Human-like adrenal features in Chinese tree shrews revealed by multi-omics analysis of adrenal cell populations and steroid synthesis.

The Chinese tree shrew ( Tupaia belangeri chinensis) has emerged as a promising model for investigating adrenal steroid synthesis, but it is unclear whether the same cells produce steroid hormones and whether their production is regulated in the same way as in humans. Here, we comprehensively mapped the cell types and pathways of steroid metabolism in the adrenal gland of Chinese tree shrews using single-cell RNA sequencing, spatial transcriptome analysis, mass spectrometry, and immunohistochemistry. We compared the transcriptomes of various adrenal cell types across tree shrews, humans, macaques, and mice. Results showed that tree shrew adrenal glands expressed many of the same key enzymes for steroid synthesis as humans, including CYP11B2, CYP11B1, CYB5A, and CHGA. Biochemical analysis confirmed the production of aldosterone, cortisol, and dehydroepiandrosterone but not dehydroepiandrosterone sulfate in the tree shrew adrenal glands. Furthermore, genes in adrenal cell types in tree shrews were correlated with genetic risk factors for polycystic ovary syndrome, primary aldosteronism, hypertension, and related disorders in humans based on genome-wide association studies. Overall, this study suggests that the adrenal glands of Chinese tree shrews may consist of closely related cell populations with functional similarity to those of the human adrenal gland. Our comprehensive results (publicly available at http://gxmujyzmolab.cn:16245/scAGMap/) should facilitate the advancement of this animal model for the investigation of adrenal gland disorders.

Immunometabolic features of natural killer cells are associated with infection outcomes in critical illness.

Immunosuppression increases the risk of nosocomial infection in patients with chronic critical illness. This exploratory study aimed to determine the immunometabolic signature associated with nosocomial infection during chronic critical illness. We prospectively recruited patients who were admitted to the respiratory care center and who had received mechanical ventilator support for more than 10 days in the intensive care unit. The study subjects were followed for the occurrence of nosocomial infection until 6 weeks after admission, hospital discharge, or death. The cytokine levels in the plasma samples were measured. Single-cell immunometabolic regulome profiling by mass cytometry, which analyzed 16 metabolic regulators in 21 immune subsets, was performed to identify immunometabolic features associated with the risk of nosocomial infection. During the study period, 37 patients were enrolled, and 16 patients (43.2%) developed nosocomial infection. Unsupervised immunologic clustering using multidimensional scaling and logistic regression analyses revealed that expression of nuclear respiratory factor 1 (NRF1) and carnitine palmitoyltransferase 1a (CPT1a), key regulators of mitochondrial biogenesis and fatty acid transport, respectively, in natural killer (NK) cells was significantly associated with nosocomial infection. Downregulated NRF1 and upregulated CPT1a were found in all subsets of NK cells from patients who developed a nosocomial infection. The risk of nosocomial infection is significantly correlated with the predictive score developed by selecting NK cell-specific features using an elastic net algorithm. Findings were further examined in an independent cohort of COVID-19-infected patients, and the results confirm that COVID-19-related mortality is significantly associated with mitochondria biogenesis and fatty acid oxidation pathways in NK cells. In conclusion, this study uncovers that NK cell-specific immunometabolic features are significantly associated with the occurrence and fatal outcomes of infection in critically ill population, and provides mechanistic insights into NK cell-specific immunity against microbial invasion in critical illness.

A Mobile Applet for Assessing Medication Adherence and Managing Adverse Drug Reactions Among Patients With Cancer: Usability and Utility Study.

