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"An, Wei"
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كل متكامل بين العالمين العقلي والمادي : الفنون والحرف الصينية التقليدية
تتناول هذه السلسلة مواضيع متنوعة، كالشخصيات الصينية، والمسرح والموسيقى والرسم، وفي هذه السلسة سيبحر القارئ مستطلعا صورا مدهشة تتراكب بشكل متقن في كتب تصل به إلى قلب الحضارة الصينية وهو في مكانه، حتى بالنسبة لأولئك الذين لم يعتادوا القراءة في هذه المواضيع، مما يجعل منها كتبا مناسبة لكل من الكبار في السن والشباب على حد سواء.
BOOK
Has the green total factor productivity increased in the early stage of the establishment of smart city
In the context of global climate change, green development has become the main goal of smart city construction. Most existing research suggests that smart cities will enhance the level of the green total factor productivity (GTFP) in cities. However, this study found that smart cities will reduce the level of green total factor production in the short term and increase it in the long term. Based on this, this article selects three batches of smart cities in China from 2013 to 2019, and uses the Malmquist index model, common frontier function, and panel data method to analyze the GTFP model in the early stage of smart city construction in China. The study found that: (1) the GTFP of the three batches of smart cities in the early stage of construction was less than 1 and showed a downward trend, indicating that smart cities will reduce the GTFP level of cities in the short term. (2) Technical efficiency is the main reason for the decline of GTFP in the early stage of smart city construction and the rise of GTFP in the medium and long term. Specifically, there is a U-shaped relationship between the technological efficiency of smart cities and their GTFP. For every 1% increase in technical efficiency in the later stages of smart cities, GTFP increases by 47.3%. (3) The GTFP in the process of smart city construction shows a trend of decreasing in the early stage and increasing in the middle and later stages. The GTFP level in the later stage of smart cities is greater than 1 and shows a fluctuating upward trend, indicating that smart cities will improve the city’s GTFP level in the long run. In view of this, we should attach importance to ecological protection in the early stage of smart city construction and take effective measures to reduce carbon emissions during this period. During this period, policies such as taxation can be implemented to encourage companies to adopt cleaner production technologies, strengthen the exchange of green technologies between cities, accelerate the flow of green knowledge, reduce redundant construction of information infrastructure, and thus minimize the decline in GTFP in the early stages of smart city construction. This study provides policy recommendations and decision-making references for further promoting the construction of new green and smart cities worldwide.
Journal Article
Highly selective cesium(I) capture under acidic conditions by a layered sulfide
Radiocesium remediation is desirable for ecological protection, human health and sustainable development of nuclear energy. Effective capture of Cs
+
from acidic solutions is still challenging, mainly due to the low stability of the adsorbing materials and the competitive adsorption of protons. Herein, the rapid and highly selective capture of Cs
+
from strongly acidic solutions is achieved by a robust K
+
-directed layered metal sulfide KInSnS
4
(InSnS-1) that exhibits excellent acid and radiation resistance. InSnS-1 possesses high adsorption capacity for Cs
+
and can serve as the stationary phase in ion exchange columns to effectively remove Cs
+
from neutral and acidic solutions. The adsorption of Cs
+
and H
3
O
+
is monitored by single-crystal structure analysis, and thus the underlying mechanism of selective Cs
+
capture from acidic solutions is elucidated at the molecular level.
The removal of radiocesium from acidic solutions is challenging. Here, the authors report the rapid and highly selective capture of cesium(I) from strongly acidic solutions by a robust layered metal sulfide.
Journal Article
Massive collapse of two glaciers in western Tibet in 2016 after surge-like instability
Surges and glacier avalanches are expressions of glacier instability, and among the most dramatic phenomena in the mountain cryosphere. Until now, the catastrophic collapse of a glacier, combining the large volume of surges and mobility of ice avalanches, has been reported only for the 2002 130 × 106 m3 detachment of Kolka Glacier (Caucasus Mountains), which has been considered a globally singular event. Here, we report on the similar detachment of the entire lower parts of two adjacent glaciers in western Tibet in July and September 2016, leading to an unprecedented pair of giant low-angle ice avalanches with volumes of 68 ± 2 × 106 m3 and 83 ± 2 × 106 m3. On the basis of satellite remote sensing, numerical modelling and field investigations, we find that the twin collapses were caused by climate- and weather-driven external forcing, acting on specific polythermal and soft-bed glacier properties. These factors converged to produce surge-like enhancement of driving stresses and massively reduced basal friction connected to subglacial water and fine-grained bed lithology, to eventually exceed collapse thresholds in resisting forces of the tongues frozen to their bed. Our findings show that large catastrophic instabilities of low-angle glaciers can happen under rare circumstances without historical precedent.
