The manipulation of the transition states of a chemical process is essential to achieve the desired selectivity. In particular, transition states of chemical reactions can be significantly modified in a confined environment. We report a catalytic reaction with remarkable amplification of stereochemical information in a confined water cage. Surprisingly, this amplification is significantly dependent on droplet size. This water-induced chirality amplification stems from the hydrophobic hydration effects, which ensures high proximity of the catalyst and substrates presumably at the transition state, leading to higher enantioselectivity. Flow and batch reactors were evaluated to confirm the generality of this water-induced chirality amplification. Our observation on efficient chiral induction in confined water cages might lead to an understanding of the chirality amplification in the prebiotic era, which is a key feature for the chemical evolution of homochirality.

Preoperative serum albumin level, age <12 months, preoperative pulmonary hypertension, and CPB duration were associated with risk for postoperative AKI in children who underwent congenital cardiac surgery.

Morphogens are signaling molecules that convey positional information and dictate cell fates during development. Although ectopic expression in model organisms suggests that morphogen gradients form through diffusion, little is known about how morphogen gradients are created and interpreted during mammalian embryogenesis due to the combined difficulties of measuring endogenous morphogen levels and observing development in utero. Here we take advantage of a human gastruloid model to visualize endogenous Nodal protein in living cells, during specification of germ layers. We show that Nodal is extremely short range so that Nodal protein is limited to the immediate neighborhood of source cells. Nodal activity spreads through a relay mechanism in which Nodal production induces neighboring cells to transcribe Nodal. We further show that the Nodal inhibitor Lefty, while biochemically capable of long-range diffusion, also acts locally to control the timing of Nodal spread and therefore of mesoderm differentiation during patterning. Our study establishes a paradigm for tissue patterning by an activator-inhibitor pair.

Background Patients with symptomatic gallbladder diseases exhibit delayed gastric emptying. We evaluated the residual gastric content in fasted patients scheduled for elective laparoscopic cholecystectomy because of symptomatic gallbladder disease using ultrasonography. Methods This prospective observational single-cohort study was approved by the Institutional Review Board, and written informed consent was obtained from all included patients. Before anesthesia induction, the gastric antrum was examined by ultrasound. Once the presence of solid content was excluded, the patients were classified using a three-point grading system (grade 0: no fluid; grade 1: fluid in the right lateral decubitus position; grade 2: fluid in both the supine and right lateral decubitus positions), and the fluid volume was measured. A stomach was considered empty if it had no contents or B 1.5 mLÁkg -1 of fluid, and was considered full if solid content or [ 1.5 mLÁkg -1 of fluid was detected. Results Among 138 patients, 18 patients (13%) presented with a full stomach, 12 (9%) of whom had solid content, and six (4%) of whom had [1.5 mLÁkg -1 of fluid in their stomach. Among the remaining 120 patients with an empty stomach, 65 patients presented with a grade 0 antrum, and 55 patients with a grade 1 or 2 antrum with B 1.5 mLÁkg -1 of fluid. Conclusion The gastric ultrasound assessment revealed that 13% of patients scheduled for elective cholecystectomy because of symptomatic gallbladder disease had a full stomach despite following the fasting guidelines. This was higher than the reported incidence of a full stomach among the general surgical population. Further studies are required to delineate the clinical implications of our findings. Trial registration www.ClinicalTrials.gov (NCT03259841); registered 4 August, 2017. RésuméContexte Les patients atteints de maladies vésiculaires symptomatiques souffrent de retard de la vidange gastrique. Nous avons évalué par échographie le contenu gastrique résiduel chez des patients à jeun devant subir une cholécystectomie non urgente par laparoscopie en raison de maladie vésiculaire symptomatique.

Background/Aim: The 14-3-3 protein family has a variety of functions in cellular responses in different organisms, including cell-cycle regulation, apoptosis, and malignant transformation. induces G2 arrest, which enables repair of damaged DNA. The purpose of this study was to identify the role of 14-3-3σ up-regulation by hepatocyte growth factor (HGF) in cancer cell proliferation and invasion in gastric cancer. Materials and Methods: In this study, cell culture, western blotting, real-time polymerase chain reaction, zymography, 14-3-3σ knock-down using short hairpin RNA (shRNA), electrophoresis mobility-shift assay, chromatin immunoprecipitation assay and standard two-chamber invasion assay were applied. Results: Firstly, we confirmed that the expression of 14-3-3σ in gastric cancer cells was up-regulated by HGF. To identify how HGF-induced 14-3-3σ expression affects matrix metalloproteinase-1 (MMP1) expression, the cells were treated with the mitogen-activated protein kinase kinase inhibitor PD098059 and analyzed using western blotting. The HGF-mediated expression of MMP1 protein decreased in the presence of PD098059. The role of 14-3-3σ in MMP1 expression was determined through 14-3-3σ knockdown using shRNA. 14-3-3σ-shRNA cells showed reduced levels of MMP1, phosphorylated extracellular signalregulated kinase, and pp38. HGF-mediated cell proliferation and in vitro invasion were reduced in 14-3-3σ knockdown cells. Serum 14-3-3σ levels were also significantly reduced following gastrectomy in patients with stage II or stage III gastric cancer (p<0.05). Conclusion: These results suggest that 14-3-3σ plays an important role in cell proliferation and metastasis in gastric cancer, and 14-3-3σ may be a novel target for detection and prevention of progression of gastric cancer. In addition, the serum 14-3-3σ level is associated with treatment status in patients with locally advanced gastric cancer.The HGF and MET proto-oncogene, receptor tyrosine kinase (MET) pathways play an important role not only in normal cell development but also in the pathogenesis of most types of human cancer (1-4). To explain the effects of HGF on the pathogenesis of gastric cancer, the gastric adenocarcinoma cell lines, NUGC3 and MKN-28, were screened using a human complementary DNA (cDNA) microarray in previous work, and many genes that are regulated by HGF were identified (5). That study suggested that calpain 12, cold-shock domain protein A, 14-3-3 proteins, cervical cancer 1 proto-oncogene, gastrin-releasing peptide, hepatoma-derived growth factor, mitogen-activated protein-binding protein-interacting protein and S100 calcium-binding protein A11 were up-regulated threefold or higher after treatment with HGF (2, 6).The 14-3-3 proteins are a large family of small, acidic polypeptides of 28-33 kDa that are encoded by at least two different 14-3-3 genes in all eukaryotic species (7, 8). 14-3-3 Proteins are an important family for research because they have diverse cellular roles in signal transduction involved in cancer development, includin...