Identification of an Oxygen Defect in Hexagonal Boron Nitride

Paramagnetic fluorescent defects in two-dimensional hexagonal boron nitride (hBN) are promising building blocks for quantum information processing. Although numerous defect-related single-photon sources and a few quantum bits have been found, except for the boron vacancy, their identification is still elusive. Here, we demonstrate that the comparison of experimental and first-principles simulated electron paramagnetic resonance (EPR) spectra is a powerful tool for defect identification in hBN, and first-principles modeling is inevitable in this process as a result of the dense nuclear spin environment of hBN. In particular, a recently observed EPR center is associated with the negatively charged oxygen vacancy complex by means of the many-body perturbation theory method on top of hybrid density functional calculations. To our surprise, the negatively charged oxygen vacancy complex produces a coherent emission around 2 eV with a well-reproducing previously recorded photoluminescence spectrum of some quantum emitters, according to our calculations

MiR-181b serves as diagnosis and prognosis biomarker in severe community-acquired pneumonia

Abstract Severe community-acquired pneumonia (SCAP) is a common critical disease in the intensive care unit (ICU). This study aims to evaluate the clinical significance of miR-181b in SCAP, which has been revealed to be dysregulated in acute respiratory distress syndrome events due to SCAP. There were 50 SCAP patients and 26 healthy volunteers were recruited in this study. The expression of miR-181b was detected by RT-qPCR and the difference between SCAP and healthy controls was evaluated. The diagnosis and prognosis value of miR-181b was assessed by the receiver operating characteristics (ROC), Kaplan-Meier, and Cox regression analysis. miR-181b was significantly downregulated in SCAP compared with healthy controls. The downregulation of miR-181b showed a significant association with the white blood cell count, absolute neutrophils, and the C-reactive protein of patients. The downregulation of miR-181b could distinguish SCAP patients from healthy controls and predicate the poor prognosis of SCAP patients. Downregulated miR-181b serves as a diagnosis and prognosis biomarker for SCAP, which may be useful biological information for the early detection and risk estimation of SCAP.</div

Two-Dimensional Covalent Organic Framework Isomers Induce Different Properties

Covalent organic frameworks (COFs) are attractive due to their predictable and tailored periodic frameworks. In the past decades, great efforts have been devoted to crystallinity control, modulation of pores, and so on; however, less attention has been given to atomic-level structural changes. This work provides a fundamental study to further understand the relationship between the periodic structures of the COFs and their unique properties. We explore the relationship of structural isomer linkages in two COFs (TAPT-TFPA and TAPA-TFPT COF). The crystal structures, stacking patterns, pore properties, optical properties, and adsorption properties of these imine-based COFs have been extensively studied and compared. Our results show that compared with TAPA-TFPT COF, TAPT-TFPA COF has superior crystallinity, reversible stacking regulation, and a significant blue shift of UV–vis absorption. These findings provide evidence that monomer pairs must be carefully considered when designing framework materials as these small structural changes can lead to large differences in properties

The M. hyorhinis p37 Protein Induces Cancer Associated Genes

<p>8 .CEL data files of the p37 Microarray analysis and 8 .XLSX data files of the qPCR analysis for the paper 'The Mycoplasma hyorhinis p37 Protein Rapidly Induces Genes in Fibroblasts Associated with Inflammation and Cancer'.</p

The Probability of ABA-Induced Closure (i.e., the Percentage of Simulations that Attain Closure) as a Function of Timesteps in the Dynamic Model

<div><p>In all panels, black triangles with dashed lines represent the normal (wild-type) response to ABA stimulus. Open triangles with dashed lines show that in wild-type, the probability of closure decays in the absence of ABA.</p> <p>(A) Perturbations in depolarization (open diamonds) or anion efflux at the plasma membrane (open squares) cause total loss of ABA-induced closure. The effect of disrupting actin reorganization (not shown) is identical to the effect of blocking anion efflux.</p> <p>(B) Perturbations in S1P (dashed squares), PA (dashed circles), or pH_c (dashed diamonds) lead to reduced closure probability. The effect of disrupting SphK is nearly identical to the effect of disrupting S1P (dashed squares); perturbations in GPA1 and PLD, KOUT are very close to perturbations in PA (dashed circles); for clarity, these curves are not shown in the plot.</p> <p>(C) <i>abi1</i> recessive mutants (black squares) show faster than wild-type ABA-induced closure (ABA hypersensitivity). The effect of blocking Ca²⁺ ATPase(s) (not shown) is very similar to the effect of the <i>abi1</i> mutation. Blocking Ca²⁺_c increase (black diamonds) causes slower than wild-type ABA-induced closure (ABA hyposensitivity). The effect of disrupting <i>atrboh</i> or ROS production (not shown) is very similar to the effect of blocking Ca²⁺_c increase.</p></div

Illustration of the Inference Rules Used in Network Reconstruction

<div><p>(1) If A → B and C → process (A → B), where A → B is not a biochemical reaction such as an enzyme catalyzed reaction or protein-protein/small molecule interaction, we assume that C is acting on an intermediary node (IN) of the A–B pathway.</p> <p>(2) If A → B, A → C, and C → process (A → B), where A → B is not a direct interaction, the most parsimonious explanation is that C is a member of the A–B pathway, i.e. A → C → B.</p> <p>(3) If A —| B and C —| process (A —| B), where A —| B is not a direct interaction, we assume that C is inhibiting an intermediary node (IN) of the A–B pathway. Note that A→ IN —| B is the only logically consistent representation of the A–B pathway.</p></div