BACKGROUND: Medication adherence and the management of adverse drug reactions (ADRs) are crucial to the efficacy of antitumor drugs. A WeChat applet, also known as a "Mini Program," is similar to the app but has marked advantages. The development and use of a WeChat applet makes follow-up convenient for patients with cancer. OBJECTIVE: This study aimed to assess the usability and utility of a newly developed WeChat applet, "DolphinCare," among patients with cancer in Shanghai. METHODS: A qualitative methodology was used to obtain an in-depth understanding of the experiences of patients with cancer when using DolphinCare from the usability and utility aspects. The development phase consisted of 2 parts: alpha and beta testing. Alpha testing combined the theory of the Fogg Behavior Model and the usability model. Alpha testing also involved testing the design of DolphinCare using a conceptual framework, which included factors that could affect medication adherence and ADRs. Beta testing was conducted using in-depth interviews. In-depth interviews allowed us to assist the patients in using DolphinCare and understand whether they liked or disliked DolphinCare and found it useful. RESULTS: We included participants who had an eHealth Literacy Scale (eHEALS) score of ≥50%, and a total of 20 participants were interviewed consecutively. The key positive motivators described by interviewers were to be reminded to take their medications and to alleviate their ADRs. The majority of the patients were able to activate and use DolphinCare by themselves. Most patients indicated that their trigger to follow-up DolphinCare was the recommendation of their known and trusted health care professionals. All participants found that labels containing the generic names of their medication and the medication reminders were useful, including timed pop-up push notifications and text alerts. The applet presented the corresponding information collection forms of ADRs to the patient to fill out. The web-based consultation system enables patients to consult pharmacists or physicians in time when they have doubts about medications or have ADRs. The applet had usabilities and utilities that could improve medication adherence and the management of ADRs among patients with cancer. CONCLUSIONS: This study provides preliminary evidence regarding the usability and utility of this type of WeChat applet among patients with cancer, which is expected to be promoted for managing follow-up among other patients with other chronic disease.

Spatial multi-omics analyses of the tumor immune microenvironment.

In the past decade, single-cell technologies have revealed the heterogeneity of the tumor-immune microenvironment at the genomic, transcriptomic, and proteomic levels and have furthered our understanding of the mechanisms of tumor development. Single-cell technologies have also been used to identify potential biomarkers. However, spatial information about the tumor-immune microenvironment such as cell locations and cell-cell interactomes is lost in these approaches. Recently, spatial multi-omics technologies have been used to study transcriptomes, proteomes, and metabolomes of tumor-immune microenvironments in several types of cancer, and the data obtained from these methods has been combined with immunohistochemistry and multiparameter analysis to yield markers of cancer progression. Here, we review numerous cutting-edge spatial 'omics techniques, their application to study of the tumor-immune microenvironment, and remaining technical challenges.

[Comparison of artificial neural network with compatible biomass model for predicting aboveground biomass of individual tree]. / 人工神经网络与相容性生物量模型预测单木地上生物量的比较.

Forest biomass is an important index in forest development planning and forest resource monitoring. In order to provide a more efficient and low-biased method for estimating individual tree biomass, we introduced artificial neural network here. We used the data of aboveground biomass of 101 Larix olgensis trees harvested from the Dongzhelenghe Forest Farm in Heilongjiang Province to develop four aggregation model systems (AMS), based on different combination of the variables (diameter at breast height, tree height, crown width). The weighted functions were used to eliminate heteroscedasticity. Then, we trained artificial neural network (ANN) biomass model based on the optimal combination. The models were tested by the leave-one-out cross-validation method to compare the accuracy of the two biomass estimation methods. The results showed that biomass model based on only one variable, diameter at breast height, could accurately estimate the biomass of L. olgensis. Adding two indices, tree height and crown width, could improve the fitting performance of models, with AMS4 performing the best among the four addictive model systems. The biomass models developed by the two methods both could estimate biomass at tree level accurately, with the coefficient of determination (R2) of each component was higher than 0.87. Compared with the AMS4, R2 of leaf biomass model was about 0.05 higher, and that of other organs were also about 0.01 higher in artificial neural network model system. In addition, the root mean square error (RMSE) and other indicators were also significantly smaller. For example, the RMSE of tree stem and aboveground biomass were smaller by 2.135 kg and 3.908 kg, respectively. The model's validation statistics mean relative error (MRE) performed better. In general, ANN was a flexible and reliable biomass estimation method, which was worthy consideration when predicting tree component biomass or aboveground biomass.

NK cell receptor and ligand composition influences the clearance of SARS-CoV-2.

