Effect of Bordered Pit Torus Position on Permeability in Chinese Yezo Spruce

The effect of different bordered pit torus positions on wood permeability was studied by air-drying and ethanol-exchange drying for green wood and by soaking in water, then followed by ethanol-exchange drying for air-dried wood of Chinese yezo spruce (Picea jezoensis var. komarovii). The results showed that different treatments caused different pit torus positions and different wood permeability. The air-drying treatment resulted in pit torus aspiration and low permeability for sapwood. The ethanol-exchange drying treatment left the pit torus in an unaspirated position and resulted in high permeability for sapwood. Soaking in water followed by ethanol-exchange drying caused deaspiration of a part of pit torus and increased permeability for both sapwood and heartwood

Multi-agent game operation of regional integrated energy system based on carbon emission flow

In the process of promoting energy green transformation, the optimization of regional integrated energy system faces many challenges such as cooperative management, energy saving and emission reduction, as well as uncertainty of new energy output. Therefore, this paper proposes a multi-agent game operation method of regional integrated energy system based on carbon emission flow. First, this paper establishes a carbon emission flow calculation model for each subject, and proposes a comprehensive tariff model based on the carbon emission flow, which discounts the carbon emissions from the power supply side to the power consumption side. Secondly, considering the interests of each subject, this paper establishes the decision-making model of each subject. And the new energy uncertainty, the cost of energy preference of prosumers, and the thermal inertia of buildings are considered in the decision model. Finally, the model is solved using differential evolution algorithm and solver. The case study verifies that the comprehensive electricity pricing model based on carbon emission flow developed in this paper can play a role in balancing economy and low carbon

Multi-objective planning of integrated energy system based on CVaR under carbon trading mechanism

In order to address the planning problem of integrated energy system (IES) under the goal of “dual-carbon”, this paper proposes a multi-objective planning method for IES with carbon trading mechanism based on CVaR (Conditional Value at Risk). Firstly, this paper establishes the IES energy supply equipment model and the improved stepped carbon trading model. Moreover, this paper proposes the IES multi-objective two-layer planning model based on the consideration of carbon trading cost. The upper layer of the planning model takes the optimization of economy and environmental as the goal to realize the rational planning of the integrated energy system. The lower layer model takes the minimum operating cost as the goal to optimize the system operating conditions and verify the rationality of the planning results. Then, the uncertainty model based on mean-CVaR is established for the uncertainty of carbon trading price and new energy output in the planning process. Finally, this paper sets up cases and solves the model using non-dominated sorting genetic algorithm-II (NSGA-II) and solver, which shows that the proposed method can realize the IES low-carbon planning while guaranteeing the economy

Glucosylceramide synthase upregulates MDR1 expression in the regulation of cancer drug resistance through cSrc and β-catenin signaling

<p>Abstract</p> <p>Background</p> <p>Drug resistance is the outcome of multiple-gene interactions in cancer cells under stress of anticancer agents. <it>MDR1 </it>overexpression is most commonly detected in drug-resistant cancers and accompanied with other gene alterations including enhanced glucosylceramide synthase (GCS). <it>MDR1 </it>encodes for P-glycoprotein that extrudes anticancer drugs. Polymorphisms of <it>MDR1 </it>disrupt the effects of P-glycoprotein antagonists and limit the success of drug resistance reversal in clinical trials. GCS converts ceramide to glucosylceramide, reducing the impact of ceramide-induced apoptosis and increasing glycosphingolipid (GSL) synthesis. Understanding the molecular mechanisms underlying <it>MDR1 </it>overexpression and how it interacts with GCS may find effective approaches to reverse drug resistance.</p> <p>Results</p> <p><it>MDR1 </it>and <it>GCS </it>were coincidently overexpressed in drug-resistant breast, ovary, cervical and colon cancer cells; silencing <it>GCS </it>using a novel mixed-backbone oligonucleotide (MBO-asGCS) sensitized these four drug-resistant cell lines to doxorubicin. This sensitization was correlated with the decreased <it>MDR1 </it>expression and the increased doxorubicin accumulation. Doxorubicin treatment induced GCS and <it>MDR1 </it>expression in tumors, but MBO-asGCS treatment eliminated "in-vivo" growth of drug-resistant tumor (NCI/ADR-RES). MBO-asGCS suppressed the expression of <it>MDR1 </it>with GCS and sensitized NCI/ADR-RES tumor to doxorubicin. The expression of P-glycoprotein and the function of its drug efflux of tumors were decreased by 4 and 8 times after MBO-asGCS treatment, even though this treatment did not have a significant effect on P-glycoprotein in normal small intestine. GCS transient transfection induced <it>MDR1 </it>overexpression and increased P-glycoprotein efflux in dose-dependent fashion in OVCAR-8 cancer cells. GSL profiling, silencing of globotriaosylceramide synthase and assessment of signaling pathway indicated that GCS transfection significantly increased globo series GSLs (globotriaosylceramide Gb3, globotetraosylceramide Gb4) on GSL-enriched microdomain (GEM), activated cSrc kinase, decreased β-catenin phosphorylation, and increased nuclear β-catenin. These consequently increased <it>MDR1 </it>promoter activation and its expression. Conversely, MBO-asGCS treatments decreased globo series GSLs (Gb3, Gb4), cSrc kinase and nuclear β-catenin, and suppressed <it>MDR-1 </it>expression in dose-dependent pattern.</p> <p>Conclusion</p> <p>This study demonstrates, for the first time, that GCS upregulates <it>MDR1 </it>expression modulating drug resistance of cancer. GSLs, in particular globo series GSLs mediate gene expression of <it>MDR1 </it>through cSrc and β-catenin signaling pathway.</p

