Mosquito brains encode unique features of human odour to drive host seeking.

A globally invasive form of the mosquito Aedes aegypti specializes in biting humans, making it an efficient disease vector1. Host-seeking female mosquitoes strongly prefer human odour over the odour of animals2,3, but exactly how they distinguish between the two is not known. Vertebrate odours are complex blends of volatile chemicals with many shared components4-7, making discrimination an interesting sensory coding challenge. Here we show that human and animal odours evoke activity in distinct combinations of olfactory glomeruli within the Ae. aegypti antennal lobe. One glomerulus in particular is strongly activated by human odour but responds weakly, or not at all, to animal odour. This human-sensitive glomerulus is selectively tuned to the long-chain aldehydes decanal and undecanal, which we show are consistently enriched in human odour and which probably originate from unique human skin lipids. Using synthetic blends, we further demonstrate that signalling in the human-sensitive glomerulus significantly enhances long-range host-seeking behaviour in a wind tunnel, recapitulating preference for human over animal odours. Our research suggests that animal brains may distil complex odour stimuli of innate biological relevance into simple neural codes and reveals targets for the design of next-generation mosquito-control strategies.

Impaired influenza A virus replication by the host restriction factor SAMHD1 which inhibited by PA-mediated dephosphorylation of the host transcription factor IRF3.

BACKGROUND: Influenza A virus (IAV) can cause severe and life-threatening illness in humans and animals. Therefore, it is important to search for host antiviral proteins and elucidate their antiviral mechanisms for the development of potential treatments. As a part of human innate immunity, host restriction factors can inhibit the replication of viruses, among which SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1 (SAMHD1) can restrict the replication of viruses, such as HIV and enterovirus EV71. Viruses also developed countermeasures in the arms race with their hosts. There are few reports about whether SAMHD1 has a restriction effect on IAV. METHODS: To investigate the impact of IAV infection on SAMHD1 expression in A549 cells, we infected A549 cells with a varying multiplicity of infection (MOI) of IAV and collected cell samples at different time points for WB and RT-qPCR analysis to detect viral protein and SAMHD1 levels. The virus replication level in the cell culture supernatant was determined using TCID50 assay. Luciferase assay was used to reveal that H5N1 virus polymerase acidic protein (PA) affected the activity of the SAMHD1 promoter. To assess the antiviral capacity of SAMHD1, we generated a knockdown and overexpressed cell line for detecting H5N1 replication. RESULTS: In this study, we observed that SAMHD1 can restrict the intracellular replication of H5N1 and that the H5N1 viral protein PA can downregulate the expression of SAMHD1 by affecting SAMHD1 transcriptional promoter activity. We also found that SAMHD1's ability to restrict H5N1 is related to phosphorylation at 592-tyrosine. CONCLUSIONS: In conclusion, we found that SAMHD1 may affect the replication of IAVs as a host restriction factor and be countered by PA. Furthermore, SAMHD1 may be a potential target for developing antiviral drugs.

Constructing graphene oxide/Au nanoparticle cellulose membranes for SERS detection of mixed pesticide residues in edible chrysanthemum.

Edible chrysanthemum is widely cultivated and used as an important ingredient of medicine, tea and multifunctional food. During the planting of chrysanthemum, pesticides are extensively used for preventing plant diseases and insect pests. To ensure the food safety of edible chrysanthemum, rapid detection methods are urgently needed for on-site inspection. In this study, a graphene oxide/Au nanoparticle (GO/Au NP) cellulose substrate was prepared through layer-by-layer assembly of GO and Au NPs on a mixed cellulose ester membrane. Surface-enhanced Raman spectroscopy (SERS) detection of four types of organophosphorus and organosulfur pesticides was achieved by filtering the extracting solution through the substrate and analysing SERS spectra. Qualitative and semi-quantitative detection of fenthion, phoxim, isocarbophos and thiram was accomplished with the detection limits of 38.01, 8.13, 48.97 and 8.74 ng mL-1, respectively. A spiking experiment further demonstrated the feasibility of this method for rapid and on-site detection of mixed pesticides in chrysanthemum. This study provides a new approach for rapid detection of multiple hazardous substances in flowering and herbal plants.

