The Distribution of Crystalline Lens Rise in High Myopia Population and Its Influence on Vault After Implanting Intraocular Collamer Lens.

INTRODUCTION: As a result of the insufficient ocular anatomical parameters used to customize implantable collamer lens (ICL), many patients still cannot achieve a suitable vault after ICL implantation surgery. This study analyzed the characteristics of a new anatomical parameter crystalline lens rise (CLR) in a population with high myopia and explored the influence of CLR on the vault after ICL implantation. METHODS: Patients (298 eyes) with high myopia who underwent ICL implantation were enrolled to study CLR characteristics. Postoperatively, patients (159 eyes) were divided into five groups according to the value of CLR (A, CLR ≤ - 150; B, - 150 < CLR ≤ 0; C, 0 < CLR < 150; D, 150 ≤ CLR < 300; E, CLR ≥ 300 µm), and to investigate the correlation between CLR and vault. RESULTS: In the 298 eyes, the CLR had a normal distribution (P = 0.35) and the mean CLR was 67.93 ± 150.66 µm. Ninety-nine eyes (33.22%) had a CLR ≤ 0 µm, of which 20 eyes (6.71%) had a CLR ≤ - 150 µm; 199 eyes (66.78%) had a CLR > 0 µm, of which 20 eyes (6.71%) had a CLR ≥ 300 µm. In 159 eyes, the CLR was negatively correlated with the vault at 1 day (R = - 0.497, P < 0.001), 3 months (R = - 0.505, P < 0.001), and 6 months (R = - 0.505, P < 0.001) postoperatively. At 6 months, the vault of group A was statistically significantly different compared to groups B-E (all P < 0.05), and that of group E was statistically significantly different compared to groups A-D (all P < 0.001). The remaining groups did not show statistically significant differences (all P > 0.05). CONCLUSION: The CLR had a normal distribution in the high myopia population, and 13.42% of the CLR values were extreme (CLR ≤ - 150 µm or CLR ≥ 300 µm). A larger ICL diameter than that recommended by the manufacturer should be considered when the CLR is ≥ 300 µm and a smaller ICL diameter should be considered when the CLR is ≤ - 150 µm.

Classification models for Tobacco Mosaic Virus and Potato Virus Y using hyperspectral and machine learning techniques.

Tobacco Mosaic Virus (TMV) and Potato Virus Y (PVY) pose significant threats to crop production. Non-destructive and accurate surveillance is crucial to effective disease control. In this study, we propose the adoption of hyperspectral and machine learning technologies to discern the type and severity of tobacco leaves affected by PVY and TMV infection. Initially, we applied three preprocessing methods - Multivariate Scattering Correction (MSC), Standard Normal Variate (SNV), and Savitzky-Golay smoothing filter (SavGol) - to corrected the leaf full-length spectral sheet data (350-2500nm). Subsequently, we employed two classifiers, support vector machine (SVM) and random forest (RF), to establish supervised classification models, including binary classification models (healthy/diseased leaves or PVY/TMV infected leaves) and six-class classification models (healthy and various severity levels of diseased leaves). Based on the core evaluation index, our models achieved accuracies in the range of 91-100% in the binary classification. In general, SVM demonstrated superior performance compared to RF in distinguishing leaves infected with PVY and TMV. Different combinations of preprocessing methods and classifiers have distinct capabilities in the six-class classification. Notably, SavGol united with SVM gave an excellent performance in the identification of different PVY severity levels with 98.1% average precision, and also achieved a high recognition rate (96.2%) in the different TMV severity level classifications. The results further highlighted that the effective wavelengths captured by SVM, 700nm and 1800nm, would be valuable for estimating disease severity levels. Our study underscores the efficacy of integrating hyperspectral technology and machine learning, showcasing their potential for accurate and non-destructive monitoring of plant viral diseases.

A glutamate-gated chloride channel as the mite-specific target-site of dicofol and other diphenylcarbinol acaricides.

