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Abstract Sevoflurane has been the most widely used inhaled anesthetics with a favorable recovery profile; however, the precise mechanisms underlying its anesthetic action are still not completely understood. Here the authors show that sevoflurane activates a cluster of urocortin 1 (UCN1+)/cocaine‐ and amphetamine‐regulated transcript (CART+) neurons in the midbrain involved in its anesthesia. Furthermore, growth hormone secretagogue receptor (GHSR) is highly enriched in sevoflurane‐activated UCN1+/CART+ cells and is necessary for sleep induction. Blockade of GHSR abolishes the excitatory effect of sevoflurane on UCN1+/CART+ neurons and attenuates its anesthetic effect. Collectively, their data suggest that anesthetic action of sevoflurane necessitates the GHSR activation in midbrain UCN1+/CART+ neurons, which provides a novel target including the nucleus and receptor in the field of anesthesia.

Summary: Background: Sensitive scalp, one of the most frequent complaints among sensitive skin syndrome, has been described as abnormal and unpleasant sensory reactions of the scalp to environmental stimulus. However, the symptoms are usually objective and hard to diagnose. Objective: This study aimed to reveal the biophysical properties and etiology of sensitive scalp. Methods: Sixty‐two healthy female subjects were enrolled and divided into nonsensitive scalp (NS) and sensitive scalp (SS) groups according to questionnaires. Noninvasive instruments were used to measure biophysical properties. Ultra‐performance liquid chromatography‐tandem mass spectrometry and gas chromatography mass spectrometry were introduced to quantify skin lipids profiles, and 16S rRNA sequencing was used to detect the composition of bacteria. Results: Sensitive scalp showed elevated pH level, more irritated skin, and more fluorescence of porphyrins. Increased sebum production was found in SS group at occiput, among which free fatty acids, cholesteryl ester, and squalene were significantly in higher amount compared with NS. SS also had significantly higher percentage of Propionibacterium, and lower bacterial diversity. Conclusions: Taken together, sensitive scalp showed disrupted barrier function, abnormal sebum amount and composition, as well as perturbed microbiome, which might be the direct cause. Products targeting these features could be helpful for the treatment of sensitive scalp. [ABSTRACT FROM AUTHOR]

Abstract Backgrounds Hereditary hemochromatosis (HH) is mainly caused by homozygous p.C282Y mutations in HFE in the Caucasians. We recently reported non-HFE mutations constitute the major cause of HH in Chinese. However, there is still a relatively high proportion of cases with primary iron overload from unexplained causes. We aimed to explore novel non-HFE mutations in Chinese patients with primary iron overload. Methods Whole exome sequence was conducted to screen mutations in novel HH-related genes in the 9 cases with unexplained primary iron overload. Then the representative candidate genes were screened for mutations in another cohort of 18 HH cases. The biological function of the selected genes and variants were analyzed in vitro. Results Whole exome sequencing of 9 cases with unexplained primary iron overload identified 42 missense variants in 40 genes associated with iron metabolism pathway genes such as UBE2O p.K689R and PCSK7 p.R711W. Subsequent Sanger sequencing of the UBE2O and PCSK7 genes in the 27 cases with primary iron overload identified p.K689R in UBE2O, p.R711W and p.V143F in PCSK7 at frequency of 2/27,1/27 and 2/27 respectively. In vitro siRNA interference of UBE2O and PCSK7 resulted in down-regulated HAMP mRNA expression. Adenovirus generation of UBE2O p.K689R in cell lines resulted in increased expression of SMAD6 and SMAD7 and downregulation of p-SMAD1/5 and HAMP expression, and the reduction of hepcidin level. Conclusions Our study identified a series of novel candidate non-HFE mutations in Chinese patients with HH. These may provide insights into the genetic basis of unexplained primary iron overload.

