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كيف يحكم الحزب الشيوعي الصيني
مع التغيرات التاريخية وتقلبات الزمن، ظل العالم يتساءل : من أين جاءت مكانة الحزب الشيوعي الصيني في قلوب الصينيين والعالم ؟ وكيف حاز ثقة الصينيين وتأييدهم ؟ وكيف يتغلب على الصعاب ؟ وكيف يقود الصين في ثبات لبدء رحلة الاشتراكية التحديثية الجديدة، مواجهة التغير العميق لأوضاع العالم والدولة والحزب ؟ يجيب هذا الكتاب على هذه التساؤلات عبر جوانب مختلفة من وجهات النظر ويدقق النظر ويستقصي أمور الحزب الشيوعي الصيني، فيرصد أفعاله ويبحث أقواله ويحلل إنجازاته خلال هذا الوقت الذي اقترب فيه من تحقيق النهضة العظيمة للأمة الصينية أكثر من أي فترة على مر التاريخ وذلك بتمشيط الحقب والخبرات التي مر بها الحزب الشيوعي الصيني خلال توليه الحكم.
BOOK
Assessing Climate Forcing From the Sea Surface Temperature‐Surface Heat Flux Relation for SST‐Coupled Oscillatory Variability
The interaction between sea surface temperatures (SST) and surface heat flux (SHF) is vital for atmospheric and oceanic variabilities. This study investigates SST‐SHF relationship in the framework of a coupled oscillatory model, extending beyond previous research that predominantly used AR‐1 type simple stochastic climate models. In contrast to the AR‐1 type model, we reveal distinct features of SST‐SHF relationships in the oscillatory model: sign reversals occur in the imaginary part of SST‐SHF coherence and the low‐pass SST tendency‐SHF correlation. However, these sign reversals are absent in the real part of SST‐SHF coherence and in the low‐pass SST‐SHF correlation. We find these features are robust across both the twentieth Century Reanalysis and GFDL SPEAR model for El Niño‐Southern Oscillation (ENSO) variability. Furthermore, we develop a new scheme to assess ENSO's climate forcing magnitude and natural frequency. Our findings thus provide novel insights into understanding ENSO dynamics from the perspective of heat flux.
Plain Language Summary
Understanding the interaction between sea surface temperature and the heat exchange between the ocean and atmosphere is crucial for predicting weather and climate patterns. Traditionally, this interaction is understood in the AR‐1 framework of stochastic model. Here, we extend the theory on sea surface temperature and surface heat flux (SHF) relation to a more advanced oscillatory model. Our new theory suggests distinct features in the sea surface temperature and SHF relationship, in contrast to those in the previous studies. These novel features are crucial for inferring climate forcing magnitude and natural frequency of the El Niño‐Southern Oscillation (ENSO). This theory sheds new light on the dynamics of ENSO variability particularly from the perspective of heat flux.
Key Points
Advanced idealized model uncovers distinct sea surface temperatures (SST)‐surface heat flux (SHF) relationship patterns
Sign reversals observed in SST tendency‐SHF correlation and SST‐SHF coherence's imaginary part
Novel schemes for assessing climate forcing magnitude and natural frequency of oscillatory variability
Journal Article
Cancer‐associated fibroblast‐derived exosomal microRNA‐24‐3p enhances colon cancer cell resistance to MTX by down‐regulating CDX2/HEPH axis
MicroRNA‐24‐3p (miR‐24‐3p) has been implicated as a key promoter of chemotherapy resistance in numerous cancers. Meanwhile, cancer‐associated fibroblasts (CAFs) can secret exosomes to transfer miRNAs, which mediate tumour development. However, little is known regarding the molecular mechanism of CAF‐derived exosomal miR‐24‐3p in colon cancer (CC). Hence, this study intended to characterize the functional relevance of CAF‐derived exosomal miR‐24‐3p in CC cell resistance to methotrexate (MTX). We identified differentially expressed HEPH, CDX2 and miR‐24‐3p in CC through bioinformatics analyses, and validated their expression in CC tissues and cells. The relationship among HEPH, CDX2 and miR‐24‐3p was verified using ChIP and dual‐luciferase reporter gene assays. Exosomes were isolated from miR‐24‐3p inhibitor–treated CAFs (CAFs‐exo/miR‐24‐3p inhibitor), which were used in combination with gain‐of‐function and loss‐of‐function experiments and MTX treatment. CCK‐8, flow cytometry and colony formation assays were conducted to determine cell viability, apoptosis and colony formation, respectively. Based on the findings, CC tissues and cells presented with high expression of miR‐24‐3p and low expression of HEPH and CDX2. CDX2 was a target gene of miR‐24‐3p and could up‐regulate HEPH. Under MTX treatment, overexpressed CDX2 or HEPH and down‐regulated miR‐24‐3p reduced cell viability and colony formation and elevated cell apoptosis. Furthermore, miR‐24‐3p was transferred into CC cells via CAF‐derived exosomes. CAF‐derived exosomal miR‐24‐3p inhibitor diminished cell viability and colony formation and increased cell apoptosis in vitro and inhibited tumour growth in vivo under MTX treatment. Altogether, CAF‐derived exosomal miR‐24‐3p accelerated resistance of CC cells to MTX by down‐regulating CDX2/HEPH axis.