Dicofol has been widely used to control phytophagous mites. Although dicofol is chemically related to DDT, its mode of action has remained elusive. Here, we mapped dicofol resistance in the spider mite Tetranychus urticae to two genomic regions. Each region harbored a glutamate-gated chloride channel (GluCl) gene that contained a mutation-G314D or G326E-known to confer resistance against the unrelated acaricide abamectin. Using electrophysiology assays we showed that dicofol and other diphenylcarbinol acaricides-bromopropylate and chlorobenzilate-induce persistent currents in Xenopus oocytes expressing wild-type T. urticae GluCl3 receptors and potentiate glutamate responses. In contrast, the G326E substitution abolished the agonistic activity of all three compounds. Assays with the wild-type Drosophila GluClα revealed that this receptor was unresponsive to dicofol. Homology modeling combined with ligand-docking confirmed the specificity of electrophysiology assays. Altogether, this work elucidates the mode of action of diphenylcarbinols as mite-specific agonists of GluCl.

Intraspecific diversity in the mechanisms underlying abamectin resistance in a cosmopolitan pest.

Pesticide resistance relies on a myriad of mechanisms, ranging from single mutations to a complex and polygenic architecture, and it involves mechanisms such as target-site insensitivity, metabolic detoxification, or a combination of these, with either additive or synergistic effects. Several resistance mechanisms against abamectin, a macrocyclic lactone widely used in crop protection, have been reported in the cosmopolitan pest Tetranychus urticae. However, it has been shown that a single mechanism cannot account for the high levels of abamectin resistance found across different mite populations. Here, we used experimental evolution combined with bulked segregant analyses to map quantitative trait loci (QTL) associated with abamectin resistance in two genetically unrelated populations of T. urticae. In these two independent QTL mapping experiments, three and four QTLs were identified, of which three were shared between experiments. Shared QTLs contained genes encoding subunits of the glutamate-gated chloride channel (GluCl) and harboured previously reported mutations, including G314D in GluCl1 and G326E in GluCl3, but also novel resistance candidate loci, including DNA helicases and chemosensory receptors. Surprisingly, the fourth QTL, present only in only one of the experiments and thus unique for one resistant parental line, revealed a non-functional variant of GluCl2, suggesting gene knock-out as resistance mechanism. Our study uncovers the complex basis of abamectin resistance, and it highlights the intraspecific diversity of genetic mechanisms underlying resistance in a cosmopolitan pest.

Incomplete reproductive barriers and genomic differentiation impact the spread of resistance mutations between green- and red-colour morphs of a cosmopolitan mite pest.

Pesticide resistance represents a clear and trackable case of adaptive evolution with a strong societal impact. Understanding the factors associated with the evolution and spread of resistance is imperative to develop sustainable crop management strategies. The two-spotted spider mite Tetranychus urticae, a major crop pest with worldwide distribution and a polyphagous lifestyle, has evolved resistance to most classes of pesticides. Tetranychus urticae exists as either a green- or a red-coloured morph. However, the extent of genetic divergence and reproductive compatibility vary across populations of these colour morphs, complicating their taxonomic resolution at the species level. Here, we studied patterns of genetic differentiation and barriers to gene flow within and between morphs of T. urticae in order to understand the factors that influence the spread of resistance mutations across its populations. We derived multiple iso-female lines from Tetranychus populations collected from agricultural crops. We generated genomic and morphological data, characterized their bacterial communities and performed controlled crosses. Despite morphological similarities, we found large genomic differentiation between the morphs. This pattern was reflected in the incomplete, but strong postzygotic incompatibility in crosses between colour morphs, while crosses within morphs from different geographical locations were largely compatible. In addition, our results suggest recent/on-going gene flow between green-coloured T. urticae and T. turkestani. By screening the sequences of 10 resistance genes, we found evidence for multiple independent origins and for single evolutionary origins of target-site resistance mutations. Our results indicate that target-site mutations mostly evolve independently in populations on different geographical locations, and that these mutations can spread due to incomplete barriers to gene flow within and between populations.