Summary of the Dynamic Effects of Calcium Disruptions

<p>All curves represent the probability of ABA-induced closure (i.e., the percentage of simulations that attain closure) as a function of time steps. Black triangles with dashed line represent the normal (wild-type) response to ABA stimulus; open triangles with dashed lines show how the probability of closure decays in the absence of ABA. CIS + PA double mutants (dashed circles) and Ca²⁺_c + pH_c double mutants (dashed diamonds) show insensitivity to ABA. Ca²⁺ ATPase + RCN1 double mutants (black circles) show hyposensitive (delayed) response to ABA. Guanyl cyclase + CIS + CaIM triple mutants (black diamonds) also show hyposensitivity; note that none of the guanyl cyclase or CIS or CaIM single knockouts show changed sensitivity (data not shown). Ca²⁺ ATPase mutants (black squares) show faster than wild-type ABA-induced closure (ABA hypersensitivity).</p

Practical and Selective Bio-Inspired Iron-Catalyzed Oxidation of Si–H Bonds to Diversely Functionalized Organosilanols

Functionalized organosilanols have found wide applications pervading the realms of chemistry, material science, and medicine. However, a practical synthesis of structurally diverse organosilanols has remained elusive. Here, a bio-inspired nonheme-iron-catalyzed preparative oxidation of Si–H bonds of organosilanes to diversely functionalized organosilanols with aqueous hydrogen peroxide as the oxidant at an iron catalyst loading of 0.1 mol % is reported. The practical and highly selective oxidation exhibits good functional group tolerance, allowing effective access to diversely functionalized alkyl-, aryl-, alkynyl-, and alkoxysilanols, silanediols, as well as mono-, oligo-, and polymeric siloxanols with various substituent patterns. Late-stage gram-scale application in functional-molecule-containing silanols is further demonstrated. Mechanistic studies suggest the involvement of high-valent Fe­(V)­oxo species and a sequence of hydrogen atom transfer and oxygen rebounds

Current Knowledge of Guard Cell ABA Signaling

<div><p>The color of the nodes represents their function: enzymes are shown in red, signal transduction proteins are green, membrane transport–related nodes are blue, and secondary messengers and small molecules are orange. Small black filled circles represent putative intermediary nodes mediating indirect regulatory interactions. Arrowheads represent activation, and short perpendicular bars indicate inhibition. Light blue lines denote interactions derived from species other than <i>Arabidopsis;</i> dashed light-blue lines denote inferred negative feedback loops on pH_c and S1P. Nodes involved in the same metabolic pathway or protein complex are bordered by a gray box; only those arrows that point into or out of the box signify information flow (signal transduction).</p> <p>The full names of network components corresponding to each abbreviated node label are: ABA, abscisic acid; ABI1/2, protein phosphatase 2C ABI1/2; ABH1, mRNA cap binding protein; Actin, actin cytoskeleton reorganization; ADPRc, ADP ribose cyclase; AGB1, heterotrimeric G protein β component; AnionEM, anion efflux at the plasma membrane; Arg, arginine; AtPP2C, protein phosphatase 2C; Atrboh, NADPH oxidase; CaIM, Ca²⁺ influx across the plasma membrane; Ca²⁺ ATPase, Ca²⁺ ATPases and Ca²⁺/H⁺ antiporters responsible for Ca²⁺ efflux from the cytosol; Ca²⁺_c, cytosolic Ca²⁺ increase; cADPR, cyclic ADP-ribose; cGMP, cyclic GMP; CIS, Ca²⁺ influx to the cytosol from intracellular stores; DAG, diacylglycerol; Depolar, plasma membrane depolarization; ERA1, farnesyl transferase ERA1; GC, guanyl cyclase; GCR1, putative G protein–coupled receptor; GPA1, heterotrimeric G protein α subunit; GTP, guanosine 5′-triphosphate; H⁺ ATPase, H⁺ ATPase at the plasma membrane; InsPK, inositol polyphosphate kinase; InsP3, inositol-1,4,5-trisphosphate; InsP6, inositol hexakisphosphate; KAP, K⁺ efflux through rapidly activating K⁺ channels (AP channels) at the plasma membrane; KEV, K⁺ efflux from the vacuole to the cytosol; KOUT, K⁺ efflux through slowly activating outwardly-rectifying K⁺ channels at the plasma membrane; NAD⁺, nicotinamide adenine dinucleotide; NADPH, nicotinamide adenine dinucleotide phosphate; NOS, Nitric oxide synthase; NIA12, Nitrate reductase; NO, Nitric oxide; OST1, protein kinase open stomata 1; PA, phosphatidic acid; PC, phosphatidyl choline; PEPC, phosphoenolpyruvate carboxylase; PIP2, phosphatidylinositol 4,5-bisphosphate; PLC, phospholipase C; PLD, phospholipase D; RAC1, small GTPase RAC1; RCN1, protein phosphatase 2A; ROP2, small GTPase ROP2; ROP10, small GTPase ROP10; ROS, reactive oxygen species; SphK, sphingosine kinase; S1P, sphingosine-1-phosphate.</p></div