Improved reference genome of Aedes aegypti informs arbovirus vector control.

Female Aedes aegypti mosquitoes infect more than 400 million people each year with dangerous viral pathogens including dengue, yellow fever, Zika and chikungunya. Progress in understanding the biology of mosquitoes and developing the tools to fight them has been slowed by the lack of a high-quality genome assembly. Here we combine diverse technologies to produce the markedly improved, fully re-annotated AaegL5 genome assembly, and demonstrate how it accelerates mosquito science. We anchored physical and cytogenetic maps, doubled the number of known chemosensory ionotropic receptors that guide mosquitoes to human hosts and egg-laying sites, provided further insight into the size and composition of the sex-determining M locus, and revealed copy-number variation among glutathione S-transferase genes that are important for insecticide resistance. Using high-resolution quantitative trait locus and population genomic analyses, we mapped new candidates for dengue vector competence and insecticide resistance. AaegL5 will catalyse new biological insights and intervention strategies to fight this deadly disease vector.

Chemokine PF4 Inhibits EV71 and CA16 Infections at the Entry Stage.

Platelet factor 4 (PF4) or the CXC chemokine CXCL4 is the most abundant protein within the α-granules of platelets. Previous studies found that PF4 regulates infections of several viruses, including HIV-1, H1N1, hepatitis C virus (HCV), and dengue virus. Here, we show that PF4 is an inhibitor of enterovirus A71 (EV71) and coxsackievirus A16 (CA16) infections. The secreted form of PF4 from transfected cells or soluble purified PF4 from Escherichia coli, even lacking signal peptide affected secretion, obviously inhibited the propagation of EV71 and CA16. Mechanistically, we demonstrated that PF4 blocked the entry of the virus into the host cells by interactions with VP3 proteins of EV71/CA16 and the interaction with SCARB2 receptor-mediated EV71 and CA16 endocytosis. As expected, the incubation of anti-PF4 antibody with PF4 blocked PF4 inhibition on EV71 and CA16 infections further supported the above conclusion. Importantly, pretreatment of EV71 viruses with PF4 significantly protected the neonatal mice from EV71 lethal challenge and promoted the survival rate of infected mice. PF4 derived from natural platelets by EV71/CA16 activation also presented strong inhibition on EV71 and CA16. In summary, our study identified a new host factor against EV71 and CA16 infections, providing a novel strategy for EV71 and CA16 treatment. IMPORTANCE The virus's life cycle starts with binding to cell surface receptors, resulting in receptor-mediated endocytosis. Targeting the entry of the virus into target cells is an effective strategy to develop a novel drug. EV71 and CA16 are the major pathogens that cause hand, foot, and mouth disease (HFMD) outbreaks worldwide since 2008. However, the treatment of EV71 and CA16 infections is mainly symptomatic because there is no approved drug. Therefore, the underlying pathogenesis of EV71/CA16 and the interaction between host-EV71/CA16 need to be further investigated to develop an inhibitor. Here, we identified PF4 as a potent entry inhibitor of EV71 and CA16 via binding to VP3 proteins of EV71 and CA16 or binding to receptor SCARB2. In the EV71 infection model, PF4 protected mice from EV71 lethal challenge and promoted the survival rate of EV71-infected mice. Our study suggests that PF4 represents a potential candidate host factor for anti-EV71 and CA16 infections.

Host Restriction Factor A3G Inhibits the Replication of Enterovirus D68 by Competitively Binding the 5' Untranslated Region with PCBP1.

