Chinese Cyber Nationalism: The 2012 Diaoyu Islands Dispute on Sina Weibo

The dissertation examined the dynamics of the 2012 Diaoyu Islands dispute on Sina Weibo across three layers: users, content, and role of platform. At the user layer, the research identifies the prominent users as elite framers on Weibo, whose discussions on the dispute dominated the framing of the issue. The most influential users are identified as predominately urban, middle class, more educated males, implying a profound inequality in the power to drive and direct the discourses on Weibo or in contemporary Chinese society. At the content layer, the dissertation discovers the major topics and frames that emerged from the discussion. It identified 11 topics via a labeled LDA topic model and then consolidated them into three major frames of Chinese cyber nationalism: nonofficial, official, and relational nationalism frames. The interactions among the social groups using the three major frames demonstrated that Chinese cyber nationalism inherited and strategically adopted the cyber nationalistic discourse from the pre-social media era; however, the dissertation found a contrasting and reconciling cyber nationalism advocated by the opinion leaders which mediated between official and popular nationalism in China. Third, the dissertation explored the roles of Weibo in the islands dispute and sought further theorization of the online space in China. As the dissertation identifies the proliferation of the “duanzi” culture among the Weibo users on the discussion of national affairs, it challenges the line of researches which only concentrate on the surveillance and censorship dynamics in Chinese internet study. A dark side of Weibo has been uncovered in the permission and promotion of fake news and misinformation on Weibo, as found elsewhere in the resurgence of nationalistic sentiments and national politics in the world. This dissertation represents the first framing study of Chinese cyber nationalism on social media. The dual rise of cyber nationalism and social media in China is not an isolated, discrete, and fragmented episode of global politics. This dissertation provides a comprehensive picture of the social players, their discourses, and power dynamics in a national/international affair of the century-long Diaoyu Islands dispute, one of the most explosive national security conflicts in the world

"Privacy" in Semantic Networks on Chinese Social Media: The Case of Sina Weibo

Unprecedented social and technological developments call into question the meanings and boundaries of privacy in contemporary China. This study examines the discourse of privacy on Sina Weibo, the country's largest social medium, by performing a semantic network analysis of 18,000 postings containing the word (privacy). The cluster analysis identifies 11 distinct yet organically related concept clusters, each representing a unique dimension of meaning of the complex concept. The interpretation of the findings is situated in the discussion of the rapidly evolving private realm in relation to emerging new contexts of the public realm. Privacy, justified for both its instrumental functions and intrinsic values, both reflects and constitutes new forms of sociality on the sociotechno space of Weibo

Carbon Nanotubes with Tailored Density of Electronic States for Electrochemical Applications

The density of electronic states (DOS) is an intrinsic electronic property that works conclusively in the electrochemistry of carbon materials. However, seldom has it been reported how the DOS at the Fermi level influences the electrochemical activity. In this work, we synthesized partially and fully unzipped carbon nanotubes by longitudinally unzipping pristine carbon nanotubes (CNTs). We then studied the electrochemical activity and biosensitivity of carbon materials by means of the CNTs and their derivatives to elucidate the effect of the DOS on their electrochemical performances. Tailoring of the DOS for the CNT derivatives could be conveniently realized by varying the sp²/sp³ ratio (i.e., graphite concentration) through manipulating the oxidative unzipping degree. Despite the diverse electron transfer mechanisms and influence factors of the four investigated redox probes (IrCl₆^2–, [Fe­(CN)₆]^3–, Fe³⁺, and ascorbic acid), the CNT derivatives exhibited consistent kinetic behaviors, wherein CNTs with a high DOS showed superior electrochemical response compared with partially and fully unzipped carbon nanotubes. For biological detection, the CNTs could simultaneously distinguish ascorbic acid, dopamine, and uric acid, while the three CNT derivatives could all differentiate phenethylamine and epinephrine existed in the newborn calf serum. Moreover, the three CNT derivatives all presented wide linear detection ranges with high sensitivities for dopamine, phenethylamine, and epinephrine

Mildly Alkaline Preparation and Methylene Blue Adsorption Capacity of Hierarchical Flower-like Sodium Titanate