The current work combines headspace solid phase microextraction-gas chromatography-mass spectrometry (HS-SPME-GC/MS) with multivariate analysis fusion metabonomics for examining metabolite profile changes. The correlation with metabolic pathways during the fermentation of kombucha tea were comprehensively explored. For optimizing the fermentation process, ultrasound-assisted factors were explored. A total of 132 metabolites released by fermented kombucha were detected by HS-SPME-GC/MS. We employed the principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) to present the relationship between aroma components and fermentation time, of which the first two principal components respectively accounted for 60.3% and 6.5% of the total variance. Multivariate statistical analysis showed that during the fermentation of kombucha tea, there were significant differences in the phenotypes of metabolites in the samples, and 25 characteristic metabolites were selected as biomarkers. Leaf alcohol was first proposed as the characteristic volatile in the fermentation process of kombucha. Furthermore, we addressed the generation pathways of characteristic volatiles, their formation mechanisms, and the transformational correlation among them. Our findings provide a roadmap for future kombucha fermentation processing to enhance kombucha flavor and aroma.

Gut microecosystem has been shown to play an important role in human health. In recent years, the concept of the gut-kidney axis has been proposed to explain the potential association between gut microbiota and chronic kidney disease (CKD). Here, a cohort of fecal samples collected from patients with CKD (n = 13) were involved. The composition of gut microbial communities and clinical features in CKD and end-stage renal disease (ESRD) were characterized. Our study focused on the changes in gut microbiome and the correlation with clinical features in patients with CKD and ESRD by analyzing high-throughput sequencing results of collected feces. We elucidated the alterations of gut microbiota in CKD patients at different stages of disease and initially identified the gut microbiota associated with CKD progression. We also combined correlation analysis to identify clinical features closely related to the gut microbiome. Our results offered the possibility of using non-invasive gut microbiome in the early diagnosis of course from CKD to ESRD and provide new insights into the association between clinical features and gut microbiota in CKD.

Bacterial resistance is becoming increasingly serious, the present study aimed to investigate the mechanism of antibacterial sensitization effect of DHA27 combined with tobramycin in tobramycin-resistant Pseudomonas aeruginosa (PA). We found that DHA27 combined with aminoglycosides had an antibacterial sensitization effect on PA. Tobramycin, owing to its lower toxic and side effects, was selected to further study the molecular mechanism of drug combination. A sublethal-dose bacterial challenge/sepsis mouse model was established to study the protective effect of DHA27 plus tobramycin. Scanning electron microscopy was used to investigate whether DHA27 exerts the antibacterial sensitization effect by directly affecting bacterial morphology. The effect of DHA27 on daunorubicin accumulation in bacteria was studied, and quantitative reverse transcription PCR was used to study the effect of DHA27 plus tobramycin on 16S rRNA methyltransferase and aminoglycoside-modifying enzyme mRNA expression. Twenty clinical isolates of PA were found to be tobramycin resistant; DHA27 plus tobramycin had a significant antibacterial sensitization effect on many of these resistant strains. DHA27 plus tobramycin reduced the bacterial load in the spleen and lungs of sepsis model mice and levels of proinflammatory cytokines interleukin-1β (IL-1β) and interferon-γ (IFN-γ). DHA27 plus tobramycin significantly inhibited the mRNA expression of aminoglycoside-modifying enzymes in bacteria. DHA27 combined with AGs had an antibacterial sensitization effect on PA; the molecular mechanism underlying this effect is closely related to the inhibition of the mRNA expression of aminoglycoside-modifying enzymes, especially aac(3)-II.

Considered as the most popular pathogen worldwide, Helicobacter pylori is intensively associated with diverse gastric diseases, including gastric ulcers, chronic progressive gastritis, and gastric cancer. Aside from its pathogenic effect on gastric diseases, growing evidences reveal that H. pylori may be related to numerous extragastric diseases. In this article, we reviewed recent studies and systematically elucidated that H. pylori may interfere with many biological processes outside the stomach and influence the occurrence of various extragastric diseases. Many epidemiological studies have indicated that H. pylori plays a pathogenic role in COVID-19, atherosclerosis, hyperemesis gravidarum and several other extragastric diseases, while the effect of H. pylori is currently under investigation in gastroesophageal reflux disease, asthma, and inflammatory bowel disease. Moreover, we also summarized the possible pathogenic mechanisms of H. pylori that may be related to chronic systemic inflammation and molecular mimicker. Taken together, this review provides a new perspective on the role of H. pylori in extragastric diseases and explores the possible mechanisms, which may help guide clinical treatment.

