Purpose This paper aims to examine the relationship between board demographic diversity and human rights reporting for a sample of large Western European companies. Design/methodology/approach Grounded on resource dependence theory, the authors hypothesize that greater gender, age and nationality diversities will translate into enhanced levels of human rights reporting. The authors use ordinal logistic regression analysis to analyze the association between these types of board diversity and such reporting. Findings The findings suggest that the companies in the sample attribute little importance to the reporting of information pertaining to the issue of human rights. They also suggest that only the diversity of nations represented in the board of directors is significant in explaining this type of reporting. Research limitations/implications The sample includes only large companies from Western Europe and the analysis covers only one year. Originality/value To the best of the authors’ knowledge, this study provides the first empirical analysis of factors influencing human rights reporting conducted on a multiple-country setting. It is also the first investigating the association between boards of directors’ demographic diversity and such reporting.

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Background: Amyloid fibrils are protein polymers. Functional amyloids play a beneficial role in a variety of physiologic processes. Amyloidosis results from the accumulation of pathogenic amyloids in a variety of tissues. Case Presentation: The authors present a case of a 60-year-old male with a pseudotumoral silicosis, a history of intermittent fever, and renal insufficiency with intermittent proteinuria (maximum of 3 g/dl). The diagnosis of amyloidosis was made from multiple biopsies. During the investigation, it was never possible to characterize the subtype of amyloidosis [the patient had findings either in favor of AL amyloidosis and AA amyloidosis (AA)]. A definite diagnosis was only obtained from an autopsy, and AA was found to be the subtype. Conclusion: At the time of this publication and to the best of authors’ knowledge, AA has never been described to be associated with pseudotumoral form of pulmonary silicosis. We believe that an inflammatory response associated with pulmonary silicosis was the trigger to the development of AA.

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