Modulation of plasmacytoid dendritic cell and CD4+ T cell differentiation accompanied by upregulation of the cholinergic anti-inflammatory pathway induced by enterovirus 71.

Enterovirus 71 (EV71) is a neurotropic enterovirus associated with hand, foot, and mouth disease (HFMD) fatalities. In this study, we investigated the impact of EV71 on plasmacytoid dendritic cells (pDCs) and CD4+ T cells. The results showed that pDCs were promptly activated, secreting interferon (IFN)-α and inducing CD4+ T cell proliferation and differentiation during early EV71 infection. This initiated adaptive immune responses and promoted proinflammatory cytokine production by CD4+ T cells. Over time, viral nucleic acids and proteins were synthesized in pDCs and CD4+ T cells. Concurrently, the cholinergic anti-inflammatory pathway (CAP) was activated, exhibiting an anti-inflammatory role. With constant viral stimulation, pDCs and CD4+ T cells showed reduced differentiation and cytokine secretion. Defects in pDCs were identified as a key factor in CD4+ T cell tolerance. CAP had a more significant regulatory effect on CD4+ T cells than on pDCs and was capable of inhibiting inflammation in these cells.

Phenotypes of a toddler with hereditary sensory and autonomic neuropathy type IV: comparing with normal: A case report.

RATIONALE: Hereditary sensory and autonomic neuropathy type IV (HSAN IV) may be misdiagnosed because of low awareness among clinical professionals and overlap with other subtypes of congenital insensitivity to pain (CIP). PATIENT: The patient was a 1-year-and-5-months-old boy whose main symptoms were delayed psychomotor development and recurrent fever. Whole-exome sequencing (WES) revealed a compound heterozygous mutation (c. 1927C > T, c. 851-33T > A) in the NTRK1 gene of the child. Pathological analysis showed decreased autonomic small nerve fibers, sparse hair follicles, and atrophy of the sweat glands. Sweat glands lack innervating nerve fibers. Brain magnetic resonance imaging (MRI) of the patient showed delayed myelination in the brain, slightly enlarged bilateral lateral ventricles, and patchy abnormal signals in the brain. DIAGNOSIS: hereditary sensory and autonomic neuropathy type IV (HSAN IV). INTERVENTION: Inform parents about the illness and take good care of the child. OUTCOMES: The children had less self-harming behavior and no painless fractures during follow-up at 2 years. LESSONS: This report describes the pathological and imaging features and clinical manifestations of a child with HSAN IV in early life to provide a reference for the early diagnosis of the disease. Early diagnosis can help avoid self-mutilation and painless injury and reduce wound infection.

Epstein-Barr virus downregulates the α7 nicotinic acetylcholine receptor of CD8+ T lymphocytes might associate with coronary artery lesions in Kawasaki disease patients.

OBJECTIVES: Kawasaki disease (KD) is a systemic vasculitis that is caused by immunological dysregulation in children exposed to pathogens like Epstein-Barr virus (EBV). Myocardial ischemia or infarction due to coronary artery lesions (CALs) might be lethal. However, it is unclear how pathogens, immunomodulation, and CALs interact, particularly in KD patients co-infected with the most widespread virus, EBV. METHODS: We investigated pathogen carriage and fundamental clinical data in 281 KD patients. Immunological differences between CALs and non-CALs in KD patients under different conditions were analyzed. Then, the effect of infection by different pathogens on the immune response was excluded, and most EBV co-infected KD patients were included to assess the incidence of CALs, the level of immune modulation, and regulatory mechanisms in different EBV infection states. RESULTS: Our results showed multiple pathogenic infections occur in KD patients, with EBV being the most prevalent. The incidence of CALs in the EBV-DNA (+) acute infection group, EBV-DNA (-) acute infection group, and EBV latent infection group was 0 (0/6), 27.27% (3/11) and 41.67% (10/24), respectively. The two groups were younger and had increased IL-6 levels and B cells, decreasing CD8+ T cells than the EBV-DNA (+) acute infection group. Interestingly, the increased B cells were not associated with immunoglobulin release. Additionally, these patients down-regulated α7 nicotinic acetylcholine receptor (α7nAChR) and downstream molecule PI3K/AKT/mTOR while activating the NF-κB. CONCLUSION: Patients with different EBV infection statuses exhibit different incidences of CALs. In acute EBV-DNA (-) infected and latent EBV-infected patients, the number of CD8+ T cells decreased and downregulated CD8+ T cells' α7nAChR and PI3K/AKT/mTOR, which may associate with CALs, while the expression of NF-κB and the pro-inflammatory factor IL-6 was upregulated by inhibiting the anti-inflammatory molecule α7nAChR.

