Some Generalised Characteristics of the Electro-dynamics of the Plasma Focus in Its Axial Phase: Illustrated by an Application to Independantly Determine the Drive Current Fraction and the Mass Swept-Up Fraction

We describe the axial phase of the Mather plasma focus by two coupled equations of motion and circuit. We non-dimensionalised these equations resulting in two coupled equations which are characterised by only three scaling parameters α, β and δ which are ratios of electrical to transit times, inductances and impedances respectively. The normalised current waveform, trajectory and speed profile are unique for each combination of α, β, δ which are the ratios of characteristic times (electrical discharge vs. axial transit), inductances (tube inductance vs. static inductance) and impedances (stray resistance vs. electrical surge impedance). This leads to important information and insight into various aspects of the axial phase. In the present work we show that in a time-matched plasma focus shot we deduce the value of axial phase current fraction f_c simply by measuring the calibrated voltage waveform and the uncalibrated current waveform. The scaling parameters β and δ are fixed; and by form-fitting the measured current waveform to the normalised current waveform using the value of α of the shot is determined uniquely; from which the peak current and the ratio of peak to average speed [the speed form factor (SFF)] are obtained. The average transit speed is measured by time-of-flight using the voltage upturn as indicator of end of axial phase. Then the SFF yields the peak speed. The measured voltage (back EMF), peak current and peak axial speed (all at the end of axial phase) allows the unambiguous measurement of f_c. The value of the mass swept-up fraction f_m is deduced from α which is the ratio of the characteristic discharge and the characteristic transit times, both deduced during the non-dimensionalisation of the equations. Analysis of a time-matched shot in the INTI PF at 15 kV, 3 Torr D₂ gave f_c = 0.68 and f_m = 0.05.     

正电子湮没研究Al、Nb共掺CaCu3Ti4O12陶瓷高介电常数机理

关于CaCu₃Ti₄O₁₂陶瓷的高介电常数机理,目前广泛接受的是非本征的内阻挡层电容模型。该模型认为在多晶中元素变价、缺陷和非化学计量比等导致的半导化晶粒被绝缘晶界层,即内阻挡层所包围。其中内阻挡层的厚度对材料的介电性能影响较大,而扫描电子显微镜（SEM）测试表明样品晶界呈稀烂的果酱状,SEM难以测量晶界区域绝缘内阻挡层厚度。本文采用正电子湮没技术表征其厚度,通过对CaCu₃Ti₄O₁₂陶瓷共掺不同浓度的Al、Nb（CaCu₃Ti_4-xAl_0.5xNb_0.5xO₁₂,x=0.2%、0.5%、5.0%）改变其晶粒和晶界的微观结构,研究CaCu₃Ti₄O₁₂陶瓷高介电常数机理。正电子湮没结果显示,掺杂样品符合多普勒展宽谱S参数的变化趋势与平均寿命的变化趋势一致。x=0.5%掺杂样品的介电常数最高,其平均寿命、S参数和湮没长寿命成分均最小,阻挡层最薄。实验结果验证了描述CaCu₃Ti₄O₁₂陶瓷高介电常数机理的内阻挡层电容模型的预测。     

基于穆斯堡尔参数的人工神经网络识别矿物的方法

采用改进型反向传播人工神经网络,以含铁矿物穆斯堡尔参数作为样本,通过神经网络的训练,能很好地识别的,从而有效地提高了对矿物的识别本领。     

Reactions with 2,3,4,5-Tetrahydro-benzo[b]thiepin-5-one and its Derivatives

2,3,4,5-Tetrahydro-benzo[b]thiepin-5-one, its 7-methyl derivative, and their S, S-dioxides condense with aromatic aldehydes to give the corresponding 4-arylidene derivatives 3 and 4 . Compounds 4 react with hydrazine and phenylhydrazine to yield 3, 3a, 4, 5-tetrahydro-2 H-benzo-[b]thiepino[4, 5-c]pyrazole S, S-dioxide derivatives 5 and 6 . Some of the arylidene derivatives 4 add GRIGNARD reagents to give 7 . The IR spectra of representative examples are discussed.     

Exposure of Mice to Thirdhand Smoke Modulates In Vitro and In Vivo Platelet Responses

Smoking is a risk factor for a variety of deleterious conditions, such as cancer, respiratory disease and cardiovascular disease. Thrombosis is an important and common aspect of several cardiovascular disease states, whose risk is known to be increased by both first- and secondhand smoke. More recently, the residual cigarette smoke that persists after someone has smoked (referred to as thirdhand smoke or THS) has been gaining more attention, since it has been shown that it also negatively affects health. Indeed, we have previously shown that 6-month exposure to THS increases the risk of thrombogenesis. However, neither the time-dependence of THS-induced thrombus formation, nor its sex dependence have been investigated. Thus, in the present study, we investigated these issues in the context of a shorter exposure to THS, specifically 3 months, in male and female mice. We show that the platelets from 3-month THS-exposed mice exhibited enhanced activation by agonists. Moreover, we also show that mice of both sexes exposed to THS have decreased tail bleeding as well as decreased thrombus occlusion time. In terms of the role of sex, intersex disparities in thrombus development and hemostasis as well as in platelet aggregation were, interestingly, observed. Together, our findings show that exposing mice to THS for 3 months is sufficient to predispose them to thrombosis; which seems to be driven, at least in part, by an increased activity in platelets, and that it does not manifest equally in both sexes.     

