Greenhouse gas emissions from extractive industries in a globalized era.

The extractive industry consumes vast amounts of energy and is a major contributor to greenhouse gas (GHG) emissions. However, its climatic impacts have not yet been fully accounted for. In this study, we estimated the GHG emissions from extractive activities globally with a focus on China, and assessed the main emission drivers. In addition, we predicted the Chinese extractive industry emissions in the context of global mineral demand and cycling. As of 2020, GHG emissions from the global extractive industry had reached 7.7 billion tons of CO2 equivalents (CO2e), accounting for approximately 15.0% of the global anthropogenic GHG emissions (excluding GHG emissions from land use, land-use change, and forestry activities (LULUCF), with China being the largest emitter, accounting for 3.5% of global emissions. Extractive industry GHG emissions are projected to peak by 2030 or even earlier to achieve low-carbon peak targets. The most critical pathway for reducing GHG emissions in the extractive industry is to control emissions from coal mining. Therefore, reducing methane emissions from mining and washing coal (MWC) should be prioritized.

Protein Kinase CK2 Maintains Reciprocal Balance Between Th17 and Treg Cells in the Pathogenesis of UC.

BACKGROUND: T helper 17 and regulatory T cells balance have crucial effects on the development of ulcerative colitis (UC). Currently, how to break this balance has not yet been found. Protein kinase CK2 is involved in the pathogenesis of immune-related disorders. However, its effects on the development of UC are obscure. METHODS: The level of CK2 in the colonic tissues of UC patients was quantified by quantitative real-time polymerase chain reaction (qRT-PCR) and immune-histochemistry. Peripheral blood CD4+ T cells were treated with CK2 inhibitor CX4945 or transfected with Csnk2-interfering lentivirus; the mRNA expression and protein levels of inflammatory cytokines were detected by qRT-PCR, enzyme-linked immunosorbent assay, and flow cytometry. Moreover, CX4945 was administered to trinitrobenzene sulfonic acid (TNBS)-induced colitis mice model for determining the function of CK2 on the regulation of intestinal inflammation. RESULTS: The CK2 level was markedly increased in inflamed mucosa of UC and highly expressed in CD4+ T cells. Blockade of CK2 by CX4945 inhibited Th17 but promoted regulatory T-cell (Treg) immune responses in CD4+ T cells from patients with UC. Moreover, CK2 blockade alleviated TNBS-induced colitis in mice. Inhibition of CK2 suppressed Th17 but promoted Treg differentiation by decreasing the phosphorylation level of signal transducer and activator of transcription (STAT) 3 and increasing the phosphorylation level of STAT5. The RNA-Seq and co-immunoprecipitation analysis further showed that CK2 could interact with Sirtuin 1 (SIRT1) and downregulate SIRT1 expression, which participated in Th17 inhibition but promoted Treg differentiation. Sirtuin 1 upregulation ameliorated TNBS-induced colitis, whereas SIRT1 blockade aggravated TNBS-induced colitis in mice. CONCLUSIONS: CK2 have crucial effects on the development of UC by maintaining reciprocal balance between Th17 and Treg cells. Protein kinase CK2 blockade might be considered as a new therapeutic approach for UC treatment.

A case report about eosinophilic enteritis presenting as abdominal pain.

RATIONALE: Eosinophilic enteritis (EE) is an immune-mediated antigen-driven disease that may lead to clinical symptoms and organ dysfunction and characterized by the presence of extensive eosinophilic infiltrates on histopathological examination of the intestinal mucosa. PATIENT CONCERNS: A 29-year-old man presented with a half-month duration of paroxysmal upper abdominal pain that gradually evolved into continuous pain accompanied by the urge to defecate. DIAGNOSES: Pathological findings of enteroscopy showed acute and chronic inflammation accompanied by eosinophilic infiltration (>20/ high-power field). INTERVENTIONS: The patient was initially treated with IV infusion of dexamethasone 10 mg per day for 3 days, which was reduced to 7.5 mg per day for 2 days once pain relief was achieved. Upon discharged from our hospital, the patient was prescribed with oral prednisolone 30 mg per day, which was reduced by 5 mg per week for 6 weeks until discontinuation. OUTCOMES: The patient was relieved from the pain after receiving dexamethasone for 5 days, and he was maintained on oral prednisolone 30 mg per day upon discharge from the hospital. On the day of discharge, the eosinophil count and derived ratios were normal. LESSONS: In patients with EE, the dynamic changes of the eosinophil count should be monitored. Clinicians must be aware that not all patients with EE have a history of allergies. In the management and treatment of the disease, multisite biopsies should be carried out if EE is suspected, and EE is responsive to steroid therapy.

