Miniaturized high signal-to-noise ratio optical air data system using a compact multi-axis parallel transceiver for airborne application.

We have developed a miniaturized multi-channel parallel optical air data system with high signal-to-noise ratio for airborne application. In the system, we designed a fiber amplifier with multi-channel high-energy output that was respectively used as the transmitting signals and a compact multi-axis transceiver with an entrance pupil diameter of 70 mm that was used to receive multi-channel signals simultaneously. We demonstrated the performance of our system both on ground and on board. On ground, the measured line-of-sight speed had an average error of 0.02 m/s and a standard deviation of 0.15 m/s. On board, the standard deviation between the true air speed, angle of attack, and angle of sideslip measured by our system and a commercial Swiss air data system was 1 kt, 0.68°, and 0.54°, respectively, and those standard deviation between our system and a system with the same design but employing multiple single-axis telescopes with entrance pupil diameter of 30 mm was 0.34 kt, 0.36°, and 0.28°, respectively. The signal-to-noise ratio of our system was 4.5 times higher than that of the system with small single-axis telescopes. Our system is very promising for airborne applications because of its small volume, high signal-to-noise ratio, and high data rate.

Microplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling.

Microplastics (MPs) are environmental pollutants and can be inhaled by humans to threaten health. The lung tissue, responsible for the gas exchange between the body and the environment, is vulnerable to MPs exposure. However, from the perspective of cellular senescence, the effect of MPs on lung cells and tissues has not yet been deeply dissected. In this study, we reported that all the four typical MPs exhibited the significant biological effects in term of inducing senescence of human lung derived cells A549 and BEAS-2B in vitro. We further found that polyvinyl chloride (PVC) increased the reactive oxygen species (ROS) level in A549 cells and that PVC-induced senescent characteristics could be largely reversed by antioxidant treatment. Importantly, intratracheal instillation of PVC MPs in mice could effectively impair their physical function, induce the increased systemic inflammation level, cause the accumulation of senescent cells. Our study demonstrates that MPs induce senescence in human lung epithelial cells and mouse lungs by activating ROS signaling, and provides new insight into the potential pathogenesis of MPs on lung diseases.

Long Noncoding RNA Regulator of Reprogramming Regulates Cell Growth, Metastasis, and Cisplatin Resistance in Gastric Cancer via miR-519d-3p/HMGA2 Axis.

Background: Gastric cancer (GC) is a common tumor found worldwide, and cisplatin is the first-line agent for the treatment of GC. However, the resistance to cisplatin is an obstacle. Here, we explored the biological mechanism of long noncoding RNA regulator of reprogramming (ROR) in the cisplatin resistance of GC. Materials and Methods: ROR, miR-519d-3p, and high mobility group protein A2 (HMGA2) expression in GC tissues and cells were measured by quantitative real-time polymerase chain reaction and Western blot. Cell viability, migration, invasion, and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, transwell assay, and flow cytometry, respectively. The relative protein expression was detected by Western blot. The interactions between miR-519d-3p and ROR, HMGA2 were predicted using miRcode and starBase v2.0 online database, and then verified by dual luciferase reporter assay and RNA immunoprecipitation assay. In addition, the xenograft tumor mouse model was constructed to verify the biological role of ROR in vivo. Results: The levels of ROR, HMGA2 were significantly upregulated, and miR-519d-3p was apparently downregulated in GC tissues and cells. The miRcode and starBase v2.0 online websites and dual luciferase reporter assay validated that miR-519d-3p directly interacted with ROR and HMGA2. Furthermore, ROR knockdown downregulated HMGA2 to restrain cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and cisplatin resistance in GC cells by targeting miR-519d-3p. In addition, the depletion of ROR repressed the xenograft tumor growth in vivo. Conclusion: In conclusion, we first found the ROR/miR-519d-3p/HMGA2 regulatory network to regulate cell proliferation, migration, invasion, EMT, and cisplatin resistance in GC, and this may shed light on the GC tumorigenesis.

Pea Albumin Attenuates Dextran Sulfate Sodium-Induced Colitis by Regulating NF-κB Signaling and the Intestinal Microbiota in Mice.

