Recently, porous hydrophobic/oleophilic materials (PHOMs) have been shown to be the most promising candidates for cleaning up oil spills; however, due to their limited absorption capacity, a large ...quantity of PHOMs would be consumed in oil spill remediation, causing serious economic problems. In addition, the complicated and time‐consuming process of oil recovery from these sorbents is also an obstacle to their practical application. To solve the above problems, we apply external pumping on PHOMs to realize the continuous collection of oil spills in situ from the water surface with high speed and efficiency. Based on this novel design, oil/water separation and oil collection can be simultaneously achieved in the remediation of oil spills, and the oil sorption capacity is no longer limited to the volume and weight of the sorption material. This novel external pumping technique may bring PHOMs a step closer to practical application in oil spill remediation.
Thirsty, thirsty PHOMs: The continuous collection of oil spills in situ from the surface of water can be accomplished through external pumping on porous hydrophobic/oleophilic materials (PHOMs). Based on this novel design, oil/water separation and oil collection can be simultaneously achieved, and the oil sorption capacity is no longer limited to the volume and weight of the sorption material.
Background
Laparoscopic hepatectomy (LH) has been proposed as a safe and feasible treatment option for liver diseases. However, the short- and long-term outcomes of LH versus open hepatectomy (OH) ...for hepatocellular carcinoma (HCC) have not been adequately assessed. Thus, as another means of surgical therapy for hepatocellular carcinoma (HCC), we assessed the feasibility of performing LH as the standard procedure for disease in the left lateral lobe and peripheral right segments for HCC in selected patients.
Methods
Literature search included PubMed, Embase, Science Citation Index, SpringerLink, and secondary sources, from inception to March 2012, with no restrictions on languages or regions. The fixed-effects and random-effects models were used to measure the pooled estimates. The test of heterogeneity was performed by the Q statistic. Subgroup and sensitivity analyses were performed to explore heterogeneity between studies and to assess the effects of study quality.
Results
A total of 1238 patients (LH 485, OH 753) from 15 studies were included. The pooled odds ratios for postoperative morbidity and incidence of negative surgical margin in LH were found to be 0.37 (95 % confidence interval CI 0.27–0.52;
P
< 0.01) and 1.63 (95 % CI 0.82–3.22;
P
= 0.16), respectively, compared with OH. Blood loss was significantly decreased in the LH (weighted mean difference −224.63; 95 % CI −384.87 to −64.39;
P
= 0.006). No significant difference was observed between the both groups for long-term outcomes of overall survival and recurrence-free survival.
Conclusions
In patients with solitary left lateral lobe/right peripheral subcapsular tumors treated with minor resection, this meta-analysis demonstrated that compared to OH, LH may have short-term advantages in terms of blood loss and postoperative morbidity for HCC. Both procedures have similar long-term outcomes. It may be time to consider changing the standard procedures for treatment of HCC in the left lateral lobe and peripheral subcapsular right segments in selected patients.
Vacuolar protein sorting-35 (VPS35) is essential for endosome-to-Golgi retrieval of membrane proteins. Mutations in the VPS35 gene have been identified in patients with autosomal dominant PD. ...However, it remains poorly understood if and how VPS35 deficiency or mutation contributes to PD pathogenesis. Here we provide evidence that links VPS35 deficiency to PD-like neuropathology. VPS35 was expressed in mouse dopamine (DA) neurons in substantia nigra pars compacta (SNpc) and STR (striatum)--regions that are PD vulnerable. VPS35-deficient mice exhibited PD-relevant deficits including accumulation of α-synuclein in SNpc-DA neurons, loss of DA transmitter and DA neurons in SNpc and STR, and impairment of locomotor behavior. Further mechanical studies showed that VPS35-deficient DA neurons or DA neurons expressing PD-linked VPS35 mutant (D620N) had impaired endosome-to-Golgi retrieval of lysosome-associated membrane glycoprotein 2a (Lamp2a) and accelerated Lamp2a degradation. Expression of Lamp2a in VPS35-deficient DA neurons reduced α-synuclein, supporting the view for Lamp2a as a receptor of chaperone-mediated autophagy to be critical for α-synuclein degradation. These results suggest that VPS35 deficiency or mutation promotes PD pathogenesis and reveals a crucial pathway, VPS35-Lamp2a-α-synuclein, to prevent PD pathogenesis. Significance statement: VPS35 is a key component of the retromer complex that is essential for endosome-to-Golgi retrieval of membrane proteins. Mutations in the VPS35 gene have been identified in patients with PD. However, if and how VPS35 deficiency or mutation contributes to PD pathogenesis remains unclear. We demonstrated that VPS35 deficiency or mutation (D620N) in mice leads to α-synuclein accumulation and aggregation in the substantia nigra, accompanied with DA neurodegeneration. VPS35-deficient DA neurons exhibit impaired endosome-to-Golgi retrieval of Lamp2a, which may contribute to the reduced α-synuclein degradation through chaperone-mediated autophagy. These results suggest that VPS35 deficiency or mutation promotes PD pathogenesis, and reveals a crucial pathway, VPS35-Lamp2a-α-synuclein, to prevent PD pathogenesis.