Association Mechanism and Conformational Changes in Trypsin on Its Interaction with Atrazine: A Multi- Spectroscopic and Biochemical Study with Computational Approach

Atrazine (ATR) is a herbicide globally used to eliminate undesired weeds. Herbicide usage leads to various adverse effects on human health and the environment. The primary source of herbicides in humans is the food laced with the herbicides. The ATR binding to trypsin (TYP) was investigated in this study to explore its binding potential and toxicity. In vitro interaction of ATR with TYP was studied using multi-spectroscopic methods, molecular docking, and enzyme kinetics to explore the mechanism of binding for the TYP-ATR system. The TYP-ATR complex revealed binding constants (10³ M⁻¹), suggesting a moderate binding. The free energy for the TYP-ATR complexes was negative, suggesting a spontaneous interaction. Thermodynamic parameters enthalpy (ΔH) and entropy (ΔS) obtained positive values for the TYP-ATR system suggesting hydrophobic interactions in the binding process. Micro-environmental and conformational changes in TYP molecules were induced on interaction with ATR. Reduced catalytic activity of TYP was observed after interaction with ATR owing to the changes in the secondary structure of the TYP.     

Genetic Elements Orchestrating Lactobacillus crispatus Glycogen Metabolism in the Vagina

Glycogen in the female lower reproductive tract is a major carbon source for colonization and acidification by common vaginal Lactobacillus species, such as Lactobacillus crispatus. Previously, we identified the amylopullulanase encoding gene pulA of Lactobacillus crispatus to correlate with the ability to autonomously utilize glycogen for growth. Here, we further characterize genetic variation and differential regulation of pulA affecting the presence of its gene product on the outer surface layer. We show that alpha-glucan degrading activity dissipates when Lactobacillus crispatus is grown on glucose, maltose and maltotriose, in agreement with carbon catabolite repression elements flanking the pulA gene. Proteome analysis of the S-layer confirmed that the amylopullulanase protein is highly abundant in an S-layer enriched fraction, but not in a strain with a defective amylopullulanase variant or in an amylopullulanase-sufficient strain grown on glucose. In addition, we provide evidence that Lactobacillus crispatus pulA mutants are relevant in vivo, as they are commonly observed in metagenome datasets of human vaginal microbial communities. Analysis of the largest publicly available dataset of 1507 human vaginal metagenomes indicates that among the 270 samples that contain a Lactobacillus crispatus pulA gene, 62 samples (23%) had a defective variant of this gene. Taken together, these results demonstrate that both environmental, as well as genetic factors explain the variation of Lactobacillus crispatus alpha-glucosidases in the vaginal environment.     

SURFACE ROUGHNESS OF SPUTTERED SILICON. II. MODEL VERIFICATION

Experimental verification of the mathematical surface roughness model for sputtered silicon was performed. The beam shape and its significant level of intensity were determined first by measuring the topography of craters sputtered by focused ion beam (FIB). Then the beam function was generated for various combinations of beam parameters. The material function was developed both by theoretical and experimental analysis. These two functions were then used in the model to calculate the theoretical surface roughness. Microsurface analysis was formed by FIB sputtering of a (100) silicon wafer. The surface roughness at the bottom of the sputtered features was then measured using an atomic force microscope. The theoretical surface roughness was found to be within ±1 and ±5 nm of the measured surface roughness with the measurement uncertainty (standard deviation) of about ±0.36 and ±0.85 nm for R_a and R_t, respectively.     

Mitochondrial Dysfunction Plays Central Role in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is a global pandemic that affects one-quarter of the world’s population. NAFLD includes a spectrum of progressive liver disease from steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis and can be complicated by hepatocellular carcinoma. It is strongly associated with metabolic syndromes, obesity, and type 2 diabetes, and it has been shown that metabolic dysregulation is central to its pathogenesis. Recently, it has been suggested that metabolic- (dysfunction) associated fatty liver disease (MAFLD) is a more appropriate term to describe the disease than NAFLD, which puts increased emphasis on the important role of metabolic dysfunction in its pathogenesis. There is strong evidence that mitochondrial dysfunction plays a significant role in the development and progression of NAFLD. Impaired mitochondrial fatty acid oxidation and, more recently, a reduction in mitochondrial quality, have been suggested to play a major role in NAFLD development and progression. In this review, we provide an overview of our current understanding of NAFLD and highlight how mitochondrial dysfunction contributes to its pathogenesis in both animal models and human subjects. Further we discuss evidence that the modification of mitochondrial function modulates NAFLD and that targeting mitochondria is a promising new avenue for drug development to treat NAFLD/NASH.