Climate change : strategies for mitigation and adaptation

The sustainability of life on Earth is under increasing threat due to humaninduced climate change. This perilous change in the Earth's climate is caused by increases in carbon dioxide and other greenhouse gases in the atmosphere, primarily due to emissions associated with burning fossil fuels. Over the next two to three decades, the effects of climate change, such as heatwaves, wildfires, droughts, storms, and floods, are expected to worsen, posing greater risks to human health and global stability. These trends call for the implementation of mitigation and adaptation strategies. Pollution and environmental degradation exacerbate existing problems and make people and nature more susceptible to the effects of climate change. In this review, we examine the current state of global climate change from different perspectives. We summarize evidence of climate change in Earth’s spheres, discuss emission pathways and drivers of climate change, and analyze the impact of climate change on environmental and human health. We also explore strategies for climate change mitigation and adaptation and highlight key challenges for reversing and adapting to global climate change

Permeability Enhancement of Coal Seam by Lower Protective Layer Mining for Gas Outburst Prevention

Risk prediction of dynamic disasters such as rock burst, gas outburst, and water inrush is closely related to the permeability evolution of coal seam. According to the characteristics of the lower protective layer mining, the basic assumption of gas-solid coupling model of the coal was proposed in this paper. The permeability enhancement coefficient of equivalent layer spacing was first put forward. Based on the three-zone-shaped dynamic evolution of the permeability of the overlying protective layer during the lower protective layer mining, the theories of seepage mechanics and damage mechanics were applied to introduce the permeability enhancement coefficient of equivalent layer spacing. A mathematical model of permeability evolution of the protected coal seam in the lower protective layer mining was established. Based on the engineering background of the lower protective layer mining in Changping Coal Mine, the numerical simulation using the proposed mathematical model was performed. The results showed that the stress and permeability of the protected layer in #3 coal seam evolved dynamically with the advancement of the working face of the protective layer in #8 coal seam. When the working face of the protective layer in #8 coal seam advanced to 80 m, the stress reduction rate in the relief area tended to be stable, and the stress in the stress reduction area was about 50% of the original rock stress. When advanced to 80 m, the permeability of the protected layer of the #3 coal seam increased sharply, and the permeability increased by 873 times. With the continuous advancement, the permeability of the protected layer in #3 coal seam tended to increase steadily, and the permeability increased by 1100–1200 times. The calculated magnitude of permeability increment is consistent with that in the engineering practice, indicating that the permeability evolution model is basically reasonable. The research provides a theoretical guidance for the gas drainage field application in the lower protective layer mining for prevention of coal and gas outburst

Correlation between neutrophil count and prognosis in STEMI patients with chronic renal dysfunction: a retrospective cohort study

Neutrophil is a key element in inflammation and stress disease, which are associated with poor clinical outcomes in various cardiac diseases. However, the clinical availability of neutrophil in patients with ST-elevation myocardial infarction (STEMI) and chronic renal dysfunction has not been known. Accordingly, we designed this retrospective cohort study to evaluate the differences of major adverse cardiovascular events incidence between renal dysfunctional STEMI patients with normal and high neutrophil levels. The primary end point was all-cause mortality. We analyzed 377 consecutive STEMI patients with chronic renal dysfunction. The results showed that during 12-48 months follow-up, death from any-cause occurred in 1.4% patients (4 of 290) in normal-level neutrophil group, as compared with 3.4% in high-level neutrophil group (3 of 87) (hazard ratio, 2.174 95% confidence interval, 1.024-10.248; P = 0.025). Kaplan-Meier survival analysis showed that there were significant differences between the two groups with respect to the risk of death (P=0.018), and heart failure (P=0.037)

Apigenin inhibits angiogenesis in retinal microvascular endothelial cells through regulating of the miR-140-5p/HDAC3-mediated PTEN/PI3K/AKT pathway

Abstract Background Diabetic retinopathy (DR) is a common cause of visual impairment. Apigenin has been shown to have antiangiogenic effects in various diseases. Our study aimed to investigate the role of apigenin in DR and elucidate the underlying mechanism. Methods Human retinal microvascular endothelial cells (HRMECs) were exposed to high glucose (HG) to establish a DR model. HRMECs were treated with apigenin. Then we knocked down or overexpressed miR-140-5p and HDAC3, and added PI3K/AKT inhibitor LY294002. The expression levels of miR-140-5p, HDAC3, and PTEN were measured using qRT-PCR. Western blot analysis was performed to assess the expression of HDAC3, PTEN, and PI3K/AKT pathway-related proteins. Finally, cell proliferation and migration were evaluated using MTT, wound-healing assay, and transwell assay, while angiogenesis was examined using the tube formation assay. Results HG treatment resulted in reduced miR-140-5p expression and overexpression of miR-140-5p suppressed proliferation, migration, and angiogenesis of the HG-induced HRMECs. Apigenin treatment significantly restored the decreased level of miR-140-5p caused by HG treatment and inhibited proliferation, migration, and angiogenesis of the HG-induced HRMECs by upregulating miR-140-5p. Moreover, miR-140-5p targeted HDAC3, and overexpression of miR-140-5p reversed the HG-inducted upregulation of HDAC3 expression. HDAC3 was found to bind to the promoter region of PTEN, inhibiting its expression. Knockdown of HDAC3 suppressed the PI3K/AKT pathway by elevating PTEN expression. Furthermore, apigenin inhibited angiogenesis in DR cell models through the regulating of the miR-140-5p/HDAC3-mediated PTEN/PI3K/AKT pathway. Conclusions Apigenin effectively suppressed angiogenesis in HG-induced HRMECs by modulating the miR-140-5p/HDAC3-mediated PTEN/PI3K/AKT pathway. Our study may contribute to the development of novel therapeutic approaches and identification of potential targets for the treatment of DR