Stretching the role of a conductor: A new kind of polyurethane sponge–Ag nanowire–poly(dimethylsiloxane) (PUS‐AgNW‐PDMS) stretchable conductors can be easily fabricated based on a novel binary ...network structure design, which greatly enhances their electronic performance. These PUS‐AgNW‐PDMS elastomeric conductors show improved electromechanical stability compared to previously reported stretchable conductors.
Fingolimod (FTY720) is used as an immunosuppressant for multiple sclerosis. Numerous studies indicated its neuroprotective effects in stroke. However, the mechanism remains to be elucidated. This ...study was intended to investigate the mechanisms of phosphorylated FTY720 (pFTY720), which was the principle active molecule in regulating astrocyte‐mediated inflammatory responses induced by oxygen‐glucose deprivation (OGD). Results demonstrated that pFTY720 could protect astrocytes against OGD‐induced injury and inflammatory responses. It significantly decreased pro‐inflammatory cytokines, including high mobility group box 1 (HMGB1) and tumour necrosis factor‐α (TNF‐α). Further, studies displayed that pFTY720 could prevent up‐regulation of Toll‐like receptor 2 (TLR2), phosphorylation of phosphoinositide 3‐kinase (PI3K) and nuclear translocation of nuclear factor kappa B (NFκB) p65 subunit caused by OGD. Sphingosine‐1‐phosphate receptor 3 (S1PR3) knockdown could reverse the above change. Moreover, administration of TLR2/4 blocker abolished the protective effects of pFTY720. Taken together, this study reveals that pFTY720 depends on S1PR3 to protect astrocytes against OGD‐induced neuroinflammation, due to inhibiting TLR2/4‐PI3K‐NFκB signalling pathway.
Transarterial chemoembolization (TACE) is the standard treatment for unresectable hepatocellular carcinoma (HCC). Hypoxia‐induced angiogenesis by TACE is linked to treatment failure; however, whether ...the chemotherapeutic damage of TACE to HCC could increase tumor angiogenesis has not been explored. The molecular effects of chemotherapy‐damaged HCC cells on the neo‐angiogenesis were investigated in vitro and in vivo. The expression of growth differentiation factor 15 (GDF15) was significantly upregulated in HCC cells exposed to chemotherapeutic agents. GDF15 from chemotherapy‐damaged HCC cells promoted the in vitro proliferation, migration, and tube formation of endothelial cells. The pro‐angiogenic effect of GDF15 was through the activation of Src and its downstream AKT, MAPK, and NF‐κB signaling, which was blocked by thalidomide. The use of thalidomide significantly attenuated the in vivo chemotherapy‐damaged HCC cells‐promoted angiogenesis in nude mice. In conclusion, the chemotherapeutic damage in TACE to HCC could promote tumor angiogenesis via the increased release of GDF15. Thalidomide could reverse these pro‐angiogenic effects.
Chemotherapeutic damage to hepatocellular carcinoma promotes tumor angiogenesis via the increased release of GDF15. Thalidomide could reverse these pro‐angiogenic effects.
By conventional ceramics sintering technique, the lead‐free 0.85Bi0.5Na0.5(1−x)Li0.5xTiO3‐0.11Bi0.5K0.5TiO3‐0.04BaTiO3 (x =0–0.15) piezoelectric ceramics were obtained and the effects of Li dopant on ...the piezoelectric, dielectric, and ferroelectric properties were studied. With increasing Li addition, the temperature‐dependent permittivity exhibited the normal ferroelectric‐to‐ergodic relaxor (FE‐to‐ER) transition temperature (TFE‐ER, abbreviated as TF‐R) decreasing down to room temperature. The increasing Li content also enhanced the diffuseness of the FE‐to‐ER transition behavior. For composition with x = 0.15, a large unipolar strain of 0.37% (d33∗ = Smax/Emax = 570 pm/V) was achieved under 6.5 kV/mm applied electric field at room temperature. Both unipolar and bipolar strain curves related to the temperature closely, and when the temperature reached the TF‐R, the normalized strain d33∗ achieved a maximum value (e.g., for x = 0.10, d33∗ = 755 pm/V) owing to the electric‐field‐induced ER‐to‐FE state transition.