WTAP promotes macrophage recruitment and increases VEGF secretion via N6-methyladenosine modification in corneal neovascularization.

BACKGROUND: Corneal neovascularization (CNV) can be caused by chemical burns. Macrophages are involved in angiogenesis and lymphangiogenesis during CNV. The aim of this study was to investigate whether Wilms' tumor 1-associated protein (WTAP) is involved in macrophage recruitment and VEGF secretion via N6-methyladenosine (m6A) modification. METHODS: A CNV mouse model was established by corneal alkali burn. Tumor necrosis factor alpha (TNF-α) was used to stimulate vascular endothelial cells. m6A immunoprecipitation qPCR was used to determine the enrichment of m6A levels in mRNAs. The H3K9me3 enrichment in the promoter region of CC motif chemokine ligand 2 (CCL2) was detected by chromatin immunoprecipitation assay. The WTAP inhibition in vivo was performed using the adeno-associated virus. RESULTS: In the alkali burn corneal tissues, angiogenesis and lymphangiogenesis were promoted as CD31 and LYVE-1 expressions were elevated, and the number of macrophages as well as WTAP expression were increased. Under the TNF-α stimulation, WTAP promoted the recruitment of endothelial cells to macrophages by promoting CCL2 secretion. Mechanistically, WTAP affected the enrichment of H3K9me3 at the CCL2 promoter by regulating the m6A level of SUV39H1 mRNA. The in vivo experiment showed that VEGFA/C/D secretion of macrophages was reduced after WTAP interference. Mechanistically, WTAP regulated the translational efficiency of HIF-1α via m6A modification. CONCLUSION: WTAP affected macrophage recruitment to endothelial cells via regulation of H3K9me3-mediated CCL2 transcription. WTAP also affected macrophage secretion of VEGFA/C/D via m6A-mediated translation regulation of HIF-1α. Both pathways were involved in the WTAP regulation of angiogenesis and lymphangiogenesis during CNV.

Abnormal obturator artery with ipsilateral inferior epigastric artery passed behind the femoral vein / Arteria obturatriz anómala con arteria epigástrica inferior ipsilateral que cruza posterior a la vena femoral

SUMMARY: Clear awareness of the vascular variations is critical in surgeries, which may cause massive hemorrhage during surgical procedures. During educational dissection of a male cadaver, we encountered a combined variation of the left obturator artery and ipsilateral aberrant inferior epigastric artery. The left obturator artery originated from the external iliac artery, then coursed inward, adherent to the superior pubic ramus. The left inferior epigastric artery originated from the femoral artery, and coursed behind the femoral vein. These anatomical variations shown in one person were extremely rare. This is particularly true with regard to these variations while performing pelvic and inguinal region surgeries.

El conocimiento claro de las variaciones vasculares es fundamental en las cirugías, ya que pueden causar una hemorragia masiva durante los procedimientos quirúrgicos. Durante la disección educativa de un cadáver de sexo masculino, encontramos una variación combinada de la arteria obturatriz izquierda y la arteria epigástrica inferior ipsilateral aberrante. La arteria obturatriz izquierda se originaba en la arteria ilíaca externa, luego discurrió hacia medial, adhiriéndose a la rama púbica superior. La arteria epigástrica inferior izquierda se originaba en la arteria femoral y discurría por detrás de la vena femoral. Estas variaciones anatómicas mostradas en una sola persona son extremadamente raras. Esto es importante de conocer estas variaciones cuando se realizan cirugías de las regiones pélvica e inguinal.

Intradiol ring cleavage dioxygenases from herbivorous spider mites as a new detoxification enzyme family in animals.