The hydrothermal preparation of flower-like layered sodium titanate architectures in a weakly alkaline medium is reported. NaCl was used as a morphology-directing agent, and a growth mechanism was proposed. The hierarchical structure is assembled from one-dimensional nanoribbons and exhibits an excellent removal capacity toward methylene blue (MB). A pseudo-second-order kinetic model was found to well describe the adsorption kinetics. Kinetic studies demonstrated that the overall rate of MB adsorption was controlled by surface adsorption and intraparticle diffusion. Results of this work are of great significance for environmental applications of flower-like layered sodium titanate architectures as a promising adsorbent material used for water purification

Cost-Effective Asymmetric Supercapacitors Based on Nickel Cobalt Oxide Nanoarrays and Biowaste-Derived Porous Carbon Electrodes

Two nanostructured electrode materials are fabricated and used to construct cost-effective asymmetric supercapacitors (ASCs). Hierarchical nickel cobalt oxide nanoarrays (NCO-NA) consisting of nanosheets (NCO-NS) or nanowires (NCO-NW) are uniformly grown on Ni foam by a simple, effective, and generally applicable method, while biowaste-derived hierarchical porous carbon (Bio-HPC) with an interconnected microstructure is fabricated by pretreatment with potassium hydroxide and followed by direct pyrolysis. Considering the mass of NiCo₂O₄, the maximum specific capacitance of the hierarchical NCO-NS and NCO-NW electrodes are 2300 and 2333 F g^–1, respectively, and the specific capacitance of the Bio-HPC electrode is 253.9 F g^–1 at a scan rate of 5 mV s^–1. NCO-NA, Bio-HPC, a piece of polypropylene membrane, and 30 wt % KOH solution are assembled into a high-performance, low-cost ASC with the capability of rapidly storing electrical energy. The NCO-NW//Bio-HPC ASC exhibits a higher energy density compared with NCO-NS//Bio-HPC ASC, while the latter shows better cycling performance (the capacitance still remains 91.12% after 2000 cycles)

Additional file 2: Figure S1. of Regulation of TRIM24 by miR-511 modulates cell proliferation in gastric cancer

Quantification of TRIM24 protein expression after indicated transfection. (DOCX 102 kb

Par-1 functionally interacts with the components of the Hpo pathway.

<p>(A–B′) Loss of Par-1 induced a phenotype that was suppressed by Yki overexpression. The protein levels of DIAP1 in the wing discs expressing <i>UAS-Par-1 RNAi</i> (A–A′) or coexpressing <i>UAS-Yki</i> and <i>UAS-Par-1 RNAi</i> (B–B′) with <i>hh-Gal4</i> were detected. Note that Yki overexpression overcame the inhibitory effect of Par-1 RNAi on <i>diap1</i> expression. The arrows indicate the P-compartment. (C) Par-1 inhibits Yki phosphorylation. S2 cells were transfected with the indicated constructs. Phosphorylated Yki was detected using the p-Yki antibody, which recognizes the phosphorylated site of Yki at Ser168. (D–E′) <i>ex</i> functions upstream of <i>par-1</i> in the Hpo pathway. Wing discs expressing <i>UAS-ex RNAi</i> (D–D′) or coexpressing <i>UAS-ex RNAi</i> and <i>UAS-Par-1 RNAi</i> (E–E′) with <i>hh-Gal4</i> were subjected to immunostaining. The transgene expression regions were marked by the lack of Ci (red) staining and are indicated by arrows. Note that ex RNAi expression resulted in an enlarged P-compartment and increased expression of <i>diap1-GFP 3.5</i>, whereas coexpression with Par-1 RNAi fully suppressed these phenotypes. (F–F′″) <i>wts</i> functions downstream of <i>par-1</i> in the Hpo pathway. Clones were generated using the MARCM system. The genotypes were the following: <i>ey-flp, Ubi-Gal4, UAS-GFP; FRT82B/FRT82B Gal80</i> (F), <i>ey-flp, Ubi-Gal4, UAS-GFP; Par-1-RNAi; FRT82B/FRT82B Gal80</i> (F′), e<i>y-flp, Ubi-Gal4, UAS-GFP; Par-1-RNAi; FRT82B wts^latsX1</i>/<i>FRT82B Gal80</i> (F″), and <i>ey-flp, Ubi-Gal4, UAS-GFP; FRT82B wts^latsX1</i>/<i>FRT82B Gal80</i> (F′″). Note that Par-1 RNAi reduced the clone size, whereas <i>wts^latsX1</i> rescued this phenotype. (G) Quantification of the relative clone size. The relative clone size was calculated as the GFP area divided by the entire disc area. All of these data were expressed as the mean ± SEM. **<i>p</i><0.01. **<i>p</i><0.001. <i>n</i>>5, for each group. (H) Par-1 modulates Wts phosphorylation status. S2 cells were transfected with the indicated plasmids. The cell lysates were harvested and followed by Western blot analysis. Note that the phosphorylation shift of Wts mediated by Hpo/Sav/Merlin/Tao-1 was partially blocked by Par-1 expression. The shifted Wts bands are indicated by the small circles. (I–I″) <i>par-1</i> functions upstream of <i>hpo</i> in the Hpo pathway. Clones were generated using the MARCM system. The genotypes were the following: <i>eyflp, ubi-Gal4, UAS-GFP; FRT42D/FRT42D Gal80</i> (I), <i>eyflp, ubi-Gal4, UAS-GFP; FRT42D hpo^BF33/FRT42DGal80</i> (I′), e<i>yflp, ubi-Gal4, UAS-GFP; FRT42D hpo^BF33/FRT42DGal80; Par-1-RNAi</i> (I″). Note that the Hpo null clones caused tumorous growth, whereas Par-1 RNAi could not rescue this phenotype.</p