To explore how the immune system controls clearance of SARS-CoV-2, we used a single-cell, mass cytometry-based proteomics platform to profile the immune systems of 21 patients who had recovered from SARS-CoV-2 infection without need for admission to an intensive care unit or for mechanical ventilation. We focused on receptors involved in interactions between immune cells and virus-infected cells. We found that the diversity of receptor repertoires on natural killer (NK) cells was negatively correlated with the viral clearance rate. In addition, NK subsets expressing the receptor DNAM1 were increased in patients who more rapidly recovered from infection. Ex vivo functional studies revealed that NK subpopulations with high DNAM1 expression had cytolytic activities in response to target cell stimulation. We also found that SARS-CoV-2 infection induced the expression of CD155 and nectin-4, ligands of DNAM1 and its paired coinhibitory receptor TIGIT, which counterbalanced the cytolytic activities of NK cells. Collectively, our results link the cytolytic immune responses of NK cells to the clearance of SARS-CoV-2 and show that the DNAM1 pathway modulates host-pathogen interactions during SARS-CoV-2 infection.

Cancer-Derived Succinate Promotes Macrophage Polarization and Cancer Metastasis via Succinate Receptor.

Macrophages form a major cell population in the tumor microenvironment. They can be activated and polarized into tumor-associated macrophages (TAM) by the tumor-derived soluble molecules to promote tumor progression and metastasis. Here, we used comparative metabolomics coupled with biochemical and animal studies to show that cancer cells release succinate into their microenvironment and activate succinate receptor (SUCNR1) signaling to polarize macrophages into TAM. Furthermore, the results from in vitro and in vivo studies revealed that succinate promotes not only cancer cell migration and invasion but also cancer metastasis. These effects are mediated by SUCNR1-triggered PI3K-hypoxia-inducible factor 1α (HIF-1α) axis. Compared with healthy subjects and tumor-free lung tissues, serum succinate levels and lung cancer SUCNR1 expression were elevated in lung cancer patients, suggesting an important clinical relevance. Collectively, our findings indicate that the secreted tumor-derived succinate belongs to a novel class of cancer progression factors, controlling TAM polarization and promoting tumorigenic signaling.

Host-Induced Gene Silencing of MoAP1 Confers Broad-Spectrum Resistance to Magnaporthe oryzae.

Rice blast caused by Magnaporthe oryzae (M. oryzae) is a major threat to global rice production. In recent years, small interference RNAs (siRNAs) and host-induced gene silencing (HIGS) has been shown to be new strategies for the development of transgenic plants to control fungal diseases and proved a useful tool to study gene function in pathogens. We here tested whether in vitro feeding artificial siRNAs (asiRNAs) could compromise M. oryzae virulence and in vivo HIGS technique could improve rice blast resistance. Our data revealed that silencing of M. oryzae MoAP1 by feeding asiRNAs targeting MoAP1 (i.e., asiR1245, asiR1362, and asiR1115) resulted in inhibited fungal growth, abnormal spores, and decreased pathogenicity. Among the asiRNAs, asiR1115 was the most inhibitory toward the rice blast fungus. Conversely, the asiRNAs targeting three other genes (i.e., MoSSADH, MoACT, and MoSOM1) had no effect on fungal growth. Transgenic rice plants expressing RNA hairpins targeting MoAP1 exhibited improved resistance to 11 tested M. oryzae strains. Confocal microscopy also revealed profoundly restricted appressoria and mycelia in rice blast-infected transgenic rice plants. Our results demonstrate that in vitro asiRNA and in vivo HIGS were useful protection approaches that may be valuable to enhance rice blast resistance.

TLR2 Promotes Vascular Smooth Muscle Cell Chondrogenic Differentiation and Consequent Calcification via the Concerted Actions of Osteoprotegerin Suppression and IL-6-Mediated RANKL Induction.

