Study on the relationship between industrialization level, economic development and environmental pollution in China

With the development of economy, environmental problems gradually outstanding in China. This article adopts the method of empirical study, have collected the data of China\u27s industrial added value, per capita GDP and emissions of the three major pollutants from 2004 to 2015. The VAR model was established on the basis of the logarithm values of the three factors mentioned above, so as to conduct impulse- response analysis to discuss the relationship between industrialization level, economic development and environmental pollution. The conclusion is as follows: (1) At present, the increase of China\u27s industrial added value can promote the decline of China\u27s environmental pollution emissions to a certain extent; (2) China is now at the left of the turning point of the Environmental Kuznets Curve, and the increase of per capita GDP will aggravate environmental pollution

Research on optimal environmental tax, sub-optimal selection and influencing factors in China

Considering the definition of the optimal environment tax, according to the sub-optimal choice under real conditions, Marginal cost of emission reduction is regarded as environmental tax payable and listed as a dependent variable. Through setting the independent variables, selecting samples and making empirical analysis, the conclusions of the paper are as follows: The actual environmental tax charged is positively correlated with government supervision and public participation, and negatively correlated with enterprise environmental investment, government environmental expenditure, upgrading of industrial structure and size of enterprise. At last, the paper puts forward some suggestions: strictly enforce the environmental tax, encourage public participation and increase the investment on environmental protection

Targeting Radioresistant Breast Cancer Cells by Single Agent CHK1 Inhibitor via Enhancing Replication Stress

Radiotherapy (RT) remains a standard therapeutic modality for breast cancer patients. However, intrinsic or acquired resistance limits the efficacy of RT. Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC). Given the critical role of ATR/CHK1 signaling in suppressing oncogene-induced replication stress (RS), we hypothesize that CHK1 inhibition leads to the specific killing for RBCC due to its abrogation in the suppression of RS induced by oncogenes. In agreement, the expression of oncogenes c-Myc/CDC25A/c-Src/H-ras/E2F1 and DNA damage response (DDR) proteins ATR/CHK1/BRCA1/CtIP were elevated in RBCC. AZD7762 exposure led to significantly higher levels of RS in RBCC, compared to the parental cells. The mechanisms by which CHK1 inhibition led to specific increase of RS in RBCC were related to the interruptions in the replication fork dynamics and the homologous recombination (HR). In summary, RBCC activate oncogenic pathways and thus depend upon mechanisms controlled by CHK1 signaling to maintain RS under control for survival. Our study provided the first example where upregulating RS by CHK1 inhibitor contributes to the specific killing of RBCC, and highlight the importance of the CHK1 as a potential target for treatment of radioresistant cancer cells

Targeting Radioresistant Breast Cancer Cells by Single Agent CHK1 Inhibitor via Enhancing Replication Stress

Radiotherapy (RT) remains a standard therapeutic modality for breast cancer patients. However, intrinsic or acquired resistance limits the efficacy of RT. Here, we demonstrate that CHK1 inhibitor AZD7762 alone significantly inhibited the growth of radioresistant breast cancer cells (RBCC). Given the critical role of ATR/CHK1 signaling in suppressing oncogene-induced replication stress (RS), we hypothesize that CHK1 inhibition leads to the specific killing for RBCC due to its abrogation in the suppression of RS induced by oncogenes. In agreement, the expression of oncogenes c-Myc/CDC25A/c-Src/H-ras/E2F1 and DNA damage response (DDR) proteins ATR/CHK1/BRCA1/CtIP were elevated in RBCC. AZD7762 exposure led to significantly higher levels of RS in RBCC, compared to the parental cells. The mechanisms by which CHK1 inhibition led to specific increase of RS in RBCC were related to the interruptions in the replication fork dynamics and the homologous recombination (HR). In summary, RBCC activate oncogenic pathways and thus depend upon mechanisms controlled by CHK1 signaling to maintain RS under control for survival. Our study provided the first example where upregulating RS by CHK1 inhibitor contributes to the specific killing of RBCC, and highlight the importance of the CHK1 as a potential target for treatment of radioresistant cancer cells

Negentropy Spectrum Decomposition and Its Application in Compound Fault Diagnosis of Rolling Bearing

The rolling bearings often suffer from compound fault in practice. Compared with single fault, compound fault contains multiple fault features that are coupled together and make it difficult to detect and extract all fault features by traditional methods such as Hilbert envelope demodulation, wavelet transform and empirical node decomposition (EMD). In order to realize the compound fault diagnosis of rolling bearings and improve the diagnostic accuracy, we developed negentropy spectrum decomposition (NSD), which is based on fast empirical wavelet transform (FEWT) and spectral negentropy, with cyclic extraction as the extraction method. The infogram is constructed by FEWT combined with spectral negentropy to select the best band center and bandwidth for band-pass filtering. The filtered signal is used as a new measured signal, and the fast empirical wavelet transform combined with spectral negentropy is used to filter the new measured signal again. This operation is repeated to achieve cyclic extraction, until the signal no longer contains obvious fault features. After obtaining the envelope of all extracted components, compound fault diagnosis of rolling bearings can be realized. The analysis of the simulation signal and the experimental signal shows that the method can realize the compound fault diagnosis of rolling bearings, which verifies the feasibility and effectiveness of the method. The method proposed in this paper can detect and extract all the fault features of compound fault completely, and it is more reliable for the diagnosis of compound fault. Therefore, the method has practical significance in rolling bearing compound fault diagnosis