BACKGROUND: Generalist herbivores such as the two-spotted spider mite Tetranychus urticae thrive on a wide variety of plants and can rapidly adapt to novel hosts. What traits enable polyphagous herbivores to cope with the diversity of secondary metabolites in their variable plant diet is unclear. Genome sequencing of T. urticae revealed the presence of 17 genes that code for secreted proteins with strong homology to "intradiol ring cleavage dioxygenases (DOGs)" from bacteria and fungi, and phylogenetic analyses show that they have been acquired by horizontal gene transfer from fungi. In bacteria and fungi, DOGs have been well characterized and cleave aromatic rings in catecholic compounds between adjacent hydroxyl groups. Such compounds are found in high amounts in solanaceous plants like tomato, where they protect against herbivory. To better understand the role of this gene family in spider mites, we used a multi-disciplinary approach to functionally characterize the various T. urticae DOG genes. RESULTS: We confirmed that DOG genes were present in the T. urticae genome and performed a phylogenetic reconstruction using transcriptomic and genomic data to advance our understanding of the evolutionary history of spider mite DOG genes. We found that DOG expression differed between mites from different plant hosts and was induced in response to jasmonic acid defense signaling. In consonance with a presumed role in detoxification, expression was localized in the mite's gut region. Silencing selected DOGs expression by dsRNA injection reduced the mites' survival rate on tomato, further supporting a role in mitigating the plant defense response. Recombinant purified DOGs displayed a broad substrate promiscuity, cleaving a surprisingly wide array of aromatic plant metabolites, greatly exceeding the metabolic capacity of previously characterized microbial DOGs. CONCLUSION: Our findings suggest that the laterally acquired spider mite DOGs function as detoxification enzymes in the gut, disarming plant metabolites before they reach toxic levels. We provide experimental evidence to support the hypothesis that this proliferated gene family in T. urticae is causally linked to its ability to feed on an extremely wide range of host plants.

The H92R substitution in PSST is a reliable diagnostic biomarker for predicting resistance to mitochondrial electron transport inhibitors of complex I in European populations of Tetranychus urticae.

BACKGROUND: Mitochondrial Electron Transport Inhibitors of complex I (METI-I), such as tebufenpyrad and fenpyroximate, are acaricides that have been used extensively to control Tetranychus urticae Koch (Acari: Tetranychidae) for more than 20 years. Because of the ability of this spider mite to rapidly develop acaricide resistance, field (cross-) resistance monitoring and elucidation of resistance mechanisms are extremely important for resistance management (RM). In the present study, 42 European T. urticae field populations were screened for tebufenpyrad and fenpyroximate resistance, and the correlation between resistance and the H92R substitution in PSST was investigated. RESULTS: According to the calculated lethal concentration values that kill 90% of the population (LC90 ), tebufenpyrad and fenpyroximate would fail to control many of the collected populations at recommended field rates. Six populations exhibited high to very high resistance levels (200- to over 1950-fold) to both METI-Is. Analysis based on the LC50 values displayed a clear correlation between tebufenpyrad and fenpyroximate resistance, further supporting cross-resistance, which is of great operational importance in acaricide RM. The previously uncovered METI-I target-site mutation H92R in the PSST homologue of complex I (NADH:ubiquinone oxidoreductase) was found with high allele frequencies in populations resistant to tebufenpyrad and fenpyroximate. Synergist assays showed this mutation is not the only factor involved in METI-I resistance and additive or synergistic effects of multiple mechanisms most likely determine the phenotypic strength. CONCLUSIONS: The predictive value of resistance by H92R is very high in European populations and offers great potential to be used as a molecular diagnostic marker for METI-I resistance. © 2022 Society of Chemical Industry.

Survival Prediction of Patients Treated With Immune Checkpoint Inhibitors via KRAS/TP53/EGFR-Single Gene Mutation.