Par-1 P-element insertion lines enlarge organ size and promote Hpo pathway-responsive gene expression.

<p>(A–B′) An EP line L[484] enhanced the Yki gain-of-function induced phenotype. Side views of <i>D. melanogaster</i> wild-type eyes (A), eyes expressing L[484] (B), eyes expressing Yki (A′), or eyes co-expressing L[484] and Yki (B′), driven by <i>GMR-Gal4</i>. (C) Schematic representation of the <i>par-1</i> gene locus and P-element insertion sites. The insertion sites of the L[484], L[507], and F[727] EP lines are at the 5′ UTR region of the Par-1 gene (marked by orange arrows). The <i>par-1</i> locus is located between <i>mei-W68</i> and <i>hpo</i>. (D–D″) L[484] promotes adult fly wing growth. Control adult fly wings (D) and wings expressing L[484] (D′) with the wing-specific driver <i>MS1096</i>. The red dashed line indicates the size of the control wing. The relative wing size was quantified using an unpaired <i>t</i>-test (D″). The results represent the mean ± SEM. ***<i>p</i><0.001 (<i>n</i>>6) for each genotype. (E) Expression of L[484] significantly increased the mRNA levels of Par-1. To detect the level of Par-1 and the transcripts of its neighboring genes, a real-time PCR analysis was performed. All of the results were expressed as the mean ± SEM.*<i>p</i><0.05, **<i>p</i><0.01. (F–G′) L[484] promotes <i>expanded</i> gene expression. Wild-type <i>D. melanogaster</i> third-instar larval wing discs (F) or wing discs expressing L[484] (G–G′) with <i>hh-Gal4</i> were immunostained to demonstrate the expression of <i>Cubitus</i> (Ci) (Red) and Ex-LacZ (EX-Z) (green). Ci marked the anterior compartment (A-compartment). The arrows indicate the P-compartment. (H–H″) L[484] elevates <i>diap1</i> gene expression. Wing discs containing flip-out clones expressing L[484] with <i>act</i>><i>CD2</i>><i>Gal4</i> were immunostained to demonstrate the expression of CD2 (red) and <i>diap1-lacZ</i> (green). Cells expressing L[484] were indicated by the lack of CD2 expression (indicated by arrows).</p

Par-1 interacts with Hpo-Sav and regulates the phosphorylation of Hpo at Ser30.