Journal Article
Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
Despite the clear association between myocardial injury, heart failure and depressed myocardial energetics, little is known about upstream signals responsible for remodeling myocardial metabolism after pathological stress. Here, we report increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial infarction (MI) surgery. By contrast, mice with genetic mitochondrial CaMKII inhibition are protected from left ventricular dilation and dysfunction after MI. Mice with myocardial and mitochondrial CaMKII overexpression (mtCaMKII) have severe dilated cardiomyopathy and decreased ATP that causes elevated cytoplasmic resting (diastolic) Ca
2+
concentration and reduced mechanical performance. We map a metabolic pathway that rescues disease phenotypes in mtCaMKII mice, providing insights into physiological and pathological metabolic consequences of CaMKII signaling in mitochondria. Our findings suggest myocardial dilation, a disease phenotype lacking specific therapies, can be prevented by targeted replacement of mitochondrial creatine kinase or mitochondrial-targeted CaMKII inhibition.
Little is known about how cardiac metabolism remodels following cardiac injury. Here, the authors show that mitochondrial CaMKII plays an important role in remodeling cardiac metabolism after injury and that replacement of mitochondrial creatine kinase improves energetics and protects against adverse remodeling.
Journal Article
Catechin attenuates TNF-α induced inflammatory response via AMPK-SIRT1 pathway in 3T3-L1 adipocytes
Chronic inflammation is a fundamental symptom of many diseases. Catechin possesses anti-oxidant and anti-inflammatory properties. However, the mechanism of catechin to prevent inflammation in 3T3-L1 adipocytes caused by TNF-α remains unknown. Therefore, the effects of catechin on the gene expression of cytokines and the activation of cell signals in TNF-α induced 3T3-L1 adipocytes were investigated. The effects of catechin on adipogenesis and cell viability were detected by Oil Red O staining and CCK-8 assay, respectively. The genes expression of cytokines was determined by real-time RT-PCR. The expression of NF-κB, AMPK, FOXO3a and SIRT1 on translation level was determined by western blotting analysis. The results demonstrated that catechin significantly enhanced adipogenesis and cell viability. catechin inhibited the gene expression of pro-inflammatory cytokines including IL-1α, IL-1β, IL-6, IL-12p35, and inflammatory enzymes including iNOS and COX-2, but enhanced the gene expression of anti-inflammatory cytokines including IL-4 and IL-10. Catechin also inhibited the activation of NF-κB, AMPK, FOXO3a and SIRT1, but increased the phosphorylation level of the above factors. All these results indicated that as a potential therapeutic strategy catechin has the ability of attenuating inflammatory response triggered by TNF-α through signaling cascades involved in inflammation and cytokines.
Journal Article
Mechanisms of the effect of fertility policies on the labor-capital income gap
This paper investigates the impact mechanism by which an incentive-based fertility policy may reduce the labor income share. First, the specific paths through which this impact mechanism is realized are analyzed using the production function. It is found that an incentive-based fertility policy triggers high savings, which implies more, cheaper, and more readily available capital to be invested in production. A distribution system that earns income based on factor contributions results in more gains for capital than labor, i.e., a lower share of labor income and a wider income gap between labor and capital. Second, the impact mechanism includes three theoretical hypotheses. They are that an encouraging fertility policy is negatively related to labor income share; this relationship is valid provided that the study subject is in a closed economy; and that capital intensification is a mediator variable of fertility policy affecting labor income share. Finally, to further corroborate the impact mechanism in this paper, a Hansen threshold panel model is applied to verify that the effect of fertility policy on labor income share has a threshold effect. This indicates that the effect of the former on the latter changes significantly before and after the change in fertility policy, confirming the existence of an impact mechanism. The established literature has paid little attention to the impact of incentivised fertility policies on the labour income gap. Using capital intensification as the mediating variable, this paper demonstrates the existence of the former effect on the latter. In view of this, under the encouraged fertility policy, this paper proposes specific measures to enhance the labor income share in order to narrow the income gap between labor and capital.