The host restriction factor APOBEC3G (A3G) inhibits an extensive variety of viruses, including retroviruses, DNA viruses, and RNA viruses. Our study shows that A3G inhibits enterovirus 71 (EV71) and coxsackievirus A16 (CA16) via competitively binding the 5' untranslated region (UTR) with the host protein poly(C)-binding protein 1 (PCBP1), which is required for the replication of multiple EVs. However, whether A3G inhibits other EVs in addition to EV71 and CA16 has not been investigated. Here, we demonstrate that A3G could inhibit the replication of EVD68, which requires PCBP1 for its replication, but not CA6, which does not require PCBP1 for replication. Further investigation revealed that the nucleic-acid-binding activity of A3G is required for EVD68 restriction, similar to the mechanism presented for EV71 restriction. Mechanistically, A3G competitively binds to the cloverleaf (1 to 123 nucleotides [nt]) and the stem-loop IV (234 to 446 nt) domains of the EVD68 5' UTR with PCBP1, thereby inhibiting the 5' UTR activity of EVD68; by contrast, A3G does not interact with CA6 5' UTR, resulting in no effect on CA6 replication. Moreover, the nonstructural protein 2C, encoded by EVD68, overcomes A3G suppression by inducing A3G degradation via the autophagy-lysosome pathway. Our findings revealed that A3G might have broad-spectrum antiviral activity against multiple EVs through this general mechanism, and they might provide important information for the development of an anti-EV strategy. IMPORTANCE As the two major pathogens causing hand, foot, and mouth disease (HFMD), enterovirus 71 (EV71) and coxsackievirus A16 (CA16) attract a lot of attention for the study of their pathogenesis, their involvement with cellular proteins, and so on. However, other EVs such as CA6 and EVD68 constantly occur sporadically or have spread worldwide in recent years. Therefore, more information related to these EVs is needed in order to develop a broad-spectrum anti-EV inhibitor. In this study, we first reveal that the protein poly(C)-binding protein 1 (PCBP1), involved in PV- and EV71 virus replication, is also required for the replication of EVD68, but not for the replication of CA6. Next, we found that the host-restriction factor A3G specifically inhibits the replication of EVD68, but not the replication of CA6, by competitively binding to the 5' UTR of EVD68 along with PCBP1. Our findings broaden knowledge related to EV replication and the interplay between EVs and host factors.

SAMHD1 Inhibits Multiple Enteroviruses by Interfering with the Interaction between VP1 and VP2 Proteins.

Sterile alpha motif and histidine-aspartic acid domain-containing protein 1 (SAMHD1) possesses multiple biological activities such as virus restriction, innate immunity regulation, and autoimmunity. Our previous study demonstrated that SAMHD1 potently inhibits the replication of enterovirus 71 (EV71). In this study, we observed that SAMHD1 also restricts multiple enteroviruses (EVs), including coxsackievirus A16 (CA16) and enterovirus D68 (EVD68), but not coxsackievirus A6 (CA6). Mechanistically, SAMHD1 competitively interacted with the same domain in VP1 that binds to VP2 of EV71 and EVD68, thereby interfering with the interaction between VP1 and VP2 , and therefore viral assembly. Moreover, we showed that the SAMHD1 T592A mutant maintained the EV71 inhibitory effect by attenuating the interaction between VP1 and VP2, whereas the T592D mutant failed to. We also demonstrated that SAMHD1 could not inhibit CA6 because a different binding site is required for the SAMHD1 and VP1 interaction. Our findings reveal the mechanism of SAMHD1 inhibition of multiple EVs, and this could potentially be important for developing drugs against a broad range of EVs. IMPORTANCE Enterovirus causes a wide variety of diseases, such as hand, foot, and mouth disease (HFMD), which is a severe public problem threatening children under 5 years. Therefore, identifying essential genes which restrict EV infection and exploring the underlying mechanisms are necessary to develop an effective strategy to inhibit EV infection. In this study, we report that host restrictive factor SAMHD1 has broad-spectrum antiviral activity against EV71, CA16, and EVD68 independent of its well-known deoxynucleoside triphosphate triphosphohydrolase (dNTPase) or RNase activity. Mechanistically, SAMHD1 restricts EVs by competitively interacting with the same domain in VP1 that binds to VP2 of EVs, thereby interfering with the interaction between VP1 and VP2, and therefore viral assembly. In contrast, we also demonstrated that SAMHD1 could not inhibit CA6 because a different binding site is required for the SAMHD1 and CA6 VP1 interaction. Our study reveals a novel mechanism for the SAMHD1 anti-EV replication activity.

Recent advances in simultaneous detection strategies for multi-mycotoxins in foods.