Background: Immune checkpoint inhibitors (ICIs) have become an effective treatment option for cancer. KRAS, EGFR and TP53 are common mutated oncogenes in cancer whose single gene status may predict the therapeutic effect of clinical ICIs. In this efficacy evaluation, we aimed to clarify whether the single gene mutation status of KRAS, EGFR or TP53 affects the survival benefits of ICIs in cancer patients. Methods: We used PubMed, Cochrane Library, web of science, and clinical trials Gov database to retrieve qualified documents, the time was up to January 2022. Hazard ratios (HRS) and 95% confidence intervals (CIs) were used to determine the single gene mutation status and no progression of KRAS, EGFR or TP53. Results: A total of 19 studies included 7029 cancer patients treated with ICIs. The results showed that KRAS, EGFR or TP53 single gene mutation could significantly improve PFS and OS in patients receiving ICIs, but the degree of improvement was different. The risk of prolongation of PFS (HR = 1.48, 95% CI = 1.19-1.85, p = 0.0004) and OS (HR = 1.68, 95% CI = 1.36-2.07, p < 0.00001) caused by TP53 single gene mutation was relatively high, the risk ratio of prolongation of PFS (HR = 1.38, 95% CI = 1.21-1.57, p < 0.00001) and OS (HR = 1.56, 95% CI = 1.20-2.04, p = 0.001) caused by EGFR single gene mutation was the second, the risk ratio of prolongation of PFS (HR = 1.33, 95% CI = 1.12-1.57, p = 0.001) and OS (HR = 1.39, 95% CI = 1.18-1.63, p < 0.00001) caused by KRAS single gene mutation was relatively low, and the results were significantly different. Conclusion: In cancer patients, KRAS, EGFR or TP53 single gene status is correlated with the benefits of immunotherapy PFS and OS, which suggests that gene sequencing should be carried out in time in the process of clinical treatment to determine the gene mutation of patients and better predict the clinical treatment effect of ICIs.

The G126S substitution in mitochondrially encoded cytochrome b does not confer bifenazate resistance in the spider mite Tetranychus urticae.

Several genetic variants of the cd1- and ef-helices of the Qo site of mitochondrial cytochrome b have been associated with bifenazate resistance in the spider mite Tetranychus urticae, an important crop pest around the world. Maternal inheritance of bifenazate resistance has provided strong evidence for the involvement of many of these mutations alone or in combination. A number of populations highly resistant to bifenazate were uncovered that carried the G126S substitution in combination with other target-site mutations. This G126S mutation has therefore been investigated in several studies in the context of resistance evolution and the development of diagnostic markers. However, experimental data that link bifenazate resistance with the presence of the G126S mutation without additional cd1- and ef-helices mutations, remain very limited. Here, we genotyped 38 T. urticae field populations for cytochrome b and uncovered nine field populations with a fixed or segregating G126S substitution without other target-site mutations in the conserved cd1- and ef-helices of the cytochrome b Qo pocket. Toxicity bioassays showed that all nine field populations were very susceptible to bifenazate, providing strong evidence that G126S alone does not confer bifenazate resistance. These findings also implicate that previous T. urticae populations with G126S found to be low to moderately resistant to bifenazate, evolved alternative mechanisms of resistance, and more importantly, that this mutation cannot be used as a molecular diagnostic for bifenazate resistance.

Role of histone deacetylase Sirt3 in the development and regression of atherosclerosis.

Atherosclerosis (AS) is the most common cause of death in cardiovascular diseases and poses severe challenges to human life and safety. Epigenetics plays a vital role in every single link of AS. Whereas, how epigenetics regulates its development and regression is still unknown. Sirt3, a recognized histone deacetylase, having been reported to be involved in other acylation processes in recent years, is broadening its role in epigenetic modifications. Sirt3 is an important factor in the normal physiology of blood vessels through deacetylation of mitochondrial proteins and participates in various metabolic activities. Besides, medical research targeting Sirt3 is in full swing as well. This review combining histone deacetylase Sirt3 with AS, aims to clarify the latest progress in the significant role of Sirt3 in the development and regression of AS and to provide a novel prospect for a new regulatory factor and potential intervention target for AS.