Transcriptomic Analyses Suggest the Adaptation of Bumblebees to High Altitudes.

Determining the adaptive mechanisms by which bumblebees adapt to high altitudes can help us to better understand their distribution, providing a basis for the future protection and utilization of bumblebee resources. For this study, the adaptive mechanisms of two dominant bumblebee species in the northeastern Qinghai-Tibet Plateau-Bombus kashmirensis and B. waltoni-were studied through transcriptomics methods. For each species, enrichment analysis of the differentially expressed genes and gene set enrichment analysis were carried out between samples collected at different altitudes (4000 m, 4500 m, and 5000 m). The results indicate that these bumblebees tend to up-regulate energy metabolism-related genes when facing extremely high-altitude environments. Of the enriched pathways up-regulated in higher altitudes, the pentose and glucuronate interconversions pathway presented the most severe up-regulation in multiple comparisons of different altitudes for B. kashmirensis, as well as the AMPK signaling pathway, which was found to be up-regulated in both species. Notably, limited by the extreme hypoxic conditions in this study, oxidative phosphorylation was found to be down-regulated with increasing altitude, which is uncommon in studies on bumblebee adaptation to high altitudes.

Potential pathogenic mechanism of type 1 X-linked lymphoproliferative syndrome caused by a mutation of SH2D1A gene in an infant: A case report.

BACKGROUND: X-linked lymphoproliferative syndrome (XLP) is a rare X-linked recessive inborn errors of immunity. The pathogenesis of XLP might be related to phophatidylinositol-3-kinase (PI3K)-associated pathways but insight details remain unclear. This study was to study an infant XLP-1 case caused by a mutation in SH2D1A gene, investigate the structural and functional alteration of mutant SAP protein, and explore the potential role of PI3K-associated pathways in the progression of XLP-1. METHODS: The proband's condition was monitored by laboratory and imagological examinations. Whole exome sequencing and Sanger sequencing were performed to detect the genetic disorder. Bioinformatics tools including PolyPhen-2, SWISS-MODEL and SWISS-PDB Viewer were used to predict the pathogenicity and estimate structural change of mutant protein. Flow cytometry was used to investigate expression of SAP and PI3K-associated proteins. RESULTS: The proband was diagnosed with XLP-1 caused by a hemizygous mutation c.96G > T in SH2D1A gene resulting in a missense substitution of Arginine to Serine at the site of amino acid 32 (p.R32S). The mutant protein contained a hydrogen bond turnover at the site of mutation and was predicted to be highly pathogenic. Expression of SH2D1A encoded protein SAP was downregulated in proband. The PI3K-AKT-mTOR signaling pathway was fully activated in XLP-1 patients, but it was inactive or only partially activated in healthy people or HLH patients. CONCLUSIONS: The mutation c.96G > T in SH2D1A gene caused structural and functional changes in the SAP protein, resulting in XLP-1. The PI3K-AKT-mTOR signaling pathway may play a role in XLP-1 pathogenesis.

The complete mitochondrial genome and phylogenetic analysis of Illiberis pruni Dyar, 1905 (Lepidoptera: Zygaenidae).