The current innovative work combines nano-optical sensors with near-infrared spectroscopy for rapid detection and quantification of polyphenols and investigates the potential of the nano-optical sensor based on chemo-selective colorants to detect the dynamic changes in aroma components during the fermentation of tea extract. The procedure examined the influence of different ultrasound-assisted sonication factors on the changes in the consumption rate of polyphenols during the fermentation of tea extract versus non-sonication as a control group. The results showed that the polyphenol consumption rate improved under the ultrasound conditions of 28 kHz ultrasound frequency, 24 min treatment time, and 40 W/L ultrasonic power density. The metal–organic framework based nano-optical sensors reported here have more adsorption sites for enhanced adsorption of the volatile organic compounds. The polystyrene-acrylic microstructure offered specific surface area for the reactants. Besides, the employed porous silica nanospheres with higher porosity administered improved gas enrichment effect. The nano-optical sensor exhibits good performance with a “chromatogram” for the identification of aroma components in the fermentation process of tea extract. The proposed method respectively enhanced the consumption rate of polyphenol by 35.57%, 11.34% and 16.09% under the optimized conditions. Based on the established polyphenol quantitative prediction models, this work demonstrated the feasibility of using a nano-optical sensor to perform in-situ imaging of the fermentation degree of tea extracts subjected to ultrasonic treatment.

MarvelD3, a recently identified tight junction membrane protein, could be associated with hepatocellular carcinoma (HCC). We aimed to investigate the role of marvelD3 in Epithelial–Mesenchymal Transition (EMT) and migration of HCC and explore the underlying molecular mechanisms. First, we assessed marvlD3 expression in HCC and normal liver tissues and found loss of marvelD3 expression was significantly correlated with the occurrence and TNM stage of HCC. Second, we detected that marvelD3 was downregulated in HCC cells with transforming growth factor β1 and snail/slug-induced EMT. Finally, we analyzed expression of marvelD3 protein was significantly associated with EMT and the NF-κB signaling pathway. Our study demonstrated that MarvelD3 inhibited EMT and migration of HCC cells along with inhibiting NF-κB signaling pathway. Abbreviations: HCC, Hepatocellular carcinoma; TJ, Tight junction; MARVEL, MAL and related proteins for vesicle trafficking and membrane link; EMT, Epithelial–mesenchymal transition; NF-κB, Nuclear factor kappa B; TAMPs, Tight junction-associated marvel proteins; TGF-β1, Transforming growth factor-β1; MMP9, matrix metallopeptidase 9; RT-PCR, Real-time PCR; IHC, Immunohistochemistry; IF, Immunofluorescence.

Chiral aldehyde catalysis is a useful strategy in the catalytic asymmetric α-functionalization of amino methyl compounds but these reaction types are limited. Here, the authors report two chiral aldehyde-catalysed diastereodivergent reactions, namely, a 1,6-conjugate addition and a bio-inspired Mannich reaction.

Abstract Background Aberrant expression of circular RNAs contributes to the initiation and progression of cancers, but the underlying mechanism remains elusive. Methods RNA-seq and qRT-PCR were performed to screen differential expressed circRNAs between gastric cancer tissues and adjacent normal tissues. Candidate circRNA (circMRPS35) was screened out and validated by qRT-PCR. Cell proliferation and invasion ability were determined by CCK-8 and cell invasion assays. RNA-seq, GO-pathway, RNA pull-down and ChIRP were further applied to search for detailed mechanism. Results Here, a novel circRNA named circMRPS35, was screened out by RNA-seq in gastric cancer tissues, whose expression is related to clinicopathological characteristics and prognosis in gastric cancer patients. Biologically, circMRPS35 suppresses the proliferation and invasion of gastric cancer cells in vitro and in vivo. Mechanistically, circMRPS35 acts as a modular scaffold to recruit histone acetyltransferase KAT7 to the promoters of FOXO1 and FOXO3a genes, which elicits acetylation of H4K5 in their promoters. Particularly, circMRPS35 specifically binds to FOXO1/3a promoter regions directly. Thus, it dramatically activates the transcription of FOXO1/3a and triggers subsequent response of their downstream target genes expression, including p21, p27, Twist1 and E-cadherin, resulting in the inhibition of cell proliferation and invasion. Moreover, circMRPS35 expression positively correlates with that of FOXO1/3a in gastric cancer tissues. Conclusions Our findings not only reveal the pivotal roles of circMRPS35 in governing histone modification in anticancer treatment, but also advocate for triggering circMRPS35/KAT7/FOXO1/3a pathway to combat gastric cancer.