Untangling a Gordian knot: the role of a GluCl3 I321T mutation in abamectin resistance in Tetranychus urticae.

BACKGROUND: The cys-loop ligand-gated ion channels, including the glutamate-gated chloride channel (GluCl) and GABA-gated chloride channel (Rdl) are important targets for drugs and pesticides. The macrocyclic lactone abamectin primarily targets GluCl and is commonly used to control the spider mite Tetranychus urticae, an economically important crop pest. However, abamectin resistance has been reported for multiple T. urticae populations worldwide, and in several cases was associated with the mutations G314D in GluCl1 and G326E in GluCl3. Recently, an additional I321T mutation in GluCl3 was identified in several abamectin resistant T. urticae field populations. Here, we aim to functionally validate this mutation and determine its phenotypic strength. RESULTS: The GluCl3 I321T mutation was introgressed into a T. urticae susceptible background by marker-assisted backcrossing, revealing contrasting results in phenotypic strength, ranging from almost none to 50-fold. Next, we used CRISPR-Cas9 to introduce I321T, G314D and G326E in the orthologous Drosophila GluCl. Genome modified flies expressing GluCl I321T were threefold less susceptible to abamectin, while CRISPRed GluCl G314D and G326E flies were lethal. Last, functional analysis in Xenopus oocytes revealed that the I321T mutation might reduce GluCl3 sensitivity to abamectin, but also suggested that all three T. urticae Rdls are affected by abamectin. CONCLUSION: Three different techniques were used to characterize the role of I321T in GluCl3 in abamectin resistance and, combining all results, our analysis suggests that the I321T mutation has a complex role in abamectin resistance. Given the reported subtle effect, additional synergistic factors in resistance warrant more investigation. © 2020 Society of Chemical Industry.

Geographical distribution and molecular insights into abamectin and milbemectin cross-resistance in European field populations of Tetranychus urticae.

BACKGROUND: Milbemectin and abamectin are frequently used to control the spider mite Tetranychus urticae. The development of abamectin resistance in this major pest has become an increasing problem worldwide, potentially compromising the use of milbemectin. In this study, a large collection of European field populations was screened for milbemectin and abamectin resistance, and both target-site and metabolic (cross-)resistance mechanisms were investigated. RESULTS: High to very high levels of abamectin resistance were found in one third of all populations, while milbemectin resistance levels were low for most populations. The occurrence of well-known target-site resistance mutations in glutamate-gated chloride channels (G314D in GluCl1 and G326E in GluCl3) was documented in the most resistant populations. However, a new mutation, I321T in GluCl3, was also uncovered in three resistant populations, while a V327G and L329F mutation was found in GluCl3 of one resistant population. A differential gene-expression analysis revealed the overexpression of detoxification genes, more specifically cytochrome P450 monooxygenase (P450) and UDP-glycosyltransferase (UGT) genes. Multiple UGTs were functionally expressed, and their capability to glycosylate abamectin and milbemectin, was tested and confirmed. CONCLUSIONS: We found a clear correlation between abamectin and milbemectin resistance in European T. urticae populations, but as milbemectin resistance levels were low, the observed cross-resistance is probably not of operational importance. The presence of target-site resistance mutations in GluCl genes was confirmed in most but not all resistant populations. Gene-expression analysis and functional characterization of P450s and UGTs suggests that also metabolic abamectin resistance mechanisms are common in European T. urticae populations. © 2020 Society of Chemical Industry.

Identification and characterization of new mutations in mitochondrial cytochrome b that confer resistance to bifenazate and acequinocyl in the spider mite Tetranychus urticae.

