Surface-enhanced Raman scattering based determination on sulfamethazine using molecularly imprinted polymers decorated with silver nanoparticles.

Molecularly imprinted polymers (MIPs) were combined with surface-enhanced Raman scattering (SERS) and AgNPs were prepared by in situ reduction within the MIP for selective and sensitive detection of sulfamethazine (SMZ). The MIP@AgNPs composites were characterized in detail by several analytical techniques, showing the generation of polymers and the formation of AgNPs hot spots. The specific affinity and rapid adsorption equilibrium rates of MIP@AgNPs composites were verified by static and kinetic adsorption studies. The MIP@AgNPs with high selectivity and excellent sensitivity were used as SERS substrates to detect SMZ. A good linear correlation (R2 = 0.996) in rang of 10-10-10-6 mol L-1 was observed between the Raman signal (1596 cm-1) and the concentration of SMZ. The limit of detection (LOD) was as low as 8.10 × 10-11 mol L-1 with relative standard deviations (RSD) of 6.32%. The good stability and reproducibility are also fully reflected in the SERS detection based on MIP@AgNPs. The method was successfully applied to the analysis of lake water samples, with recoveries in the range 85.1% to 102.5%. In summary, SERS detection based on MIP@AgNPs can be developed for a wider and broader range of practical applications. Schematic illustration of MIP@AgNPs sensor for the SERS detection of sulfamethazine.

The Binding of PD-L1 and Akt Facilitates Glioma Cell Invasion Upon Starvation via Akt/Autophagy/F-Actin Signaling.

Glioma, especially glioblastoma, is pathologically characterized by high aggressiveness, which largely contributed to the ineffectiveness of current therapies. It has been recently reported that intrinsic PD-L1 can regulate tumor malignancy, whereas underlying mechanisms remain mostly unclear. Here, we report a novel mechanism by which PD-L1 promotes glioma cell infiltration. In orthotopic glioma models, PD-L1 expression was up-regulated predominantly in glioma cells in the infiltrating front. For PD-L1-overexpressed glioma cells, PI3K/Akt and actin regulations were among the top six most altered signaling pathways as detected by RNA-sequencing. PD-L1 significantly activated Akt/F-actin signaling while suppressed autophagic signaling upon cell starvation. Mechanistically, PD-L1 preferentially bound to Akt among various PI3K/Akt signaling proteins. Serial truncation identified the interaction between the 128-237aa fragment of PD-L1 and the 112-480aa fragment of Akt, which facilitates the membrane translocation/activation of Akt, and was unaffected by Perifosin (specific p-Akt inhibitor targeting Akt PH-domain). Taken together, our data indicate that in glioma cells, PD-L1 is induced to prevent autophagic cytoskeleton collapse via Akt binding/activation, facilitating glioma cell invasion upon starvation stress.

[Tomato R-protein Tm-2(2) gene interacting with ToMV movement protein triggered programmed cell death in tobacco transformants].

Tomato Tm-2(2) and ToMV MP gene are a pair of R-Avr mediated response genes. Tm-2(2) and MP gene expressed in tobacco transformants with single-copy integration respectively. Tm-2(2) transformants displayed virus-resistant specificity as the reaction of original Tm-2(2) tomato species in virus-inoculation test. The results of agro-infiltration experiment and transformant-crossing test between Tm-2(2) plants and MP plants indicated that: (1) Tm-2(2) and ToMV-MP maintained "Gene for Gene" characters in transgenic tobacco; (2) The interaction between Tm-22 and MP of ToMV could induce the programmed cell death in the host tobacco by exo-ethylene stimulation. This result will be useful in furthering understanding of molecular mechanism of Tm-2(2) interaction with ToMV-MP.