Who is Responsible? Attribution of Responsibility in the Context of Dementia: A Content-Analysis of Framing in Media Coverage.

Dementia is currently one of the most significant public health challenges from a medical as well as a societal perspective. The number of people living with dementia is increasing, and there is conflicting evidence in terms of preventive measures and risk factors. The available therapies can slow down but neither stop nor reverse the condition. Educating the public about these circumstances is thus of utmost relevance. As the mass media are a major source of health-related information, this study uses a quantitative content analysis to examine the extent to which responsibility framing occurs concerning risk and protection factors for dementia. Besides the established levels of individual and society, this study considers the level "social network" as an independent level to account for the supporting role of relatives and friends in the care of people living with dementia. The results show that protection factors for dementia are reported more frequently than the risk factors of the condition. Further, attribution of responsibility for risk factors tended to be at the individual level, while protection was the responsibility of society and the social network.

Expression of serum amyloid A4 in human trophoblast-like choriocarcinoma cell lines and human first trimester/term trophoblast cells.

Trophoblast invasion into uterine tissues represents a hallmark of first trimester placental development. As expression of serum amyloid A4 (SAA4) occurs in tumorigenic and invasive tissues we here investigated whether SAA4 is present in trophoblast-like human AC1-M59/Jeg-3 cells and trophoblast preparations of human first trimester and term placenta. SAA4 mRNA was expressed in non-stimulated and cytokine-treated AC1-M59/Jeg-3 cells. In purified trophoblast cells SAA4 mRNA expression was upregulated at weeks 10 and 12 of pregnancy. Western-blot and immunohistochemical staining of first trimester placental tissue revealed pronounced SAA4 expression in invasive trophoblast cells indicating a potential role of SAA4 during invasion.

[The perils of risk communication and the role of the mass media]. / Die Risiken der Risikokommunikation und die Rolle der Massenmedien.

Based on theories and empirical results from communication science, the present paper provides an overview of the role of mass media in risk communication. It is guided by the following questions: How do risk issues find their way into the media and how does the media depict them? How do mass-mediated risk messages affect people's perception of risks, knowledge, attitudes, and behavior? What potential does the media have in disseminating health risk information in campaigns? Hence, the present paper aims to provide a basis for the appropriate use of mass media in health risk communication so as to make use of the potential of mass media without neglecting its limits.

Expression and purification of recombinant, glycosylated human interferon alpha 2b in murine myeloma NSo cells.

We have expressed recombinant human interferon-alpha 2b in mammalian cells and isolated cell lines constitutively secreting very high levels of biologically active protein. The expression system takes advantage of the strong human cytomegalovirus immediate early promoter in mouse myeloma NSo cells and glutamine synthetase as a selectable marker; spontaneous mutants with amplified gene copy numbers were selected by growth of primary transfectants in the presence of methionine sulfoximine. Using this procedure, we have isolated a recombinant NSo cell line which secretes human interferon at the rate of 20 micrograms/10(6) cells/24 h and accumulates up to 120 micrograms/ml (approximately 2.4 x 10(7) U/ml) following prolonged undiluted culture. The interferon (IFN) could be efficiently purified on a polyclonal bovine anti-human IFN alpha specific antibody column and the glycosylation pattern was found to be similar to that of nonrecombinant IFN alpha 2b purified from virus-induced human Namalwa cells. The biological activity of the recombinant material was indistinguishable from that of natural IFN from Namalwa cells, and the specific antiviral activity, as assayed on human HeLa cells challenged with encephalomyocarditis virus, was 2 x 10(8) IU/mg, similar to that of nonrecombinant IFN preparations. This represents the highest reported level of glycosylated, recombinant IFN expression in a stable mammalian system and is a significant advance in the large-scale production of these clinically important cytokines.

Interferon system defects in human malignant melanoma.

We have examined the ability of melanoma cell lines and normal human melanocytes, which have demonstrable intact IFN genes, to secrete both IFN-alpha and IFN-beta in response to induction with virus. Normal melanocytes were found to secrete both IFN-alpha and IFN-beta after virus induction. In contrast, although all but one of the melanoma lines tested were capable of secreting IFN-beta, none were capable of IFN-alpha secretion. This phenomenon was not due to defects in either translation of IFN-alpha mRNA or secretion of IFN-alpha proteins, since transfection of melanoma lines with a constitutive IFN-alpha 2b expression vector resulted in the secretion of high levels of IFN. On further examination, this inability to express natural IFN-alpha appeared to be due to a defect in activation of the IFN-alpha promoters, since constructs containing the IFN-alpha promotor were completely unresponsive to viral infection in melanoma cells but inducible in melanocytes. These results show that there is a specific disruption of IFN-alpha gene activation rather than IFN-beta in melanoma lines and suggest that this is due to disruption of a trans-acting IFN-alpha gene transcription factor. Disruption of this factor and its consequences may be important in the development of malignant melanoma.

Preincubation with anti-CD4 influences activation of human T cells by subsequent co-cross-linking of CD4 with CD3.

Under physiological conditions, T cell activation by major histocompatibility complex (MHC)-antigen complexes requires engagement of both the T cell receptor (TcR) and the CD4 (or CD8) accessory molecules. It has been shown, however, that ligation of CD4 and CD8 can also inhibit T cell activation in an MHC-independent way. Therefore, the role of CD4 in T cell activation and the mechanism of the suppression of T cell functions by anti-CD4 are as yet unclear. We activated T cells by CD4/CD3 co-cross-linking and studied the effect of preincubation with anti-CD4 on this activation. We show here that anti-CD4 effects T cell activation in a complex, time-dependent manner. Whereas short preincubations with anti-CD4 usually enhanced T cell proliferation in response to subsequent co-cross-linking of CD3 with CD4, longer preincubations led to its decrease. The observed suppression of proliferation after a long preincubation with anti-CD4 was apparently due to impairment of TcR signaling, as assessed by measurement of Ca2+ mobilization and tyrosine phosphorylation in T cells. These results add a temporal element to the previously observed synergism between the TcR and CD4 in T cell activation.