scholarly journals Comparison of Clinical Manifestations, Antimicrobial Susceptibility Patterns, and Mutations of Fluoroquinolone Target Genes between Elizabethkingia meningoseptica and Elizabethkingia anophelis Isolated in Taiwan

2018 ◽  
Vol 7 (12) ◽  
pp. 538 ◽  
Author(s):  
Jiun-Nong Lin ◽  
Chung-Hsu Lai ◽  
Chih-Hui Yang ◽  
Yi-Han Huang
Keyword(s):  
Ribosomal Rna ◽  
Target Gene ◽  
Target Genes ◽  
Clinical Manifestations ◽  
Gene Mutations ◽  
Clinical Microbiology Laboratory ◽  
Elizabethkingia Meningoseptica ◽  
Major Pathogens ◽  
Susceptibility Patterns ◽  
Multiple Antibiotics

Elizabethkingia meningoseptica and Elizabethkingia anophelis are two major pathogens in the genus Elizabethkingia. Studies have revealed that Elizabethkingia anophelis is frequently misidentified as E. meningoseptica. Therefore, our aim was to explore the clinical and molecular differences between these two species. The database of a clinical microbiology laboratory in a university-affiliated hospital of Taiwan was searched to identify patients with Elizabethkingia infections between January 2005 and June 2018. Species were reidentified using 16S ribosomal RNA gene sequencing. Twenty E. meningoseptica and 72 E. anophelis samples were collected from consecutive patients. E. meningoseptica was significantly more frequently isolated from the cerebrospinal fluid than was E. anophelis. The most susceptible antibiotic for all Elizabethkingia isolates was minocycline (91.3%), followed by levofloxacin (52.2%), tigecycline (23.9%), and piperacillin tazobactam (23.9%). Compared with E. anophelis, E. meningoseptica was significantly less susceptible to piperacillin tazobactam, minocycline, and levofloxacin. Regarding nonsynonymous substitutions in the quinolone-resistance determining regions of DNA gyrase, six sites were recognized in E. meningoseptica and one site was recognized in E. anophelis. E. meningoseptica had a significantly higher rate of fluoroquinolone target gene mutations than did E. anophelis. Because of less susceptibility to multiple antibiotics than E. anophelis, empirical antimicrobial therapy of E. meningoseptica should be more rigorous.

scholarly journals Differences in Clinical Manifestations, Antimicrobial Susceptibility Patterns, and Mutations of Fluoroquinolone Target Genes betweenChryseobacterium gleumandChryseobacterium indologenes

2019 ◽  
Vol 63 (5) ◽  
Author(s):  
Jiun-Nong Lin ◽  
Chung-Hsu Lai ◽  
Chih-Hui Yang ◽  
Yi-Han Huang
Keyword(s):  
Antimicrobial Susceptibility ◽  
Target Genes ◽  
Clinical Manifestations ◽  
Case Fatality ◽  
16S Rrna Gene Sequencing ◽  
Fluoroquinolone Resistance ◽  
Clinical Microbiology Laboratory ◽  
Rrna Gene ◽  
Content Type ◽  
Susceptibility Patterns

ABSTRACTChryseobacteriuminfections are uncommon, and previous studies have revealed thatChryseobacterium gleumis frequently misidentified asChryseobacterium indologenes. We aimed to explore the differences in clinical manifestations and antimicrobial susceptibility patterns betweenC. gleumandC. indologenes. The database of a clinical microbiology laboratory was searched to identify patients withChryseobacteriuminfections between 2005 and 2017. Species were reidentified using 16S rRNA gene sequencing, and patients withC. gleumandC. indologenesinfections were included in the study. A total of 42C. gleumand 84C. indologenesisolates were collected from consecutive patients. A significant increase inC. indologenesincidence was observed.C. gleumwas significantly more associated with bacteremia thanC. indologenes. Patients withC. gleuminfections had more comorbidities of malignancy and liver cirrhosis than those withC. indologenesinfections. The overall case fatality rate was 19.8%. Independent risk factors for mortality were female sex andC. indologenesinfection. These isolates were most susceptible to minocycline (73%), followed by trimethoprim-sulfamethoxazole (47.6%), tigecycline (34.1%), and levofloxacin (32.5%).C. gleumexhibited a significantly higher rate of susceptibility thanC. indologenesto piperacillin, piperacillin-tazobactam, ceftazidime, tigecycline, and levofloxacin. Alterations in DNA gyrase subunit A were identified to be associated with fluoroquinolone resistance inC. indologenes. No nonsynonymous substitutions were observed in the quinolone resistance-determining regions (QRDRs) ofC. gleum. Differences in epidemiology, clinical manifestations, and antimicrobial susceptibility patterns exist betweenC. gleumandC. indologenes. Additional investigations are needed to explore the significance of these differences.

