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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.socscimed.2010.01.013 Byline: Jackie M. Street (a), Wendy A. Rogers (b)(c), Mark Israel (d)(e), Annette J. Braunack-Mayer (a) Abstract: Despite attempts at clear direction in international, national and journal guidelines, attribution of authorship can be a confusing area for both new and established researchers. As journal articles are valuable intellectual property, authorship can be hotly contested. Individual authors' responsibilities for the integrity of article content have not been well explored. Semi-structured interviews (n = 17) were conducted with staff, student advocates and doctoral candidates working in health research in two universities in Australia. Stratified sampling ensured participants reflected a range of experience across biomedical, clinical and social science disciplines. Participants were asked about their experience with research publication and their views on the responsibilities of authorship. Participants gave a variety of reasons for attribution of authorship including: writing the paper; seniority; and student supervision. Gift authorship was seen by some participants as: a way of maintaining relationships; a reward; a means to increase a paper's credibility; or a demonstration of collaboration between authors. Norms and beliefs differed markedly between disciplines for authorship attribution and, to a lesser extent, for authors' responsibility for content integrity. Discussions about the effect of power differentials on authorship were common across disciplines. This paper describes a broad range of beliefs, values and practice norms held by health science researchers with respect to attribution of authorship and author responsibility for scientific publications. The findings support the need for clarity in relation to authorship, and a research environment which is supportive of ethical behaviour in the publication of research. Author Affiliation: (a) School of Population Health and Clinical Practice, University of Adelaide, Adelaide 5005, Australia (b) Philosophy Department, Australian School of Advanced Medicine, Macquarie University, Sydney, Australia (c) School of Medicine, Flinders University, Adelaide, Australia (d) Faculty of Law, University of Western Australia, Perth, Australia (e) School of Law, Flinders University, Adelaide, Australia

Effects of consumer learning about product quality on automobile insurance purchasing decisions are presented.

Glioblastoma multiforme (GBM) is the most common form of malignant glioma, characterized by genetic instability, intratumoral histopathological variability, and unpredictable clinical behavior. We investigated global gene expression in surgical samples of brain tumors. Gene expression profiling revealed large differences between normal brain samples and tumor tissues and between GBMs and lower-grade oligodendroglial tumors. Extensive differences in gene expression were found among GBMs, particularly in genes involved in angiogenesis, immune cell infiltration, and extracellular matrix remodeling. We found that the gene expression patterns in paired specimens from the same GBM invariably were more closely related to each other than to any other tumor, even when the paired specimens had strikingly divergent histologies. Survival analyses revealed a set of [approximately equal to] 70 genes more highly expressed in rapidly progressing tumors that stratified GBMs into two groups that differed by >4-fold in median duration of survival. We further investigated one gene from the group, FABP7, and confirmed its association with survival in two unrelated cohorts totaling 105 patients. Expression of FABP7 enhanced the motility of glioma-derived cells in vitro. Our analyses thus identify and validate a prognostic marker of both biologic and clinical significance and provide a series of putative markers for additional evaluation. brain | glioma | tumor | FABP7 | prognosis

A typical pattern in markets featuring long-term consumer-firm relationships is for departure probabilities to decline with tenure. A crucial question is whether this actually implies increasing consumer preference for firms, [...]

The vulnerability of backpackers to crime has not been studied. This article looks at possible crimes which backpackers face in Australia and highlights the need for victimological and criminological studies.

Basic helix-loop-helix (bHLH) DNA-binding proteins have been demonstrated to regulate tissue-specific transcription within multiple cell lineages. The Id family of helix-loop-helix proteins does not possess a basic DNA-binding domain and functions as a negative regulator of bHLH proteins. Overexpression of Id proteins within a variety of cell types has been shown to inhibit their ability to differentiate under appropriate conditions. We demonstrate that ectopic expression of Id-1 leads to activation of telomerase activity and immortalization of primary human keratinocytes. These immortalized cells have a decreased capacity to differentiate as well as activate phosphorylation of the retinoblastoma protein. Additionally, these cells acquire an impaired p53-mediated DNA-damage response as a late event in immortalization. We conclude that bHLH proteins play a pivotal role in regulating normal keratinocyte growth and differentiation, which can be disrupted by the immortalizing functions of Id-1 through activation of telomerase activity and inactivation of the retinoblastoma protein.

The author examines various models of jury selection, how they reflect competing and diverse concepts of community, and the consequences they have on the representation of ethnic and racial minorities.

