Underground Excavation in Jointed Rocks

Master'sMASTER OF ENGINEERIN

Finger Citron Extract Ameliorates Glycolipid Metabolism and Inflammation by Regulating GLP-1 Secretion via TGR5 Receptors in Obese Rats

Finger citron (FC) is one of many traditional Chinese herbs that have been used to treat obesity. The aim of this study was to elucidate the pharmacological effects and mechanisms of FC on obese rats. Rats were fed with a high-fat diet as a model of obesity and treated with FC at three different dosages for 6 weeks. Pathology in liver tissue was observed. Glucose levels, lipids levels, and inflammatory indicators in serum were evaluated by enzyme‐linked immunosorbent assay. Furthermore, the expression of G protein-coupled receptor 5 (TGR5) pathway genes in rat colon tissue was detected by reverse transcription-polymerase chain reaction analysis (RT-PCR). Our result revealed that FC alleviates obesity by reducing body weight (BW) and waist circumference, managing inflammation and improving glycolipid metabolism, liver function, and liver lipid peroxidation in vivo. In addition, the mechanism of FC on obesity is possibly the stimulation of glucagon-like peptide-1 (GLP-1) secretion by activating the TGR5 pathway in intestinal endocrine cells. Our studies highlight the obesity reduction effects of FC and one of the mechanisms may be the activation of the TGR5 pathway in intestinal endocrine cells

mTOR acts as a pivotal signaling hub for neural crest cells during craniofacial development.

mTOR is a highly conserved serine/threonine protein kinase that is critical for diverse cellular processes in both developmental and physiological settings. mTOR interacts with a set of molecules including Raptor and Rictor to form two distinct functional complexes, namely the mTORC1 and mTORC2. Here, we used novel genetic models to investigate functions of the mTOR pathway for cranial neural crest cells (NCCs), which are a temporary type of cells arising from the ectoderm layer and migrate to the pharyngeal arches participating craniofacial development. mTOR deletion elicited a proliferation deficit and excessive apoptosis of post-migratory NCCs, leading to growth arrest of the facial primordia along with midline orofacial clefts. Furthermore, NCC differentiation was impaired. Thus, NCC derivatives, such as skeletons, vasculatures and neural tissues were either rudimentary or malformed. We further demonstrate that disruption of mTOR caused P53 hyperactivity and cell cycle arrest in cranial NCCs, and lowering P53 activity by one copy reduction attenuated the severity of craniofacial phenotype in NCC-mTOR knockout mice. Remarkably, NCC-Rptor disruption caused a spectrum of defects mirroring that of the NCC-mTOR deletion, whereas NCC-Rictor disruption only caused a mild craniofacial phenotype compared to the mTOR and Rptor conditional knockout models. Altogether, our data demonstrate that mTOR functions mediated by mTORC1 are indispensable for multiple processes of NCC development including proliferation, survival, and differentiation during craniofacial morphogenesis and organogenesis, and P53 hyperactivity in part accounts for the defective craniofacial development in NCC-mTOR knockout mice

Effects of Exposed Artificial Substrate on the Competition between Phytoplankton and Benthic Algae: Implications for Shallow Lake Restoration

Phytoplankton and benthic algae coexist in shallow lakes and the outcome of the competition between these two photoautotrophs can markedly influence water clarity. It is well established that exposed artificial substrate in eutrophic waters can remove nutrients and fine particles from the water column via the attached periphyton canopy. However, the effects of the introduction of artificial substrate on the competition between planktonic and benthic primary producers remain to be elucidated. We conducted a short-term outdoor mesocosm experiment to test the hypothesis that the nutrient and light changes induced by exposed artificial substrate (polythene nets) would benefit the benthic algae. Artificial substrate significantly reduced total nitrogen and phosphorus concentrations and water clarity improved, the latter due to the substrate-induced reduction of both organic and inorganic suspended solids. Consequently, as judged from changes in chlorophyll a (Chl-a) concentrations in water and sediment, respectively, exposed artificial substrate significantly reduced the phytoplankton biomass, while benthic algae biomass increased. Our results thus indicate that exposed artificial substrate may be used as a tool to re-establish benthic primary production in eutrophic shallow lakes after an external nutrient loading reduction, paving the way for a benthic- or a macrophyte-dominated system. Longer term and larger scale experiments are, however, needed before any firm conclusions can be drawn on this

