Emergence in Taiwan of novel imipenem-resistant Acinetobacter baumannii ST455 causing bloodstream infection in critical patients

BackgroundAcinetobacter baumannii is one of the most important noscomial pathogens worldwide. The study aimed to use multilocus sequence typing (MLST) for epidemiological surveillance of A. baumannii isolates in Taiwan and analyze the clinical presentations and patients' outcomes.MethodsMLST according to both Bartual's PubMLST and Pasteur's MLST schemes was applied to characterize bloodstream imipenem-resistant A. baumannii (IRAB) infection in intensive care units in a medical center. A total of 39 clinical IRAB bloodstream isolates in 2010 were enrolled. We also collected 13 imipenem-susceptible A. baumannii bloodstream isolates and 30 clinical sputum isolates (24 IRAB and 6 imipenem-susceptible A. baumannii) for comparison. Clinical presentations and outcome of the patients were analyzed.ResultsWe found that infection by ST455B/ST2P and inappropriate initial therapy were statistically significant risk factors for mortality. More than one third of the IRAB isolates belonged to ST455B/ST2P. Most ST455B/ST2P (80%) carried ISAba1–blaOXA-23, including 10 (66.7%) with Tn2006 (ISAba1–blaOXA-23–ISAba1) in an AbaR4-type resistance island. ST455B/ST2P appears to evolve from ST208B/ST2P of clonal complex (CC) 92B/CC2P. In this hospital-based study, A. baumannii ST455 accounted for 38.5% of IRAB bacteremia, with a high mortality of 86.7%. Approximately 85% of ST455B/ST2P bacteremia had a primary source of ventilation-associated pneumonia.ConclusionWe report the emergence in Taiwan of IRAB ST455B/ST2P, which is the current predominant clone of IRAB in our hospital and has been causing bacteremia with high mortality in critical patients

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

Increasing Ceftriaxone Resistance in Salmonellae, Taiwan

In Taiwan, despite a substantial decline of Salmonella enterica serotype Choleraesuis infections, strains resistant to ciprofloxacin and ceftriaxone persist. A self-transferable blaCMY-2-harboring IncI1 plasmid was identified in S. enterica serotypes Choleraesuis, Typhimurium, Agona, and Enteritidis and contributed to the overall increase of ceftriaxone resistance in salmonellae

A Zinc Oxide Nanorod Ammonia Microsensor Integrated with a Readout Circuit on-a-Chip

A zinc oxide nanorod ammonia microsensor integrated with a readout circuit on-a-chip fabricated using the commercial 0.35 μm complementary metal oxide semiconductor (CMOS) process was investigated. The structure of the ammonia sensor is composed of a sensitive film and polysilicon electrodes. The ammonia sensor requires a post-process to etch the sacrificial layer, and to coat the sensitive film on the polysilicon electrodes. The sensitive film that is prepared by a hydrothermal method is made of zinc oxide. The sensor resistance changes when the sensitive film adsorbs or desorbs ammonia gas. The readout circuit is used to convert the sensor resistance into the voltage output. Experiments show that the ammonia sensor has a sensitivity of about 1.5 mV/ppm at room temperature

Clonal dissemination of the multi-drug resistant Salmonella enterica serovar Braenderup, but not the serovar Bareilly, of prevalent serogroup C1 Salmonella from Taiwan

