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Our attention is known to be intrinsically variable over time, especially when divided over multiple sources of information. Individuals differ in their ability to divide and focus attention on relevant information, so it is important to know which factors play a role in this ability, whether it can be trained or reflects fundamentally limitations that cannot be overcome. Typically, most people have great difficulty to identify the second of two targets when presented within 500 ms, a phenomenon known as the attentional blink (AB). We found evidence that the AB can be diminished by training one’s ability to time attention, but this learning ability is dependent on emotional disposition (depression) which was reflected in beta-gamma oscillation as measured with EEG. In a subsequent study, it was found that the oscillatory nature of attention can account for individual differences, explaining why some people show a large attentional blink (i.e. large blinkers) while others show no restrictions whatsoever (non-blinkers). We finally considered the self-relevance of the presented stimuli in the AB task. We revealed a processing advantage for highly self-relevant stimuli, which interestingly came at either a subsequent cost or benefit in temporal attention, dependent on one’s mental disposition. In conclusion, the current thesis could shed new light on the fundamental processing of temporal attention, suggesting that temporal attention is oscillatory and trainable, and can be modulated by depression. Our robust findings have the potential to be helpful in the preliminary screening and diagnosis of depression.

Yuan-Run Deng,1* Xiao-Jing Chen,2* Wei Chen,1 Lan-Fang Wu,1 Hui-Ping Jiang,1 Dan Lin,1 Li-Jing Wang,1 Wei Wang*,2,3 Sui-Qun Guo1,1Department of Obstetrics and Gynecology, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China; 2Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China; 3Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, People’s Republic of China*These authors contributed equally to this work Background/aims: Radioresistance remains a significant obstacle in the therapy of cervical cancer, and the mechanism of it is still unclear. We aimed to investigate the role of specificity protein 1 (Sp1) in radioresistance of cervical cancer.Methods: Sp1 was examined immunohistochemically on tissues from 36 human cervical cancer patients. We used RT-qPCR and Western blot to examine the expression of Sp1 in irradiated cervical cancer cell lines SiHa and HeLa. The role of Sp1 in radioresistance of cervical cancer cells was assessed by colony-formation assay and cell cycle analysis. Dual-luciferase reporter assay was performed to detect the downstream of Sp1.Results: High Sp1 expression was positively correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and lymphovascular space invasion (LVSI) of cervical cancer. The expression of Sp1 was dose-dependently increased in irradiated cervical cancer cell lines at both mRNA and protein levels. Colony-formation assay showed that alteration of Sp1 expression affected the survival of cervical cancer cells with radiotherapy (RT) treatment. Knockdown of Sp1 significantly strengthened the cellular response to radiation by inducing G2/M arrest in cervical cancer cells. Overexpression of Sp1 significantly decreased G2/M arrest in cervical cancer cells, which was related to upregulation of CDK1 expression. Dual-luciferase reporter assay showed the direct effect of Sp1 on the transcriptional activation of CDK1.Conclusion: Sp1 may contribute to radioresistance through inhibiting G2/M phase arrest by targeting CDK1, and be considered as a potential therapeutic target to promote the effect of RT for patients with cervical cancer.Keywords: cervical cancer, Sp1, radioresistance, G2/M phase, CDK1

NF-kappaB (NF-κB) signaling is involved in regulating a great number of normal and abnormal cellular events. However, little is known about its role in ovarian follicular development. In this study, we found NF-κB signaling is activated during the transition from secondary to antral follicles. We generated active NF-κB mice and found that antral follicular numbers were higher than wild-types ovaries. Activation of NF-κB signaling could enhance granulosa cell proliferation and regress granulosa cell apoptosis of mouse ovarian follicles. Higher FSHR and LHCGR expressions were observed in active NF-κB ovaries compared to wild-type. Furthermore, we confirmed that NF-κB signaling was indeed involved in the granulosa cell viability and proliferation through FSHR using COV434 cell line. This is the first experimental evidence that NF-κB signaling is implicated in the control of follicular development through FSHR and its corresponding target molecules, which might be achieved by targeting proliferation and apoptosis in follicular granulosa cells.