Journal Article
Distribution and risk assessment of phthalates in water and sediment of the Pearl River Delta
Phthalate esters (PAEs) are widely used industrial raw materials that are well known for their environmental contamination and toxicological effects as “endocrine disruptors.” In this study, environmental levels of PAEs and eco-toxicological risk assessments were determined in the eight estuaries of the Pearl River (Estuaries), main upstream tributary (Xijiang River), urban river network (River network), and nature reserve reservoir (Reservoirs). Water and sediment samples from the above water systems were collected during the low-water period (May) and the high-water period (August) between 2012 and 2014. Solid phase and ultrasonic methods were used to extract 14 different PAEs that were analyzed by gas chromatography. The analytical average recovery of PAEs in water and sediment was 75.4% ± 4.9% and 121.5% ± 8.9%, respectively. The results showed that PAEs were detected in all of the samples, and the di-n-butyl phtalate (DBP) and benzyl butyl phthalate (BBP) monomers had a detection rate of 100% in water. Similarly, in sediment samples, the detection rates of diisobutyl phthalate (D
i
BP), DBP, dimethoxyethyl phthalate (DMEP), BBP, di-n-octyl phthalate (D
n
OP), and DNP ranged from 66.7 to 100%. Among these, in sediment samples, di(2-ethylhexyl) phthalate (DEHP) and phthalic acid bis(2-butoxyethyl) ester (DBEP) had detection rates of 95.8% to 100% in the Estuaries, Xijiang River, and River network. The concentrations of Σ
14
PAEs in water samples and sediments ranged from 12.95 ± 1.97 to 6717.29 ± 112.37 ng/L and 71.99 ± 8.72 to 17,340.04 ± 227.83 ng/g-dw, respectively. During the low-water period, the average concentration of Σ
14
PAEs in water and sediment was 1159.58 ± 97.22 ng/L and 2842.50 ± 178.21 ng/g-dw, respectively, and during the high-water period, 822.83 ± 53.19 ng/L and 1936.42 ± 111.31 ng/g-dw, respectively. In water, the average concentration of Σ
14
PAEs in 2013 and 2014 was 963.39 ± 19.55 ng/L and 2815.35 ± 176.32 ng/L, respectively. In sediment, the average concentrations of Σ
14
PAEs in 2012 to 2014 were 990.10 ± 23.33 ng/g-dw, 1084.20 ± 112.12 ng/g-dw, and 1816.89 ± 79.97 ng/g-dw, respectively, with concentrations showing an increasing trend year after year (2014 > 2013 > 2012). Potential risk assessment of water ecological, the results show that exceeding environmental risk level (ERL) value in higher molecular weight plasticizer (DEHP, DMEP, DNOP, DNP) was mainly distributed in water, the lower molecular weight plasticizer (BMP, D
i
BP) was mainly distributed in sediment.
