Effects of phthalic acid esters on the liver and thyroid

The effects, over periods from 3 days to 9 months of administration, of diets containing di-2-ethylhexyl phthalate are very similar to those observed in rats administered diets containing hypolipidemic drugs such as clofibrate. Changes occur in a characteristic order commencing with alterations in the distribution of lipid within the liver, quickly followed by proliferation of hepatic peroxisomes and induction of the specialized P-450 isoenzyme(s) catalyzing omega oxidation of fatty acids. There follows a phase of mild liver damage indicated by induction of glucose-6-phosphatase activity and a loss of glycogen, eventually leading to the formation of enlarged lysosomes through autophagy and the accumulation of lipofuscin. Associated changes are found in the kidney and thyroid. The renal changes are limited to the proximal convoluted tubules and are generally similar to changes found in the liver. The effects on the thyroid are more marked. Although the levels of thyroxine in plasma fail to about half normal values, serum triiodothyronine remains close to normal values while the appearance of the thyroid varies, very marked hyperactivity being noted 7 days after commencement of treatment, this is less marked at 14 days, but even after 9 months treatment there is clear cut evidence for hyperactivity with colloid changes which indicate this has persisted for some time. Straight chain analogs of di-2-ethylhexyl phthalate, di-n-hexyl phthalate and di-n-oxtyl phthalate differ entirely in their short-term effects on the liver and kidney but have similar effects on the thyroid. The short-term in vivo hepatic effects of the three phthalate esters can be reproduced in hepatocytes in tissue culture. All three phthalate esters, as well as clofibrate, have early marked effects on the metabolism of fatty acids in isolated hepatocytes. The nature of these changes is such as to increase storage of lipid in the liver. A hypothesis is presented to explain the progress from these initial metabolic effects to the final formation of liver tumors.

Towards (more) integrity in academia: transcending neo-liberal assumption of research and knowledge creation and the “rules” supressing academic freedom

European researchers across heterogeneous disciplines voice concerns and argue for new paths towards a brighter future regarding scientific and knowledge creation and communication. Recently, in biological and natural sciences concerns have been expressed that major threats are intentionally ignored. These threats are challenging Europe’s future sustainability towards creating knowledge that effectively deals with emerging social, environmental, health, and economic problems of a planetary scope. Within social science circles however, the root cause regarding the above challenges, have been linked with macro level forces of neo-liberal ways of valuing and relevant rules in academia and beyond which we take for granted. These concerns raised by heterogeneous scholars in natural and the applied social sciences concern the ethics of today’s research and academic integrity. Applying Bourdieu’s sociology may not allow an optimistic lens if change is possible. Rather than attributing the replication of neo-liberal habitus in intentional agent and institutional choices, Bourdieu’s work raises the importance of thoughtlessly internalised habits in human and social action. Accordingly, most action within a given paradigm (in this case, neo-liberalism) is understood as habituated, i.e. unconsciously reproducing external social fields, even ill-defined ways of valuing. This essay analyses these and how they may help critically analyse the current habitus surrounding research and knowledge production, evaluation, and communication and related aspects of academic freedom. Although it is acknowledged that transformation is not easy, the essay presents arguments and recent theory paths to suggest that change nevertheless may be a realistic hope once certain action logics are encouraged.