scholarly journals Role of Active Efflux in Association with Target Gene Mutations in Fluoroquinolone Resistance in Clinical Isolates of Vibrio cholerae

2002 ◽  
Vol 46 (8) ◽  
pp. 2676-2678 ◽  
Author(s):  
Somesh Baranwal ◽  
Keya Dey ◽  
T. Ramamurthy ◽  
G. Balakrish Nair ◽  
Manikuntala Kundu
Keyword(s):  
Vibrio Cholerae ◽  
Target Gene ◽  
Target Genes ◽  
Gene Mutations ◽  
Proton Motive Force ◽  
Quinolone Resistance ◽  
Clinical Isolates ◽  
Fluoroquinolone Resistance ◽  
Active Efflux

ABSTRACT Quinolones are among the drugs of choice in the management of cholera caused by Vibrio cholerae. In this study, we demonstrate that, in addition to mutations detected in the target genes gyrA and parC, proton motive force-dependent efflux is involved in quinolone resistance in clinical isolates of V. cholerae.

scholarly journals Elizabethkingia Infections in Humans: From Genomics to Clinics

2019 ◽  
Vol 7 (9) ◽  
pp. 295 ◽  
Author(s):  
Jiun-Nong Lin ◽  
Chung-Hsu Lai ◽  
Chih-Hui Yang ◽  
Yi-Han Huang
Keyword(s):  
Target Gene ◽  
Gene Mutations ◽  
Housekeeping Gene ◽  
Molecular Techniques ◽  
Fluoroquinolone Resistance ◽  
Emerging Pathogens ◽  
Ionization Time ◽  
Flight Mass Spectrometry ◽  
Elizabethkingia Meningoseptica ◽  
Life Threatening

The genus Elizabethkingia has recently emerged as a cause of life-threatening infections in humans, particularly in immunocompromised patients. Several new species in the genus Elizabethkingia have been proposed in the last decade. Numerous studies have indicated that Elizabethkingia anophelis, rather than Elizabethkingia meningoseptica, is the most prevalent pathogen in this genus. Matrix-assisted laser desorption/ionization–time of flight mass spectrometry systems with an extended spectrum database could reliably identify E. anophelis and E. meningoseptica, but they are unable to distinguish the remaining species. Precise species identification relies on molecular techniques, such as housekeeping gene sequencing and whole-genome sequencing. These microorganisms are usually susceptible to minocycline but resistant to most β-lactams, β-lactam/β-lactam inhibitors, carbapenems, and aminoglycosides. They often exhibit variable susceptibility to piperacillin, piperacillin-tazobactam, fluoroquinolones, and trimethoprim-sulfamethoxazole. Accordingly, treatment should be guided by antimicrobial susceptibility testing. Target gene mutations are markedly associated with fluoroquinolone resistance. Knowledge on the genomic characteristics provides valuable insights into in these emerging pathogens.

scholarly journals Analysis of Mutation Spectra of 28 Pathogenic Genes Associated With Congenital Hypothyroidism in the Chinese Han Population

2021 ◽  
Vol 12 ◽  
Author(s):  
Miao Huang ◽  
Xiyan Lu ◽  
Guoqing Dong ◽  
Jianxu Li ◽  
Chengcong Chen ◽  
...  
Keyword(s):  
Congenital Hypothyroidism ◽  
Detection Rate ◽  
Target Genes ◽  
Clinical Manifestations ◽  
Gene Mutations ◽  
Compound Heterozygous ◽  
Chinese Han ◽  
High Detection Rate ◽  
Published Evidence ◽  
Pathogenic Genes