Journal Article
Ultrafast charge transfer in mixed-dimensional WO3-x nanowire/WSe2 heterostructures for attomolar-level molecular sensing
Developing efficient noble-metal-free surface-enhanced Raman scattering (SERS) substrates and unveiling the underlying mechanism is crucial for ultrasensitive molecular sensing. Herein, we report a facile synthesis of mixed-dimensional heterostructures via oxygen plasma treatments of two-dimensional (2D) materials. As a proof-of-concept, 1D/2D WO
3-
x
/WSe
2
heterostructures with good controllability and reproducibility are synthesized, in which 1D WO
3-x
nanowire patterns are laterally arranged along the three-fold symmetric directions of 2D WSe
2
. The WO
3-x
/WSe
2
heterostructures exhibited high molecular sensitivity, with a limit of detection of 5 × 10
−18
M and an enhancement factor of 5.0 × 10
11
for methylene blue molecules, even in mixed solutions. We associate the ultrasensitive performance to the efficient charge transfer induced by the unique structures of 1D WO
3-x
nanowires and the effective interlayer coupling of the heterostructures. We observed a charge transfer timescale of around 1.0 picosecond via ultrafast transient spectroscopy. Our work provides an alternative strategy for the synthesis of 1D nanostructures from 2D materials and offers insights on the role of ultrafast charge transfer mechanisms in plasmon-free SERS-based molecular sensing.
2D materials are promising substrates for surface-enhanced Raman scattering (SERS)-based molecular sensing, but their performance is usually inferior to their plasmonic counterparts. Here, the authors report the synthesis of 1D/2D WO
3-x
/WSe
2
heterostructures, showing high molecular sensitivity associated to ultrafast charge transfer timescales of ~1 ps.
Journal Article
A novel robust interacting multiple model filter for manoeuvering target tracking
A robust interacting multiple model approach is proposed to address the problem of accuracy and non‐Gaussian measurement noise in manoeuvering target tracking. The proposed approach introduces multiple fading factors into the prediction covariance matrix and adjusts each channel of the gain matrix in real time to improve the accuracy caused by model mismatch and enhance state transition capability. Considering the non‐Gaussian noise, an improved IMM filter is constructed to further improve the robustness using the maximum correntropy criterion. The simulation results show that the proposed approach can effectively suppress the non‐Gaussian noise and improve the accuracy with adaptability and robustness.
The multiple fading factors are constructed for adjusting prediction covariance matrix in the IMM prediction process, and a cost function based on the maximum correntropy criterion is designed in the IMM update step to obtain an iterative state estimation solution by maximizing this function.
Journal Article
Strong Oceanic Forcing on Decadal Surface Temperature Variability Over Global Ocean
Sea surface temperature (SST) variability on decadal timescales has been associated with global and regional climate variability and impacts. The mechanisms that drive decadal SST variability, however, remain highly uncertain. Many previous studies have examined the role of atmospheric variability in driving decadal SST variations. Here we assess the strength of oceanic forcing in driving decadal SST variability in observations and state‐of‐the‐art climate models by analyzing the relationship between surface heat flux and SST. We find a largely similar pattern of decadal oceanic forcing across all ocean basins, characterized by oceanic forcing about twice the strength of the atmospheric forcing in the mid‐ and high latitude regions, but comparable or weaker than the atmospheric forcing in the subtropics. The decadal oceanic forcing is hypothesized to be associated with the wind‐driven oceanic circulation, which is common across all ocean basins.
Plain Language Summary
Decadal variabilities in SST create large climate responses, ranging from heat waves to droughts to enhanced hurricanes. However, there has been considerable uncertainty over whether decadal SST variations are driven primarily by atmospheric forcing or ocean forcing related to ocean circulation. Using a newly developed theoretical framework, we provide the first quantitative estimation of decadal oceanic forcing across the global ocean in observations and state‐of‐the‐art climate model. Our estimation shows that decadal ocean forcing is stronger than the atmospheric forcing by about 2–3 times in the mid‐ and high latitude, but comparable or even weaker than atmospheric forcing in the subtropics.
