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The aquaculture industry in China is not complete without the freshwater industry. The scientific assessment of the regional competitiveness of the freshwater aquaculture industry has significant theoretical and practical implications for fostering the industry's sustainable development. Based on the diamond model, this study developed a competitiveness evaluation index system for Chinese freshwater aquaculture industry which included six primary indicators and sixteen secondary indicators. The primary indicators included resource endowment, production capacity, science and technology promotion capacity, related and supporting industries, market demand and guiding development policy. The study analyzed freshwater aquaculture industrial competitiveness during 2012-2020 and classified the Chinese 18 major freshwater aquaculture provinces into five competitive levels. The results showed that the development of related and supporting industries has the greatest contribution to the competitiveness, followed by resource endowment and market demand capacity. The analysis and tier classification showed that the competitiveness of Jiangsu Province and Hubei Province has always been at the forefront, and the province of Guangdong, Fujian, Hunan, Jiangxi, Zhejiang, Anhui, Liaoning, and Guangxi were above the middle level. Moreover, the results indicated that the competitiveness of most provinces showed an upward trend. [ABSTRACT FROM AUTHOR]

A novel dynamic multistage hybrid swarm intelligence optimization algorithm is introduced, which is abbreviated as DM-PSO-ABC. The DM-PSO-ABC combined the exploration capabilities of the dynamic multiswarm particle swarm optimizer (PSO) and the stochastic exploitation of the cooperative artificial bee colony algorithm (CABC) for solving the function optimization. In the proposed hybrid algorithm, the whole process is divided into three stages. In the first stage, a dynamic multiswarm PSO is constructed to maintain the population diversity. In the second stage, the parallel, positive feedback of CABC was implemented in each small swarm. In the third stage, we make use of the particle swarm optimization global model, which has a faster convergence speed to enhance the global convergence in solving the whole problem. To verify the effectiveness and efficiency of the proposed hybrid algorithm, various scale benchmark problems are tested to demonstrate the potential of the proposed multistage hybrid swarm intelligence optimization algorithm. The results show that DM-PSO-ABC is better in the search precision, and convergence property and has strong ability to escape from the local suboptima when compared with several other peer algorithms. [ABSTRACT FROM AUTHOR]

A biodegradable polymer network hydrogel with both hydrophobic and hydrophilic components was synthesized and characterized. The hydrophobic and hydrophilic components were a three-arm poly(ε-caprolactone) maleic acid (PGCL-Ma, as the hydrophobic constituent) and poly(ethylene glycol) diacrylate macromer (PEGDA, as a hydrophilic constituent), respectively. These two polymers were chemically photo-crosslinked to generate a three-dimensional network structure, which were characterized by FT-IR, DSC and SEM. The swelling property of the networks was studied in phosphate-buffered saline (PBS, pH 7.4). The results of this study showed that a wide-range swelling property was obtained by changing the composition ratio of PGCL-Ma to PEGDA. The in vitro release of bovine serum albumin (BSA) from these hydrogels as a function of the PEGDA to PGCL-Ma composition ratio and incubation time was examined and we found that the incorporation of PEGDA into PGCL-Ma increased the initial burst release of BSA. As the PEGDA component increased, the rate of formation of a loose three-dimensional (3D) network structure increased; consequently, the sustained rate and extent of BSA release increased. We suggest that the release of BSA was controlled by both diffusion of BSA through swelling of the hydrophilic phase during an early stage and degradation of the hydrophobic phase during a late stage; and that the relative magnitude of diffusion versus degradation controlled release depended on composition ratio and immersion time. [ABSTRACT FROM AUTHOR]

In this work, titanomagnetite was used as a heterogeneous Fenton catalyst for the degradation of methylene blue (MB). The degradation of MB on synthetic titanomagnetite at neutral pH values was studied in comparison with the adsorption of MB on titanomagnetite using UV−vis, FTIR, and the analyses of element C on titanomagnetite and DOC in reaction solution. Meanwhile, important factors affecting catalytic activity were investigated, that is, titanomagnetite load, H2O2concentration, and reaction temperature. Titanomagnetite decomposed H2O2yielding highly reactive hydroxyl radicals, and MB adsorbed on titanomagnetite was degraded. With the increases of titanomagnetite load, H2O2concentration, and reaction temperature, the degradation of MB was promoted. Moreover, titanomagnetite was proved to be durable with a stable MB removal efficiency after five consecutive cycles. [ABSTRACT FROM AUTHOR]