PurposeCongenital hypothyroidism (CH) is the most common neonatal endocrine disease; its early detection ensures successful treatment and prevents complications. However, its molecular etiology remains unclear.MethodsWe used second-generation sequencing to detect 28 pathogenic genes in 15 Chinese Han patients with CH in Shenzhen, China, and analyzed the genetic pattern of the pathogenic genes through their pedigrees. The pathogenicity assessment of gene mutations was performed based on the American College of Medical Genetics and Genomics (ACMG) classification guidelines, inheritance models, and published evidence.ResultsMutations in several target genes were identified in 14 of 15 patients (93.33%); these mutations were distributed in eight genes (DUOX2, DUOXA2, TPO, TG, TSHR, FOXE1, KDM6A, and POU1F1). DUOX2 exhibited the highest mutation frequency (44%, 11/25), followed by TPO (16%, 4/25) and TG (16%, 4/25). DUOX2 exhibited the highest biallelic mutation (7/15). Eight out of 25 variants verified by the ACMG guidelines were classified as pathogenic (P, category 1) or possibly pathogenic (LP, Type 2), namely six variants of DUOX2, and one variant of TPO and DUOXA2. Five new mutations were detected: one in DUOX2, which was located in the splicing region of mRNA (c.1575-1G>A), three new missense mutants, p.A291T, p.R169W, and p. S1237dup, and one new TPO missense variant c.2012G>T (p.W671L). The main criteria for determining the genotype–phenotype relationship were a diagnostic detection rate of 53.33% (8/15) and combination of three or more gene mutations.ConclusionsCH gene mutations in the population may be mainly manifested in genes influencing thyroid hormone synthesis, such as DUOX2 compound heterozygous mutations, which exhibited a high detection rate. The clinical manifestations are diverse, and mainly include transient CH. Therefore, genetic screening is recommended for CH patients to determine the correlation between clinical phenotypes and gene mutations, which will assist in clinical management.

Artificial microRNA (amiRNA) induced gene silencing in alfalfa (Medicago sativa)

Botany ◽  
2013 ◽  
Vol 91 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Julian C. Verdonk ◽  
Michael L. Sullivan
Keyword(s):  
Gene Silencing ◽  
Medicago Sativa ◽  
Target Gene ◽  
Target Genes ◽  
Mirna Precursor ◽  
Crop Species ◽  
Forage Crop ◽  
Ribonucleic Acids ◽  
Endogenous Gene ◽  
Medicago Sativa L

Gene silencing is a powerful technique that allows the study of the function of specific genes by selectively reducing their transcription. Several different approaches can be used, however they all have in common the artificial generation of single stranded small ribonucleic acids (RNAs) that are utilized by the endogenous gene silencing machinery of the organism. Artificial microRNAs (amiRNA) can be used to very specifically target genes for silencing because only a short sequence of 21 nucleotides of the gene of interest is used. Gene silencing via amiRNA has been developed for Arabidopsis thaliana (L.) Heynh. and rice using endogenous microRNA (miRNA) precursors and has been shown to also work effectively in other dicot species using the arabidopsis miRNA precursor. Here, we demonstrate that the arabidopsis miR319 precursor can be used to silence genes in the important forage crop species alfalfa (Medicago sativa L.) by silencing the expression of a transgenic beta-glucuronidase (GUSPlus) target gene.

scholarly journals CHOP-Dependent Stress-Inducible Expression of a Novel Form of Carbonic Anhydrase VI

1999 ◽  
Vol 19 (1) ◽  
pp. 495-504 ◽  
Author(s):  
John Sok ◽  
Xiao-Zhong Wang ◽  
Nikoleta Batchvarova ◽  
Masahiko Kuroda ◽  
Heather Harding ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Target Gene ◽  
Target Genes ◽  
Direct Evidence ◽  
Nuclear Protein ◽  
Intracellular Form ◽  
Carbonic Anhydrase Vi ◽  
Responsive Element

