Intelligent Hotel ROS-based Service Robot

With the advances of artificial intelligence (AI) technology, many studies and work have been carried out on how robots could replace human labor. In this paper, we present a ROS based intelligence hotel robot, which simplifies the check-in process. We use pioneer 3dx robot and considered different environment settings. The robot combined with Hokuyo Lidar and Kinect Xbox camera, can plan the routes accurately and reach rooms in different floors. In addition, we added an intelligent voice system which provides an assistant for the customers

The symbiotic bacterial surface factor polysaccharide A on Bacteroides fragilis inhibits IL-1β-induced inflammation in human fetal enterocytes via toll receptors 2 and 4

Colonizing bacteria interacting with the immature, unlike the mature, human intestine favors inflammation over immune homeostasis. As a result, ten percent of premature infants under 1500 grams weight develop an inflammatory necrosis of the intestine after birth, e.g., necrotizing enterocolitis (NEC). NEC is a major health problem in this population causing extensive morbidity and mortality and an enormous expenditure of health care dollars. NEC can be prevented by giving preterm infants their mother’s expressed breast milk or ingesting selective probiotic organisms. Vaginally delivered, breast fed newborns develop health promoting bacteria (“pioneer” bacteria) which preferentially stimulate intestinal host defense and anti-inflammation. One such “pioneer” organism is Bacteroides fragilis with a polysaccharide (PSA) on its capsule. B. fragilis has been shown developmentally in intestinal lymphocytes and dendritic cells to produce a balanced T-helper cell (TH1/TH2) response and to reduce intestinal inflammation by activity through the TLR2 receptor stimulating IL-10 which inhibits IL-17 causing inflammation. No studies have been done on the role of B. fragilis PSA on fetal enterocytes and its increased inflammation. Accordingly, using human and mouse fetal intestinal models, we have shown that B. fragilis with PSA and PSA alone inhibits IL-1β-induced IL-8 inflammation in fetal and NEC intestine. We have also begun to define the mechanism for this unique inflammation noted in fetal intestine. We have shown that B. fragilis PSA anti-inflammation requires both the TLR2 and TLR4 receptor and is in part mediated by the AP1 transcription factor (TLR2) which is developmentally regulated. These observations may help to devise future preventative treatments of premature infants against NEC

Cul4-Ddb1 ubiquitin ligases facilitate DNA replication-coupled sister chromatid cohesion through regulation of cohesin acetyltransferase Esco2.

Cohesin acetyltransferases ESCO1 and ESCO2 play a vital role in establishing sister chromatid cohesion. How ESCO1 and ESCO2 are controlled in a DNA replication-coupled manner remains unclear in higher eukaryotes. Here we show a critical role of CUL4-RING ligases (CRL4s) in cohesion establishment via regulating ESCO2 in human cells. Depletion of CUL4A, CUL4B or DDB1 subunits substantially reduces the normal cohesion efficiency. We also show that MMS22L, a vertebrate ortholog of yeast Mms22, is one of DDB1 and CUL4-associated factors (DCAFs) involved in cohesion. Several lines of evidence show selective interaction of CRL4s with ESCO2 through LxG motif, which is lost in ESCO1. Depletion of either CRL4s or ESCO2 causes a defect in SMC3 acetylation, which can be rescued by HDAC8 inhibition. More importantly, both CRL4s and PCNA act as mediators for efficiently stabilizing ESCO2 on chromatin and catalyzing SMC3 acetylation. Taken together, we propose an evolutionarily conserved mechanism in which CRL4s and PCNA promote ESCO2-dependent establishment of sister chromatid cohesion

PSA reduced IL-1βinduced IL-8 in H4 cells.

<p>H4 cells were pretreated with or without PSA at an optimal dose and then exposed to IL-1β or treated with PSA alone. The supernatants were collected to measure IL8 levels by Elisa. The mean and SEM were from triplicate wells and were representative of three separate experiments with similar results. **P<0.01 (one-way ANOVA and post-hoc tests).</p

PSA reduced IL-1β induced P-c-Jun expression is TLR2 dependent.

<p>P-c-Jun (green color) was detected by immunofluorescent staining in control (A1), TLR2 knockdown (B1) and TLR4 knockdown (C1) H4 cells which were pretreated with or without PSA for 24 hrs and then exposed to IL-1β for 2 hrs The nuclei were counterstained by Dapi (blue), and the cell membrane was stained red. Amplified x600; scale bar = 20 μm; n = 60–70 cells/treatment. The images were representative of three separate experiments with similar results. The analysis (A2, B2 and C2) applied by corrected total cell fluorescence (CTCF) was determined.** P<0.01, ***P<0.001(one-way ANOVA and post-hoc tests).</p

TLR4 and TLR2 are required for PSA reduction of IL-1β-induced IL8 in fetal mouse small intestinal organ cultures.

<p>Embryonic 18.5 day (E18.5) mouse fetal small intestinal organ culture were pretreated with or without PSA in (A) wild type (WT), (B) TLR2^-/-and (C) TLR4^-/- mice. The supernatant IL8 levels were detected 24 hrs after IL-1 β stimulation. The mean and SEM were from triplicate wells and were representative of three separate experiments with similar results. **P<0.01, ***P<0.001(one-way ANOVA and post-hoc tests).</p

Wild type (WT) <i>B</i>. <i>fragilis</i> with polysaccharides A (PSA dossa) reduced IL-1 β triggered IL8 in immature human fetal intestinal epithelial cell line (H4 cells).

<p>H4 cells were pretreated with WT <i>B</i>. <i>fragilis</i> PSA (dossa) or mutant type without PSA (delta) at an indicated dosage for 1 hour. Then the cells were stimulated with or without IL-1β for 24 hrs. The supernatant IL8 levels were determined by Elisa. Data are represented as mean ± SD (n = 3, *P< 0.05, one-way ANOVA and post-hoc tests). Three experiments with similar results were analyzed.</p

PSA reduced IL-1 β triggered IL-8 in necrotizing enterocolitis intestinal epithelial cells (NEC-IEC).

<p>NEC-IEC cells were pretreated with or without PSA and then exposed to IL-1 β for 24 hrs or treated with PSA alone. The supernatant IL8 levels induced by IL-1 β were reduced by PSA pretreatment. The mean and SEM were from triplicate wells and were representative of three separate experiments with similar results. **P<0.01, ***P<0.001(one-way ANOVA and post-hoc tests).</p

Laser-Induced Flash-Evaporation Printing CH₃NH₃PbI₃ Thin Films for High-Performance Planar Solar Cells

Organic–inorganic hybrid perovskites have been emerging as promising light-harvesting materials for high-efficiency solar cells recently. Compared to solution-based methods, vapor-based deposition technologies are more suitable in preparing compact, uniform, and large-scale perovskite thin films. Here, we utilized flash-evaporation printing (FEP), a laser-induced ultrafast single source evaporation method employing a carbon nanotube evaporator, to fabricate high-quality methylammonium lead iodide perovskite thin films. Stoichiometric films with pure tetragonal perovskite phase can be achieved using a controlled methylammonium iodide to lead iodide ratio in evaporation precursors. The film crystallinity and crystal grain growth could further be promoted after postannealing. Planar solar cells (0.06 cm²) employing these perovskite films exhibit a champion power conversion efficiency (PCE) of 16.8% with insignificant hysteresis, which is among the highest reported PCEs using vapor-based deposition methods. Large-area (1 cm²) devices based on such perovskite films also achieved a stabilized PCE of 11.2%, indicating the feasibility and scalability of our FEP method in fabricating large-area perovskite films for other optoelectronic applications