BackgroundProtein disulfide isomerase A3 (PDIA3) is a member of the protein disulfide isomerase (PDI) family that participates in protein folding through its protein disulfide isomerase function. It has been reported to regulate the progression of several cancers, but its function in cancer immunotherapy is unknown.MethodsThe RNA-seq data of cancer and normal tissues were downloaded from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases. The Cbioportal dataset was used to explore the genomic alteration information of PDIA3 in pan-cancer. Human Protein Atlas (HPA) and ComPPI websites were employed to mine the protein information of PDIA3, and western blot assay was performed to monitor the upregulated PDIA3 expression in clinical GBM samples. The univariate Cox regression and the Kaplan–Meier method were utilized to appraise the prognostic role of PDIA3 in pan-cancer. Gene Set Enrichment Analysis (GSEA) was applied to search the associated cancer hallmarks with PDIA3 expression. TIMER2.0 was the main platform to investigate the immune cell infiltrations related to PDIA3 in pan-cancer. The associations between PDIA3 and immunotherapy biomarkers were performed by Spearman correlation analysis. The immunoblot was used to quantify the PDIA3 expression levels, and the proliferative and invasive ability of glioma cells was determined by colony formation and transwell assays.FindingsPDIA3 is overexpressed in most cancer types and exhibits prognosis predictive ability in various cancers, and it is especially expressed in the malignant cells and monocytes/macrophages. In addition, PDIA3 is significantly correlated with immune-activated hallmarks, cancer immune cell infiltrations, and immunoregulators, and the most interesting finding is that PDIA3 could significantly predict anti-PDL1 therapy response. Besides, specific inhibitors that correlated with PDIA3 expression in different cancer types were also screened by using Connectivity Map (CMap). Finally, knockdown of PDIA3 significantly weakened the proliferative and invasive ability of glioma cells.InterpretationThe results revealed that PDIA3 acts as a robust tumor biomarker. Its function in protein disulfide linkage regulation could influence protein synthesis, degradation, and secretion, and then shapes the tumor microenvironment, which might be further applied to develop novel anticancer inhibitors.

Specific interaction between the postsynaptic density protein 95 (PSD95) and synapse-associated protein 90/postsynaptic density 95–associated protein (SAPAP) is crucial for excitatory synaptic development and plasticity. Designing inhibitors that target the guanylate kinase (GK) domain of PSD95, which is responsible for the interaction, is a promising manipulation tool for the investigation of the function of PSD95 GK and the etiology of its related psychiatric disorders. Herein, we designed new peptide inhibitors of PSD95 GK/SAPAP with higher binding affinity by using molecular dynamics simulations. First, the interactions between PSD95 GK and their reported phosphorylated and unphosphorylated peptides were explored by molecular dynamics simulations. Besides the hydrogen bonding interactions mediated by the phospho-serine (p-Ser) or corresponding phosphomimic residue Asp/Glu, the hydrophobic interactions from the other amino acids also contribute to the PSD95 GK/SAPAP interaction. As an unphosphorylated synthetic peptide with moderate binding affinity and relatively lower molecular weight, the QSF inhibitory peptide was selected for further modification. Based on per-residue energy decomposition results of the PSD95 GK/QSF complex, ten peptides were designed to enhance the binding interactions, especially the hydrophobic interactions. The top-ranked five peptides with lower binding energy were eventually synthesized. The binding affinities of the synthesized peptides were determined using fluorescence polarization (FP) assay. As expected, all peptides have higher binding affinity than the QSF peptide (Ki = 5.64 ± 0.51 μM). Among them, F10W was the most potent inhibitor (Ki = 0.75 ± 0.25 μM), suggesting that enhancement of the hydrophobic interactions is an important strategy for the design of new inhibitory peptides targeting PSD95 GK.