The high prevalence and long latency period of prostate cancer (PCa) provide a unique opportunity to control disease progression with dietary and nutraceutical approaches. We developed ProFine, a standardized composition of luteolin, quercetin, and kaempferol, and investigated its potential as a nutraceutical for PCa in preclinical models. The three ingredients of ProFine demonstrated synergistic in vitro cytotoxicity and effectively induced apoptosis in PCa cells. ProFine markedly affected the transcriptome of PCa cells, suppressed the expression of androgen receptor, and inhibited androgen-regulated genes. Oral administration of ProFine did not exhibit obvious toxicities in mice, and the three ingredients retained their individual pharmacokinetic and bioavailability profiles. Importantly, ProFine significantly retarded the growth of PCa xenografts in athymic nude mice and extended the survival of animals. This study provides preclinical evidence supporting the promise of ProFine as a safe, efficacious, and affordable intervention to control PCa progression and improve clinical outcomes. [ABSTRACT FROM AUTHOR]

Aberrant expression of EGF receptors has been associated with hormone-refractory and metastatic prostate cancer (PCa). However, the molecular mechanism for EGF signaling in promoting PCa metastasis remains elusive. Using experimental models of PCa metastasis, we demonstrated that EGF could induce robust epithelial-mesenchymal transition (EMT) and increase invasiveness. Interestingly, EGF was found to be capable of promoting protein turnover of epithelial protein lost in neoplasm (EPLIN), a putative suppressor of EMT and tumor metastasis. Mechanistic study revealed that EGF could activate the phosphorylation, ubiquitination, and degradation of EPLIN through an extracellular signal-regulated kinase 1/2 (ERK1/2)-dependent signaling cascade. Pharmacological inhibition of the ERK1/2 pathway effectively antagonized EGF-induced EPLIN degradation. Two serine residues, i.e. serine 362 and serine 604, were identified as putative ERK1/2 phosphorylation sites in human EPLIN, whose point mutation rendered resistance to EGF-induced protein turnover. This study elucidated a novel molecular mechanism for EGF regulation of EMT and invasiveness in PCa cells, indicating that blockade of EGF signaling could be beneficial in preventing and retarding PCa metastasis at early stages. [ABSTRACT FROM AUTHOR]

Background: Aberrant platelet derived growth factor (PDGF) signaling has been associated with prostate cancer (PCa) progression. However, its role in the regulation of PCa cell growth and survival has not been well characterized. Methodology/Principal Findings: Using experimental models that closely mimic clinical pathophysiology of PCa progression, we demonstrated that PDGF is a survival factor in PCa cells through upregulation of myeloid cell leukemia- 1 (Mcl-1). PDGF treatment induced rapid nuclear translocation of β-catenin, presumably mediated by c-Abl and p68 signaling. Intriguingly, PDGF promoted formation of a nuclear transcriptional complex consisting of β-catenin and hypoxiainducible factor (HIF)-1α, and its binding to Mcl-1 promoter. Deletion of a putative hypoxia response element (HRE) within the Mcl-1 promoter attenuated PDGF effects on Mcl-1 expression. Blockade of PDGF receptor (PDGFR) signaling with a pharmacological inhibitor AG-17 abrogated PDGF induction of Mcl-1, and induced apoptosis in metastatic PCa cells. Conclusions/Significance: Our study elucidated a crucial survival mechanism in PCa cells, indicating that interruption of the PDGF-Mcl-1 survival signal may provide a novel strategy for treating PCa metastasis. [ABSTRACT FROM AUTHOR]

