16层螺旋CT三维重建与DR平片检查对外伤性肋骨骨折的诊断价值比较研究

目的:研究16层螺旋电子计算机断层扫描(CT)三维重建与数字化摄影(DR)平片检查对外伤性肋骨骨折的诊断价值,为临床诊治提供参考。方法:将2017年6月至2018年6月期间于本院接受诊治的82例外伤性肋骨骨折患者作为研究对象,所有患者均接受16层螺旋CT三维重建与DR平片检查,观察并记录患者的骨折发生部位,并比较两种诊断方法对外伤性肋骨骨折诊断的准确率、灵敏度、特异性、阳性预测值、阴性预测值以及漏诊情况。结果:82例外伤性肋骨骨折患者经影像学与临床诊断明确发生骨折179处,多发性骨折发生率为62.20%,单发性骨折发生率为37.80%,骨折肋骨段位中4-10段骨折发生率最高为69.83%,骨折肋骨水平阶段中腋肋骨折发生率最高为59.78%。相较于DR平片,16层螺旋CT三维重建诊断外伤性肋骨骨折的准确率、灵敏度、特异性、阳性预测值、阴性预测值更高,漏诊率更低,差异有统计学意义(P0.05)。结论:相较于DR平片检查,应用16层螺旋CT三维重建检查外伤性肋骨骨折能明显提高临床诊断的准确率、灵敏度和特异性,减少漏诊,可为临床诊治提供更可靠的信息,值得临床推广。     

Inverse Optical Cavity Design for Ultrabroadband Light Absorption Beyond the Conventional Limit in Low‐Bandgap Nonfullerene Acceptor–Based Solar Cells

In the subwavelength regime, several nanophotonic configurations have been proposed to overcome the conventional light trapping or light absorption enhancement limit in solar cells also known as the Yablonovitch limit. It has been recently suggested that establishing such limit should rely on computational inverse electromagnetic design instead of the traditional approach combining intuition and a priori known physical effect. In the present work, by applying an inverse full wave vector electromagnetic computational approach, a 1D nanostructured optical cavity with a new resonance configuration is designed that provides an ultrabroadband (≈450 nm) light absorption enhancement when applied to a 107 nm thick active layer organic solar cell based on a low‐bandgap (1.32 eV) nonfullerene acceptor. It is demonstrated computationally and experimentally that the absorption enhancement provided by such a cavity surpasses the conventional limit resulting from an ergodic optical geometry by a 7% average over a 450 nm band and by more than 20% in the NIR. In such a cavity configuration the solar cells exhibit a maximum power conversion efficiency above 14%, corresponding to the highest ever measured for devices based on the specific nonfullerene acceptor used.     

Bringing Conducting Polymers to High Order: Toward Conductivities beyond 105 S cm−1 and Thermoelectric Power Factors of 2 mW m−1 K−2

Here, an effective design strategy of polymer thermoelectric materials based on structural control in doped polymer semiconductors is presented. The strategy is illustrated for two archetypical polythiophenes, e.g., poly(2,5‐bis(3‐dodecyl‐2‐thienyl)thieno[3,2‐b]thiophene) (C₁₂‐PBTTT) and regioregular poly(3‐hexylthiophene) (P3HT). FeCl₃ doping of aligned films results in charge conductivities up to 2 × 10⁵ S cm^?1 and metallic‐like thermopowers similar to iodine‐doped polyacetylene. The films are almost optically transparent and show strongly polarized near‐infrared polaronic bands (dichroic ratio >10). The comparative study of structure–property correlations in P3HT and C₁₂‐PBTTT identifies three conditions to obtain conductivities beyond 10⁵ S cm^?1: i) achieve high in‐plane orientation of conjugated polymers with high persistence length; ii) ensure uniform chain oxidation of the polymer backbones by regular intercalation of dopant molecules in the polymer structure without disrupting alignment of π‐stacked layers; and iii) maintain a percolating nanomorphology along the chain direction. The highly anisotropic conducting polymer films are ideal model systems to investigate the correlations between thermopower S and charge conductivity σ. A scaling law S ∝ σ^?1/4 prevails along the chain direction, but a different S ∝ ?ln(σ) relation is observed perpendicular to the chains, suggesting different charge transport mechanisms. The simultaneous increase of charge conductivity and thermopower along the chain direction results in a substantial improvement of thermoelectric power factors up to 2 mW m^?1 K^?2 in C₁₂‐PBTTT.     

