significant reduction in the vitro ability of recipient splenocytes to respond to Concanavalin A (ConA) was observed; this was not seen with lipopolysaccharide (LPS) stimulation. Elevated levels of NO2- were found in the ConA culture supernatants from transfused mice at day 3 PT. Serum antidonor alloantibodies were detected by the fifth platelet transfusion. AMG treatment of recipient mice significantly inhibited the transfusion. Induced cytotoxicity and ConA-stimulated NO2- production, and restored ConA-induced proliferation to normal levels. AMG appeared to selectively inhibit platelet-induced alloantibody production in that it did not affect antibody production induced by transfusions with 10(5) allogeneic leukocytes or by immunization with a foreign protein antigen, human gamma globulin, in adjuvant therapy. These results indicate that an in vivo AMG-sensitive mechanism is essential for recipients to initiate a humoral IgG immune response against allogeneic platelets.     

Codon insertion mutants of the adenovirus terminal protein.

A series of codon insertion mutants was isolated following restriction site-directed linker insertion mutagenesis of the open reading frame for the type 5 adenovirus terminal protein precursor. The conditionally lethal mutant H5sub100 bears an insertion mutation upstream of the first AUG in the reading frame, fails to replicate its DNA under nonpermissive conditions, and was assigned to the terminal protein complementation group. These data establish that terminal protein is an essential polypeptide required for DNA replication in vivo and indicate that the NH2-terminal region of the precursor is encoded in an upstream mRNA leader. The extended eclipse period of the viral replication cycle in H5in179-infected cells is probably a consequence of delayed onset of DNA replication. Analysis of DNA replication in coinfections with wild-type virus shows that the in179 mutation has cis and trans effects. The trans-dominant, negative-complementing in179 terminal protein precursor inhibits wild-type DNA replication in a dose-dependent manner. Replication of parental in179 templates is not stimulated by an excess of coinfecting wild-type virus, indicating that the mutant terminal protein covalently bound to the in179 template in some way interferes with the replication of that template. The implications of these results for the structure and function of the terminal protein are discussed.     

Hemoglobin M equon beta 41 (C7) phenylalanine leads to tyrosine

A severe hemolytic crisis was observed in a 34-yr-old female of English- Irish extraction following a viral illness treated with acetaminophen. Heinz bodies and heat instability were present only during a transient hemolytic event. A challenge dose of acetaminophen caused no detectable hematologic abnormality. Structural studies of the hemoglobin during hemolysis and again after complete recovery localized the abnormality to tryptic peptide beta Tp-5, and automated sequencing of I 125-labeled beta chains indicated a replacement of phenylalanine (C7) beta 41 by tyrosine. Substitution of the next residue, phenylalanine (CD1) beta 42 by serine (Hb Hammersmith), has resulted in chronic severe Heinz body hemolytic anemia. The lack of chronic anemia in the present disorder may reflect the different relationships of beta41 and beta 42 and/or the similarities in volume and hydrophobicity of tyrosine and phenylalanine. It is suggested that substitution of tyrosine for phenylalanine in Hb Mequon may disturb the critical environment around the heme group and render it susceptible to oxidative denaturation in the presence of infections and/or drugs.