Objective- Vascular smooth muscle cell (VSMC) transformation to an osteochondrogenic phenotype is an initial step toward arterial calcification, which is highly correlated with cardiovascular disease-related morbidity and mortality. TLR2 (Toll-like receptor 2) plays a pathogenic role in the development of vascular diseases, but its regulation in calcification of arteries and VSMCs remains unclear. We postulate that TLR2-mediated inflammation participates in mediating atherosclerotic arterial calcification and VSMC calcification. Approach and Results- We found that ApoE-/- Tlr2-/- genotype in mice suppressed high-fat diet-induced atherosclerotic plaques formation during initiation but progressively lost its preventative capacity, compared with ApoE-/- mice. However, TLR2 deficiency prohibited high-fat diet-induced advanced atherosclerotic calcification, chondrogenic metaplasia, and OPG (osteoprotegerin) downregulation in the calcified lesions. Incubation of VSMCs in a calcifying medium revealed that TLR2 agonists significantly increased VSMC calcification and chondrogenic differentiation. Furthermore, TLR2 deficiency suppressed TLR2 agonist-mediated VSMC chondrogenic differentiation and consequent calcification, which were triggered via the concerted actions of IL (interleukin)-6-mediated RANKL (receptor activator of nuclear factor κB ligand) induction and OPG suppression. Inhibition experiments with pharmacological inhibitors demonstrated that IL-6-mediated RANKL induction is signaled by p38 and ERK1/2 (extracellular signal-regulated kinase 1/2) pathways, whereas the OPG is suppressed via NF-κB (nuclear factor κB) dependent signaling mediated by ERK1/2. Conclusions- We concluded that on ligand binding, TLR2 activates p38 and ERK1/2 signaling to selectively modulate the upregulation of IL-6-mediated RANKL and downregulation of OPG. These signaling pathways act in concert to induce chondrogenic transdifferentiation of VSMCs, which in turn leads to vascular calcification during the pathogenesis of atherosclerosis.

Mitigation of membrane biofouling by d-amino acids: Effect of bacterial cell-wall property and d-amino acid type.

Development of novel approaches for biofouling mitigation is of crucial importance for membrane-based technologies. d-amino acids (d-AAs) have been proposed as a potential strategy to mitigate biofouling. However, the effect of bacterial cell-wall properties and d-AAs type on biofouling mitigation remains unclear. This study assesses the effect of d-AAs type on membrane biofouling control, towards Gram positive (G+) and Gram negative (G-) bacteria. Three kinds of d-AAs were found to inhibit both G+ and G- bacterial attachment in short-term attachment and dead-end filtration experiments. The existence of d-AAs reduces extracellular polysaccharides and proteins on the membrane, which may decrease membrane biofouling. Cross-flow filtration tests further indicated that d-AAs could effectively reduce membrane biofouling. The permeate flux recovery post chemical cleaning, improved for both P. aeruginosa and B. subtilis treated with d-AAs. The results obtained from this study enable better understanding of the role of d-AAs species on bacterial adhesion and biofilm formation. This may provide a new way to regulate biofilm formation by manipulating the species of d-AAs membrane systems.

Inhomogeneity of Free Volumes in Metallic Glasses under Tension.

In this work, the deformation of Zr2Cu metallic glass (MG) under uniaxial tensile stress was investigated at the atomic level using a series of synchrotron radiation techniques combined with molecular dynamics simulation. A new approach to the quantitative detection of free volumes in MGs was designed and it was found that free volumes increase in the elastic stage, slowly expand in the yield stage, and finally reach saturation in the plastic stage. In addition, in different regions of the MG model, free volumes exhibited inhomogeneity under stress, in terms of size, density, and distribution. In particular, the expansion of free volumes in the center region was much more rapid than those in the other regions. It is interesting that the density of free volumes in the center region abnormally decreased with strain. It was revealed that the atomic-level stress between different regions may contribute to the inhomogeneity of free volumes under stress. In addition, the inhomogeneous change of free volumes during the deformation was confirmed by the evolution of local atomic shear strains in different regions. The present work provides in-depth insight into the deformation mechanisms of MGs.

Modelling of XCO2 Surfaces Based on Flight Tests of TanSat Instruments.

The TanSat carbon satellite is to be launched at the end of 2016. In order to verify the performance of its instruments, a flight test of TanSat instruments was conducted in Jilin Province in September, 2015. The flight test area covered a total area of about 11,000 km² and the underlying surface cover included several lakes, forest land, grassland, wetland, farmland, a thermal power plant and numerous cities and villages. We modeled the column-average dry-air mole fraction of atmospheric carbon dioxide (XCO2) surface based on flight test data which measured the near- and short-wave infrared (NIR) reflected solar radiation in the absorption bands at around 760 and 1610 nm. However, it is difficult to directly analyze the spatial distribution of XCO2 in the flight area using the limited flight test data and the approximate surface of XCO2, which was obtained by regression modeling, which is not very accurate either. We therefore used the high accuracy surface modeling (HASM) platform to fill the gaps where there is no information on XCO2 in the flight test area, which takes the approximate surface of XCO2 as its driving field and the XCO2 observations retrieved from the flight test as its optimum control constraints. High accuracy surfaces of XCO2 were constructed with HASM based on the flight's observations. The results showed that the mean XCO2 in the flight test area is about 400 ppm and that XCO2 over urban areas is much higher than in other places. Compared with OCO-2's XCO2, the mean difference is 0.7 ppm and the standard deviation is 0.95 ppm. Therefore, the modelling of the XCO2 surface based on the flight test of the TanSat instruments fell within an expected and acceptable range.