Effects of the cardiomyopathy-causing E244D mutation of troponin T on the structures of cardiac thin filaments studied by small-angle X-ray scattering

Small-angle X-ray scattering experiments were carried out to investigate the structural changes of cardiac thin filaments induced by the cardiomyopathy-causing E244D mutation in troponin T (TnT). We examined native thin filaments (NTF) from a bovine heart, reconstituted thin filaments containing human cardiac wild-type Tn (WTF), and filaments containing the E244D mutant of Tn (DTF), in the absence and presence of Ca²⁺. Analysis by model calculation showed that upon Ca²⁺-activation, tropomyosin (Tm) and Tn in the WTF and NTF moved together in a direction to expose myosin-binding sites on actin. On the other hand, Tm and Tn of the DTF moved in the opposite directions to each other upon Ca²⁺-activation. These movements caused Tm to expose more myosin-binding sites on actin than the WTF, suggesting that the affinity of myosin for actin is higher for the DTF. Thus, the mutation-induced structural changes in thin filaments would increase the number of myosin molecules bound to actin compared with the WTF, resulting in the force enhancement observed for the E244D mutation.     

Evidence for a role of glycosphingolipids in CXCR4-dependent cell migration

Chemotaxis induction is a major effect evoked by stimulation of the chemokine receptor CXCR4 with its sole ligand CXCL12. We now report that treatment of CHP-100 human neuroepithelioma cells with the glucosylceramide synthase (GCS) inhibitor DL-threo-1-phenyl-2-hexadecanoylamino-3-pyrrolidino-1-propanol inhibits CXCR4-dependent chemotaxis. We provide evidence that the phenomenon is not due to unspecific effects of the inhibitor employed and that inhibition of GCS neither affects total or plasmamembrane CXCR4 expression, nor CXCL12-induced Ca(2+) mobilization. The effects of the GCS inhibitor on impairment of CXCL12-induced cell migration temporally correlated with a pronounced downregulation of neutral glycosphingolipids, particularly glucosylceramide, and with a delayed and more moderate downregulation of gangliosides; moreover, exogenously administered glycosphingolipids allowed resumption of CXCR4-dependent chemotaxis. Altogether our results provide evidence, for the first time, for a role glycosphingolipids in sustaining CXCL12-induced cell migration.     

EDTA-induced Membrane Fluidization and Destabilization： Biophysical Studies on Artificial Lipid Membranes

The molecular mechanism of ethylenediaminetetraacetic acid （EDTA）-induced membrane destabilization has been studied using a combination of four biophysical techniques on artificial lipid membranes. Data from Langmuir film balance and epifluorescence microscopy revealed the fluidization and expansion effect of EDTA on phase behavior of monolayers of either 1,2-dipalmitoyl-sn-glycero-3-phosphocholine （DPPC） or mixtures of DPPC and metal-chelating lipids, such as N^a,N^a-Bis[carboxymethyl]-N^ε [（dioctadecylamino）succinyl]-L-lysine or 1,2-dioleoyl-sn-glycero-3-[N-（5-amino- 1 -carboxypentyl iminodiacetic acid） succinyl]. A plausible explanation could be drawn from the electrostatic interaction between negatively charged groups of EDTA and the positively charged choline head group of DPPC. Intercalation of EDTA into the lipid membrane induced membrane curvature as elucidated by atomic force microscopy. Growth in size and shape of the membrane protrusion was found to be time-dependent upon exposure to EDTA. Further loss of material from the lipid membrane surface was monitored in real time using a quartz crystal microbalance. This indicates membrane restabilization by exclusion of the protrusions from the surface. Loss of lipid components facilitates membrane instability, leading to membrane permeabilization and lysis.     