Illiberis pruni is a leaf-eating pest that infests pear trees across all pear-producing regions of China. The present study, aimed to sequence the I. pruni mitochondrial genome (GenBank accession no. MZ726799) using the Illumina NovaSe Sequencing System to understand the population genetics, evolution, and taxonomy of I. pruni and other related species. The circular I. pruni mitochondrial genome was found to be 15,252 bps in length and comprised 38 sequence elements including 13 protein-coding genes (PCGs), 22 transfer RNA (tRNA) genes, 2 ribosomal RNA (rRNA) genes, and a putative control region (CR). Phylogenetic analysis revealed that I. pruni and Illiberis ulmivora are closely related, thereby indicating that their mitochondrial genes may share common ancestry.

Analysis of complete mitochondrial genome sequence of Pontania dolichura (Hymenoptera: Tenthredinidae) (Thomson, 1871).

Pontania dolichura is a leaf-eating pest that mainly damages willow trees and is widely distributed in northern regions. In this study, we sequenced the entire mitochondrial genome of P. dolichura (GenBank accession number: MZ726800). The circular gene was 16,104 bp in length and comprised 38 column elements, including 13 protein-coding genes (PCGs), 22 transfer RNA genes, two ribosomal RNA genes, and a non-coding control region. Most of the PCGs of P. dolichura have typical ATN (Met) start codons and typical TAN stop codons. The A + T contents of the genome, PCGs, transfer RNAs (tRNAs), and ribosomal RNAs (rRNAs) were 80.32%, 78.66%, 81.94%, and 82.59%, respectively. Phylogenetic analysis supported the close genetic relationship between P. dolichura and Mesoneura rufonota indicating that the two species share more recent common ancestor gene. These data will be useful for further molecular identification and population genetics studies.

[High quality standard of Scutellariae Radix based on plant metabolomics and index components].

Scutellariae Radix(SR), derived from the dried root of Scutellaria baicalensis in the family Lamiaceae, commonly serves as Chinese medicinal material. Affected by producing areas, growing years, and harvesting periods, the quality of SR fluctuates in the market. However, baicalin≥9% in SR required in the Chinese Pharmacopoeia(2020 edition) can only determine the qualified SR but cannot identify high-quality SR. To improve the quality control methods of SR, the present study analyzed the accumulation of metabolites in SR of different growth years by plant metabolomics, and identified 28 metabolites increasing with growth years(1-3 years). Subsequently, 14 main metabolites were quantitatively analyzed by ultra-high performance liquid chromatography-tandem triple quadrupole mass spectrometry(UPLC-QQQ-MS). Among them, baicalin, wogonoside, baicalein, and wogonin with high content and good activity were selected as the index components of SR for quality evaluation. A high-performance liquid chromatography(HPLC) method was established to determine the content of four index components in 32 batches of SR from different producing areas, harvesting perio-ds, and growth years. The results showed that the growth years could greatly affect the content of index components. The total content of four index components in 2-year SR was the highest, followed by the 3-/4-year SR and 1-year SR. Based on HPLC data and verification results by enterprises, baicalin ≥12.0%, wogonoside ≥2.3%, baicalein ≥0.1%, and wogonin ≥0.03% were proposed as the evaluation criteria for the high-quality SR. The findings of this study are expected to provide a basis for improving the quality of SR.

A novel mutation in the homogentisate 1,2 dioxygenase gene identified in Chinese Hani pediatric patients with Alkaptonuria.