Key Points
In the mid‐ and high latitude, decadal oceanic forcing is stronger than atmospheric forcing by about 2–3 times across world ocean basins
In the subtropics, decadal oceanic forcing is comparable to or even weaker than atmospheric forcing
Decadal oceanic forcing is likely contributed predominantly by the wind‐driven oceanic circulation
Journal Article
lncRNA HOXD-AS1 Regulates Proliferation and Chemo-Resistance of Castration-Resistant Prostate Cancer via Recruiting WDR5
Castration-resistant prostate cancer (CRPC) that occurs after the failure of androgen deprivation therapy is the leading cause of deaths in prostate cancer patients. Thus, there is an obvious and urgent need to fully understand the mechanism of CRPC and discover novel therapeutic targets. Long noncoding RNAs (lncRNAs) are crucial regulators in many human cancers, yet their potential roles and molecular mechanisms in CRPC are poorly understood. In this study, we discovered that an lncRNA HOXD-AS1 is highly expressed in CRPC cells and correlated closely with Gleason score, T stage, lymph nodes metastasis, and progression-free survival. Knockdown of HOXD-AS1 inhibited the proliferation and chemo-resistance of CRPC cells in vitro and in vivo. Furthermore, we identified several cell cycle, chemo-resistance, and castration-resistance-related genes, including PLK1, AURKA, CDC25C, FOXM1, and UBE2C, that were activated transcriptionally by HOXD-AS1. Further investigation revealed that HOXD-AS1 recruited WDR5 to directly regulate the expression of target genes by mediating histone H3 lysine 4 tri-methylation (H3K4me3). In conclusion, our findings indicate that HOXD-AS1 promotes proliferation, castration resistance, and chemo-resistance in prostate cancer by recruiting WDR5. This sheds a new insight into the regulation of CRPC by lncRNA and provides a potential approach for the treatment of CRPC.
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Huang, Lin, and colleagues show that long noncoding RNA HOXD-AS1 is upregulated in castration-resistant prostate cancer (CRPC) and correlated with disease progression. HOXD-AS1 promotes proliferation, castration resistance, and chemo-resistance of prostate cancer cells via interacting with WDR5, which in turn activates the transcription of downstream genes.
Journal Article
KDM5A silencing transcriptionally suppresses the FXYD3‐PI3K/AKT axis to inhibit angiogenesis in hepatocellular cancer via miR‐433 up‐regulation
Hepatocellular cancer (HCC) has been reported to belong to one of the highly vascularized solid tumours accompanied with angiogenesis of human umbilical vein endothelial cells (HUVECs). KDM5A, an attractive drug target, plays a critical role in diverse physiological processes. Thus, this study aims to investigate its role in angiogenesis and underlying mechanisms in HCC. ChIP‐qPCR was utilized to validate enrichment of H3K4me3 and KDM5A on the promotor region of miR‐433, while dual luciferase assay was carried out to confirm the targeting relationship between miR‐433 and FXYD3. Scratch assay, transwell assay, Edu assay, pseudo‐tube formation assay and mice with xenografted tumours were conducted to investigate the physiological function of KDM5A‐miR‐433‐FXYD3‐PI3K‐AKT axis in the progression of HCC after loss‐ and gain‐function assays. KDM5A p‐p85 and p‐AKT were highly expressed but miR‐433 was down‐regulated in HCC tissues and cell lines. Depletion of KDM5A led to reduced migrative, invasive and proliferative capacities in HCC cells, including growth and a lowered HUVEC angiogenic capacity in vitro. Furthermore, KDM5A suppressed the expression of miR‐433 by demethylating H3K4me3 on its promoterregion. miR‐433 negatively targeted FXYD3. Depleting miR‐433 or re‐expressing FXYD3 restores the reduced migrative, invasive and proliferative capacities, and lowers the HUVEC angiogenic capacity caused by silencing KDM5A. Therefore, KDM5A silencing significantly suppresses HCC tumorigenesis in vivo, accompanied with down‐regulated miR‐433 and up‐regulated FXYD3‐PI3K‐AKT axis in tumour tissues. Lastly, KDM5A activates the FXYD3‐PI3K‐AKT axis to enhance angiogenesis in HCC by suppressing miR‐433.
Journal Article