α-bisabolol β-D-fucopyranoside as a potential modulator of β-amyloid peptide induced neurotoxicity: An in vitro & in silico study

Alzheimer’s disease (AD) is a multifaceted neurodegenerative disorder affecting the elderly people. For the AD treatment, there is inefficiency in the existing medication, as these drugs reduce only the symptoms of the disease. Since multiple pathological proteins are involved in the development of AD, searching for a single molecule targeting multiple AD proteins will be a new strategy for the management of AD. In view of this, the present study was designed to synthesize and evaluate the multifunctional neuroprotective ability of the sesquiterpene glycoside α-bisabolol β-D-fucopyranoside (ABFP) against multiple targets like acetylcholinesterase, oxidative stress and β-amyloid peptide aggregation induced cytotoxicity. In silico computational docking and simulation studies of ABFP with acetylcholinesterase (AChE) showed that it can interact with Asp74 and Thr75 residues of the enzyme. The in vitro studies showed that the compound possess significant ability to inhibit the AChE enzyme apart from exhibiting antioxidant, anti-aggregation and disaggregation properties. In addition, molecular dynamics simulation studies proved that the interacting residue between Aβ peptide and ABFP was found to be involved in Leu34 and Ile31. Furthermore, the compound was able to protect the Neuro2 a cells against Aβ_25-35 peptide induced toxicity. Overall, the present study evidently proved ABFP as a neuroprotective agent, which might act as a multi-target compound for the treatment of Alzheimer’s disease.     

Growth and Characterization of Epitaxial Insulating CaF2 Layers on Silicon by MBE

In the course of the present work CaF₂ epitaxialfilms were grown on Si(111) substrates by means ofMBE. The Si substrates were chemically cleaned priorto insertion into the system. The final volatile oxidewas desorbed in situ by heating to 850. CaF₂ was evaporated from aKnudsen-type cell by use of a graphite crucible, whilethe growth temperature was held at 650 .RHEED (Reflection High Energy Electron Diffraction)has been used to monitor the film growth in situand to study the epitaxial quality. Also we have usedthe MeV He⁺ RBS channeling technique to look atdefects and to measure strain in the CaF₂ layer.Usually good crystallographic properties are achievedunder optimum growth conditions, with values of_min < 5%. Electrical properties aremeasured by use of a special MIS structure.     

UNC-60B, an ADF/cofilin family protein, is required for proper assembly of actin into myofibrils in Caenorhabditis elegans body wall muscle

The Caenorhabditis elegans unc-60 gene encodes two functionally distinct isoforms of ADF/cofilin that are implicated in myofibril assembly. Here, we show that one of the gene products, UNC-60B, is specifically required for proper assembly of actin into myofibrils. We found that all homozygous viable unc-60 mutations resided in the unc-60B coding region, indicating that UNC-60B is responsible for the Unc-60 phenotype. Wild-type UNC-60B had F-actin binding, partial actin depolymerizing, and weak F-actin severing activities in vitro. However, mutations in UNC-60B caused various alterations in these activities. Three missense mutations resulted in weaker F-actin binding and actin depolymerizing activities and complete loss of severing activity. The r398 mutation truncated three residues from the COOH terminus and resulted in the loss of severing activity and greater actin depolymerizing activity. The s1307 mutation in a putative actin-binding helix caused greater activity in actin-depolymerizing and severing. Using a specific antibody for UNC-60B, we found varying protein levels of UNC-60B in mutant animals, and that UNC-60B was expressed in embryonic muscles. Regardless of these various molecular phenotypes, actin was not properly assembled into embryonic myofibrils in all unc-60 mutants to similar extents. We conclude that precise control of actin filament dynamics by UNC-60B is required for proper integration of actin into myofibrils.