A New Mixed-Backbone Oligonucleotide against Glucosylceramide Synthase Sensitizes Multidrug-Resistant Tumors to Apoptosis

Enhanced ceramide glycosylation catalyzed by glucosylceramide synthase (GCS) limits therapeutic efficiencies of antineoplastic agents including doxorubicin in drug-resistant cancer cells. Aimed to determine the role of GCS in tumor response to chemotherapy, a new mixed-backbone oligonucleotide (MBO-asGCS) with higher stability and efficiency has been generated to silence human GCS gene. MBO-asGCS was taken up efficiently in both drug-sensitive and drug-resistant cells, but it selectively suppressed GCS overexpression, and sensitized drug-resistant cells. MBO-asGCS increased doxorubicin sensitivity by 83-fold in human NCI/ADR-RES, and 43-fold in murine EMT6/AR1 breast cancer cells, respectively. In tumor-bearing mice, MBO-asGCS treatment dramatically inhibited the growth of multidrug-resistant NCI/ADR-RE tumors, decreasing tumor volume to 37%, as compared with scrambled control. Furthermore, MBO-asGCS sensitized multidrug-resistant tumors to chemotherapy, increasing doxorubicin efficiency greater than 2-fold. The sensitization effects of MBO-asGCS relied on the decreases of gene expression and enzyme activity of GCS, and on the increases of C18-ceramide and of caspase-executed apoptosis. MBO-asGCS was accumulation in tumor xenografts was greater in other tissues, excepting liver and kidneys; but MBO-asGCS did not exert significant toxic effects on liver and kidneys. This study, for the first time in vivo, has demonstrated that GCS is a promising therapeutic target for cancer drug resistance, and MBO-asGCS has the potential to be developed as an antineoplastic agent

Spatiotemporal Changes of Ecosystem Service Values in Response to Land Cover Dynamics in China from 1992 to 2020

Global land cover changed significantly in the last several decades due to strong climate warming and intensive human activities, and those changes greatly affected ecosystem services all over the world. Using CCI-LC land cover data from 1992 to 2020, the spatiotemporal characteristics of land cover change in China were investigated, and the annual ecosystem service values (ESVs) were estimated with the equivalent factor method. The results showed that: (1) The overall accuracy and Kappa coefficient of CCI-LC products in China were 71.1% and 0.65, respectively. (2) From 1992 to 2020, the area of cropland in China increased generally first before 2004 then decreased after 2008; the area of forest land decreased before 2003 then increased after 2015; the area of grassland and bare land consistently decreased; and the area of built-up land continuously increased, with a total increase of 113,000 km2. The primary characteristics of land cover transitions in China were the mutual conversion of cropland, forestland, and grassland as well as the continuous increase of built-up land. (3) Forest land was the most significant contributor of ESV in China, making 62.9% of the total ESV by multi-year average, followed by grassland (18.5%) and water (10.3%); the ESV was roughly high in the southeast China and low in the northwest. (4) The total ESV in China decreased generally before 2015 and got stable in the last five years. The hot spots with rising ESV were mainly concentrated in the western, northern and southwestern parts of China, while the cold spots with declining ESV were mainly concentrated in the economically developed eastern and southern China. (5) Cropland, forest land, grassland, and water were the positive contributors to ESV change in China, while built-up land and bare land were the negative contributors. The findings provide a theoretical foundation for China’s harmonized socioeconomic and environmental development

Novel Evidence for the Increasing Prevalence of Unique Names in China: A Reply to Ogihara