Mycotoxin contamination has become a challenge in the field of food safety testing, given the increasing emphasis on food safety in recent years. Mycotoxins are widely distributed, in heavily polluted areas. Food contamination with these toxins is difficult to prevent and control. Mycotoxins, as are small-molecule toxic metabolites produced by several species belonging to the genera Aspergillus, Fusarium, and Penicillium growing in food. They are considered teratogenic, carcinogenic, and mutagenic to humans and animals. Food systems are often simultaneously contaminated with multiple mycotoxins. Due to the additive or synergistic toxicological effects caused by the co-existence of multiple mycotoxins, their individual detection requires reliable, accurate, and high-throughput techniques. Currently available, methods for the detection of multiple mycotoxins are mainly based on chromatography, spectroscopy (colorimetry, fluorescence, and surface-enhanced Raman scattering), and electrochemistry. This review provides a comprehensive overview of advances in the multiple detection methods of mycotoxins during the recent 5 years. The principles and features of these techniques are described. The practical applications and challenges associated with assays for multiple detection methods of mycotoxins are summarized. The potential for future development and application is discussed in an effort, to provide standards of references for further research.

TRIM21-mediated proteasomal degradation of SAMHD1 regulates its antiviral activity.

SAMHD1 possesses multiple functions, but whether cellular factors regulate SAMHD1 expression or its function remains not well characterized. Here, by investigating why cultured RD and HEK293T cells show different sensitivity to enterovirus 71 (EV71) infection, we demonstrate that SAMHD1 is a restriction factor for EV71. Importantly, we identify TRIM21, an E3 ubiquitin ligase, as a key regulator of SAMHD1, which specifically interacts and degrades SAMHD1 through the proteasomal pathway. However, TRIM21 has no effect on EV71 replication itself. Moreover, we prove that interferon production stimulated by EV71 infection induces increased TRIM21 and SAMHD1 expression, whereas increasing TRIM21 overrides SAMHD1 inhibition of EV71 in cells and in a neonatal mouse model. TRIM21-mediated degradation of SAMHD1 also affects SAMHD1-dependent restriction of HIV-1 and the regulation of interferon production. We further identify the functional domains in TRIM21 required for SAMHD1 binding and the ubiquitination site K622 in SAMHD1 and show that phosphorylation of SAMHD1 at T592 also blocks EV71 restriction. Our findings illuminate how EV71 overcomes SAMHD1 inhibition via the upregulation of TRIM21.

GBP5 Is an Interferon-Induced Inhibitor of Respiratory Syncytial Virus.

Guanylate binding protein 5 (GBP5) belongs to the GTPase subfamily, which is mainly induced by interferon gamma (IFN-γ) and is involved in many important cellular processes, including inflammasome activation and innate immunity against a wide variety of microbial pathogens. However, it is unknown whether GBP5 inhibits respiratory syncytial virus (RSV) infection. In this study, we identified GBP5 as an effector of the anti-RSV activity of IFN-γ and found that in children, the weaker immune response, especially the weaker IFN-γ response and the decreased GBP5 expression, leads to RSV susceptibility. Furthermore, we revealed that GBP5 reduced the cell-associated levels of the RSV small hydrophobic (SH) protein, which was identified as a viroporin. In contrast, overexpression of the SH protein rescued RSV replication in the presence of GBP5. The GBP5-induced decrease in intracellular SH protein levels is because GBP5 promotes the release of the SH protein into the cell culture. Moreover, the GBP5 C583A mutants with changes at the C terminus or the GBP5 ΔC mutant lacking the C-terminal region, which impairs GBP5 localization in the Golgi, could not inhibit RSV infection, whereas the GTPase-defective GBP5 maintained RSV inhibition, suggesting that Golgi localization but not the GTPase activity of GBP5 is required for RSV inhibition. Interestingly, we found that RSV infection or RSV G protein downregulates GBP5 expression by upregulating DZIP3, an E3 ligase, which induces GBP5 degradation through the K48 ubiquitination and proteasomal pathways. Thus, this study reveals a complicated interplay between host restrictive factor GBP5 and RSV infection and provides important information for understanding the pathogenesis of RSV.IMPORTANCE RSV is a highly contagious virus that causes multiple infections in infants within their first year of life. It can also easily cause infection in elderly or immunocompromised individuals, suggesting that individual differences in immunity play an important role in RSV infection. Therefore, exploring the pathogenic mechanisms of RSV and identifying essential genes which inhibit RSV infection are necessary to develop an effective strategy to control RSV infection. Here, we report that the IFN-inducible gene GBP5 potently inhibits RSV replication by reducing the cell-associated levels of the RSV small hydrophobic (SH) protein, which is a viroporin. In contrast, the RSV G protein was shown to upregulate the expression of the DZIP3 protein, an E3 ligase that degrades GBP5 through the proteasomal pathway. Our study provides important information for the understanding of the pathogenic mechanisms of RSV and host immunity as well as the complicated interplay between the virus and host.