Third harmonic generation in tapered photonic crystal fiber

International audienc

Robust Stability of Efficient Lead-Free Formamidinium Tin Iodide Perovskite Solar Cells Realized by Structural Regulation

The instability issue of Pb-free Sn-based perovskite is one of the biggest challenges for its application in optoelectronic devices. Herein, a structural regulation strategy is demonstrated to regulate the geometric symmetry of formamidiniumtin iodide (FASnI3) perovskite. Experimental and theoretical works show that the introduction of cesium cation (Cs+) could improve the geometric symmetry, suppress the oxidation of Sn2+, and enhance the thermodynamical structural stability of FASnI3. As a result, the inverted planar Cs-doped FASnI3-based perovskite solar cell (PSC) is shown to maintain 90% of its initial power-conversion efficiency (PCE) after 2000 h stored in N2, which is the best durability to date for 3D Sn-based PSCs. Most importantly, the air, thermal, and illumination stabilities of the PSCs are all improved after Cs doping. The PCE of the Cs-doped PSC shows a 63% increase compared to that of the control device (from 3.74% to 6.08%) due to the improved quality of the Cs-doped FASnI3 film.Peer reviewe

Lowering P53 activity by <i>P53</i> copy reduction attenuates the craniofacial phenotype in the NCC-<i>mTOR</i> cKO mice.

<p>(A) Gross examination of NCC-<i>mTOR</i> cKO mice by <i>P53</i> copy deduction. (B) Alcian blue staining in parasagittal sections of E12.5 heads. (C) Histology in frontal sections of E12.5 heads. (D) Quantification of the length of snout/frontonasal prominence, which is represented by the length from the brain-nose turning point to the most anterior plane of the snout. (E) PHH3 staining in frontal sections of E11.5 FN. (F) Apoptosis in frontal sections of E11.5 heads (arrow heads). (G, H) Quantification of cell proliferation and apoptosis. * P<0.05; **P<0.01. bc: basicranium; br; brain; ctr: control; fn: frontonasal prominence; ls: length of the snout; mc: Meckel’ cartilage; md: mandibular arch; mx: maxillary arch; ne: nasal epithelium; pl: palatal shelf; sn: snout; tb: tooth bud; ton: tongue; vd: vessel dilation. Scale bar: 200μm.</p

Apoptosis and proliferation assays.

<p>(A-D) Apoptosis at E10.5 and E11.5. (E) Quantification of apoptotic cells. (F, F’) Dual staining of TUNEL and Runx2 shows that apoptotic cells are predominantly NCC descendants. (G, H) Immunofluorescence for PHH3 in E10.5 facial primordia. (I, J) Immunofluorescence for PHH3 in the FN at E11.5. (K, L) Immunofluorescence for PHH3 in the mandibular arch at E11.5. Arrowheads indicate groove in the tongue. (M) Quantification of PHH3+ cells. (N, O) O9 NCCs cultured with and without rapamycin (100nM). (P) PHH3 staining of O9 cells. (Q)Western blot for mTORC1 downstream target p-S6K1/S6K1 upon rapamycin treatment. (R) Percentage of PHH3+ cells and cell live/death assay. (S) Phase contrast images of cultured PA cells. (T) Phalloidin and Dapi staining of PA cells. (U) PHH3 and Phalloidin double staining of PA cells. br: brain; ctr: control; fn: frontonasal prominence; md: mandibular prominence; mx: maxillary prominence; rapa: rapamycin; ton: tongue. Scale bars in (A-D): 100 μm.; scale bars in (L-U): 200 μm; scale bar in (L) applies to (G-K).</p