In this study, we aimed to address three comments proposed by Ogihara on a recent study where we found that unique names in China have become increasingly popular from 1950 to 2009. Using a large representative sample of Chinese names (N = 2.1 million), we replicated the increase in uniqueness of Chinese names from 1920 to 2005, especially since the 1970s, with multiple uniqueness indices based on name-character frequency and name-length deviation. Over the years, Chinese characters that are rare in daily life or naming practice were more often used in given names, and the length of given names became more deviant from typical practice (i.e., more one-character and three-character given names and higher standard deviation of name length). Taken together, these findings not only reconfirmed the increasing prevalence of unique names but also demonstrated the validity of various indices in assessing name uniqueness in China.</p

Identification of Gene Markers for Survival Prediction of Lung Adenocarcinoma Patients Based on Integrated Multibody Data Analysis

We constructed a prognostic-related risk prediction for patients with lung adenocarcinoma by integrating multiple omics information of lung adenocarcinoma clinical information group and genome and transcriptome. Blood samples and cancer and paracancerous lung tissue samples were collected from 480 patients with lung adenocarcinoma. DNA and RNA sequencing was performed on DNA samples and RNA samples. The first follow-up was carried out 3 months after discharge. Clinical information of patients including age, gender, smoking history, and TNM stage was collected. The Cox proportional hazard model evaluated more than 600 potential SNPs related to the prognosis of lung adenocarcinoma. After LASSO analysis, we obtained 4 SNPs related to the prognosis of lung adenocarcinoma (including rs1059292, rs995343, rs2013335, and rs8078328). Through the Cox proportional hazard model, 260 candidate genes related to the prognosis of lung adenocarcinoma were evaluated. After subsequent analysis, 3 genes related to the prognosis of lung adenocarcinoma (LDHA, SDHC, and TYMS) were obtained. All survived patients were spilt into a high-risk group (n=170) and a low-risk group (n=170) according to 4 SNPs and 3 genes related to the prognosis of lung adenocarcinoma. The overall survival rate of patients in the high-risk group was lower than that in the low-risk group. The prognostic risk prediction index constructed by combining clinical information group and genomic and transcriptome characteristics of multiomics information can effectively distinguish the prognosis of patients with lung adenocarcinoma, which will provide effective support for the precise treatment of patients with lung adenocarcinoma

Glucosylceramide synthase upregulates MDR1 expression in the regulation of cancer drug resistance through cSrc and beta-catenin signaling

Abstract Background Drug resistance is the outcome of multiple-gene interactions in cancer cells under stress of anticancer agents. MDR1 overexpression is most commonly detected in drug-resistant cancers and accompanied with other gene alterations including enhanced glucosylceramide synthase (GCS). MDR1 encodes for P-glycoprotein that extrudes anticancer drugs. Polymorphisms of MDR1 disrupt the effects of P-glycoprotein antagonists and limit the success of drug resistance reversal in clinical trials. GCS converts ceramide to glucosylceramide, reducing the impact of ceramide-induced apoptosis and increasing glycosphingolipid (GSL) synthesis. Understanding the molecular mechanisms underlying MDR1 overexpression and how it interacts with GCS may find effective approaches to reverse drug resistance. Results MDR1 and GCS were coincidently overexpressed in drug-resistant breast, ovary, cervical and colon cancer cells; silencing GCS using a novel mixed-backbone oligonucleotide (MBO-asGCS) sensitized these four drug-resistant cell lines to doxorubicin. This sensitization was correlated with the decreased MDR1 expression and the increased doxorubicin accumulation. Doxorubicin treatment induced GCS and MDR1 expression in tumors, but MBO-asGCS treatment eliminated "in-vivo" growth of drug-resistant tumor (NCI/ADR-RES). MBO-asGCS suppressed the expression of MDR1 with GCS and sensitized NCI/ADR-RES tumor to doxorubicin. The expression of P-glycoprotein and the function of its drug efflux of tumors were decreased by 4 and 8 times after MBO-asGCS treatment, even though this treatment did not have a significant effect on P-glycoprotein in normal small intestine. GCS transient transfection induced MDR1 overexpression and increased P-glycoprotein efflux in dose-dependent fashion in OVCAR-8 cancer cells. GSL profiling, silencing of globotriaosylceramide synthase and assessment of signaling pathway indicated that GCS transfection significantly increased globo series GSLs (globotriaosylceramide Gb3, globotetraosylceramide Gb4) on GSL-enriched microdomain (GEM), activated cSrc kinase, decreased β-catenin phosphorylation, and increased nuclear β-catenin. These consequently increased MDR1 promoter activation and its expression. Conversely, MBO-asGCS treatments decreased globo series GSLs (Gb3, Gb4), cSrc kinase and nuclear β-catenin, and suppressed MDR-1 expression in dose-dependent pattern. Conclusion This study demonstrates, for the first time, that GCS upregulates MDR1 expression modulating drug resistance of cancer. GSLs, in particular globo series GSLs mediate gene expression of MDR1 through cSrc and β-catenin signaling pathway