Dosimetric feasibility of stereotactic ablative radiotherapy in pulmonary vein isolation for atrial fibrillation using intensity-modulated proton therapy.

PURPOSE: To evaluate dosimetric properties of intensity-modulated proton therapy (IMPT) for simulated treatment planning in patients with atrial fibrillation (AF) targeting left atrial-pulmonary vein junction (LA-PVJ), in comparison with volumetric-modulated arc therapy (VMAT) and helical tomotherapy (TOMO). METHODS: Ten thoracic 4D-CT scans with respiratory motion and one with cardiac motion were used for the study. Ten respiratory 4D-CTs were planned with VMAT, TOMO, and IMPT for simulated AF. Targets at the LA-PVJ were defined as wide-area circumferential ablation line. A single fraction of 25 Gy was prescribed to all plans. The interplay effects from cardiac motion were evaluated based on the cardiac 4D-CT scan. Dose-volume histograms (DVHs) of the ITV and normal tissues were compared. Statistical analysis was evaluated via one-way Repeated-Measures ANOVA and Friedman's test with Bonferroni's multiple comparisons test. RESULTS: The median volume of ITV was 8.72cc. All plans had adequate target coverage (V23.75Gy  ≥ 99%). Compared with VMAT and TOMO, IMPT resulted in significantly lower dose of most normal tissues. For VMAT, TOMO, and IMPT plans, Dmean of the whole heart was 5.52 ± 0.90 Gy, 5.89 ± 0.78 Gy, and 3.01 ± 0.57 Gy (P < 0.001), mean dose of pericardium was 4.74 ± 0.76 Gy, 4.98 ± 0.62 Gy, and 2.59 ± 0.44 Gy (P < 0.001), and D0.03cc of left circumflex artery (LCX) was 13.96 ± 5.45 Gy, 14.34 ± 5.91 Gy, and 8.43 ± 7.24 Gy (P < 0.001), respectively. However, no significant advantage for one technique over the others was observed when examining the D0.03cc of esophagus and main bronchi. CONCLUSIONS: IMPT targeting LA-PVJ for patients with AF has high potential to reduce dose to surrounding tissues compared to VMAT or TOMO. Motion mitigation techniques are critical for a particle-therapy approach.

MicroRNA duplication accelerates the recruitment of new targets during vertebrate evolution.

The repertoire of miRNAs has considerably expanded during metazoan evolution, and duplication is an important mechanism for generating new functional miRNAs. However, relatively little is known about the functional divergence between paralogous miRNAs and the possible coevolution between duplicated miRNAs and the genomic contexts. By systematically examining small RNA expression profiles across various human tissues and interrogating the publicly available miRNA:mRNA pairing chimeras, we found that changes in expression patterns and targeting preferences are widespread for duplicated miRNAs in vertebrates. Both the empirical interactions and target predictions suggest that evolutionarily conserved homo-seed duplicated miRNAs pair with significantly higher numbers of target sites compared to the single-copy miRNAs. Our birth-and-death evolutionary analysis revealed that the new target sites of miRNAs experienced frequent gains and losses during function development. Our results suggest that a newly emerged target site has a higher probability to be functional and maintained by natural selection if it is paired to a seed shared by multiple paralogous miRNAs rather than being paired to a single-copy miRNA. We experimentally verified the divergence in target repression between two paralogous miRNAs by transfecting let-7a and let-7b mimics into kidney-derived cell lines of four mammalian species and measuring the resulting transcriptome alterations by extensive high-throughput sequencing. Our results also suggest that the gains and losses of let-7 target sites might be associated with the evolution of repressiveness of let-7 across mammalian species.

