Virtual and augmented reality: New tools for visualizing, analyzing, and communicating complex morphology.

Virtual and augmented reality (VR/AR) are new technologies with the power to revolutionize the study of morphology. Modern imaging approaches such as computed tomography, laser scanning, and photogrammetry have opened up a new digital world, enabling researchers to share and analyze morphological data electronically and in great detail. Because this digital data exists on a computer screen, however, it can remain difficult to understand and unintuitive to interact with. VR/AR technologies bridge the analog-to-digital divide by presenting 3D data to users in a very similar way to how they would interact with actual anatomy, while also providing a more immersive experience and greater possibilities for exploration. This manuscript describes VR/AR hardware, software, and techniques, and is designed to give practicing morphologists and educators a primer on using these technologies in their research, pedagogy, and communication to a wide variety of audiences. We also include a series of case studies from the presentations and workshop given at the 2019 International Congress of Vertebrate Morphology, and suggest best practices for the use of VR/AR in comparative morphology.

Resveratrol reduces drug resistance of SCLC cells by suppressing the inflammatory microenvironment and the STAT3/VEGF pathway.

DNA-damaging agents, such as doxorubicin (Adriamycin), are widely used for the treatment of small cell lung cancer (SCLC). However, drug resistance is one of the major challenges for treatment of SCLC. Herein, we investigated the mechanisms underlying drug resistance in SCLC cells and the effects of resveratrol (Res) on drug resistance. We report that Adriamycin treatment of H69AR (multidrug resistance phenotype) cells resulted in a lower rate of growth inhibition, up-regulation of MRP1 and P-glycoprotein (P-gp), and higher P-gp activity as compared with susceptible H69 cells treated with Adriamycin. Moreover, the signal transducer and activator of transcription 3/vascular endothelial growth factor (STAT3/VEGF) pathway was overactivated in H69AR cells, especially after interleukin-23 treatment. The inflammatory microenvironment promoted the drug resistance of H69AR cells by activating the STAT3/VEGF pathway. The addition of Res suppressed the expression levels of inflammatory mediators, inhibited the STAT3/VEGF pathway, impeded P-gp activity, and decreased the drug resistance of H69AR cells. H69AR cells exhibited Adriamycin resistance through activation of the STAT3/VEGF pathway, and Res ameliorated the inflammatory microenvironment to suppress the STAT3/VEGF pathway to reduce drug resistance. Our results suggest that Res may have therapeutic potential for SCLC treatment.

Exosomal long non-coding RNA LINC00662 promotes non-small cell lung cancer progression by miR-320d/E2F1 axis.

Non-small cell lung cancer (NSCLC) is the most common tumor affecting modern people and is associated with severe morbidity and high mortality. Exosomal long non-coding RNAs as crucial regulators are involved in cancer progression. However, the role of exosomal lncRNA LINC00662 in the development of NSCLC remains unclear. Here, we aimed to explore the impact of exosomal lncRNA LINC00662 on the NSCLC progression and the underlying mechanism. Significantly, we revealed that the expression of lncRNA LINC00662 was elevated in the plasma exosome of NSCLC patients. Exosomal LINC00662 promoted proliferation, invasion, and migration, and inhibited apoptosis and cell cycle arrest of NSCLC cells. Mechanically, LINC00662 was able to serve as a miR-320d sponge in NSCLC cells. MiR-320d could target E2F1 in NSCLC cells. Exosomal LINC00662 contributed to the progression of NSCLC by miR-320d/E2F1 axis in vitro. Remarkably, exosomal LINC00662 enhanced the tumor growth of NSCLC in vivo. Thus, we conclude that exosomal lncRNA LINC00662 promotes NSCLC progression by modulating miR-320d/E2F1 axis. Our finding provides new insights into the mechanism by which exosomal lncRNA LINC00662 contributes to the development of NSCLC. LncRNA LINC00662, miR-320d, and E2F1 may serve as potential targets for NSCLC therapy.

[Determination of the total amount of maleic acid and maleic anhydride in starch and its products by high performance liquid chromatography-tandem mass spectrometry].

A high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/ MS) method was established for the determination of the total amount of maleic acid and maleic anhydride in starch and its products. The samples were extracted with 50% (v/v) methanol and hydrolyzed by alkaline, then analyzed by HPLC-MS/MS, and quantified with the external standard method. The mass spectrometry was operated with electrospray in negative ionization mode. The multiple reaction monitoring (MRM) mode was employed involving the transition of the precursor ion to two selected product ions, in which one pair was for quantification (m/z 115.0 > 71.1) and the other pair was for identification (m/z 115.0 > 27.1). The results indicated that no significant matrix effect was found for the spiked samples. The recoveries of maleic acid spiked in starch and its products were 80.2%-115.3% at spiked levels of 0.5-1,000 mg/kg. The relative standard deviations (RSDs) were less than 12% (n = 6). The limits of detection (LOD) and quantification (LOQ) were 0.1 and 0.5 mg/kg for maleic acid and maleic anhydride, respectively. The method is rapid, sensitive and reproducible for the determination of the total amount of maleic acid and maleic anhydride in starch and its products and shows great potential for routine analysis