Circadian Rhythms in Socializing Propensity

Using large-scale interaction data from a virtual world, we show that people’s propensity to socialize (forming new social connections) varies by hour of the day. We arrive at our results by longitudinally tracking people’s friend-adding activities in a virtual world. Specifically, we find that people are most likely to socialize during the evening, at approximately 8 p.m. and 12 a.m., and are least likely to do so in the morning, at approximately 8 a.m. Such patterns prevail on weekdays and weekends and are robust to variations in individual characteristics and geographical conditions.     

Exercise‐induced α‐ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1‐dependent adrenal activation

The authors approached the journal to correct a mistake in the data presented in Appendix␣Fig S3D. The authors state that the mouse images in Appendix␣Fig S3D mistakenly displayed images from Fig 2F and Appendix␣Fig S1F. The images in Appendix␣Fig S3D are herewith corrected. The authors state that this change does not affect the conclusions or the statistics. The source data for these panels have been added to the original publication.The authors note that the following sentence needs to be corrected from: Appendix Figure S3D. Original. Appendix Figure S3D. Corrected. “Interestingly, several well‐established accumulation signatures of succinate, malate, hypoxanthine, and xanthine induced by endurance exercise (Lewis et␣al, 2010) were found to be decreased by endurance exercise (Figs 1D and EV1A–D)”.to“Interestingly, several well‐established accumulation signatures of succinate, malate, hypoxanthine, and xanthine induced by endurance exercise (Lewis et␣al, 2010) were found to be decreased by resistance exercise (Figs 1D and EV1A–D)”.Further, the authors requested to amend the legend of Appendix␣Fig S3R to indicate that the same sample for the iWAT group, “WT+2%AKG” treatment, is shown in Fig 3P. The corrected legend reads: “(R‐S). Representative images (R) and quantification (S) of p‐HSL DAB staining from male OXGR1OE^AG mice treated with AKG for 12 weeks (n = 6 per group). The same sample is shown as in Fig 3P ”.The authors regret these errors and any confusion they may have caused. All authors approve of this correction.     

MicroRNA-21 accelerates hepatocyte proliferation in vitro via PI3K/Akt signaling by targeting PTEN

MicroRNAs (miRNAs) are involved in controlling hepatocyte proliferation during liver regeneration. In this study, we established the miRNAs-expression patterns of primary hepatocytes in vitro under stimulation of epidermal growth factor (EGF), and found that microRNA-21 (miR-21) was appreciably up-regulated and peaked at 12 h. In addition, we further presented evidences indicating that miR-21 promotes primary hepatocyte proliferation through in vitro transfecting with miR-21 mimics or inhibitor. We further demonstrated that phosphatidylinositol 3′-OH kinase (PI3K)/Akt signaling was altered accordingly, it is, by targeting phosphatase and tensin homologue deleted on chromosome 10, PI3K/Akt signaling is activated by miR-21 to accelerate hepatocyte rapid S-phase entry and proliferation in vitro.     

Regulation of vascular smooth muscle cell proliferation by nuclear orphan receptor Nur77

Endothelium-derived nitric oxide (NO) is a cytoprotective molecule to prevent endothelial cells (ECs) from apoptosis. CREB-binding protein (CBP) is involved in the apoptotic pathway in several tumor cells, however, little is known whether CBP is associated with apoptosis in ECs and the apoptotic effect of CBP on ECs is regulated by NO. Therefore, the purpose of the present study was to investigate whether silencing CBP expression could affect the sensitivity of ECs toward apoptotic stimuli and determined the role of NO. In this study, we found that when CBP expression was silenced by RNA interference, ECs were more prone to apoptosis under serum deprivation, whereas the apoptosis was not significantly induced in the serum-containing condition. The increased apoptosis is paralleled by a reduction of NO, and the apoptosis was reversed by NO donors, suggesting an important role of NO. Furthermore, CBP silencing decreased NO production by downregulating the endothelial NO synthase (eNOS) expression in a dose-dependent manner. These results indicated that CBP silencing is associated with decreased eNOS expression and NO production, and therefore concomitantly increased the sensitivity of ECs toward apoptosis.     

Biodelignification of rice straw by <Emphasis Type="Italic">Phanerochaete chrysosporium</Emphasis> in the presence of dirhamnolipid

Lignin degradation by white-rot fungi has received considerable attention as a means for reducing accumulation of lignocellulosic wastes in the environment. The stimulatory effect of surfactants on fungal lignocellulose bioconversion also has attracted wide interest. In this study the influence of dirhamnolipid biosurfactant on biodegradation of rice straw by Phanerochaete chrysosporium was investigated. It was shown that the biodelignification process of rice straw can be significantly enhanced by the presence of dirhamnolipid biosurfactant. In particular, the dirhamnolipid at the concentration of 0.007% increased the peak activity of lignin peroxidase (LiP) by 86% without affecting the manganese peroxidase (MnP) activity. The water-soluble organic carbon (WSOC) contents in the straw substrates as well as the microbial growth and activity were effectively improved by dirhamnolipid, while the degradation rate of lignin increased by 54% with dirhamnolipid of 0.007%. Observed chemical structural and morphological changes showed that the straw substrates were delignified in the presence of dirhamnolipid with the formation of terrace-like fragments separated from the inner cellular fibers and the release of simple compounds. Variation partitioning analysis revealed that the dirhamnolipid addition induced a significant straw biodelignification which explained 22.1% (P = 0.013) of the variance.