BACKGROUND: Alkaptonuria (AKU) is a rare tyrosine metabolism disorder caused by homogentisate 1,2-dioxygenase (HGD) mutations and homogentisic acid (HGA) accumulation. In this study, we investigated the genotype-phenotype relationship in AKU patients with a novel HGD gene mutation from a Chinese Hani family. METHODS: Routine clinical examination and laboratory evaluation were performed, urine alkalinization test and urinary gas chromatography-mass spectrometry were used to assess HGA. Gene sequencing was utilized to study the defining features of AKU. NetGene2-2.42 and BDGP software was used to predict protein structure online. Flow cytometry and RT-PCR were used to analyze HGD proteins and HGD mRNA, respectively. RESULTS: Two pediatric patients fulfilled diagnostic criteria for AKU with eddish-brown or black diapers and urine HGA testing. Sequencing testing revealed that all members of this family had a novel samesense mutation c.15G > A at the edge of exon 1 of the HGD. By flow cytometry, the expression of HGD protein in the pediatric patients' peripheral blood mononuclear cells was barely expressed. NetGene2-2.42 and BDGP software showed that the mutation reduced the score of the 5' splice donor site and disrupted its normal splicing, and the RT-PCR product also demonstrated that the defect in the HGD protein was due to the lack of the first exon containing the start codon ATG after the mutation. CONCLUSIONS: The novel mutation c.15G > A in HGD is associated with the AKU phenotype. It may affect the splicing of exon 1, leading to exon skipping, which impairs the structure and function of the protein.

A novel frameshift c.22_25dupGCAT mutation of the NDP gene in a Chinese infant with Norrie disease: A case report.

RATIONALE: Norrie disease (ND) is a rare X-linked recessive disease characterized by bilateral congenital blindness and auditory impairments. According to the previous studies, Norrin cystine knot growth factor (NDP) gene have been found to be responsible for ND. Herein, we report a case of ND with a novel mutation in NDP and elucidate the clinical and molecular characteristics of this patient. PATIENT CONCERNS: A 2-month-old Chinese male infant presented with gray-white opacification in the bilateral cornea. Vitreous opacity and retinal detachment were observed on ocular ultrasound. Furthermore, a novel de novo hemizygous mutation (c.22_25dupGCAT, p.S9Cfs∗18) in exon 2 of the NDP gene was identified by next-generation sequencing. SWISS-MODEL predicted that the c.22_25dupGCAT mutation truncated the NDP protein. DIAGNOSIS: Based on the above clinical and genetic evidence, this patient was eventually diagnosed with ND. INTERVENTIONS: Currently, no clinical therapy is available for ND. OUTCOMES: In addition to the typical ocular symptoms, no other abnormalities were observed. The patient's vital signs remained stable and normal. LESSON: A novel causative mutation of NDP was identified using next-generation sequencing. Our report expands the pathogenic mutation spectrum of NDP and facilitates genetic counseling and prenatal diagnosis. Additionally, we emphasize the importance of molecular genetic testing in the diagnosis of ND.

A novel homozygous mutation of the PCNT gene in a Chinese patient with microcephalic osteodysplastic primordial dwarfism type II.

BACKGROUND: Microcephalic osteodysplastic primordial dwarfism type II (MOPD II) is a rare autosomal recessive disorder characterized by severe pre- and postnatal growth restrictions, microcephaly, skeletal dysplasia, severe teeth deformities, and typical facial features. Previous studies have shown that MOPD II is associated with mutations in the pericentrin (PCNT) gene. METHODS: We evaluated the clinical features of a 10-year and 7-month-old Chinese girl with MOPD II. Subsequently, next-generation sequencing and flow cytometry were performed to investigate genetic characteristics and the expression of PCNT protein respectively. RESULTS: The patient presented with short stature, microcephaly, typical craniofacial features, teeth deformity, thrombocytosis, and a delayed bone age (approximately 7 years). No abnormality in growth hormone or insulin-like growth factor 1 was detected. Notably, the patient was found to carry a novel homozygous PCNT mutation (c.6157G>T, p.Glu2053Ter), which was inherited from her healthy heterozygous parents. Meanwhile, significant deficiency of PCNT expression was identified in the patient. CONCLUSION: Our study identified a novel PCNT mutation associated with MOPD II, expanded the mutation spectrum of the PCNT gene and improved our understanding of the molecular basis of MOPD II.

Two novel mutations of the LPL gene in two Chinese family cases with familial chylomicronemia syndrome.

