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Even though peer process feedback is an often used tool to enhance the effectiveness of collaborative learning environments like PBL, the conditions under which it is best facilitated still need to be investigated. Therefore, this study investigated the effects of individual versus shared reflection and goal setting on students' individual contributions to the group and their academic achievement. In addition, the influence of prior knowledge on the effectiveness of peer feedback was studied. In this pretest-intervention-posttest study 242 first year students were divided into three conditions: condition 1 (individual reflection and goal setting), condition 2 (individual and shared reflection and goal setting), and condition 3 (control group). Results indicated that the quality of individual contributions to the tutorial group did not improve after receiving the peer feedback, nor did it differ between the three conditions. With regard to academic achievement, only males in conditions 1 and 2 showed better academic achievement compared with condition 3. However, there was no difference between both ways of reflection and goal setting with regard to achievement, indicating that both ways are equally effective. Nevertheless, it is still too early to conclude that peer feedback combined with reflection and goal setting is not effective in enhancing students' individual contributions. Students only had a limited number of opportunities to improve their contributions. Therefore, future research should investigate whether an increase in number of tutorial group meetings can enhance the effectiveness of peer feedback. In addition, the effect of quality of reflection and goal setting could be taken into consideration in future research.

Although increasing apolipoprotein A-I (apoA-I) might lower the cardiovascular disease risk, knowledge on natural compounds that elevate apoA-I transcription is limited. Therefore, the aim of this study was to discover natural compounds that increase apoA-I transcription in HepG2 cells. Since BRD4 inhibition is known to elevate apoA-I transcription, we focused on natural BRD4 inhibitors. For this, the literature was screened for compounds that might increase apoA-I and or inhibit BRD4. This resulted in list A, (apoA-I increasers with unknown BRD4 inhibitor capacity), list B (known BRD4 inhibitors that increase apoA-I), and list C (BRD4 inhibitors with unknown effect on apoA-I). These compounds were compared with the compounds in two natural compound databases. This resulted in (1) a common substructure (ethyl-benzene) in 60% of selected BRD4-inhibitors, and (2) four compounds that increased ApoA-I: hesperetin, equilenin, 9(S)-HOTrE, and cymarin. Whether these increases are regulated via BRD4 inhibition and the ethyl-benzene structure inhibits BRD4 requires further study., (© 2019 The Authors. Lipids published by Wiley Periodicals, Inc. on behalf of American Oil Chemists' Society.)

Activating transcription factor peroxisome proliferator-activated receptor alpha (PPARα) may increase apoA-I transcription. Furthermore, Bromodomain and Extra-Terminal domain (BET) protein inhibitors increase, whereas Endoplasmic Reticulum (ER) stress decreases apoA-I transcription. We examined possible links between these processes as related to apoA-I transcription in HepG2 cells. JQ1(+), thapsigargin, and GW7647 were used to induce, respectively BET inhibition, ER-stress, and PPARα activation. Expression of ER-stress markers (CHOP, XBP1s) was analyzed by western blotting. PPARα, KEAP1 (marker for BET inhibition), and apoA-I mRNAs were measured using qPCR. ER-stress and BET inhibition both decreased PPARα mRNA expression and activity, but did not interfere with each other, as ER-stress did not change KEAP1 and JQ1(+) did not influence ER-stress marker production. Interestingly, PPARα activation and BET-inhibition diminished ER-stress marker production and rescued apoA-I transcription during existing ER-stress. We conclude that the ER-stress mediated reduction in apoA-I transcription could be partly mediated via the inhibition of PPARα mRNA expression and activity. In addition, BET inhibition increased apoA-I transcription, even if PPARα production and activity were decreased. Finally, both BET inhibition and PPARα activation ameliorate the apoA-I lowering effect of ER-stress and are therefore interesting targets to elevate apoA-I transcription. J. Cell. Biochem. 118:2161-2167, 2017. © 2016 Wiley Periodicals, Inc., (© 2016 Wiley Periodicals, Inc.)