BACKGROUND: Inflammatory bowel disease remains a global burden with rapidly increasing incidence and prevalence in both industrialized countries and developing countries. In this study, we prepared pea albumin from pea seeds and determined its beneficial effects being anti-inflammatory and on gut microbiota modulation in dextran sulfate sodium (DSS)-challenged mice. METHOD: Six-week-old C57BL/6N male mice received an equivalent volume (200 µL) of sterile phosphate balanced solution, 0.375, 0.75, or 1.50 g/kg body weight (BW) of pea albumin that was subjected to 2.0% DSS for 7 days to induce colitis. On day 17 of the experiment, all mice were sacrificed after blood sample collection, and colon tissue and colon contents were collected. BW change curve, colon length, myeloperoxidase (MPO) activity, mucus staining, immunofluorescence staining of T cells and macrophages, cytokines, pro-inflammatory genes expression, nuclear factor-κB (NF-κB) and signal transducer, and activator of transcription 3 (STAT3) signaling pathways as well as 16S DNA sequence were measured. RESULTS: Our results show that pea albumin alleviates DSS-induced BW loss, colon length shortening, enhanced MPO activity, cytokines secretion, mucus deficiency, and inflammatory cell infiltration, as well as enhanced pro-inflammatory genes expression. In addition, the overactivation of NF-κB and STAT3 following DSS exposure is attenuated by pea albumin administration. Of particular interest, pea albumin oral administration restored gut microbiota dysbiosis as evidenced by enhanced α-diversity, restored ß-diversity, and promoted relative abundance of Lactobacillus and Lachnospiraceae_NK4A136_group. CONCLUSION: Taken together, the data provided herein demonstrated that pea albumin plays a protective role in DSS-induced colitis by reducing inflammatory cell infiltration, pro-inflammatory genes expression and pro-inflammatory cytokines release, inactivation of NF-κB signal, and gut microbiota modulation.

Enzymatic enrichment of n-3 polyunsaturated fatty acid glycerides by selective hydrolysis.

Most natural oils are low in n-3 polyunsaturated fatty acids (n-3 PUFAs) content, which limits their application in health products. In this study, n-3 PUFAs in glyceride form were selectively enriched by lipase-mediated hydrolysis of n-3 PUFA-containing oils. First, commercial lipases were screened, and the lipase AY "Amano" 400SD from Candida cylindracea was the best choice in producing n-3 PUFA glycerides from tuna oil. Subsequently, the hydrolysis conditions were optimized. Under the optimal conditions, the highest n-3 PUFA content in the glyceride fraction was found to be 57.7% after enzymatic hydrolysis. Addition of Ca2+ to the system significantly shortened the reaction time from 10 to 4 h. When algal oil was used as substrate, total PUFA contents in the glyceride fraction were 89.9%. This study provides an efficient enzymatic process to produce n-3 PUFA-enriched glyceride concentrates and demonstrates that AY "Amano" 400SD can effectively discriminate against n-3 PUFAs during hydrolysis.

Linkage of a locus determining familial progressive hyperpigmentation (FPH) to chromosome 19p13.1-pter in a Chinese family.

Familial progressive hyperpigmentation (FPH) is a rare autosomal dominantly inherited disorder characterized by patches of hyperpigmentation in the skin which are present at birth or in early infancy and increase in size and number with age. Although previous studies showed that FPH is a monogenic trait, the genetic basis for this disease is unknown. Using a genome screening with 182 STR markers from autosomes in a three-generation Chinese family with 17 members, including 6 affected individuals, we identified a locus linked to chromosome 19p13.1-pter responsible for FPH, spanning 45.48 cM between D19S593 and 19pter. Interestingly, this region harbors the LKB1 gene, in which germline mutations were shown to be associated with Peutz-Jeghers Syndrome (PJS). PJS and FPH share the disorder of hyperpigmentation, the fine mapping of the FPH gene is expected to lead to a better understanding of the etiology for both FPH and PJS. The linkage of FPH locus to human chromosome 19p13.1-pter provides a genetic basis for further fine mapping.