The aim of this study was to investigate the clinical features and genetic causes of two family cases with familial chylomicronemia syndrome (FCS). Clinical manifestations of proband 1 and her families, and also proband 2 showed severe hypertriglyceridemia, especially the triglycerides levels of two probands were extremely high. Gene sequencing results showed that the LPL genes in each of the two probands had a new mutation site. For the proband 1, a compound heterozygous mutation at c.429 (c.429 + 1G > T) was detected in the LPL gene, which was splicing mutation and inherited from her mother. Homozygous mutation was detected in the LPL gene of proband 2, the nucleotide mutation at c.802 (c.802C > T) exhibited missense mutation, his parents and brother had a heterozygous mutation at the same site. It was confirmed that the conservative lipoprotein lipase superfamily domain changed an amino acid from histidine to tyrosine at p. 268 (p. His268Tyr). Flow cytometry confirmed the deficient expression of LPL protein in two families. These results indicated that the mutation in LPL gene might be the cause of familial chylomicronemia syndrome.

Clinical and genetic analysis of 2 rare cases of Wiskott-Aldrich syndrome from Chinese minorities: Two case reports.

RATIONALE: Wiskott-Aldrich syndrome (WAS) is a rare X-linked recessive disease characterized by thrombocytopenia, small platelets, eczema, immunodeficiency, and an increased risk of autoimmunity and malignancies. X-linked thrombocytopenia (XLT), the milder phenotype of WAS, is always limited to thrombocytopenia with absent or slight infections and eczema. Here, we illustrated the clinical and molecular characteristics of 2 unrelated patients with WAS from Chinese minorities. PATIENT CONCERNS: Patient 1, a 13-day-old male newborn of the Chinese Lahu minority, showed a classic WAS phenotype, including thrombocytopenia, small platelets, buttock eczema, and recurrent infections. Patient 2, an 8-year-and 8-month-old boy of the Chinese Zhuang minority, presented an XLT phenotype without eczema and repeated infections. DIAGNOSIS: Next-generation sequencing was performed to investigate the genetic variations. Flow cytometry was used to quantify the expression of WAS protein and analyze the lymphocyte subsets. A novel frameshift WAS mutation (c.927delC, p.Q310Rfs∗135) and a known nonsense WAS mutation (c.1090C>T, p.R364X) were identified in Patient 1 and Patient 2, respectively. Both patients were confirmed to have WAS protein deficiency, which was more severe in Patient 1. Meanwhile, the analysis of lymphocyte subsets revealed an abnormality in Patient 1, but not in Patient 2. Combined with the above clinical data and genetic characteristics, Patient 1 and Patient 2 were diagnosed as classic WAS and XLT, respectively. In addition, many miliary nodules were accidentally found in abdominal cavity of Patient 2 during appendectomy. Subsequently, Patient 2 was confirmed with pulmonary and abdominal tuberculosis through further laboratory and imaging examinations. To our knowledge, there have been only a few reports about WAS/XLT with tuberculosis. INTERVENTIONS: Both patients received anti-infection therapy, platelet transfusions, and intravenous immunoglobulins. Moreover, Patient 2 also received antituberculosis treatment with ethambutol and amoxicillin-clavulanate. OUTCOMES: The clinical symptoms and hematological parameters of these 2 patients were significantly improved. Regrettably, both patients discontinued the treatment for financial reasons. LESSONS: Our report expands the pathogenic mutation spectrum of WAS gene and emphasizes the importance of molecular genetic testing in diagnosing WAS. Furthermore, researching and reporting rare cases of WAS from different populations will facilitate diagnosis and treatment of this disease.

Complete mitochondrial genome of Polyphylla gracilicornis (Coleoptera：Scarabaeoidea).

Polyphylla gracilicornis is one of the important underground pest species that damage agricultural and forestry plants and often requires chemical control during outbreak. Here, we determined the complete mitochondrial genome sequence of P. gracilicornis (GenBank accession no. MW143080) using Illumina NovaSe Sequencing System with a read length of 150 bp. The complete mitogenome consists of a 16,793 bp circular DNA molecule and the overall base composition was 36.97% A, 31.95% T, 10.41% G and 20.67% C. The full mitochondrial genome contains 38 sequence elements: 13 protein-coding genes (PCGs), 22 transfer RNA (tRNA) genes, two ribosomal RNA (rRNA) genes, and a putative control region (CR). All protein-coding genes of P. gracilicornis have the typical ATN (Met) start codons and typical TAN stop codons. Phylogenetic analysis revealed that P. gracilicornis clustered into a clade with homologous species with high bootstrap support.

