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Silencing of the Slt2-Type Road Kinase Bmp3 throughout Botrytis cinerea through Application of Exogenous dsRNA Has an effect on Fungal Progress and Virulence upon Lactuca sativa.
Background Inflammation and apoptosis play a crucial role in the progression of nonalcoholic steatohepatitis (NASH). Suppressor of cytokine signaling 2 (SOCS2) is one of classic negative regulators of cytokine signaling, which has recently been described as anti-inflammatory mediators. However, the role of SOCS2 in macrophages during NASH progression and the relationship among SOCS2, inflammation, apoptosis and NASH is largely unknown. Herein, we aimed to study the function of SOCS2 in NASH progression. Methods We detected SOCS2 expression in macrophages in human subjects without steatosis, with simple steatosis and with NASH to confirm the relationship between SOCS2 and NASH. Free fatty acids was used to establish stress environment in RAW 264.7 cell lines stably overexpressing or knockdown SOCS2. In vitro and vivo assays also performed to study the molecular function of SOCS2 in NASH progression. Findings Our human samples illustrated that SOCS2 was decreased in macrophages during NASH progression and was negatively correlated to NASH level. Meanwhile, In vitro assays showed SOCS2 overexpression in macrophages suppressed inflammation and apoptosis via inhibiting NF-κB signaling pathway, while SOCS2 knock-down in macrophages caused an increased activation of NF-κB, which could be blocked by ammonium 1-pyrrolidinedithiocarbamate (PDTC). In addition, SOCS2 in macrophages also suppressed inflammation via limiting the activation of inflammasomes. Consistent with these, our BMT model also confirmed the SOCS2 function in macrophages during NASH. Interpretation Our data strongly indicate that SOCS2 plays a role in inhibiting inflammation and apoptosis via NF-κB and inflammasome signaling pathway in macrophages during NASH. Further studies are required to explore the potential preventive and therapeutic strategies of SOCS2 for this common liver disease.Gastroesophageal reflux disease (GERD) is a common clinical disease associated with upper gastrointestinal motility disorders. Recently, with improvements in living standards and changes in lifestyle and dietary habits, the incidence of GERD has been increasing yearly. However, the mechanism of GERD has not been fully elucidated due to its complex pathogenesis, and this had led to unsatisfactory therapeutic outcomes. Currently, the occurrence and development of GERD involve multiple factors. Its pathogenesis is mainly thought to be related to factors, such as lower esophageal sphincter pressure, transient lower esophageal sphincter relaxation, crural diaphragmatic dysfunction, hiatus hernia, and impaired esophageal clearance. Therefore, explaining the pathogenesis of GERD more clearly and systematically, exploring potential and effective therapeutic targets, and choosing the best treatment methods have gradually become the focus of scholars' attention. Herein, we reviewed current advancements in the dynamic mechanism of GERD to better counsel patients on possible treatment options.Systemic application of glucocorticoids is an essential anti-inflammatory and immune-modulating therapy for severe inflammatory or autoimmunity conditions. However, its long-term effects on articular cartilage of patients' health need to be further investigated. see more In this study, we studied the effects of dexamethasone (Dex) on the homeostasis of articular cartilage and the progress of destabilization of medial meniscus (DMM)-induced osteoarthritis (OA) in adult mice. Long-term administration of Dex aggravates the proteoglycan loss of articular cartilage and drastically accelerates cartilage degeneration under surgically induced OA conditions. In addition, Dex increases calcium content in calcified cartilage layer of mice and the samples from OA patients with a history of long-term Dex treatment. Moreover, long term usage of Dex results in decrease subchondral bone mass and bone density. Further studies showed that Dex leads to calcification of extracellular matrix of chondrocytes partially through activation of AKT, as well as promotes apoptosis of chondrocytes in calcified cartilage layer. Besides, Dex weakens the stress-response autophagy with the passage of time. Taken together, our data indicate that long-term application of Dex may predispose patients to OA and or even accelerate the OA disease progression development of OA patients.Objective Angiogenesis is involved in multiple biological processes, including atherosclerosis (AS) and cancer. Dickkopf1 (DKK1) plays many roles in both tumors and AS and has emerged as a potential biomarker of cancer progression and prognosis. Targeting DKK1 is a good choice for oncological treatments. Many anticancer therapies are associated with specific cardiovascular toxicity. However, the effects of DKK1 neutralizing therapy on AS are unclear. We focused on how DKK1 affected angiogenesis in AS and ox-LDL-induced human umbilical vein endothelial cells (HUVECs). Methods ApoE-/- mice were fed a high-fat diet and then injected with DKK1i or DKK1 lentivirus to study the effects of DKK1. In vitro, promoter assays, protein analysis, database mining, dual-luciferase reporter assay (DLR), electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP), and coimmunoprecipitation (co-IP) were used to study the mechanism of DKK1 biogenesis. Cell migration and angiogenesis assays were performed tocular protection.Laron syndrome (LS) is an autosomal recessive genetic disease mainly caused by mutations in the human growth hormone receptor (GHR) gene. Previous studies have focused on Ghr mutant mice, but compared with LS patients, Ghr knockout (KO) mice exhibit differential lipid metabolism. To elucidate the relationship between GHR mutation and lipid metabolism, the role of GHR in lipid metabolism was examined in GHR KO pigs and hepatocytes transfected with siGHR. We observed high levels of free fatty acids