Blockade of CXCR2 suppresses proinflammatory activities of neutrophils in ulcerative colitis.

Ulcerative colitis (UC) is one chronically remittent and progressive inflammatory disorder. Chemokine receptor CXCR2 is reported to be involved in the pathogenesis of several inflammatory diseases. However, how CXCR2 modulate mucosal inflammation in UC is still obscure. In this study, CXCR2 expression was determined in inflamed mucosa and peripheral blood cells from patients with UC by qRT-PCR. Neutrophils isolated from peripheral blood were pretreated with CXCR2 inhibitor (SB225002), and proinflammatory mediators were examined by qRT-PCR, ELISA and IF. The migratory capacity of neutrophils after SB225002 treatment was examined by using Transwell plate. Furthermore, SB225002 was administrated daily in DSS-induced colitis mice. We found that CXCR2 expression was significantly increased in colonic mucosal tissues and peripheral blood cells from patients with active UC. Besides, CXCR2 was highly expressed in neutrophils, and was positively correlated with disease activity. Inhibition of CXCR2 in neutrophils decreased the production of proinflammatory mediators, such as reactive oxygen species (ROS), MPO, S100a8, S100a9, TNF-α, IL-1ß, IL-8 and IL-6, and the migratory capacity of neutrophils was markedly impaired after SB225002 treatment. Moreover, blockade of CXCR2 with SB225002 could markedly ameliorate DSS-induced colitis in mice. In summary, CXCR2 plays a critical role in the pathogenesis of UC through modulating immune responses of neutrophils. Blockade of CXCR2 may serve as a new therapeutic approach for treatment of UC.

Kaempferol suppresses human gastric cancer SNU-216 cell proliferation, promotes cell autophagy, but has no influence on cell apoptosis.

Gastric cancer remains a serious threat to human health worldwide. Kaempferol is a plant-derived flavonoid compound with a wide range of pharmacological activities. This study aimed to investigate the effects of kaempferol on gastric cancer SNU-216 cell proliferation, apoptosis, and autophagy, as well as underlying potential mechanisms. Viability, proliferation, and apoptosis of SNU-216 cells after kaempferol treatment were evaluated using cell counting kit-8 assay, 5-btomo-2'-deoxyuridine incorporation assay, and annexin V-FITC/PI staining, respectively. Quantitative reverse transcription PCR was performed to measure the mRNA expressions of cyclin D1 and microRNA-181a (miR-181a) in SNU-216 cells. Cell transfection was used to down-regulate the expression of miR-181a. The protein expression levels of cyclin D1, bcl-2, bax, caspase 3, caspase 9, autophagy-related gene 7, microtubule-associated protein 1 light chain 3-I (LC3-I), LC3-II, Beclin 1, p62, mitogen-activated protein kinase (MAPK), extracellular regulated protein kinases (ERK), and phosphatidylinositol 3 kinase (PI3K) in SNU-216 cells were detected using western blotting. Results showed that kaempferol significantly suppressed SNU-216 cell viability and proliferation but had no influence on cell apoptosis. Further results suggested that kaempferol significantly induced SNU-216 cell autophagy. The expression of miR-181a in SNU-216 cells after kaempferol treatment was enhanced. Kaempferol significantly inactivated MAPK/ERK and PI3K pathways in SNU-216 cells. Suppression of miR-181a significantly reversed the kaempferol-induced MAPK/ERK and PI3K pathways inactivation in SNU-216 cells. This research demonstrated that kaempferol suppressed proliferation and promoted autophagy of human gastric cancer SNU-216 cells by up-regulating miR-181a and inactivating MAPK/ERK and PI3K pathways.

