Transcriptome profiling of the fifth-stage larvae of Angiostrongylus cantonensis by next-generation sequencing

Angiostrongylus cantonensis is an important zoonotic nematode. It is the causative agent of eosinophilic meningitis and eosinophilic meningoencephalitis in humans. However, information of this parasite at the genomic level is very limited. In the present study, the transcriptomic profiles of the fifth-stage larvae (L5) of A. cantonensis were investigated by next-generation sequencing (NGS). In the NGS database established from the larvae isolated from the brain of Sprague–Dawley rats, 31,487 unique genes with a mean length of 617 nucleotides were assembled. These genes were found to have a 46.08 % significant similarity to Caenorhabditis elegans by BLASTx. They were then compared with the expressed sequence tags of 18 other nematodes, and significant matches of 36.09–59.12 % were found. Among these genes, 3,338 were found to participate in 124 Kyoto Encyclopedia of Genes and Genomes pathways. These pathways included 1,514 metabolisms, 846 genetic information processing, 358 environmental information processing, 264 cellular processes, and 91 organismal systems. Analysis of 30,816 sequences with the gene ontology database indicated that their annotations included 5,656 biological processes (3,364 cellular processes, 3,061 developmental processes, and 3,191 multicellular organismal processes), 7,218 molecular functions (4,597 binding and 3,084 catalytic activities), and 4,719 cellular components (4,459 cell parts and 4,466 cells). Moreover, stress-related genes (112 heat stress and 33 oxidation stress) and genes for proteases (159) were not uncommon. This study is the first NGS-based study to set up a transcriptomic database of A. cantonensis L5. The results provide new insights into the survival, development, and host–parasite interactions of this blood-feeding nematode. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00436-013-3495-z) contains supplementary material, which is available to authorized users

Allele Size Miscalling due to the Pull-Up Effect Influencing Size Standard Calibration in Capillary Electrophoresis: A Case Study Using HEX Fluorescent Dye in Microsatellites

Microsatellites are important genetic markers and have been broadly employed in many genetic studies. Currently, polymorphisms in microsatellites are often detected by an automated system of capillary electrophoresis with fluorescent dyes. In this situation, different dye combinations may cause pull-up/bleed-through problems, which introduce noise signals from one dye channel into another, causing genotyping errors. Here, we report the detection of such a problem at two microsatellite loci that used the HEX dye. Using three datasets, we tested for noise effects in four allele-scoring programmes: Genemapper, Genemarker, Gelquest and Fragman. We found that, because some allele sizes were identical or close to the size of one of the internal size standards, all four programmes gave allele size calling errors due to wrongly identifying pull-up signals as the internal size standard. In addition, because allele miscalling in this study was caused by the fluorescent dye that the microsatellites used introducing noise of the same colour as the internal size standard used, the pull-up correction function in Genemapper, Genemarker and Fragman failed to deal with this. Considering that pull-up peak scoring errors can occur with any dye colour, the phenomenon is not limited to the current HEX dye. Using different software and visual scoring of each result will allow accurate sizing of microsatellite alleles

Application of semiochemical releasers and intercropping to control aphid and related virus in east China

Peer reviewe

Decreased Blood Levels of Oxytocin in Ketamine-Dependent Patients During Early Abstinence

Background: Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, is a common drug of abuse worldwide. Existing evidence suggest a disruption of oxytocin system involves in the development of addiction. In this study, we aimed to investigate the role of oxytocin in ketamine addiction by measuring the blood oxytocin levels in ketamine-dependent (KD) patients.Methods: Sixty-five KD patients and 65 controls were enrolled. Fasting plasma levels of oxytocin were determined at baseline and 1 and 2 weeks after ketamine withdrawal. Ketamine use variables, Beck Depression Inventory, Beck Anxiety Inventory (BAI), Visual Analog Scale for craving, and Childhood Trauma Questionnaire-short form were assessed in KD patients.Results: KD patients had significantly lower levels of oxytocin at baseline compared to controls (5.89 ± 2.13 vs. 9.53 ± 4.17 ng/mL, P < 0.001). Oxytocin levels increased after one (6.74 ± 2.63, P < 0.002) and 2 weeks (6.89 ± 2.69, P = 0.01) of withdrawal in KD patient despite the levels were still lower than controls (P = 0.001 and 0.002, respectively). The clinical variables did not correlate with baseline oxytocin levels except BAI scores, which showed a negative correlation with the levels (r = −0.263; P = 0.039).Conclusion: We found a distinctively reduced oxytocin level in KD patients and the level did not normalize after early abstinence. Lower oxytocin might be associated with anxious phenotype of ketamine dependence. These results suggest that oxytocin system dysregulated following chronic ketamine abuse and might provide insight in evaluating the potential therapeutic use of oxytocin for treating ketamine dependence