BACKGROUND: In spider mites, mutations in the mitochondrial cytochrome b Qo pocket have been reported to confer resistance to the Qo inhibitors bifenazate and acequinocyl. In this study, we surveyed populations of the two-spotted spider mite Tetranychus urticae for mutations in cytochrome b, linked newly discovered mutations with resistance and assessed potential pleiotropic fitness costs. RESULTS: We identified two novel mutations in the Qo site: G132A (equivalent to G143A in fungi resistant to strobilurins) and G126S + A133T (previously reported to cause bifenazate and acequinocyl resistance in Panonychus citri). Two T. urticae strains carrying G132A were highly resistant to bifenazate but not acequinocyl, whereas a strain with G126S + A133T displayed high levels of acequinocyl resistance, but only moderate levels of bifenazate resistance. Bifenazate and acequinocyl resistance were inherited maternally, providing strong evidence for the involvement of these mutations in the resistance phenotype. Near isogenic lines carrying G132A revealed several fitness penalties in T. urticae; a lower net reproductive rate (R0 ), intrinsic rate of increase (rm) and finite rate of increase (LM); a higher doubling time (DT); and a more male-biased sex ratio. CONCLUSIONS: Several lines of evidence were provided to support the causal role of newly discovered cytochrome b mutations in bifenazate and acequinocyl resistance. Because of the fitness costs associated with the G132A mutation, resistant T. urticae populations might be less competitive in a bifenazate-free environment, offering opportunities for resistance management. © 2019 Society of Chemical Industry.

Differential Expression Analysis of Olfactory Genes Based on a Combination of Sequencing Platforms and Behavioral Investigations in Aphidius gifuensis.

Aphidius gifuensis Ashmead is a dominant endoparasitoid of aphids, such as Myzus persicae and Sitobion avenae, and plays an important role in controlling aphids in various habitats, including tobacco plants and wheat in China. A. gifuensis has been successfully applied for the biological control of aphids, especially M. persicae, in green houses and fields in China. The corresponding parasites, as well as its mate-searching behaviors, are subjects of considerable interest. Previous A. gifuensis transcriptome studies have relied on short-read next-generation sequencing (NGS), and the vast majority of the resulting isotigs do not represent full-length cDNA. Here, we employed a combination of NGS and single-molecule real-time (SMRT) sequencing of virgin females (VFs), mated females (MFs), virgin males (VMs), and mated males (MMs) to comprehensively study the A. gifuensis transcriptome. Behavioral responses to the aphid alarm pheromone (E-ß-farnesene, EBF) as well as to A. gifuensis of the opposite sex were also studied. VMs were found to be attracted by female wasps and MFs were repelled by male wasps, whereas MMs and VFs did not respond to the opposite sex. In addition, VFs, MFs, and MMs were attracted by EBF, while VMs did not respond. According to these results, we performed a personalized differential gene expression analysis of olfactory gene sets (66 odorant receptors, 25 inotropic receptors, 16 odorant-binding proteins, and 12 chemosensory proteins) in virgin and mated A. gifuensis of both sexes, and identified 13 candidate genes whose expression levels were highly consistent with behavioral test results, suggesting potential functions for these genes in pheromone perception.

Endothelium-dependent relaxation induced by etomidate in the aortas of insulin-resistant rats.

INTRODUCTION: Few reports have mentioned the effect of etomidate on the aortas of insulin-resistant (IR) rats. In this study, we investigated the effect of etomidate on isolated IR aortas of rats, and explored its underlying mechanism. MATERIAL AND METHODS: The IR rat model was established through feeding with a high-fructose diet. The systolic blood pressure (SBP) was measured by the tail-cuff method before grouping and at the end of the 8-week feeding; blood samples were also obtained for analysis. Thoracic aorta rings of IR rats were isolated and suspended in a tissue bath. The tensile force was recorded isometrically. The effect of etomidate on provoked contraction of the rings was assessed with or without a potassium channel blocker or NO synthase inhibitor. RESULTS: Etomidate-induced relaxation in IR rings was greater than normal control (NC) rings (all p < 0.001 with etomidate log M of -4 to -6). NG-nitro-L-arginine methyl ester (L-NAME, an NO synthase inhibitors) inhibited etomidate-induced relaxation in NC rings, but had no effect on the IR rings (all p < 0.001 with etomidate log M of -4 to -6). Pre-incubation with glibenclamide (Gli, a potassium channel blocker) significantly inhibited etomidate-induced relaxation in NC and IR rings (all p < 0.001 with etomidate log M of -4 to -6), and had no inhibited effect on endothelial denuded aortic rings. CONCLUSIONS: Insulin resistance increased etomidate-induced relaxation in rat aortas. Etomidate causes vasodilation in IR rat aortas via both endothelium-dependent and independent ways; impaired NO-mediated relaxation was disrupted and ATP-sensitive potassium (KATP) channel-mediated relaxation may be involved in the endothelium-dependent relaxation of etomidate in IR rats.

