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In conclusion, the MCP-1 A-2518 G polymorphism correlates with an elevated risk of AD and increased MCP-1 serum levels. The interaction between the MCP-1 A-2518 G polymorphism and smoking contributes to the increased risk for AD in Chinese Han individuals.Heroin use disorder is a chronic relapsing brain disease containing multiple phenotypes. These phenotypes vary among heroin users and might be influenced by genetic factors. Single-nucleotide polymorphisms (SNPs) of catechol-O-methyltransferase (COMT) and alpha-1-adrenergic receptor (ADRA1A) genes are associated with heroin use disorder. However, it has not been clarified which phenotypes of heroin use disorder are related to these genes. To address this question, we recruited 801 unrelated heroin users and divided them into different subgroups according to four important phenotypes of heroin use disorder. Then 7 SNPs in the functional region of these genes were systematically screened and genotyped using a SNaPshot assay. We found that the A allele of ADRA1A rs1048101 was associated with a shorter duration of transition from first use to addiction. Subjects with the C allele of ADRA1A rs3808585 were more susceptible to memory impairment after heroin use disorder. Subjects with the G allele of COMT rs769224 were more likely to take a higher dose of heroin every day. Our study confirmed the association between polymorphisms of COMT and ADRA1A with those specific phenotypes of heroin use disorder, which will be instructive for the precise treatment of the disease.

Pseudomonas is a Gram-negative bacterial genus with numerous member species. In this study, using whole-genome sequencing, we characterized a novel Pseudomonas sp. strain TUM18999, isolated as a pathogen from a human patient.

The TUM18999 strain was isolated from a patient's burn wound. Minimum inhibitory concentrations (MICs) were determined using the broth microdilution method. The whole-genome sequence was obtained using Miseq and MinION, and we conducted phylogenetic analysis based on single nucleotide polymorphisms of the core genome.

Antimicrobial susceptibility testing revealed a high ceftazidime MIC (32 mg/L). Moreover, carbapenemase production was confirmed using the modified carbapenem inactivation method. We found that the complete genome of TUM18999 was 6,826,062 bp long, with 6175 coding sequences (CDS) and a DNA G+C content (non-plasmid) of 66.4 mol%. Consistent with the high similarities with the 16S rRNA sequences of P. otitidis MCC10330 (98.6%) and P. alcaligenes NBRC 14159 (99.2%), similarities (<90%) were also observed with the gyrB genes of both strains. The average nucleotide identities for P. alcaligenes NBRC 14159 and P. otitidis MCC10330 were also <90%. The core-genome single nucleotide polymorphism phylogenetic tree indicated that the TUM18999 strain was most closely related to P. otitidis MCC10330. In addition, the TUM18999 strain carried the novel gene, species-specific subclass B3 metallo-β-lactamase (MBL), and its similarities with P. alcaligenes metallo-β-lactamase-1 (PAM-1) and P. otitidis metallo-β-lactamase-1 (POM-1) were 90.24% and 73.14%, respectively.

We characterized the complete whole genome sequence of the novel Pseudomonas sp. TUM18999 carrying the novel gene species-specific subclass B3 MBL.

We characterized the complete whole genome sequence of the novel Pseudomonas sp. TUM18999 carrying the novel gene species-specific subclass B3 MBL.Working memory (WM) engagement produces pain inhibition. However, it remains unclear whether higher WM load increases this effect. The aim of this study was to investigate the interaction between WM load and pain inhibition by WM and examine the contribution of cerebrospinal mechanism. Thirty-eight healthy volunteers were assigned to one of 2 n-back groups for which WM load was different (2-back or 3-back). The experimental protocol comprised 5 counterbalanced conditions (0-back, n-back, pain, 0-back with pain, and n-back with pain). Pain and the nociceptive flexion reflex (NFR) were evoked by transcutaneous electrical stimulation of the sural nerve. Pain was significantly different between conditions, but not between n-back groups. Both the 0-back and n-back tasks reduced pain compared with pain alone, but the n-back task produced stronger pain inhibition compared with the 0-back task. see more NFR amplitude was significantly different between conditions but not between n-back groups. NFR was inhibited by the 0-back and n-back tasks, with no difference between the 2 tasks. These findings indicate that pain inhibition by WM is increased by WM load, but only to a certain point. NFR inhibition by WM suggests that inhibition of pain by WM depends, at least in part, on cerebrospinal mechanism. PERSPECTIVE This behavioral and electrophysiological study shows that engaging in a cognitive task reduces pain by decreasing spinal nociceptive transmission, depending on task difficulty. These findings may yield better nonpharmacological pain therapies based on individual differences in working memory performance and capacity as well as several factors that regulate working memory.Copy number variants (CNVs) and gene mutations are important for diagnosis and treatment of myeloid malignancies. In a routine clinical setting, somatic gene mutations are detected by targeted next-generation sequencing (NGS) assay, but CNVs are commonly detected by conventional chromosome analysis and fluorescence in situ hybridization (FISH). The aim of this proof-of-principle study was to investigate the feasibility of using targeted NGS to simultaneously detect both somatic mutations and CNVs. Herein, we sequenced 406 consecutive patients with myeloid malignancies by targeted NGS and performed a head-to-head comparison with the results from a myelodysplastic syndrome (MDS) FISH and conventional chromosome analysis to detect CNVs. Among 91 patients with abnormal MDS FISH results, the targeted NGS revealed all 120 CNVs detected by MDS FISH (including -5/5q-, -7/7q-, +8, and 20q-) and 193 extra CNVs detected by conventional chromosome analysis. The targeted NGS achieved 100% concordance with the MDS FISH. The lower limit of detection of MDS CNVs by the targeted NGS was generally 5% variant allele fraction for DNA, based on the lowest percentages of abnormal cells detected by MDS FISH in this study.