Alanine-serine-cysteine transporter 2 (ASCT2, SLC1A5) is the primary transporter of glutamine in cancer cells and regulates the mTORC1 signaling pathway. The SLC1A5 function involves finely tuned ...orchestration of two domain movements that include the substrate-binding transport domain and the scaffold domain. Here, we present cryo-EM structures of human SLC1A5 and its complex with the substrate, L-glutamine in an outward-facing conformation. These structures reveal insights into the conformation of the critical ECL2a loop which connects the two domains, thus allowing rigid body movement of the transport domain throughout the transport cycle. Furthermore, the structures provide new insights into substrate recognition, which involves conformational changes in the HP2 loop. A putative cholesterol binding site was observed near the domain interface in the outward-facing state. Comparison with the previously determined inward-facing structure of SCL1A5 provides a basis for a more integrated understanding of substrate recognition and transport mechanism in the SLC1 family.
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•Soluble PD-L1 was secreted by glioma cells to glioma microenvironment.•PD-1/PD-L1 promotes M2-type polarization of microglia by regulating STAT3 signaling pathway.•Blocking ...PD-1/PD-L1 axis suppresses M2-type polarization of microglia and reduces invasion of glioblastoma.
The tumor microenvironment plays a vital role in glioblastoma growth and invasion. PD-1 and PD-L1 modulate the immunity in the brain tumor microenvironment. However, the underlying mechanisms remain unclear. In the present study, in vivo and in vitro experiments were conducted to reveal the effects of PD-1/PD-L1 on the crosstalk between microglia and glioma. Results showed that glioma cells secreted PD-L1 to the peritumoral areas, particularly microglia containing highly expressed PD-1. In the early stages of glioma, microglia mainly polarized into the pro-inflammatory subtype (M1). Subsequently, the secreted PD-L1 accumulated and bound to PD-1 on microglia, facilitating their polarization toward the microglial anti-inflammatory (M2) subtype primarily via the STAT3 signaling pathway. The role of PD-1/PD-L1 in M2 polarization of microglia was partially due to PD-1/PD-L1 depletion or application of BMS-1166, a novel inhibitor of PD-1/PD-L1. Consistently, co-culturing with microglia promoted glioma cell growth and invasion, and blocking PD-1/PD-L1 significantly suppressed these processes. Our findings reveal that the PD-1/PD-L1 axis engages in the microglial M2 polarization in the glioma microenvironment and promotes tumor growth and invasion.
Background:Lipoprotein lipase (LPL) expressed in macrophages plays an important role in promoting the development of atherosclerosis or atherogenesis. MicroRNA-182 (miR-182) is involved in the ...regulation of lipid metabolism and inflammation. However, it remains unclear how miR-182 regulates LPL and atherogenesis.Methods and Results:Using bioinformatics analyses and a dual-luciferase reporter assay, we identified histone deacetylase 9 (HDAC9) as a target gene of miR-182. Moreover, miR-182 upregulated LPL expression by directly targetingHDAC9in THP-1 macrophages. Hematoxylin-eosin (H&E), Oil Red O and Masson’s trichrome staining showed that apolipoprotein E (ApoE)-knockout (KO) mice treated with miR-182 exhibited more severe atherosclerotic plaques. Treatment with miR-182 increased CD68 and LPL expression in atherosclerotic lesions in ApoE-KO mice, as indicated by double immunofluorescence staining in the aortic sinus. Increased miR-182-induced increases in LPL expression in ApoE-KO mice was confirmed by real-time quantitative polymerase chain reaction and western blotting analyses. Treatment with miR-182 also increased plasma concentrations of proinflammatory cytokines and lipids in ApoE-KO mice.Conclusions:The results of the present study suggest that miR-182 upregulates LPL expression, promotes lipid accumulation in atherosclerotic lesions, and increases proinflammatory cytokine secretion, likely through targetingHDAC9, leading to an acceleration of atherogenesis in ApoE-KO mice.
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