TLR4-Activated MAPK-IL-6 Axis Regulates Vascular Smooth Muscle Cell Function.

Migration of vascular smooth muscle cells (VSMCs) into the intima is considered to be a vital event in the pathophysiology of atherosclerosis. Despite substantial evidence supporting the pathogenic role of Toll-like receptor 4 (TLR4) in the progression of atherogenesis, its function in the regulation of VSMC migration remains unclear. The goal of the present study was to elucidate the mechanism by which TLR4 regulates VSMC migration. Inhibitor experiments revealed that TLR4-induced IL-6 secretion and VSMC migration were mediated via the concerted actions of MyD88 and TRIF on the activation of p38 MAPK and ERK1/2 signaling. Neutralizing anti-IL-6 antibodies abrogated TLR4-driven VSMC migration and F-actin polymerization. Blockade of p38 MAPK or ERK1/2 signaling cascade inhibited TLR4 agonist-mediated activation of cAMP response element binding protein (CREB). Moreover, siRNA-mediated suppression of CREB production repressed TLR4-induced IL-6 production and VSMC migration. Rac-1 inhibitor suppressed TLR4-driven VSMC migration but not IL-6 production. Importantly, the serum level of IL-6 and TLR4 endogenous ligand HMGB1 was significantly higher in patients with coronary artery diseases (CAD) than in healthy subjects. Serum HMGB1 level was positively correlated with serum IL-6 level in CAD patients. The expression of both HMGB1 and IL-6 was clearly detected in the atherosclerotic tissue of the CAD patients. Additionally, there was a positive association between p-CREB and HMGB1 in mouse atherosclerotic tissue. Based on our findings, we concluded that, upon ligand binding, TLR4 activates p38 MAPK and ERK1/2 signaling through MyD88 and TRIF in VSMCs. These signaling pathways subsequently coordinate an additive augmentation of CREB-driven IL-6 production, which in turn triggers Rac-1-mediated actin cytoskeleton to promote VSMC migration.

sn-1,2-diacylglycerols protect against lethal endotoxemia by controlling systemic inflammation.

Systemic inflammation has emerged as a key pathophysiological process that induces multiple organ injuries and causes serious human diseases. Despite substantial evidence supporting the role of diacylglycerols (DAG) in modulating chronic inflammation and chronic diseases, the potential mechanisms of its involvement in TLRs-mediated inflammation are still unclear. Here, we show that sn-1,2-diacylglycerols modulate LPS/TLR4-mediated inflammation in vitro and in vivo. ELISA and western blotting experiments indicated that sn-1,2-diacylglycerols suppress LPS-induced responses, including IL-6 and TNF-α production, and COX-2 expression in mouse RAW264.7 macrophages and human endothelial cells, in a dose-dependent manner. Using LPS-induced murine model of systemic inflammation, we show that sn-1,2-diacylglycerols block the cytokine storm, the expression of inflammatory mediators, and LPS-induced septic lung damage and mortality. sn-1,2-diacylglycerols reduce systemic inflammation by inhibiting LPS-induced p38 MAPK- and PI3K/AKT-mediated NF-κB activation in macrophages. These results suggest that exogenous DAG probably acts by blocking p38 MAPK or PI3K/AKT signal transduction, thereby down-regulating NF-κB activation and NF-κB-mediated transcription of genes encoding cytokines and pro-inflammatory oxidative enzymes. Our findings demonstrate that exogenous sn-1,2-diacylglycerol protects mice from LPS-induced lethal endotoxemia by suppressing TLR4-driven inflammatory responses, suggesting that 1,2-diacylglycerols may be used as dietary health supplements for the prevention or therapy of systemic inflammatory diseases.