<p>(A–B) Par-1 interacts with Hpo and Sav <i>in vitro</i>. S2 cells were transfected with HA-tagged full-length or truncated Par-1 and Hpo (A) or Sav (B) constructs. The cell lysates were immunoprecipitated, followed by Western blot analysis with the indicated antibodies. Note that weak binding (asterisk indicated) between full-length Par-1/Par-1-C and Hpo and Sav were detected, whereas the N-terminal truncation of Par-1, which contained the kinase domain, showed a much stronger interaction signal. (C) Par-1 induces phosphorylation shift of Hpo-KD <i>in vitro</i>. S2 cells were transfected with the indicated constructs. The cell lysates were subjected to phosphorylation mobility shift assays. Note the phosphorylation shift of Hpo-KD in the presence of Par-1. Phos-tag was used to enhance the phosphorylation shift (see <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1001620#s4" target="_blank">Materials and Methods</a> for further details). (D) Par-1 regulates phosphorylation of Hpo-KD at Ser30 in S2 cells. S2 cells were transfected with the indicated constructs. The cell lysates were subjected to a phosphorylation mobility shift assay. The Hpo Ser30 site was mutated to an alanine. Note that the Hpo(S30A) mutant did not shift in the presence of Par-1. (E–F) Par-1 induces the phosphorylation of Hpo-KD at Ser30 in S2 cells. S2 cells were transfected with the indicated constructs. The cell lysates were subjected to Western blot analyses. Note that the phospho Hpo(Ser30) antibody could only detect Par-1-induced phosphorylation in the Hpo-KD samples but not in the Hpo(Ser30) mutant samples. The asterisks indicate non-specific bands. Lambda-PP indicates λ-phosphatase. (G) Par-1 inhibits Hpo(Thr195) phosphorylation. S2 cells were transfected with the indicated constructs. The cell lysates were immunoprecipitated, followed by Western blot analyses to detect p-Hpo(Thr195) levels. Note that Par-1 inhibited Hpo(Thr195) phosphorylation in a kinase-dependent manner, whereas the Hpo(S30A) mutant could not be inhibited. (H) Quantification of p-Hpo(Thr195) levels. p-Hpo(Thr195) levels were quantified using densitometry. The results were expressed as the mean ± SEM from three independent experiments. *<i>p</i><0.05. (I) Hpo(S30A) results in a higher phosphorylation shift of Yki. S2 cells were transfected with the indicated constructs. The cell lysates were subjected to a phosphorylation mobility shift assay. Note that the phosphorylation shift of Yki was enhanced in the presence of Hpo(S30A) and that the Hpo(S30A) mutant was resistant to Par-1 induced Yki dephosphorylation. (J–K) Hpo(S30A) shows enhanced activity compared with wild-type Hpo <i>in vivo</i>. Control wings (J) or wings expressing <i>UAS-Hpo</i> (J′) or <i>UAS-Hpo(S30A)</i> (J″) with <i>C765</i> were shown. The relative wing size was quantified using an unpaired <i>t</i>-test (K). The results represented the mean ± SEM.*<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001 (<i>n</i>>6) for each genotype. Note that the Hpo(S30A) flies exhibited smaller wings than the Hpo flies.</p

Par-1 disrupts the association of the Hpo-Sav complex in a kinase-dependent manner.

<p>(A) Par-1 could destabilize Hpo-induced accumulation of Sav in a kinase-dependent manner. S2 cells were transfected with the indicated constructs followed by a Western blot analysis. CFP served as a loading control. (B) Par-1 inhibits the phosphorylation of Sav induced by Hpo. The mobility shift assay was employed. The loading volume was adjusted according to the total Sav protein level. (C) Par-1 disrupts the interaction of the Hpo-Sav complex. S2 cells were transfected with the indicated constructs followed by immunoprecipitation to test whether the interaction between Sav and endogenous Hpo was affected by Par-1. Note that less Sav interacted with Hpo in the presence of Par-1. (D–D″) Par-1 RNAi is incapable of inhibiting <i>sav</i> mutant-induced adult eye overgrowth. The clones were generated using the MARCM system. The genotypes are as following: <i>eyflp, ubi-Gal4, UAS-GFP; FRT82B/FRT82BGal80</i> (D), e<i>yflp, ubi-Gal4, UAS-GFP; FRT82B Sav^SH13</i>/<i>FRT82B Gal80</i> (D′), and <i>eyflp, ubi-Gal4, UAS-GFP; Par-1-RNAi; FRT82B Sav^SH13</i>/<i>FRT82B Gal80</i> (D″). (E) The proposed mechanism of Par-1 regulation of the Hpo pathway (see text for further detail).</p