Background: Non-small-cell lung cancer (NSCLC) with STK11 mutation showed primary resistance to immune checkpoint inhibitors (ICIs). The glucose-lowering drug metformin exerted anti-cancer effect and enhanced efficacy of chemotherapy in NSCLC with KRAS/STK11 co-mutation, yet it is unknown whether metformin may enhance ICI efficacy in STK11 mutant NSCLC.Methods: We studied the impact of metformin on ICI efficacy in STK11 mutant NSCLC in vitro and in vivo using colony formation assay, cell viability assay, Ki67 staining, ELISA, CRISPR/Cas9-mediated knockout, and animal experiments.Results: Through colony formation assay, Ki67 incorporation assay, and CCK-8 assay, we found that metformin significantly enhanced the killing of H460 cells and A549 cells by T cells. In NOD-SCID xenografts, metformin in combination with PD-1 inhibitor pembrolizumab effectively decreased tumor growth and increased infiltration of CD8+ T cells. Metformin enhanced stabilization of STING and activation of its downstream signaling pathway. siRNA-mediated knockdown of STING abolished the effect of metformin on T cell-mediated killing of tumor cells. Next, we found that CRISPR/Cas9-mediated knockout of the scaffold protein AXIN-1 abolished the effect of metformin on T cell-mediated killing and STING stabilization. Immunoprecipitation and confocal macroscopy revealed that metformin enhanced the interaction and colocalization between AXIN-1 and STING. Protein-protein interaction modeling indicated that AXIN-1 may directly bind to STING at its K150 site. Next, we found that metformin decreased K48-linked ubiquitination of STING and inhibited the interaction of E3-ligand RNF5 and STING. Moreover, in AXIN-1−/− H460 cells, metformin failed to alter the interaction of RNF5 and STING.Conclusion: Metformin combining PD-1 inhibitor enhanced anti-tumor efficacy in STK11 mutant lung cancer through inhibition of RNF5-mediated K48-linked ubiquitination of STING, which was dependent on AXIN-1.

Background Sensitive scalp which has been recently proposed and assessed by several questionnaires is one of the most cosmetic concerns in sensitive skin syndrome by consumers. Objective This study is to investigate the prevalence and factors related to the scalp sensitivity in China. Methods Two well-known questionnaires including four-grade self-assessment and 3S, and a new questionnaire we proposed (10Q), were used to evaluate the severity and symptoms of sensitive scalp. Results The proportions of sensitive scalp according to self-assessment and 3S were 35.77% and 57.45%, respectively. Distributions of severity and tendency of proportion along ages were significantly different between the two methods. The 10Q questionnaire which we designed could discriminate different grade of severity of sensitive scalp with superior reliability. Moreover, triggering factors which have significant impacts on the symptoms of sensitive scalp were elucidated by logistic regression analysis, including air dryness, exercises, humidity, heat, and sun. Conclusion Questionnaires with more dimensions and details such as 10Q and 3S should be used for the diagnosis, prognosis, and treatment monitoring on sensitive scalp in Chinese female. [ABSTRACT FROM AUTHOR]

The Asia-Pacific Working Group on inflammatory bowel disease (IBD) was established in Cebu, Philippines, under the auspices of the Asian Pacific Association of Gastroenterology with the goal of improving IBD care in Asia. This consensus is carried out in collaboration with Asian Organization for Crohn’s and Colitis. With biologic agents and biosimilars becoming more established, it is necessary to conduct a review on existing literature and establish a consensus on when and how to introduce biologic agents and biosimilars in the conjunction with conventional treatments for ulcerative colitis (UC) and Crohn’s disease (CD) in Asia. These statements also address how pharmacogenetics influence the treatments of UC and CD and provide guidance on response monitoring and strategies to restore loss of response. Finally, the review includes statements on how to manage treatment alongside possible hepatitis B and tuberculosis infections, both common in Asia. These statements have been prepared and voted upon by members of IBD workgroup employing the modified Delphi process. These statements do not intend to be all-encompassing and future revisions are likely as new data continue to emerge.