Identification of an intraspecific alarm pheromone and two conserved odorant-binding proteins associated with (E)-ß-farnesene perception in aphid Rhopalosiphum padi.

(E)-ß-farnesene (EBF) is the common active component of aphid alarm pheromone. Either or both of two orthologs of ordorant-binding proteins (OBPs), OBP3 and OBP7, recently reported in aphids, may be involved in EBF perception. The aim of this study was to investigate the respondence of the aphid Rhopalosiphum padi to its intraspecific alarm pheromone and which OBP is responsible for that response. We tested the olfactory response of the aphid R. padi to EBF and freshly crushed aphids. Then, we extracted the volatiles from crushed aphids using solid phase microextraction (SPME) for analysis with GC×GC-TOF/MS. We also cloned two OBPs cDNAs in R. padi (RpadOBP3 and RpadOBP7) and expressed them in competent Escherichia coli cells. Both recombinant proteins, RpadOBP3 and RpadOBP7, bound EBF well, with RpadOBP7 having specifically stronger affinity for EBF than for other volatiles. Based on the crystal structure of the OBPs with high identity, we performed homology modeling and analyzed the interactions between RpadOBPs and EBF. In conclusion, R. padi was repelled by both EBF and crushed aphids. EBF was identified as the only volatile that acted as the alarm pheromone. Our results indicated that OBP7 is a potential molecular target to control wheat aphids by disturbing their behaviors to the alarm pheromone.

Protective effects of ginsenoside Rg1 against oxygen-glucose-deprivation-induced apoptosis in neural stem cells.

Oxygen-glucose deprivation (OGD) causes neural damages through stroke-induced ischemia. Neural stem cells (NSCs) have been shown to alleviate ischemia-induced neural damages. However, ischemia reduces NSC survival. Ginsenoside Rg1 exerts anti-inflammatory and anti-oxidative effects, and repairs brain injury-related neural damages. We aimed to investigate whether ginsenoside Rg1 could prevent NSCs from OGD insult. Using multiple techniques, we explored neuroprotective effects of ginsenoside Rg1 on OGD-insulted NSCs. 6h treatment of OGD most significantly decreased NSC viability, and 10-20µM ginsenoside Rg1 efficiently protected NSCs against OGD insult. Annexin V-FITC/propidium iodide (PI) double staining results confirmed that ginsenoside Rg1 significantly reduced the OGD-induced apoptosis in NSCs. OGD-insulted NSCs with ginsenoside Rg1 treatment displayed reduced expressions of pro-apoptotic proteins cleaved Caspase3 and Bax, and elevated expression of anti-apoptotic protein Bcl-2 than the NSCs with OGD insult. Moreover, ginsenoside Rg1 reduced OGD-induced oxidative stress, and inhibited the expression of p-p38 and p-JNK2. Ginsenoside Rg1 protects NSCs against OGD-induced cell apoptosis through regulating the expression of apoptotic signal proteins. In addition, ginsenoside Rg1 attenuates OGD-induced oxidative stress and inhibits p38/JNK2 phosphorylation in NSCs. Our study provides solid evidence for neuroprotective effects of ginsenoside Rg1 and reveals the underlying mechanisms.