Prognostic significance of Spinster homolog gene family in acute myeloid leukemia

Acute myeloid leukemia (AML) is a clonal and heterogeneous disease characterized by proliferation of immature myeloid cells, with impaired differentiation and maturation. Spinster homolog (SPNS) is a widely distributed transmembrane transporter, which assists sphingolipids in playing their roles through the cell membrane. However, the expression and clinical implication of the SPNS family has not been investigated in AML. From the Cancer Genome Atlas database, a total of 155 AML patients with complete clinical characteristics and SPNS1-3 expression data were contained in our study. In patients who received chemotherapy only, high expressions of SPNS2 and SPNS3 had adverse effects on event-free survival (EFS) and overall survival (OS) (all P＜0.05). However, in the allogeneic hematopoietic stem cell transplantation (allo-HSCT) group, we only found a significant difference in OS between the high and low SPNS3 expression groups (P=0.001), while other SPNS members showed no effect on survival. Multivariate analysis indicated that high SPNS2 expression was an independent risk factor for both EFS and OS in chemotherapy patients. The results confirmed that high expression of SPNS2 and SPNS3 were poor prognostic factors, and the effect of SPNS2 can be neutralized by allo-HSCT

Global Phosphoproteomic Analysis Reveals Significant Metabolic Reprogramming in the Termination of Liver Regeneration in Mice

Phosphorylation is crucial in regulating various biological processes. However, comprehensive phosphoproteomic profiling in the termination of liver regeneration (LR) is still missing. Here, we used Tandem Mass Tag (TMT) labeling coupled with phosphopeptide enrichment and two-dimensional (2D) liquid chromatography-mass spectrometry (LC-MS)/MS analysis to establish a global phosphoproteomic map in the liver of mice at day 5 after partial hepatectomy (PH). Altogether, 9731 phosphosites from 3443 proteins were identified and 7802 phosphosites from 2980 proteins were quantified. Motif analysis of the identified phosphosites revealed a diverse array of consensus sequences, suggesting that multiple kinase families including ERK/MAPK, PKA/PKC, CaMK-II, CKII, and CDK may be involved in the termination of LR. Functional clustering analysis of proteins with dysregulated phosphosites showed that they mainly participate in metabolic pathways, DNA replication, and tight junction. More importantly, the deletion of PP2Acα in the liver remarkably changes the overall phosphorylation profile, indicating its critical role in regulating the termination of LR. Finally, several differentially phosphorylated sites were validated by co-immunoprecipitation and Western blot. Taken together, our data unravel the first comprehensive phosphoproteomic map in the termination of LR in mice, which greatly expands our knowledge in the complicated regulation of this process and provides new directions for the treatment of liver cancer using liver resection

High IFITM3 expression predicts adverse prognosis in acute myeloid leukemia

Acute myeloid leukemia (AML) is a malignancy caused by the uncontrolled and dysregulated clonal expansion of abnormal myeloid primordial cells. In general, the prognosis of AML remains poor despite new discoveries in its pathogenesis and treatment. It is crucial to find early and sensitive biomarkers and continue to explore active targeted treatments. Interferon-induced transmembrane protein (IFITM) family is an important part of the interferon signaling pathway and participate in the regulation of immune cell signaling, adhesion, cancer, and liver cell migration. However, the clinical and prognostic value of the IFITM family in AML has rarely been studied. We screened The Cancer Genome Atlas database and found 155 AML patients with IFITM family (IFITM1-5) expression data. In patients who only received chemotherapy, those with high IFITM3 expression had significantly shorter event-free survival (EFS) and overall survival (OS) than patients with low expression (all P <0.05). Multivariate analysis demonstrated that high IFITM3 expression was an independent risk factor for EFS and OS in patients only received chemotherapy (all P <0.05). In patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT), however, all IFITM members had no impact on either EFS or OS. In conclusion, our study elucidated that high IFITM3 expression could be an adverse prognostic factor for AML, whose effect might be overcome by allo-HSCT