One-step fabrication of alkali-acid modified three-dimensional magnetic biochar for the determination of pesticides in pigment-rich vegetables.

Magnetic biochar was successfully synthesized via a one-step method through simultaneous activation and magnetization with alkali-acid modified citrus peel as the raw material, which could effectively penetrate interfering substances. The characterization analysis showed that the magnetic biochar exhibited high graphitic degree, higher specific surface area and smaller pore diameter, which resulted in superior adsorption performance. The magnetic biochar was used as an adsorbent for the cleanup and extraction of 22 pesticides (consisting of insecticides, fungicides and herbicides) from vegetables and the quantitative detection was completed by gas chromatography-mass spectrometry (GC-MS). The Plackett-Burman experimental design (PBD), central composite design (CCD) and response surface methodology (RSM) were employed to identify significant factors and optimal experimental conditions. Under optimal conditions, the methodological linearity was in the range of 1-100 µg kg-1 with the coefficients of determination ranging from 0.9969-0.9999, while the limits of detection (LODs) and limits of quantification (LOQs) were 0.31-0.91 µg kg-1 and 1.03-3.05 µg kg-1, respectively. The recoveries of the analytes from spiked samples were in the range of 78.1-112.5%. It was confirmed that the method established by using magnetic graphitic biochar as the adsorbent is an efficient pretreatment procedure and could be successfully applied for analysis of food safety.

Waardenburg syndrome type II in a Chinese pedigree caused by frameshift mutation in the SOX10 gene.

Waardenburg syndrome (WS) is a congenital hereditary disease, attributed to the most common symptoms of sensorineural deafness and iris hypopigmentation. It is also known as the hearing-pigmentation deficient syndrome. Mutations on SOXl0 gene often lead to congenital deafness and has been shown to play an important role in the pathogenesis of WS. We investigated one family of five members, with four patients exhibiting the classic form of WS2, whose DNA samples were analyzed by the technique of Whole-exome sequencing (WES). From analysis of WES data, we found that both the mother and all three children in the family have a heterozygous mutation on the Sex Determining Region Y - Box 10 (SOX10) gene. The mutation was c.298_300delinsGG in exon 2 of SOX10 (NM_006941), which leads to a frameshift of nine nucleotides, hence the amino acids (p. S100Rfs*9) are altered and the protein translation may be terminated prematurely. Further flow cytometry confirmed significant down-regulation of SOX10 protein, which indicated the SOX10 gene mutation was responsible for the pathogenesis of WS2 patients. In addition, we speculated that some other mutated genes might be related to disease phenotype in this family, which might also participate in promoting the progression of WS2.

Three Chemosensory Proteins Involved in Chemoreception of Oedaleus asiaticus (Orthopera: Acridoidea).

Chemosensory proteins (CSPs) are thought to play roles in the insect olfactory system by binding and carrying hydrophobic odorants across the aqueous sensillar lymph. The band-winged grasshopper, Oedaleus asiaticus Bei-Bienko, is one of the most important grasshopper pests in northern China, but there is little information about its olfactory system. In order to investigate the olfactory functions of CSPs in this pest, three CSP genes (OasiCSP4, OasiCSP11 and OasiCSP12) were expressed in Escherichia coli, and the binding affinities of the three recombinant CSP proteins were measured for 16 volatiles from the host plant (Stipa krylovii), fecal material and body of live adult O. asiaticus using fluorescence competitive binding assays. To further verify their olfactory functions, RNA interference (RNAi) and electrophysiological recording were conducted. The three recombinant proteins displayed different degrees of binding to various volatiles in ligand-binding assays, with OasiCSP12 having higher binding affinities for more volatiles than OasiCSP4 and OasiCSP11. OasiCSP12 exhibited strong binding affinities (Ki < 20 µΜ) for five host plant volatiles and one volatile from the live body of adult O. asiaticus. The transcript levels of the three OasiCSP genes were significantly lower after silencing the individual genes by RNAi, which in turn reduced the EAG responses in adults of both sexes to most tested compounds. Our study indicates that these three OasiCSPs are involved in the detection of volatile semiochemicals, and may play important roles in finding host plants and in aggregation in O. asiaticus.