The activation of oncogenes and the loss of tumor suppressor genes are believed to play critical roles in the pathogenesis of human hepatocellular carcinoma (HCC). Metaherin (MTDH), also called astrocyte elevated gene-1 (AEG-1), is frequently amplified in a variety of cancers, but the roles of MTDH with regard to growth and apoptosis in HCC have not yet been studied. In the present study, we first analyzed the expression of MTDH in HCC samples. We found that MTDH protein levels are higher in most HCC cancerous tissues compared with their matched adjacent non-tumor tissues. Additionally, the MTDH mRNA was also higher in HCC tissues compared to their matched adjacent non-tumor tissues. Knockdown of the endogenous MTDH using small interfering RNA further showed that deficiency of MTDH suppressed cell growth and caused apoptosis in HCC cells. Knockdown MTDH promoted PTEN and p53 expression in HCC cells and inhibited AKT phosphorylation. Knockdown MTDH also inhibited tumor growth in vivo. All these results indicated that MTDH protein levels in most HCC tissues are higher than non-tumor tissues, and knockdown of MTDH inhibited growth and induced apoptosis in HCC cells through the activation of PTEN. Therefore, MTDH might be an effective targeted therapy gene for HCC. [ABSTRACT FROM AUTHOR]

A family of novel efficient non-oxime compounds exhibited promising reactivation efficacy for VX and sarin inhibited human acetylcholinesterase was discovered. It was found that aromatic groups coupled to Mannich phenols and the introduction of imidazole to the ortho position of phenols would dramatically enhance reactivation efficiency. Moreover, the in vivo experiment was conducted, and the results demonstrated that Mannich phenol L10R1 (30 mg/kg, ip) could afford 100% 48 h survival for mice of 2*LD50 sarin exposure, which is promising for the development of non-oxime reactivators with central efficiency.

Background/AimsTo examine the association between use of oral contraceptive pills (OCPs) and the risk of developing inflammatory bowel diseases (IBD), in a modern cohort.MethodsA prospective nested case-control study across sites in the Asia-Pacific region was conducted; involving female IBD cases and asymptomatic controls. Subjects completed a questionnaire addressing questions related to OCP use. Primary outcome was the risk of development of IBD of those exposed to OCP versus non-exposure. Secondary outcomes were development of Crohn's disease (CD) versus ulcerative colitis (UC), and whether age of first use of OCP use may be associated with risk of IBD.ResultsThree hundred and forty-eight female IBD cases (41% CD, median age: 43 years) and 590 female age-matched controls were recruited. No significant association was found between OCP use and the risk of IBD (odds ratio [OR], 1.65; 95% confidence interval, 0.77–3.13; P=0.22), CD (OR, 1.55) or UC (OR, 1.01). The lack of association persisted when results were adjusted for age and smoking. IBD cases commenced OCP use at a younger age than controls (18 years vs. 20 years, P=0.049).ConclusionsIn this large cohort of subjects from the Asia-Pacific region, we found a modest but not significantly increased risk of developing IBD amongst OCP users.

Discs-large (DLG) is a member that belongs to the membrane-associated guanylate kinase (MAGUK) family. The GK domain of DLGs has evolved into a protein–protein interaction module that could bind with kinds of proteins to regulate diverse cellular functions. Previous reports have demonstrated the GK domain of DLGs functioned as a phosphor-peptide-binding module by resolving the crystal structures. Here we investigated into the interactions of DLG1 and DLG4 with their reported phosphor-peptides by molecular dynamics simulations. Post-dynamics analysis showed that DLG1/4 formed extensive interactions with phosphorylated ligands, including hydrophobic and hydrogen bonding interactions. Among them, the highly conserved residues among the DLGs in phosphor-site and β5 sheet were crucial for the binding according to the energy decomposition calculations. Additionally, the binding interactions between DLG4 and reported unphosphorylated peptides including MAP1A and designed GK inhibitory (GKI-QSF) peptides were analyzed. We found the key residues that played important roles in DLG4/unphosphorylated peptide systems were very similar as in DLG4/phosphor-peptide systems. Moreover, the molecular dynamic simulation for the complex of DLG1 and GKI-QSF was carried out and predicted that the GKI-QSF could bind with DLG1 with similar Kd value compared to DLG4/GKI-QSF, which was verified by using ITC assay (Kd = 1.20 ± 0.29 μM). Our study might be helpful for the better understanding of the structural and biological function of DLGs GK domain and encourage the discovery of new binders.