Correction to: Evolution of olfactory circuits in insects.

Authors would like to correct the typo found in the fourth sentence of the introduction from "organisional" to "organismal". The original article has been corrected.

Evolution of olfactory circuits in insects.

Recent years have seen an explosion of interest in the evolution of neural circuits. Comparison of animals from different families, orders, and phyla reveals fascinating variation in brain morphology, circuit structure, and neural cell types. However, it can be difficult to connect the complex changes that occur across long evolutionary distances to behavior. Luckily, these changes accumulate through processes that should also be observable in recent time, making more tractable comparisons of closely related species relevant and complementary. Here, we review several decades of research on the evolution of insect olfactory circuits across short evolutionary time scales. We describe two well-studied systems, Drosophila sechellia flies and Heliothis moths, in detailed case studies. We then move through key types of circuit evolution, cataloging examples from other insects and looking for general patterns. The literature is dominated by changes in sensory neuron number and tuning at the periphery-often enhancing neural response to odorants with new ecological or social relevance. However, changes in the way olfactory information is processed by central circuits is clearly important in a few cases, and we suspect the development of genetic tools in non-model species will reveal a broad role for central circuit evolution. Moving forward, such tools should also be used to rigorously test causal links between brain evolution and behavior.

[Discrimination of Plum Browning with Near Infrared Spectroscopy].

Flesh browning mostly happens in plum fruit during the post-harvest storage period, which is an important factor affecting the storage quality of plum fruits. Traditional methods used to discriminate plum browning involve the destruction of the intact fruit, which are highly subjective and error-prone. Therefore, the near-infrared (NIR) spectroscopy technique was applied to achieve rapid and non-destructive identification of plum browning and non-browning in this paper. The near infrared diffuse reflectance spectroscopy of 124 plum samples were collected in the band number of 4 000~12 500 cm-1. These samples were classified into two groups, browning (n=70) and non-browning (n=54). In order to find a new way to effectively discriminate plum fruits with flesh browning, three qualitative identification methods: the qualitative test, Mahalanobis distances discriminate analysis (DA) and Back Propagation-artificial neural networks (BP-ANN) were used to compare their capacity of recognizing browning plums and non-browning oneswhile the last two approaches were based on the principal component analysis (PCA) method. These results showed that DA and BP-ANN could be used to conctruct effective classification models for identifying plum browning, and the first ten principal components extracted from original spectra were applied as input variables to build DA and BP-ANN models. The optimal method was obtained with BP-ANN, which gained an accuracy of 100% for calibration set and 97.56% for prediction set, and the identification accuracy rate reached 100% and 98.57% for non-browning samples and browning ones, respectively. It could be concluded that NIR spectroscopy technique combined with chemometrics methods has great potential to recognize plums of browning and non-browning rapidly, non-destructively and effectively.

Contribution of the hydration force to vesicle adhesion on titanium oxide.

Titanium oxide is a biocompatible material that supports vesicle adhesion. Depending on experimental parameters, adsorbed vesicles remain intact or rupture spontaneously. Vesicle rupture has been attributed to electrostatic attraction between vesicles and titanium oxide, although the relative contribution of various interfacial forces remains to be clarified. Herein, we investigated the influence of vesicle surface charge on vesicle adsorption onto titanium oxide and observed that electrostatic attraction is insufficient for vesicle rupture. Following this line of evidence, a continuum model based on the DLVO forces and a non-DLVO hydration force was applied to investigate the role of different interfacial forces in modulating the lipid-substrate interaction. Within an experimentally significant range of conditions, the model shows that the magnitude of the repulsive hydration force strongly influences the behavior of adsorbed vesicles, thereby supporting that the hydration force makes a strong contribution to the fate of adsorbed vesicles on titanium oxide. The findings are consistent with literature reports concerning phospholipid assemblies on solid supports and nanoparticles and underscore the importance of the hydration force in influencing the behavior of phospholipid films on hydrophilic surfaces.

Vesicle adhesion and rupture on silicon oxide: influence of freeze-thaw pretreatment.

