广东省科技期刊编辑个性心理特征的分析

目的探索广东省科技期刊编辑的个性特征,为管理部门对其进行继续教育提供依据。方法2004年10月至2005年5月采用艾森克个性问卷(EPQ)和症状自评量表(SCL-90),对广东省65家科技期刊的编辑人员进行问卷调查,并进行统计学分析。结果共调查129名编辑人员,其SCL-90总分(123±39)、强迫症状、人际关系敏感、焦虑、敌对、恐怖、偏执因子评分均低于全国成人常模(P<0.05或P<0.01);心理症状阳性检出率为22.5%;男性的强迫症状、偏执因子评分高于女性(P<0.05);编辑组男、女性与成人常模组比较,EPQ中精神质因子(P)与神经质因子(N)得分较低,而内外向因子(E)与掩饰性因子(L)得分较高(P<0.05或P<0.01);EPQ中N因子是编辑心理健康的影响因素(P<0.01)。结论广东省科技期刊编辑总体心理健康状况较好,但少部分编辑存在心理问题,仍需对编辑群体加强编辑心理与心理健康方面的教育。     

Multimodal imaging in photic retinopathy

Letter to the Editor     

Letter to editor ‘Gastroenteropathy in gastric cancer patients concurrent with diabetes mellitus’

The present letter to the editor is related to the study titled “Diabetic gastroenteropathy: An underdiagnosed complication”. Diabetic gastroenteropathy contributes to a decline in quality of life. In addition, gastroenteropathy is generally observed in patients with concurrent gastric cancer and diabetes mellitus before surgery, and the occurrence of the symptoms might be due not only to cancer but also to the complications of diabetes mellitus.     

基于SF-36的学术期刊编辑生存质量初步调查及影响因素探析

【目的】 初步了解学术期刊编辑生存质量状况,并探析其可能的影响因素,为改善学术期刊编辑身心健康、促进期刊可持续发展提供参考。【方法】 基于SF-36健康调查量表,在问卷星网站创建《学术期刊编辑生存质量调查问卷》,并发送至多个期刊编辑QQ群和微信群,在线下载答卷后进行分析。【结果】 在SF-36量表的8个维度中,生理角色维度的得分最高,总体健康维度的得分最低,与常模一致;生理职能维度的得分高于常模,躯体疼痛和精神健康维度的得分低于常模。多因素分析结果表明,每周加班频次≥3次、男性、工作年限在0~<10年、无职务、未与家人同住,以及所在期刊未被《中文核心期刊要目总览(2017年版)》、中国科学引文数据库、《中国科技论文统计源期刊》中的任一种收录可能是编辑生存质量的关键影响因素。【结论】 学术期刊编辑生存质量状况总体与国内常模接近,男性、独居、编龄短、加班频次高、期刊未被任一国内核心数据库收录可能与学术期刊编辑生存质量相关。     

PER extended-spectrum β-lactamases originate from Pararheinheimera spp

To investigate the origin of PER extended-spectrum β-lactamases, publicly available sequence databases were searched for bla_PER-like genes. Three genomes from Pararheinheimera, a genus associated with water and soil environments, were found to carry bla_PER-like genes but lacked the ISCR1/ISPa12/ISPa13 insertion sequences commonly associated with bla_PER in clinical isolates. Sequence analysis revealed 78–96% nucleotide identity and conserved synteny between the clinical mobile genetic elements (MGEs) encoding bla_PER-1 and the bla_PER locus in the Pararheinheimera genomes. Notably, bla_PER genes were only identified in 3 of 21 Pararheinheimera and Rheinheimera genomes, whereas the genetic environment of bla_PER genes as found in clinical MGEs was conserved in all Pararheinheimera and Rheinheimera genomes. These findings indicate that bla_PER genes were likely acquired by a branch of the Pararheinheimera genus long before the antibiotic era. Later, bla_PER genes were mobilised, likely through the involvement of insertion sequences, from one or several Pararheinheimera species, allowing their dissemination into human pathogens.     