and hepatic steatosis in GHR KO pigs, which recapitulates the abnormal lipid metabolism in LS patients. RNAseq analysis revealed that genes related to the fatty acid oxidation pathway were significantly altered in GHR KO pigs. AHR, a transcription factor related to lipid metabolism, was significantly downregulated in GHR KO pigs and siGHR-treated human hepatocytes. We found that AHR directly regulated fatty acid oxidation by directly binding to the promoters of ACOX1 and CPT1A and activating their expression. These data indicate that loss of GHR disturbs the ERK-AHR-ACOX1/CPT1A pathway and consequently leads to hepatic steatosis. Our results established AHR as a modulator of hepatic steatosis, thereby providing a therapeutic target for lipid metabolism disorder.Diabetic nephropathy (DN) has become the common and principal microvascular complication of diabetes that could lead to end-stage renal disease. It was reported endothelial-to-mesenchymal transition (EndMT) in glomeruli plays an important role in DN. Enolase1 (ENO1) and Lysine Methyltransferase 5A (KMT5A) were found to modulate epithelial-to-mesenchymal transition in some situations. In the present study, we speculated KMT5A regulates ENO1 transcript, thus participating in hyperglycemia-induced EndMT in glomeruli of DN. Our study represented vimentin, αSMA and ENO1 expression elevated, and CD31 expression decreased in glomeruli of DN participants and rats. In vitro, high glucose induced EndMT by increase of ENO1 levels. Moreover, high glucose downregulated KMT5A levels and increased regulatory factor X1 (RFX1) levels. KMT5A upregulation or si-RFX1 decreased high glucose-induced ENO1 expression and EndMT. RFX1 overexpression- or sh-KMT5A-induced EndMT was attenuated by si-ENO1. Further, the association between KMT5A and RFX1 was verified. Furthermore, histone H4 lysine20 methylation (the direct target of KMT5A) and RFX1 positioned on ENO1 promoter region. sh-KMT5A enhanced positive action of RFX1 on ENO1 promoter activity. KMT5A reduction and RFX1 upregulation were verified in glomeruli of DN patients and rats. KMT5A associated with RFX1 to modulate ENO1, thus involved in hyperglycemia-mediated EndMT in glomeruli of DN.[This retracts the article DOI 10.7150/ijbs.7723.].We review the recent progress made in using holographic QCD to study hadronic contributions to the anomalous magnetic moment of the muon, in particular the hadronic light-by-light scattering contribution, where the short-distance constraints associated with the axial anomaly are notoriously difficult to satisfy in hadronic models. This requires the summation of an infinite tower of axial vector mesons, which is naturally present in holographic QCD models, and indeed takes care of the longitudinal short-distance constraint due to Melnikov and Vainshtein. Numerically the results of simple hard-wall holographic QCD models point to larger contributions from axial vector mesons than assumed previously, while the predicted contributions from pseudo-Goldstone bosons agree nicely with data-driven approaches.Streams and rivers form dense networks that drain the terrestrial landscape and are relevant for biodiversity dynamics, ecosystem functioning, and transport and transformation of carbon. Yet, resolving in both space and time gross primary production (GPP), ecosystem respiration (ER) and net ecosystem production (NEP) at the scale of entire stream networks has been elusive so far. Here, combining Random Forest (RF) with time series of sensor data in 12 reach sites, we predicted annual regimes of GPP, ER, and NEP in 292 individual stream reaches and disclosed properties emerging from the network they form. We further predicted available light and thermal regimes for the entire network and expanded the library of stream metabolism predictors. We found that the annual network-scale metabolism was heterotrophic yet with a clear peak of autotrophy in spring. In agreement with the River Continuum Concept, small headwaters and larger downstream reaches contributed 16% and 60%, respectively, to the annual network-scale GPP. Our results suggest that ER rather than GPP drives the metabolic stability at the network scale, which is likely attributable to the buffering function of the streambed for ER, while GPP is more susceptible to flow-induced disturbance and fluctuations in light availability. Furthermore, we found large terrestrial subsidies fueling ER, pointing to an unexpectedly high network-scale level of heterotrophy, otherwise masked by simply considering reach-scale NEP estimations. Our machine learning approach sheds new light on the spatiotemporal dynamics of ecosystem metabolism at the network scale, which is a prerequisite to integrate aquatic and terrestrial carbon cycling at relevant scales.
The online version contains supplementary material available at (10.1007/s10021-021-00618-8).
The online version contains supplementary material available at (10.1007/s10021-021-00618-8).This paper presents an approach how to create FAIR data for prehistoric mining archaeology, based on the CIDOC CRM ontology and semantic web standards. The interdisciplinary Research Centre HiMAT (History of mining activities in the Tyrol and adjacent areas, University of Innsbruck) investigates mining history from prehistoric to modern times with an interdisciplinary approach. One of the projects carried out at the research centre is the multinational DACH project "Prehistoric copper production in the eastern and central Alps". For a specific geographical region of the project, the data transformation to open and re-usable data is investigated in a separate Open Research Data pilot project. The methodological approach will use the FAIR principles to make data Findable, Accessible, Interoperable and Re-usable. Every archaeological investigation in Austria has to be documented according to the requirements of the Austrian Federal Monuments Office. This documentation is deposited in the CERN-based EU supported research data repository ZENODO.
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