Exploration of intrinsic brain activity in migraine with and without comorbid depression

Abstract Background Major depressive disorder is a common comorbidity in migraineurs. Depression may affect the progression and prognosis of migraine. Few studies have examined the brain function in migraineurs that may cause this comorbidity. Here, we aimed to explore depression-related abnormalities in the intrinsic brain activity of interictal migraineurs with comorbid depression using resting-state functional magnetic resonance imaging. Results Significant main effects of migraine and depression provided evidence that migraine and depression jointly affected the left medial prefrontal cortex, which was thought to be the neural basis of self-referential mental activity in previous studies. Abnormalities in this region may contribute to determining the common symptoms of migraine and depression and even result in comorbidity. Additionally, migraineurs with comorbid depression had different developmental trajectories in the right thalamus and fusiform, which were associated with recognizing, transmitting, controlling and remembering pain and emotion. Conclusions Based on our findings, the abnormal mPFC which may contribute to determining the common symptoms in migraine and depression and may be a therapeutic target for migraineurs comorbid depression. The different developmental trajectory in thalamus and fusiform indicates that the comorbidity may arise through a specific mechanism rather than simple superposition of migraine and depression

Efficacy and safety of human umbilical cord-derived mesenchymal stem cells for COVID-19 pneumonia: a meta-analysis of randomized controlled trials

Abstract Background Elevated levels of inflammatory factors are associated with poor prognosis in coronavirus disease-19 (COVID-19). However, mesenchymal stem cells (MSCs) have immunomodulatory functions. Accordingly, this meta-analysis aimed to determine the efficacy and safety of MSC-based therapy in patients with COVID-19 pneumonia. Methods Online global databases were used to find relevant studies. Two independent researchers then selected and evaluated the studies for suitability while the Cochrane risk of bias tool determined the quality of all articles and Cochran's Q test and I2 index assessed the degree of heterogeneity in the principal studies. Statistical analysis was performed using Review Manager software, and the effect of each study on the overall estimate was evaluated by sensitivity analysis. Results Seven studies were included in the meta-analysis, and all MSCs used in the trials were acquired from the umbilical cord. The results of these studies (n = 328) indicated that patients with COVID-19 pneumonia who received MSCs had a 0.58 risk of death compared with controls (95% CI = 0.38, 0.87; P = 0.53; I2 = 0%). In terms of inflammatory biomarkers, MSCs reduced the levels of C-reactive protein (n = 88; MD =  − 32.49; 95% CI =  − 48.43, − 16.56; P = 0.46; I2 = 0%) and interferon-gamma (n = 44; SMD =  − 1.23; 95% CI =  − 1.89, − 0.57; P = 0.37; I2 = 0%) in severe COVID-19 patients but had no significant effect on interleukin-6 (n = 185; MD =  − 0.75; 95% CI =  − 7.76, 6.27; P = 0.57; I2 = 0%). A summary of the data revealed no significant differences in adverse events (n = 287) or serious adverse events (n = 229) between the MSC and control groups. Conclusions Infusion of umbilical cord-derived MSCs is an effective strategy for treating patients with COVID-19 pneumonia, with no noticeable adverse effects

Suppression of insulin receptor substrate 1 (IRS-1) promotes mammary tumor metastasis

The insulin receptor substrate (IRS) proteins are cytoplasmic adaptors that organize signaling complexes downstream of activated cell surface receptors. Here, we show that IRS-1 and IRS-2, despite significant homology, play critical yet distinct functions in breast cancer, and we identify specific signaling pathways that are influenced by IRS-1 using the polyoma virus middle-T (PyV-MT) transgenic mouse model of mammary carcinoma and Irs-1 null (Irs1(-/-)) mice. The absence of Irs-1 expression enhanced metastatic spread significantly without a significant effect on primary tumor growth. Orthotopic transplant studies revealed that the increased metastatic potential of Irs1-deficient tumor cells is cell autonomous. Mammary tumors that developed in PyV-MT::Irs1(-/-) mice exhibited elevated Irs-2 function and enhanced phosphatidylinositol 3-kinase/Akt/mTor activity, suggesting that one mechanism by which Irs-1 impedes metastasis is to suppress Irs-2-dependent signaling. In support of this mechanism, reduction of Irs-2 expression in Irs1(-/-) tumor cells restored mTor signaling to wild-type levels. PyV-MT::Irs1(-/-) tumors also exhibited a significant increase in vascular endothelial growth factor expression and microvessel density, which could facilitate their dissemination. The significance of our findings for human breast cancer is heightened by our observation that Irs-1 is inactivated in wild-type, metastatic mammary tumors by serine phosphorylation. Collectively, our findings reveal that inactivation of IRS-1 enhances breast cancer metastasis and support the novel hypothesis that IRS-1 has metastasis suppressor functions for breast cancer