TGF-ß/Smad3 pathway enhances the cardio-protection of S1R/SIPR1 in in vitro ischemia-reperfusion myocardial cell model.

Ischemia-reperfusion (IR) injury is usually associated with a high risk of cardiomyocyte death in patients with acute myocardial infarction. Sphingosine 1-phosphate (S1P) and transforming growth factor (TGF)-ß are thought to be involved in the protection of cardiomyocyte and heart function following IR-induced injury. However, the possible association of S1P and S1P receptor 1 (S1PR1) with the TGF-ß/Smad3 pathway as the potential protective mechanism has remained to be investigated. In the present study, an in vitro ischemia/reperfusion injury model was established and evaluated by analysis of apoptosis, lactate dehydrogenase (LDH) release and caspase3 activity. The mRNA and protein levels of S1PR1, TGF-ß and Smad3 after treatment with 1 µM S1P alone or combined with 0.4 µM W146 (a specific S1PR1 antagonist) were assessed. The mRNA expression of five S1PRs (S1PR1-5) and the protein levels of S1PR1 were also assayed following treatment with 1 ng/ml TGF-ß for 0, 4 or 24 h. The mRNA expression of S1PR1 and the levels of S1P were further assessed following exposure to 10 µM SB4 (TGFßR1 inhibitor) plus 1 ng/ml TGF-ß and 2 µM SIS3 (Smad3 inhibitor) plus 1 ng/ml TGF-ß. The results indicated that apoptosis, LDH release and caspase3 activity were all increased in the established IR model. Exogenous S1P increased the mRNA and protein levels of S1PR1, TGF-ß and Smad3, which was abolished by addition of W146. Extraneous TGF-ß resulted in the stimulation of several S1PRs, most prominently of S1PR1, while supplementation with SB4 and SIS3 offset the stimulation by TGF-ß. These results suggested that the TGF-ß/Smad3 pathway was closely associated with S1P/S1PR1 in the protection of myocardial cells from IR injury.

Kaempferol suppresses human gastric cancer SNU-216 cell proliferation, promotes cell autophagy, but has no influence on cell apoptosis

Gastric cancer remains a serious threat to human health worldwide. Kaempferol is a plant-derived flavonoid compound with a wide range of pharmacological activities. This study aimed to investigate the effects of kaempferol on gastric cancer SNU-216 cell proliferation, apoptosis, and autophagy, as well as underlying potential mechanisms. Viability, proliferation, and apoptosis of SNU-216 cells after kaempferol treatment were evaluated using cell counting kit-8 assay, 5-btomo-2′-deoxyuridine incorporation assay, and annexin V-FITC/PI staining, respectively. Quantitative reverse transcription PCR was performed to measure the mRNA expressions of cyclin D1 and microRNA-181a (miR-181a) in SNU-216 cells. Cell transfection was used to down-regulate the expression of miR-181a. The protein expression levels of cyclin D1, bcl-2, bax, caspase 3, caspase 9, autophagy-related gene 7, microtubule-associated protein 1 light chain 3-I (LC3-I), LC3-II, Beclin 1, p62, mitogen-activated protein kinase (MAPK), extracellular regulated protein kinases (ERK), and phosphatidylinositol 3 kinase (PI3K) in SNU-216 cells were detected using western blotting. Results showed that kaempferol significantly suppressed SNU-216 cell viability and proliferation but had no influence on cell apoptosis. Further results suggested that kaempferol significantly induced SNU-216 cell autophagy. The expression of miR-181a in SNU-216 cells after kaempferol treatment was enhanced. Kaempferol significantly inactivated MAPK/ERK and PI3K pathways in SNU-216 cells. Suppression of miR-181a significantly reversed the kaempferol-induced MAPK/ERK and PI3K pathways inactivation in SNU-216 cells. This research demonstrated that kaempferol suppressed proliferation and promoted autophagy of human gastric cancer SNU-216 cells by up-regulating miR-181a and inactivating MAPK/ERK and PI3K pathways.