Journal Article
MicroRNA160 Modulates Plant Development and Heat Shock Protein Gene Expression to Mediate Heat Tolerance in Arabidopsis
Global warming is causing a negative impact on plant growth and adversely impacts on crop yield. MicroRNAs (miRNAs) are critical in regulating the expression of genes involved in plant development as well as defense responses. The effects of miRNAs on heat-stressed
warrants further investigation. Heat stress increased the expression of miR160 and its precursors but considerably reduced that of its targets,
, and
. To study the roles of miR160 during heat stress, transgenic
plants overexpressing
a (160OE) and artificial miR160 (MIM160), which mimics an inhibitor of miR160, were created. T-DNA insertion mutants of miR160 targets were also used to examine their tolerances to heat stress. Results presented that overexpressing miR160 improved seed germination and seedling survival under heat stress. The lengths of hypocotyl elongation and rachis were also longer in 160OE than the wild-type (WT) plants under heat stress. Interestingly, MIM160 plants showed worse adaption to heat. In addition,
, and
mutants presented similar phenotypes to 160OE under heat stress to advance abilities of thermotolerance. Moreover, transcriptome and qRT-PCR analyses revealed that
, and
expression levels were regulated by heat in 160OE, MIM160,
, and
plants. Hence, miR160 altered the expression of the heat shock proteins and plant development to allow plants to survive heat stress.
Journal Article
Transcriptome and machine learning analysis of the impact of COVID-19 on mitochondria and multiorgan damage
The effects of coronavirus disease 2019 (COVID-19) primarily concern the respiratory tract and lungs; however, studies have shown that all organs are susceptible to infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 may involve multiorgan damage from direct viral invasion through angiotensin-converting enzyme 2 (ACE2), through inflammatory cytokine storms, or through other secondary pathways. This study involved the analysis of publicly accessible transcriptome data from the Gene Expression Omnibus (GEO) database for identifying significant differentially expressed genes related to COVID-19 and an investigation relating to the pathways associated with mitochondrial, cardiac, hepatic, and renal toxicity in COVID-19. Significant differentially expressed genes were identified and ranked by statistical approaches, and the genes derived by biological meaning were ranked by feature importance; both were utilized as machine learning features for verification. Sample set selection for machine learning was based on the performance, sample size, imbalanced data state, and overfitting assessment. Machine learning served as a verification tool by facilitating the testing of biological hypotheses by incorporating gene list adjustment. A subsequent in-depth study for gene and pathway network analysis was conducted to explore whether COVID-19 is associated with cardiac, hepatic, and renal impairments via mitochondrial infection. The analysis showed that potential cardiac, hepatic, and renal impairments in COVID-19 are associated with ACE2, inflammatory cytokine storms, and mitochondrial pathways, suggesting potential medical interventions for COVID-19-induced multiorgan damage.
Journal Article
FTY720 in resistant human epidermal growth factor receptor 2-positive breast cancer
The prognosis of patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer has considerably improved. However, no reliable treatment besides anti-HER2 strategies has been available. FTY720, a small-molecule compound used for treating refractory multiple sclerosis, has been reported to have beneficial effects against cancers. We therefore evaluated the efficacy of FTY720 in trastuzumab-resistant breast cancer cells and investigated the possible mechanism involved. This study evaluated morphological changes after FTY720 treatment. Antiproliferative WST-1 assays and LDH Cytotoxicity Assay Kits were used to determine the treatment effects of drugs, whereas Western blot analysis was used to evaluate protein expression. Apoptotic events were investigated through annexin V staining and TUNEL assays using flow cytometry. FTY720 was effective in trastuzumab-resistant breast cancer cell lines despite the presence of
PIK3CA
mutation. Studied on a xenograft mouse model, FTY720-treated groups had statistically significantly poorer HCC1954 xenograft growth in vivo compared with the control group. Our findings suggest that FTY720 can overcome resistance to trastuzumab therapy in patients with HER2-positive breast cancer, with FTY720 plus trastuzumab might offer even better efficacy in vitro and in vivo.
Journal Article