A series of nanosized (Fe3-xMnx)1-δO4 (x = 0, 0.2, 0.5, and 0.8) were synthesized for elemental mercury capture from the flue gas. Cation vacancies on (Fe3-xMnx)1-δO4 can provide the active sites for elemental mercury adsorption, and Mn4+ cations on (Fe3-xMnx)1-δO4 may be the oxidizing agents for elemental mercury oxidization. With the increase of Mn content in the spinel structure, the percents of Mn4+ cations and cation vacancies on the surface increased. As a result, elemental mercury capture by (Fe3-xMnx)1-δO4 was obviously promoted with the increase of Mn content. (Fe2.2Mn0.8)1-δO4 showed an excellent capacity for elemental mercury capture (>1.5 mg g-1 at 100-300 °C) in the presence of SO2 and HCl. Furthermore, (Fe2.2Mn0.8)1-δO4 with the saturation magnetization of 45.6 emu g-1 can be separated from the fly ash using magnetic separation, leaving the fly ash essentially free of sorbent and adsorbed Hg. Therefore, nanosized (Fe2.2Mn0.8)1-δO4 may be a promising sorbent for the control of elemental mercury emission. [ABSTRACT FROM AUTHOR]

Background: Myeloid cell leukemia-1 (Mcl-1) is a member of the Bcl-2 family, which inhibits cell apoptosis by sequestering pro-apoptotic proteins Bim and Bid. Mcl-1 overexpression has been associated with progression in leukemia and some solid tumors including prostate cancer (PCa). However, the regulatory mechanism for Mcl-1 expression in PCa cells remains elusive. Results: Immunohistochemical analyses revealed that Mcl-1 expression was elevated in PCa specimens with high Gleason grades and further significantly increased in bone metastasis, suggesting a pivotal role of Mcl-1 in PCa metastasis. We further found that vascular endothelial growth factor (VEGF) is a novel regulator of Mcl-1 expression in PCa cells. Inhibition of endogenous Mcl-1 induced apoptosis, indicating that Mcl-1 is an important survival factor in PCa cells. Neuropilin-1 (NRP1), the "co-receptor" for VEGF165 isoform, was found to be highly expressed in PCa cells, and indispensible in the regulation of Mcl-1. Intriguingly, VEGF165 promoted physical interaction between NRP1 and hepatocyte growth factor (HGF) receptor c-MET, and facilitated c-MET phosphorylation via a NRP1-dependent mechanism. VEGF165 induction of Mcl-1 may involve rapid activation of Src kinases and signal transducers and activators of transcription 3 (Stat3). Importantly, NRP1 overexpression and c-MET activation were positively associated with progression and bone metastasis in human PCa specimens and xenograft tissues. Conclusions: This study demonstrated that Mcl-1 overexpression is associated with PCa bone metastasis. Activation of VEGF165-NRP1-c-MET signaling could confer PCa cells survival advantages by up-regulating Mcl-1, contributing to PCa progression. [ABSTRACT FROM AUTHOR]

Prostatic glandular epithelial cells express protein kinase C? (PKC?), an oncoprotein that coordinately disrupts the reactivation of the tumor suppressor Rb, derepressess transcriptional elongation of the c-myc oncogene, and propagates survival signals in LNCaP cells. Since the activation of such a program may contribute to the progression of human prostate cancer, a proteomic analysis was performed to gain a more global perspective on the signaling network that PKC? might be capable of engaging in prostate cancer cells. Using CWR22 xenografts, we identified at least 18 different structural, signaling, and stress-related proteins that associated with PKC?, including an interaction with the proapoptotic protein Bax that was novel to recurrent CWR22 tumors. An investigation into the biological significance of the PKC? association with Bax provided the first evidence of an inverse relationship between endogenous levels of PKC? and susceptibility of prostate cancer cells to the apoptotic effects of phorbol esters. Western blot and antisense experiments demonstrated that CWR-R1 cells expressed moderate levels of PKC? and relied on this protein to survive in the presence of phorbol esters, while the apoptosis normally induced by phorbol esters in PKC?-deficient LNCaP cells was dependent on the presence of Bax. Forced expression of PKC? in LNCaP cells was sufficient to confer a significant resistance to phorbol esters and this resistance was associated with an inhibition of phorbol ester-induced Bax conformational rearrangements that are important for Bax oligomerization, mitochondrial integration, and cytochrome c release. Considered in their entirety, our data suggest that an association of PKC? with Bax may neutralize apoptotic signals propagated through a mitochondrial death-signaling pathway.Oncogene (2003) 22, 6014-6024. doi:10.1038/sj.onc.1206795 [ABSTRACT FROM AUTHOR]