Endothelium-Derived 5-Methoxytryptophan Is a Circulating Anti-Inflammatory Molecule That Blocks Systemic Inflammation.

RATIONALE: Systemic inflammation has emerged as a key pathophysiological process that induces multiorgan injury and causes serious human diseases. Endothelium is critical in maintaining cellular and inflammatory homeostasis, controlling systemic inflammation, and progression of inflammatory diseases. We postulated that endothelium produces and releases endogenous soluble factors to modulate inflammatory responses and protect against systemic inflammation. OBJECTIVE: To identify endothelial cell-released soluble factors that protect against endothelial barrier dysfunction and systemic inflammation. METHODS AND RESULTS: We found that conditioned medium of endothelial cells inhibited cyclooxgenase-2 and interleukin-6 expression in macrophages stimulated with lipopolysaccharide. Analysis of conditioned medium extracts by liquid chromatography-mass spectrometry showed the presence of 5-methoxytryptophan (5-MTP), but not other related tryptophan metabolites. Furthermore, endothelial cell-derived 5-MTP suppressed lipopolysaccharide-induced inflammatory responses and signaling in macrophages and endotoxemic lung tissues. Lipopolysaccharide suppressed 5-MTP level in endothelial cell-conditioned medium and reduced serum 5-MTP level in the murine sepsis model. Intraperitoneal injection of 5-MTP restored serum 5-MTP accompanied by the inhibition of lipopolysaccharide-induced endothelial leakage and suppression of lipopolysaccharide- or cecal ligation and puncture-mediated proinflammatory mediators overexpression. 5-MTP administration rescued lungs from lipopolysaccharide-induced damages and prevented sepsis-related mortality. Importantly, compared with healthy subjects, serum 5-MTP level in septic patients was decreased by 65%, indicating an important clinical relevance. CONCLUSIONS: We conclude that 5-MTP belongs to a novel class of endothelium-derived protective molecules that defend against endothelial barrier dysfunction and excessive systemic inflammatory responses.

Endothelium-Derived 5-Methoxytryptophan Protects Endothelial Barrier Function by Blocking p38 MAPK Activation.

The endothelial junction is tightly controlled to restrict the passage of blood cells and solutes. Disruption of endothelial barrier function by bacterial endotoxins, cytokines or growth factors results in inflammation and vascular damage leading to vascular diseases. We have identified 5-methoxytryptophan (5-MTP) as an anti-inflammatory factor by metabolomic analysis of conditioned medium of human fibroblasts. Here we postulated that endothelial cells release 5-MTP to protect the barrier function. Conditioned medium of human umbilical vein endothelial cells (HUVECs) prevented endothelial hyperpermeability and VE-cadherin downregulation induced by VEGF, LPS and cytokines. We analyzed the metabolomic profile of HUVEC conditioned medium and detected 5-MTP but not melatonin, serotonin or their catabolites, which was confirmed by enzyme-linked immunosorbent assay. Addition of synthetic pure 5-MTP preserved VE-cadherin and maintained barrier function despite challenge with pro-inflammatory mediators. Tryptophan hydroxylase-1, an enzyme required for 5-MTP biosynthesis, was downregulated in HUVECs by pro-inflammatory mediators and it was accompanied by reduction of 5-MTP. 5-MTP protected VE-cadherin and prevented endothelial hyperpermeability by blocking p38 MAPK activation. A chemical inhibitor of p38 MAPK, SB202190, exhibited a similar protective effect as 5-MTP. To determine whether 5-MTP prevents vascular hyperpermeability in vivo, we evaluated the effect of 5-MTP administration on LPS-induced murine microvascular permeability with Evans blue. 5-MTP significantly prevented Evans blue dye leakage. Our findings indicate that 5-MTP is a new class of endothelium-derived molecules which protects endothelial barrier function by blocking p38 MAPK.

D-amino acids inhibit initial bacterial adhesion: thermodynamic evidence.