Radiation is the primary modality of therapy for all commonly occurring malignant brain tumors, including medulloblastoma and glioblastoma. These two brain tumors, however, have a distinctly different response to radiation therapy. Medulloblastoma is very sensitive to radiation therapy, whereas glioblastoma is highly resistant, and the long-term survival of medulioblastoma patients exceeds 50%, while there are few long-term survivors among glioblastoma patients. p53-mediated apoptosis is thought to be an important mechanism mediating the cytotoxic response of tumors to radiotherapy. In this study, we compared the response to radiation of five cell lines that have wild-type p53: three derived from glioblastoma and two derived from medulloblastoma. We found that the medulloblastoma-derived cell lines underwent extensive radiation-induced apoptotic cell death, while those from glioblastomas did not exhibit significant radiation-induced apoptosis. p53-mediated induction of [p21.sup.BAX] is thought to be a key component of the pathway mediating apoptosis after the exposure of cells to cytotoxins, and the expression of mRNA encoding [p21.sup.BAX] was correlated with these cell lines undergoing radiation-induced apoptosis. The failure of p53 to induce [p21.sup.BAX] expression in glioblastoma-derived cell lines is likely to be of biologic significance, since inhibition of [p21.sup.BAX] induction in medulloblastoma resulted in a loss of radiation-induced apoptosis, while forced expression of [p21.sup.BAX] in glioblastoma was sufficient to induce apoptosis. The failure of p53 to induce [p21.sup.BAX] in glioblastoma-derived cell lines suggests a distinct mechanism of radioresistance and may represent a critical factor in determining therapeutic responsiveness to radiation in glioblastomas.

Britain's South African immigrants have been allowed to grow in number even though other groups, such as those from the New Commonwealth, have been carefully controlled. Britain's favourable historical links to South Africa are offered as an explanation for this leniency. White South Africans find it easier to enter the country than black South Africans, even if they are of no relation to immigration workers.

Herpes simplex virus thymidine kinase (HSV-tk)/ganciclovir (GCV) viral-directed enzyme prodrug gene therapy causes potent, tumor-selective cytotoxicity in animal models in which HSV-tk gene transduction is limited to a minority of tumor cells. The passage of toxic molecules from HSV-[tk.sup.+] cells to neighboring HSV-[tk.sup.-] cells during GCV therapy is one mechanism that may account for this 'bystander' cytotoxicity. To investigate whether gap junction-mediated intercellular coupling could mediate this bystander effect, we used a flow cytometry assay to quantitate the extent of heterocellilar coupling between HSV-[tk.sup.+] murine fibroblasts and both rodent and human tumor cell lines. Bystander tumor cytotoxicity during GCV treatment in a coculture assay was highly correlated (P < 0.001) with the extent of gap junction-mediated coupling. These findings show that gap junction-mediated intercellular coupling contributes to the in vitro bystander effect during HSV-TK/GCV therapy and that retroviral transduction of tumor cells is not required for bystander cytotoxicity.

Cholecystokinin (CCK) is a peptide hormone that has been detected in two tumor cell lines derived from human neuroepitheliomas. An investigation was conducted to determine the expression of CCK in a larger subset of human tumor lines. The results showed that CCK is also expressed in neuroeptihelioma, Ewing sarcoma and human rhabdomyosarcoma cell lines. The expression of CCK was not detected in any of the neuroblastoma cell lines tested. The expression of CCK in these cell lines may serve as a marker to distinguish these types of tumors.

The developmental regulation of genes may be mediated by transcription factors like Id, which contains a helix-loop-helix (HLH) motifand inhibits myogenic differentiation. The gene coding for a new factor, termedId-2 was isolated. Id-2 is composed of 134 amino acids whose sequence shows 90%homology to Id in the HLH region. However, Id-2 shows a different pattern of expression compared to Id, and is modulated in association with retinoic acid-induced ganglionic differentiation. It is highly expressed in several fetal tissues, but not expressed in the corresponding mature tissues.

Single-strand conformation polymorphism analysis was used to examine the tumor suppressor gene, p53 gene, in genomic DNA from tumor and normal tissues of four patients with multifocal osteogenic sarcoma (mOS). The results revealed the occurrence of somatic p53 mutations from all four mOS patients and of a germ-line mutation in one of them. p53 germ-line mutations can contribute to enhanced cancer predisposition in patients with mOS.

INTRODUCTION Since the publication of William Julius Wilson's The Truly Disadvantaged in 1987, poverty research has reemerged as a major focus of economics and sociology. An important portion of this [...]

An overview of the way in which ethics committees tend to treat social science research, with particular attention paid to the situation in Australia and the UK's Economic and Social Research Council's research ethics framework. It is suggested that the UK system manages to avoid many of the problems of the Australian system but that there are still areas in which arguments may occur.