Identification and expression profiling of candidate chemosensory membrane proteins in the band-winged grasshopper, Oedaleus asiaticus.

The band-winged grasshopper Oedaleus asiaticus (Orthoptera: Acridoidea) is an important insect pest in north China. Chemosensory membrane proteins are believed to be crucial factors in direct interactions with odorants in the chemosensory process. However, there is much limited information on the chemosensory system in this pest. In this study, a total of 69 candidate chemosensory membrane protein genes, including 60 olfactory receptors (ORs), 6 ionotropic receptors (IRs) and 3 sensory neuron membrane proteins (SNMPs), were identified for the first time from the antennal transcriptomes of O. asiaticus. Blastp match and phylogenetic analysis demonstrated that these chemosensory membrane proteins were the closest to their orthologous species, Locusta migratoria. The qRT-PCR analysis revealed that all tested 14 OR and two SNMP genes (OasiSNMP1 and OasiSNMP2a) were strongly expressed in adult antennae, and nearly all tested genes (15/16) displayed significant differences in the expression levels between both sexes. Moreover, two IR genes (OasiIR25a and OasiIR76b) had uniquely high expression levels in the antennae, labial palps and maxillary palps, while three IR genes (OasiIR1, OasiIR2 and OasiIR3) were highly expressed in most tested tissues (heads without antennae and mouthparts, labial palps, maxillary palps, labia without labial palps, thoraxes, tarsi, and abdomens) except for antennae, labra, and wings but OasiIR5a was just faintly expressed in the antennae, labia without labial palps, labial palps, maxillary palps and abdomen. Our results provide important molecular information for further investigation on the chemoreception mechanisms in O. asiaticus.

Controllable synthesis of magnetic nanoporous carbon with tunable porosity for the efficient cleanup of vegetable samples.

Highly graphitic nanoporous carbon (NPC) was obtained from an agricultural waste-citrus peel at optimum condition. Then, a low-cost and pore size-controlled magnetic graphitic nanoporous carbon (MNPC) with ultrahigh specific surface area (1064 m2 g-1) was successfully fabricated by coprecipitation of Fe3O4 particles onto NPC. The prepared MNPC was characterized by Brunauer-Emmett-Teller (BET), Raman spectrum, scanning electron microscope (SEM) and Fourier transform infrared spectrometry (FT-IR). BET results showed a significant increase in the micropores volume and specific surface area of MNPCs following the increase of carbonization temperature, which implied that highly efficient carbonization made NPC an excellent active phase for MNPC. Besides, the adsorption mechanism was investigated and turned out that π-π interactions between interfering substances and MNPC were considered to be the major driving force for the adsorption process. The experimental parameters affecting the cleanup efficiency was optimized through Response surface methodology (RSM) in detail. Under the optimal cleanup condition, the MNPC was applied for determination of 16 insecticides in vegetables coupled with gas chromatography-mass spectrometry (GC-MS), a satisfactory performance was obtained. Good linearity was observed in the investigated concentration range of 1-100 µg kg-1 with correlation coefficients (r2) between 0.9963 and 0.9999. The limits of detection (LODs) were in the range of 0.03-0.33 µg kg-1. The recoveries ranged from 81.9 to 112.3% with relative standard deviations (RSDs) less than 10.9%. To summary up, the MNPC could potentially be used as a super adsorbent to efficiently remove pigments from vegetables, so that the proposed method was an efficient cleanup and enrichment procedure.