The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites

Double-strand breaks (DSBs) are repaired through two major pathways, homology-directed recombination (HDR) and non-homologous end joining (NHEJ). While HDR can only occur in S/G2, NHEJ can happen in all cell cycle phases (except mitosis). How then is the repair choice made in S/G2 cells? Here we provide evidence demonstrating that APCCdh1 plays a critical role in choosing the repair pathways in S/G2 cells. Our results suggest that the default for all DSBs is to recruit 53BP1 and RIF1. BRCA1 is blocked from being recruited to broken ends because its recruitment signal, K63-linked poly-ubiquitin chains on histones, is actively destroyed by the deubiquitinating enzyme USP1. We show that the removal of USP1 depends on APCCdh1 and requires Chk1 activation known to be catalysed by ssDNA-RPA-ATR signalling at the ends designated for HDR, linking the status of end processing to RIF1 or BRCA1 recruitment.We thank S.-Y. Lin (MD Anderson Cancer Center) for cell lines; J. Rosen (Baylor College of Medicine) for reagents; H. Masai (Tokyo Metropolitan Institute of Medical Science) for U2OS-Fucci cell line; D. Durocher (University of Toronto) for HeLa-Fucci cell line; E. Citterio (Netherlands Cancer Institute) for GFP-USP3 construct; M.S.Y. Huen (The University of Hong Kong) for RNF168 antibody. This work was performed with facilities and instruments in the Imaging Core of National Center for Protein Science (Beijing), the Cytometry and Cell Sorting Core at Baylor College of Medicine with funding from the NIH (P30 AI036211, P30 CA125123 and S10 RR024574), the Integrated Microscopy Core at Baylor College of Medicine with funding from the NIH (HD007495, DK56338 and CA125123), and the John S. Dunn Gulf Coast Consortium for Chemical Genomics. We also thank other members of the Zhang lab for helpful discussion and support. This work was supported in part by an international collaboration grant (# 2013DFB30210) and a 973 Project grant (# 2013CB910300) from Chinese Minister of Science and Technology, in part by a Chinese National Natural Science Foundation grant (# 81171920), in part by a grant from The Committee of Science and Technology of Beijing Municipality, China (# Z141100000214015), and in part by NIH grants CA116097 and CA122623 to P.Z. J.J. is supported by grants from National Institutes of Health (R01GM102529) and the Welch Foundation (AU-1711). S.H. is supported by grants (# 81272488 and 81472795) from Chinese National Natural Science Foundation. Y.Z. is supported by grants from the National Natural Scientific Foundation of China (No. 81430055), Programs for Changjiang Scholars and Innovative Research Team in University (No. IRT_15R13).S

Return of 4U~1730--22 after 49 years silence: the peculiar burst properties of the 2021/2022 outbursts observed by Insight-HXMT

After in quiescence for 49 years, 4U~1730--22 became active and had two outbursts in 2021 \& 2022; ten thermonuclear X-ray bursts were detected with Insight-HXMT. Among them, the faintest burst showed a double-peaked profile, placing the source as the 5th accreting neutron star (NS) exhibiting double/triple-peaked type-I X-ray bursts; the other bursts showed photospheric radius expansion (PRE). The properties of double-peaked non-PRE burst indicate that it could be related to a stalled burning front. For the five bright PRE bursts, apart from the emission from the neutron star (NS) surface, we find the residuals both in the soft ($$10 keV) X-ray band. Time-resolved spectroscopy reveals that the excess can be attributed to an enhanced pre-burst/persistent emission or the Comptonization of the burst emission by the corona/boundary-layer. We find, the burst emission shows a rise until the photosphere touches down to the NS surface rather than the theoretical predicted constant Eddington luminosity. The shortage of the burst emission in the early rising phase is beyond the occlusion by the disk. We speculate that the findings above correspond to that the obscured part (not only the lower part) of the NS surface is exposed to the line of sight due to the evaporation of the obscured material by the burst emission, or the burst emission is anisotropic ($\xi>1$) in the burst early phase. In addition, based on the average flux of PRE bursts at their touch-down time, we derive a distance estimation as 10.4 kpc.Comment: arXiv admin note: substantial text overlap with arXiv:2208.13556; text overlap with arXiv:2208.1212

A neural network model for constructing endophenotypes of common complex diseases: an application to male young-onset hypertension microarray data

Motivation: Identification of disease-related genes using high-throughput microarray data is more difficult for complex diseases as compared with monogenic ones. We hypothesized that an endophenotype derived from transcriptional data is associated with a set of genes corresponding to a pathway cluster. We assumed that a complex disease is associated with multiple endophenotypes and can be induced by their up/downregulated gene expression patterns. Thus, a neural network model was adopted to simulate the gene–endophenotype–disease relationship in which endophenotypes were represented by hidden nodes

Structure of a putative NTP pyrophosphohydrolase: YP_001813558.1 from Exiguobacterium sibiricum 255-15.

The crystal structure of a putative NTPase, YP_001813558.1 from Exiguobacterium sibiricum 255-15 (PF09934, DUF2166) was determined to 1.78 Å resolution. YP_001813558.1 and its homologs (dimeric dUTPases, MazG proteins and HisE-encoded phosphoribosyl ATP pyrophosphohydrolases) form a superfamily of all-α-helical NTP pyrophosphatases. In dimeric dUTPase-like proteins, a central four-helix bundle forms the active site. However, in YP_001813558.1, an unexpected intertwined swapping of two of the helices that compose the conserved helix bundle results in a `linked dimer' that has not previously been observed for this family. Interestingly, despite this novel mode of dimerization, the metal-binding site for divalent cations, such as magnesium, that are essential for NTPase activity is still conserved. Furthermore, the active-site residues that are involved in sugar binding of the NTPs are also conserved when compared with other α-helical NTPases, but those that recognize the nucleotide bases are not conserved, suggesting a different substrate specificity