Abstract In this study, a partially bio‐based carbon fiber (CF) precursor is prepared by blending 32 wt% of pyrolytic lignin (PyL) with 68 wt% of poly(acrylonitrile‐co‐itaconic acid) (PANIA), and the effect of PyL on forming conjugated ladder structure during stepwise thermal stabilization is studied. The results of X‐ray photoelectron spectroscopy (XPS) reveal that PyL accelerates the formation of conjugated ladder structure at 230 °C during thermal stabilization for PANIA/PyL, which is 15 °C lower and 13 min earlier than PANIA. The acceleration on forming thermally stable conjugated ladder structure can be confirmed through Fourier‐transform infrared spectroscopy (FTIR), differential scanning calorimetry (DSC), and thermogravimetric analysis (TGA). Moreover, the fiber stabilized at 230 °C is subsequently made into PANIA/PyL‐230 CF, which has relatively higher‐ordered graphitic structure and dense morphology without voids. The mechanism of PyL accelerating the formation of conjugated ladder structure during thermal stabilization is discussed.

It is crucial for the efficacy of the apple storage to apply methods like electronic nose systems for detection and prediction of spoilage or infection by Penicillium expansum. Based on the acquisition of electronic nose signals, selected sensitive feature sensors of spoilage apple and all sensors were analyzed and compared by the recognition effect. Principal component analysis (PCA), principle component analysis-discriminant analysis (PCA-DA), linear discriminant analysis (LDA), partial least squares discriminate analysis (PLS-DA) and K-nearest neighbor (KNN) were used to establish the classification model of apple with different degrees of corruption. PCA-DA has the best prediction, the accuracy of training set and prediction set was 100% and 97.22%, respectively. synergy interval (SI), genetic algorithm (GA) and competitive adaptive reweighted sampling (CARS) are three selection methods used to accurately and quickly extract appropriate feature variables, while constructing a PLS model to predict plaque area. Among them, the PLS model with unique variables was optimized by CARS method, and the best prediction result of the area of the rotten apple was obtained. The best results are as follows: Rc = 0.953, root mean square error of calibration (RMSEC) = 1.28, Rp = 0.972, root mean square error of prediction (RMSEP) = 1.01. The results demonstrated that the electronic nose has a potential application in the classification of rotten apples and the quantitative detection of spoilage area.

Utilizing renewable resources and accelerating thermal stabilization have been two main effective technical means to reduce the cost of poly(acrylonitrile) (PAN) based carbon fibre (CF). In this work, cross-linked poplar lignin (CPPL) with higher carbon content and 15 times the weight-average molecular weight of poplar lignin (PPL) was formed by doping boron phosphate (BP) in situ composites, which was blended with poly(acrylonitrile-co-vinyl acetate) (PANVA) to prepare a low-cost partially bio-based composite PANVA/CPPL-BP. During thermal stabilization, the C1s curve-fitting of x-ray photoelectron spectroscopy (XPS) spectra showed that the conjugated ladder structure of PANVA/CPPL-BP started to form at 230 °C, which was 20 °C lower than PANVA. And the acceleration in forming conjugated ladder structures was further confirmed by Fourier transform infrared spectroscopy (FTIR), differential scanning calorimetry (DSC), thermogravimetric (TG), and TG-FTIR. During simulated low-temperature carbonization for composites stabilized at 230 °C in advance, the addition of CPPL-BP greatly improved the order of graphitic structure for PANVA. The mechanical property of CF mats has also been obviously improved by CPPL-BP. The possible mechanism that CPPL-BP accelerating the formation of conjugated ladder structures for PANVA/CPPL-BP during thermal stabilization was proposed. With such improvement on accelerating thermal stabilization and utilizing cheap bio-material at the same time, this PANVA/CPPL-BP composite has a great potential in developing low-cost CF.

An abstract of the paper "Identification and characterization of novel B-cell epitopes within EBV latent membrane protein 2 (LMP2)," by Xiangyang Xue and colleagues is presented.