Bacterial biofilms are structured communities of cells enclosed in a self-produced hydrated polymeric matrix that can adhere to inert or living surfaces. D-Amino acids were previously identified as self-produced compounds that mediate biofilm disassembly by causing the release of the protein component of the polymeric matrix. However, whether exogenous D-amino acids could inhibit initial bacterial adhesion is still unknown. Here, the effect of the exogenous amino acid D-tyrosine on initial bacterial adhesion was determined by combined use of chemical analysis, force spectroscopic measurement, and theoretical predictions. The surface thermodynamic theory demonstrated that the total interaction energy increased with more D-tyrosine, and the contribution of Lewis acid-base interactions relative to the change in the total interaction energy was much greater than the overall nonspecific interactions. Finally, atomic force microscopy analysis implied that the hydrogen bond numbers and adhesion forces decreased with the increase in D-tyrosine concentrations. D-Tyrosine contributed to the repulsive nature of the cell and ultimately led to the inhibition of bacterial adhesion. This study provides a new way to regulate biofilm formation by manipulating the contents of D-amino acids in natural or engineered systems.

[Preliminary study of atomic emission spectrometry of Ti (H) plasma produced by vacuum arc ion source].

In order to study the discharge process of vacuum arc ion source, make a detail description of the discharge plasma, and lay the foundation for further research on ion source, atomic emission spectrometry was used to diagnose the parameters of plasma produced by vaccum arc ion source. In the present paper, two kinds of analysis method for the emission spectra data collected by a spectrometer were developed. Those were based in the stark broadening of spectral lines and Saba-Boltzmann equation. Using those two methods, the electron temperature, electron number density and the ion temperature of the plasma can be determined. The emission spectroscopy data used in this paper was collected from the plasma produced by a vacuum are ion source whose cathode was made by Ti material (which adsorbed hydrogen during storage procedure). Both of the two methods were used to diagnose the plasma parameters and judge the thermal motion state of the plasma. Otherwise, the validity of the diagnostic results by the two methods were analyzed and compared. In addition, the affection from laboratory background radiation during the spectral acquisition process was discussed.

Influences of D-tyrosine on the stability of activated sludge flocs.

The sludge floc stability is essential for the solid/liquid separation in biological wastewater treatment. In this study, the effect of an exogenous d-tyrosine on the shear stability and surface characteristics of activated sludge flocs was investigated. Sludge flocs were found to be less stable in the addition of d-tyrosine. d-Tyrosine inhibited the production of extracellular polymeric substances (EPS) especially for the proteins. A high correlation coefficient was observed between the composition of EPS fraction and d-tyrosine content. In addition, the hydrophobicity of sludge flocs was reduced and the zeta potential was more negative with the content of d-tyrosine increased. A linear relationship between the extracellular polymeric substances and surface characteristics for sludge flocs indicated that the inhibited EPS production may be responsible for the instability of sludge upon the addition of d-tyrosine.

[Two-temperature diagnostic studies by emission spectra for nonequilibrium Ti-H plasma].

Using the T-H solid solution made by titanium absorbed hydrogen as the cathode, the Ti-H plasma produced by the pulsed vacuum are ion source was nonequilibrium: it contained both the component of titanium and hydrogen; there existed gradient in the radiaL, the horizontal and the time. As a result, it could not be described by a single temperature. The present paper assumed that the subsystem consisting of electrons and the subsystem consisting of other heavy particles reached equilibrium respectively, meaning that the Ti-H plasma was described by the two temperatures as electron temperature and heavy ion temperature, it was non-equilibrium two-temperature plasma Using Culdberg-Waage dissociation equation to describe the molecular dissociation process in the system, using Saha ionization equation to describe the atomic ionization process, combining plasma's charge quasi-neutral condition and introducing atomic emission spectroscopy as a plasma diagnostic method which would not interfere the plasma at the same time; the temperature and the particle number density of the Ti-H plasma were diagnosed. Using MATLAB as a tool, both the titanium atoms and monovalent titanium ions' ionization were considered, and the calculated results showed that with the electtron density determined by the Stark broadening of spectral lines in advance, except the heavy particle temperature and the hydrogen number density, the Ti-H plasma's parameters could be diagnosed fairly accurately; the accuracy of the electron density values had a great effect on the calculation results; if the heavy particle temperature could be determined in advance, the temperature and the particle number density of the Ti-H plasma could be accurately analyzed quantitatively.