Intracerebral hemorrhage (ICH) is a subtype of stroke and causes disability and death worldwide. The roles of long noncoding RNAs (lncRNAs) in brain function and neurological diseases have been revealed. LncRNA maternally expressed gene 3 (MEG3) is involved in neurological impairment, but its role in ICH remains unknown.

The aim of this research is to explore the role of MEG3 in ICH.

Here, we established an ICH mouse model via intracerebral injection of autologous blood. Primary brain microvascular endothelial cells (BMECs) were treated with oxygen-and-glucose-deprivation (OGD) plus hemin to establish the model in vitro. We observed that MEG3 expression was significantly upregulated in both ICH mouse model and OGD/hemin (OGD/H) induced BMECs. The downregulation of MEG3 suppressed cell apoptosis and the activation of NOD-like receptor family protein 3 (NLRP3) inflammasome in OGD/H-induced BMECs. In ICH mice, MEG3 downregulation inhibited cell apoptosis and improved brain dysfunction. Mechanistically, MEG3 was confirmed to act as a molecular sponge for microRNA (miR)-1930-5p, and Mllt1 was a downstream target for miR-1930-5p. MEG3 competitively bound with miR-1930-5p to upregulate Mllt1. We further verified that Mllt1 overexpression reversed the inhibitory effect of miR-1930-5p in OGD/H-induced BMECs.

In conclusion, lncRNA MEG3 promoted the dysfunction of BMECs by modulating the miR-1930-5p/Mllt1 axis, which provides a potential target in gene therapy for brain injury following ICH.

In conclusion, lncRNA MEG3 promoted the dysfunction of BMECs by modulating the miR-1930-5p/Mllt1 axis, which provides a potential target in gene therapy for brain injury following ICH.Pancreatic cancer (PC) is one the deadliest cancers worldwide. It is characterized by elevated mortality rates because of the lack of effective diagnostic methods, the dense stroma that shields the tumor from effective drug penetration, and the emergence of chemoresistance. Recent research has elucidated the role of PC-derived exosomes in driving and fueling PC progression, metastasis, and chemoresistance by transporting key molecules from tumor cells to recipient cells in the tumor microenvironment (TME). In this review, we delineate some of the key exosomal molecules involved in immune suppression and reprogramming of the TME, the establishment of metastatic niches, and drug resistance. We also explore the potential of exosomes as both diagnostic tools for early PC detection and management and as therapeutic targets.

Canola oil (CO) is a plant-based oil with the potential to improve several cardiometabolic risk factors. We systematically reviewed controlled clinical trials investigating the effects of CO on lipid profiles, apo-lipoproteins, glycemic indices, inflammation, and blood pressure compared to other edible oils in adults.

Online databases were searched for articles up to January 2020. Forty-two articles met the inclusion criteria. CO significantly reduced total cholesterol (TC, -0.27mmol/l, n=37), low-density lipoprotein cholesterol (LDL-C, -0.23mmol/l, n=35), LDL-C to high-density lipoprotein cholesterol ratio (LDL/HDL, -0.21, n=10), TC/HDL (-0.13, n=15), apolipoprotein B (Apo B, -0.03g/l, n=14), and Apo B/Apo A-1 (-0.02, n=6) compared to other edible oils (P < 0.05). Compared to olive oil, CO decreased TC (-0.23mmol/l, n=9), LDL-C (-0.17mmol/l, n=9), LDL/HDL (-0.39, n=2), and triglycerides in VLDL (VLDL-TG, -0.10mmol/l, n=2) (P < 0.05). Compared to sunflower oil, CO improved LDL-C (-0.14mmol/l, n=11), and LDL/HDL (-0.30, n=3) (P < 0.05). In comparison with saturated fats, CO improved TC (-0.59mmol/l, n=11), TG (-0.08mmol/l, n=11), LDL-C (-0.49mmol/l, n=10), TC/HDL (-0.29, n=5), and Apo B (-0.09g/l, n=4) (P < 0.05). Based on the nonlinear dose-response curve, replacing CO with ~15% of total caloric intake provided the greatest benefits.

CO significantly improved different cardiometabolic risk factors compared to other edible oils. Further well-designed clinical trials are warranted to confirm the dose-response associations.

CO significantly improved different cardiometabolic risk factors compared to other edible oils. Further well-designed clinical trials are warranted to confirm the dose-response associations.Chlorinated ethenes (CEs) are most problematic pollutants in groundwater. Dehalogenating bacteria, and in particular organohalide-respiring bacteria (OHRB), can transform PCE to ethene under anaerobic conditions, and thus contribute to bioremediation of contaminated sites. check details Current approaches to characterize in situ biodegradation of CEs include hydrochemical analyses, quantification of the abundance of key species (e.g. Dehalococcoides mccartyi) and dehalogenase genes (pceA, vcrA, bvcA and tceA) involved in different steps of organohalide respiration (OHR) by qPCR, and compound-specific isotope analysis (CSIA) of CEs. Here we combined these approaches with sequencing of 16S rRNA gene amplicons to consider both OHRB and bacterial taxa involved in CE transformation at a multi-contaminated site. Integrated analysis of hydrogeochemical characteristics, gene abundances and bacterial diversity shows that bacterial diversity and OHRB mainly correlated with hydrogeochemical conditions, suggesting that pollutant exposure acts as a central driver of bacterial diversity. CSIA, abundances of four reductive dehalogenase encoding genes and the prevalence of Dehalococcoides highlighted sustained PCE, DCE and VC degradation in several wells of the polluted plume. These results suggest that bacterial taxa associated with OHR play an essential role in natural attenuation of CEs, and that representatives of taxa including Dehalobacterium and Desulfosporosinus co-occur with Dehalococcoides. Overall, our study emphasizes the benefits of combining several approaches to evaluate the interplay between the dynamics of bacterial diversity in CE-polluted plumes and in situ degradation of CEs, and to contribute to a more robust assessment of natural attenuation at multi-polluted sites.Controlling the morphology of noble metal-based nanostructures is a powerful strategy for optimizing their catalytic performance. Here, we report a one-pot aqueous synthesis of versatile NiPd nanostructures at room temperature without employing organic solvents or surfactants. The synthesis can be tuned to form zero-dimensional (0D) architectures, such as core-shell and hollow nanoparticles (NPs), as well as nanostructures with higher dimensionality, such as extended nanowire networks and three-dimensional (3D) nanodendrites. The diverse morphologies were successfully obtained through modification of the HCl concentration in the Pd precursor solution, and the reaction aging time. An in-depth understanding of the formation mechanism and morphology evolution are described in detail. A key factor in the structural evolution of the nanostructures was the ability to tune the reduction rate and to protonate the citrate stabiliser by adding HCl. Spherical core-shell NPs were formed by the galvanic replacement-free deposition of Pd on Ni NPs which can be transformed to hollow NPs via a corrosion process.