Features for Hate? Using the Delphi Method to Explore Digital Determinants for Online Hate Perpetration and Possibilities for Intervention.

Online hate speech on social media platforms causes harm to those who are victimized as well as society at large. The prevalence of hateful content has, thus, prompted numerous calls for improved countermeasures and prevention. For such interventions to be effective, it is necessary to gain a nuanced understanding of influences that facilitate the spread of hate speech. This study does so by investigating what are relevant digital determinants for online hate perpetration. Moreover, the study explores possibilities of different technology-driven interventions for prevention. Thereby, the study specifically considers the digital environments in which online hate speech is most often produced and disseminated, namely social media platforms. We apply frameworks related to the concept of digital affordances to focus on the role that technological features of these platforms play in the context of online hate speech. Data were collected using the Delphi method in which a selected sample of experts from both research and practice answered multiple rounds of surveys with the goal of reaching a group consensus. The study encompassed an open-ended collection of initial ideas, followed by a multiple-choice questionnaire to identify, and rate the most relevant determinants. Usefulness of the suggested intervention ideas was assessed through the three lenses of human-centered design. The results of both thematic analysis and non-parametric statistics yield insights on how features of social media platforms can be both determinants that facilitate online hate perpetration as well as crucial mechanisms of preventive interventions. Implications of these findings for future intervention development are discussed.

The role of kinesin, dynein and microtubules in pancreatic secretion.

The regulated secretion of pancreatic zymogens depends on a functional cytoskeleton and intracellular vesicle transport. To study the dynamics of tubulin and its motor proteins dynein and kinesin during secretion in pancreatic acinar cells, we infused rats with 0.1 mug/kg/h caerulein. Electron and fluorescence microscopy detected neither dynein nor kinesin at the apical secretory pole, nor on the surface of mature zymogen granules. After 30 min of secretagogue stimulation, kinesin and the Golgi marker protein 58 K were reallocated towards the apical plasma membrane and association of kinesin with tubulin was enhanced. Disruption of acinar cell microtubules had no effect on initial caerulein-induced amylase release but completely blocked secretion during a second stimulus. Our results suggest that mature zymogen granule exocytosis is independent of intact microtubules, kinesin and dynein. However, microtubule-dependent mechanisms seem to be important for the replenishment of secretory vesicles by redistribution of Golgi elements towards the apical cell pole.

No carry over of unmetabolised deoxynivalenol in milk of dairy cows fed high concentrate proportions.

To examine the carry over of deoxynivalenol (DON) and its metabolite de-epoxy DON (DOM-1) in milk, lactating German Holstein cows (n = 13) were fed an isoenergetic total mixed ration in Period 1 with 50% concentrates and 5.3 mg DON/kg dry matter (DM) over 11 wk and were compared with control cows (n = 14). In Period 2 (18 wk), an elevated concentrate proportion was compared to a low concentrate ration by dividing the cows into four Groups (n = 8): Control-30 (30% concentrates), Myco-30 (30% concentrates, 4.4 mg DON/kg DM), Control-60 (60% concentrates) and Myco-60 (60% concentrates, 4.6 mg DON/kg DM). Taken both periods together, no unmetabolised DON was detected in milk samples using the HPLC-UV method. DOM-1 concentrations ranged between below the LOD and 3.2 microg/kg milk in mycotoxin fed cows, while control cows did not excrete any measurable amounts of DOM-1. Regarding the concentrate effects, the carry over of DON as DOM-1 in milk was negligible (between 0.0001 and 0.0011) but significantly higher in Group Myco-30 than in Group Myco-60. This effect may result from an altered bioavailability of DON from maize silage which made up a higher proportion of the daily ration.

Early changes in pancreatic acinar cell calcium signaling after pancreatic duct obstruction.

Intracellular Ca(2+)-changes not only participate in important signaling pathways but have also been implicated in a number of disease states including acute pancreatitis. To investigate the underlying mechanisms in an experimental model mimicking human gallstone-induced pancreatitis, we ligated the pancreatic duct of Sprague-Dawley rats and NMRI mice for up to 6 h and studied intrapancreatic changes including the dynamics of [Ca(2+)](i) in isolated acini. In contrast to bile duct ligation, pancreatic duct obstruction induced intra-pancreatic trypsinogen activation, leukocytosis, hyperamylasemia, and pancreatic edema and increased lung myeloperoxidase activity. Although resting [Ca(2+)](i) in isolated acini rose by 45% to 205 +/- 7 nmol, the acetylcholine- and cholecystokinin (CCK)-stimulated calcium peaks as well as the amylase secretion declined, but neither the [Ca(2+)](i)-signaling pattern nor the amylase output in response to the Ca(2+)-ATPase inhibitor thapsigargin nor the secretin-stimulated amylase release were impaired by pancreatic duct ligation. On the single cell level pancreatic duct ligation reduced the percentage of cells in which submaximal secretagogue stimulation was followed by a physiological response (i.e. Ca(2+) oscillations) and increased the percentage of cells with a pathological response (i.e. peak plateau or absent Ca(2+) signal). Moreover, it reduced the frequency and amplitude of Ca(2+) oscillation as well as the capacitative Ca(2+) influx in response to secretagogue stimulation. Serum pancreatic enzyme elevation as well as trypsinogen activation was significantly reduced by pretreatment of animals with the calcium chelator BAPTA-AM. These experiments suggest that pancreatic duct obstruction rapidly changes the physiological response of the exocrine pancreas to a Ca(2+)-signaling pattern that has been associated with premature digestive enzyme activation and the onset of pancreatitis, both of which can be prevented by administration of an intracellular calcium chelator.