Expansion of KPC-producing Klebsiella pneumoniae with various mgrB mutations giving rise to colistin resistance: the role of ISL3 on plasmids

mcr-1 has been reported as the first plasmid-encoded gene conferring colistin resistance. In KPC-producing Klebsiella pneumoniae (KPC-KP), however, colistin resistance is rapidly emerging through other mechanisms. Resistance is frequently due to disruption of the mgrB gene by insertion sequences, e.g. ISL3. The aim of this study was to investigate the expansion of mgrB-mutated KPC-KP isolates. In addition, the localisation and targets of ISL3 sequences within the core and accessory genome of common KPC-KP lineages were identified. A total of 29 clinical K. pneumoniae isolates collected from Italian patients were randomly selected. Whole genome sequences were analysed for resistance genes, plasmids and insertion sequences. In addition, 27 colistin-resistant KPC-KP isolates from a previous study from Crete (Greece) were assessed. Clonal expansion of KPC-KP isolates with various mutations in mgrB among all lineages was observed. In two Italian MLST ST512 isolates and eight Greek ST258 isolates, an identical copy of ISL3 was inserted in mgrB nucleotide position 133. ISL3, a transposable restriction–modification system of 8154 nucleotides, was located on pKpQIL-like plasmids and may transpose into the chromosome. In four isolates, chromosomal integration of ISL3 in diverse inner membrane proteins other than mgrB was identified. Colistin resistance is most often explained by clonal expansion of isolates with mutated mgrB. pKpQIL-like plasmids, which are omnipresent in KPC-KP, carry insertion sequences such as ISL3 that have mgrB as a target hotspot for transposition. Transposition of insertion sequences from plasmids and subsequent clonal expansion may contribute to the emerging colistin resistance in KPC-KP.     

Genetic basis of chromosomally-encoded mcr-1 gene

Compared with plasmid-borne mcr-1, the occurrence of chromosomally-encoded mcr-1 is rare although it has been reported in several cases. This study aimed to investigate the genetic features of chromosomally-encoded mcr-1 among Escherichia coli strains as well as the potential genetic basis governing mobilisation of mcr-1 in bacterial chromosomes. The genome sequences of 16 E. coli strains containing a chromosomal mcr-1 gene were obtained and analysed. Phylogenetic and whole-genome sequencing (WGS) analysis demonstrated that mcr-1 was associated with four major types of genetic arrangements, namely ISApl1–mcr1–orf, Tn6330, complex Tn6330 and ΔTn6330 in chromosomes of genetically unrelated E. coli strains. The mcr-1-carrying mobile elements were shown to insert into the AT-rich region, which was also the case for ISApl1. Analysis of complete E. coli genome sequences showed that there were multiple copies of ISApl1 present in E. coli chromosomes that also carried mcr-1, whilst all mcr-1-negative chromosomes were absent of any copy of ISApl1, suggesting the strong association of ISApl1 and mcr-1. Insertion of ISApl1 into E. coli chromosomes may be a prerequisite for the insertion of mcr-1-carrying mobile elements. Insertion of mcr-1 into E. coli chromosomes would enable it to become intrinsically resistant, which is expected to become more prevalent. Policy on the prudent use of colistin both in veterinary and clinical settings should be imposed globally to further prevent dissemination of mcr-1 in E. coli and other bacterial pathogens.     

Insertion sequences in the CRISPR-Cas system regulate horizontal antimicrobial resistance gene transfer in Shigella strains

Multidrug-resistant (MDR) Shigella strains are an enormous threat to public health. Antimicrobial resistance genes are frequently located on plasmids, phages and integrons, which enter bacterial cells by horizontal gene transfer (HGT). CRISPR-Cas systems are adaptive prokaryotic immune systems in bacteria that confer resistance to foreign genetic material such as phages and other mobile genetic elements. However, this may come at a cost of inhibiting the acquisition of other beneficial genes through HGT. This study investigated how Shigella strains regulate the activity of the CRISPR-Cas system spontaneously when they require an exogenous gene necessary for survival. Insertion sequence (IS) elements were identified in cas genes, such as IS600 in cse2, ISSfl2 in cas6e and IS629 in cse1–cas3. The number of spacers in CRISPR-Cas arrays in strains containing an IS was less than that for strains with no IS. Interestingly, fewer spacers were also found in MDR Shigella isolates. Furthermore, an antimicrobial-resistant strain was constructed by electrotransformation of a resistance plasmid in order to detect changes in the CRISPR-Cas system. It was found that the cse2 gene had a new IS (IS600) in the antimicrobial-resistant strain. Bioinformatics analyses showed that the IS600 insertion hotspot was TGC-GGC in the cse2 gene, and the tertiary structure of the Cse2 protein was different with IS600. IS600 caused a five-order of magnitude decrease in relative expression of the cse2 gene. This study sheds mechanistic light on CRISPR-Cas-mediated HGT of antimicrobial resistance genes in Shigella spp. isolates.