ABSTRACT CHOP (also called GADD153) is a stress-inducible nuclear protein that dimerizes with members of the C/EBP family of transcription factors and was initially identified as an inhibitor of C/EBP binding to classic C/EBP target genes. Subsequent experiments suggested a role for CHOP-C/EBP heterodimers in positively regulating gene expression; however, direct evidence that this is the case has so far not been uncovered. Here we describe the identification of a positively regulated direct CHOP-C/EBP target gene, that encoding murine carbonic anhydrase VI (CA-VI). The stress-inducible form of the gene is expressed from an internal promoter and encodes a novel intracellular form of what is normally a secreted protein. Stress-induced expression of CA-VI is both CHOP and C/EBPβ dependent in that it does not occur in cells deficient in either gene. A CHOP-responsive element was mapped to the inducibleCA-VI promoter, and in vitro footprinting revealed binding of CHOP-C/EBP heterodimers to that site. Rescue of CA-VIexpression in c/ebpβ−/− cells by exogenous C/EBPβ and a shorter, normally inhibitory isoform of the protein known as LIP suggests that the role of the C/EBP partner is limited to targeting the CHOP-containing heterodimer to the response element and points to a preeminent role for CHOP in CA-VI induction during stress.

scholarly journals Mutant Alleles of the Drosophila trithorax Gene Produce Common and Unusual Homeotic and Other Developmental Phenotypes

Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 319-344
Author(s):  
Thomas R Breen
Keyword(s):  
Target Gene ◽  
Target Genes ◽  
Protein Isoforms ◽  
Homeotic Genes ◽  
Set Domain ◽  
Human Homologue ◽  
Terminal Set ◽  
Hypomorphic Alleles ◽  
Different Levels ◽  
Target Gene Transcription

Abstract trithorax (trx) encodes chromosome-binding proteins required throughout embryogenesis and imaginal development for tissue- and cell-specific levels of transcription of many genes including homeotic genes of the ANT-C and BX-C. trx encodes two protein isoforms that contain conserved motifs including a C-terminal SET domain, central PHD fingers, an N-terminal DNA-binding homology, and two short motifs also found in the TRX human homologue, ALL1. As a first step to characterizing specific developmental functions of TRX, I examined phenotypes of 420 combinations of 21 trx alleles. Among these are 8 hypomorphic alleles that are sufficient for embryogenesis but provide different levels of trx function at homeotic genes in imaginal cells. One allele alters the N terminus of TRX, which severely impairs larval and imaginal growth. Hypomorphic alleles that alter different regions of TRX equivalently reduce function at affected genes, suggesting TRX interacts with common factors at different target genes. All hypomorphic alleles examined complement one another, suggesting cooperative TRX function at target genes. Comparative effects of hypomorphic genotypes support previous findings that TRX has tissue-specific interactions with other factors at each target gene. Some hypomorphic genotypes also produce phenotypes that suggest TRX may be a component of signal transduction pathways that provide tissue- and cell-specific levels of target gene transcription.

scholarly journals Novel missense mutation of SASH1 in a Chinese family with dyschromatosis universalis hereditaria

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Lu Cao ◽  
Ruixue Zhang ◽  
Liang Yong ◽  
Shirui Chen ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Missense Mutation ◽  
Sequence Alignment ◽  
Multiple Sequence Alignment ◽  
Molecular Genetic ◽  
Family Members ◽  
Clinical Manifestations ◽  
Gene Mutations ◽  
Mendelian Inheritance ◽  
Chinese Family ◽  
Multiple Sequence

Abstract Background Dyschromatosis universalis hereditaria (DUH) is a pigmentary dermatosis characterized by generalized mottled macules with hypopigmention and hyperpigmention. ABCB6 and SASH1 are recently reported pathogenic genes related to DUH, and the aim of this study was to identify the causative mutations in a Chinese family with DUH. Methods Sanger sequencing was performed to investigate the clinical manifestation and molecular genetic basis of these familial cases of DUH, bioinformatics tools and multiple sequence alignment were used to analyse the pathogenicity of mutations. Results A novel missense mutation, c.1529G>A, in the SASH1 gene was identified, and this mutation was not found in the National Center for Biotechnology Information Database of Short Genetic Variation, Online Mendelian Inheritance in Man, ClinVar, or 1000 Genomes Project databases. All in silico predictors suggested that the observed substitution mutation was deleterious. Furthermore, multiple sequence alignment of SASH1 revealed that the p.S510N mutation was highly conserved during evolution. In addition, we reviewed the previously reported DUH-related gene mutations in SASH1 and ABCB6. Conclusion Although the affected family members had identical mutations, differences in the clinical manifestations of these family members were observed, which reveals the complexity of the phenotype-influencing factors in DUH. Our findings reveal the mutation responsible for DUH in this family and broaden the mutational spectrum of the SASH1 gene.

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