We have investigated the effect of freeze-thaw (FT) pretreatment on the adhesion and rupture of extruded vesicles over a wide range of vesicle sizes. To characterize the size distributions of vesicles obtained with and without FT pretreatment, dynamic light scattering (DLS) experiments were performed. The interaction between extruded vesicles and a silicon oxide substrate was investigated by quartz crystal microbalance with dissipation (QCM-D) monitoring, with a focus on comparative analysis of similar-sized vesicles with and without FT pretreatment. Under this condition, there was a smaller mass load at the critical coverage associated with untreated vesicles, as compared to vesicles which had been subjected to FT pretreatment. In addition, the rupture of treated vesicles generally resulted in formation of a complete planar bilayer, while the adlayer was more heterogeneous when employing untreated vesicles. Combined with kinetic analysis and extended-DLVO model calculations, the experimental evidence suggests that the differences arising from FT pretreatment are due to characteristics of the vesicle size distribution and also multilamellarity of an appreciable fraction of untreated vesicles. Taken together, our findings clarify the influence of FT pretreatment on model membrane fabrication on solid supports.

[Discrimination of donkey meat by NIR and chemometrics].

Donkey meat samples (n = 167) from different parts of donkey body (neck, costalia, rump, and tendon), beef (n = 47), pork (n = 51) and mutton (n = 32) samples were used to establish near-infrared reflectance spectroscopy (NIR) classification models in the spectra range of 4,000~12,500 cm(-1). The accuracies of classification models constructed by Mahalanobis distances analysis, soft independent modeling of class analogy (SIMCA) and least squares-support vector machine (LS-SVM), respectively combined with pretreatment of Savitzky-Golay smooth (5, 15 and 25 points) and derivative (first and second), multiplicative scatter correction and standard normal variate, were compared. The optimal models for intact samples were obtained by Mahalanobis distances analysis with the first 11 principal components (PCs) from original spectra as inputs and by LS-SVM with the first 6 PCs as inputs, and correctly classified 100% of calibration set and 98. 96% of prediction set. For minced samples of 7 mm diameter the optimal result was attained by LS-SVM with the first 5 PCs from original spectra as inputs, which gained an accuracy of 100% for calibration and 97.53% for prediction. For minced diameter of 5 mm SIMCA model with the first 8 PCs from original spectra as inputs correctly classified 100% of calibration and prediction. And for minced diameter of 3 mm Mahalanobis distances analysis and SIMCA models both achieved 100% accuracy for calibration and prediction respectively with the first 7 and 9 PCs from original spectra as inputs. And in these models, donkey meat samples were all correctly classified with 100% either in calibration or prediction. The results show that it is feasible that NIR with chemometrics methods is used to discriminate donkey meat from the else meat.

Altruistic seagull optimization algorithm enables selection of radiomic features for predicting benign and malignant pulmonary nodules.

Accurately differentiating indeterminate pulmonary nodules remains a significant challenge in clinical practice. This challenge becomes increasingly formidable when dealing with the vast radiomic features obtained from low-dose computed tomography, a lung cancer screening technique being rolling out in many areas of the world. Consequently, this study proposed the Altruistic Seagull Optimization Algorithm (AltSOA) for the selection of radiomic features in predicting the malignancy risk of pulmonary nodules. This innovative approach incorporated altruism into the traditional seagull optimization algorithm to seek a global optimal solution. A multi-objective fitness function was designed for training the pulmonary nodule prediction model, aiming to use fewer radiomic features while ensuring prediction performance. Among global radiomic features, the AltSOA identified 11 interested features, including the gray level co-occurrence matrix. This automatically selected panel of radiomic features enabled precise prediction (area under the curve = 0.8383 (95 % confidence interval 0.7862-0.8863)) of the malignancy risk of pulmonary nodules, surpassing the proficiency of radiologists. Furthermore, the interpretability, clinical utility, and generalizability of the pulmonary nodule prediction model were thoroughly discussed. All results consistently underscore the superiority of the AltSOA in predicting the malignancy risk of pulmonary nodules. And the proposed malignant risk prediction model for pulmonary nodules holds promise for enhancing existing lung cancer screening methods. The supporting source codes of this work can be found at: https://github.com/zzl2022/PBMPN.