<p>Abstract</p> <p>Background</p> <p>Nontyphoidal <it>Salmonella </it>is the main cause of human salmonellosis. In order to study the prevalent serogroups and serovars of clinical isolates in Taiwan, 8931 <it>Salmonellae </it>isolates were collected from 19 medical centers and district hospitals throughout the country from 2004 to 2007. The pulsed-field eletrophoresis types (PFGE) and antibiotic resistance profiles of <it>Salmonella enterica </it>serovars Bareilly (<it>S</it>. Bareilly) and Braenderup (<it>S</it>. Braenderup) were compared, and multi-drug resistance (MDR) plasmids were characterized.</p> <p>Results</p> <p>Over 95% of human salmonellosis in Taiwan was caused by five <it>Salmonella </it>serogroups: B, C1, C2-C3, D1, and E1. <it>S</it>. Typhymurium, <it>S</it>. Enteritidis, <it>S</it>. Stanley and <it>S</it>. Newport were the four most prevalent serovars, accounting for about 64% of isolates. While only one or two major serovars from four of the most prevalent serogroups were represented, four predominant serovars were found in serogroup C1 <it>Salmonellae</it>. The prevalence was decreasing for <it>S</it>. Choleraeuis and <it>S</it>. Braenderup, and S. Virchow and increasing for <it>S</it>. Bareilly. <it>S</it>. Braenderup mainly caused gastroenteritis in children; in contrast, <it>S</it>. Bareiley infected children and elderly people. Both serovars differed by <it>Xba</it>I-PFGE patterns. Almost all <it>S</it>. Bareilly isolates were susceptible to antibiotics of interest, while all lacked plasmids and belonged to one clone. Two distinct major clones in <it>S</it>. Braenderup were cluster A, mainly including MDR isolates with large MDR plasmid from North Taiwan, and cluster B, mainly containing susceptible isolates without R plasmid from South Taiwan. In cluster A, there were two types of conjugative R plasmids with sizes ranging from 75 to 130 kb. Type 1 plasmids consisted of replicons F1A/F1B, <it>bla</it>_TEM, IS<it>26</it>, and a class 1 integron with the genes <it>dfrA12</it>-<it>orfF</it>-<it>aadA2-qacE</it>Δ1-<it>sulI</it>. Type 2 plasmids belonged to incompatibility group Inc<it>I</it>, contained <it>tnpA</it>-<it>bla</it>_CMY-2-<it>blc</it>-<it>sugE </it>genetic structures and lacked both IS<it>26 </it>and class 1 integrons. Although type 2 plasmids showed higher conjugation capability, type 1 plasmids were the predominant plasmid.</p> <p>Conclusions</p> <p>Serogroups B, C1, C2-C3, D1, and E1 of <it>Salmonella </it>caused over 95% of human salmonellosis. Two prevalent serovars within serogroup C1, <it>S</it>. Bareilly and cluster B of S. Braenderup, were clonal and drug-susceptible. However, cluster A of <it>S</it>. Braenderup was MDR and probably derived from susceptible isolates by acquiring one of two distinct conjugative R plasmids.</p

Transcriptome Changes in Relation to Manic Episode

Bipolar disorder (BD) is highly heritable and well known for its recurrent manic and depressive episodes. The present study focused on manic episode in BD patients and aimed to investigate state-specific transcriptome alterations between acute episode and remission, including messenger RNAs (mRNAs), long noncoding RNAs (lncRNAs), and micro-RNAs (miRNAs), using microarray and RNA sequencing (RNA-Seq) platforms. BD patients were enrolled with clinical information, and peripheral blood samples collected at both acute and remission status spanning for at least 2 months were confirmed by follow-ups. Symptom severity was assessed by Young Mania Rating Scale. We enrolled six BD patients as the discovery samples and used the Affymetrix Human Transcriptome Array 2.0 to capture transcriptome data at the two time points. For replication, expression data from Gene Expression Omnibus that consisted of 11 BD patients were downloaded, and we performed a mega-analysis for microarray data of 17 patients. Moreover, we conducted RNA sequencing (RNA-Seq) in additional samples of 7 BD patients. To identify intraindividual differentially expressed genes (DEGs), we analyzed data using a linear model controlling for symptom severity. We found that noncoding genes were of majority among the top DEGs in microarray data. The expression fold change of coding genes among DEGs showed moderate to high correlations (∼0.5) across platforms. A number of lncRNAs and two miRNAs (MIR181B1 and MIR103A1) exhibited high levels of gene expression in the manic state. For coding genes, we reported that the taste function-related genes, including TAS2R5 and TAS2R3, may be mania state-specific markers. Additionally, four genes showed a nominal p-value of less than 0.05 in all our microarray data, mega-analysis, and RNA-Seq analysis. They were upregulated in the manic state and consisted of MS4A14, PYHIN1, UTRN, and DMXL2, and their gene expression patterns were further validated by quantitative real-time polymerase chain reaction (PCR) (qRT-PCR). We also performed weight gene coexpression network analysis to identify gene modules for manic episode. Genes in the mania-related modules were different from the susceptible loci of BD obtained from genome-wide association studies, and biological pathways in relation to these modules were mainly related to immune function, especially cytokine–cytokine receptor interaction. Results of the present study elucidated potential molecular targets and genomic networks that are involved in manic episode. Future studies are needed to further validate these biomarkers for their roles in the etiology of bipolar illness

Cobalt oxide nanosheet and CNT micro carbon monoxide sensor integrated with readout circuit on chip

100學年度研究獎補助論文[[abstract]]The study presents a micro carbon monoxide (CO) sensor integrated with a readout circuit-on-a-chip manufactured by the commercial 0.35 μm complementary metal oxide semiconductor (CMOS) process and a post-process. The sensing film of the sensor is a composite cobalt oxide nanosheet and carbon nanotube (CoOOH/CNT) film that is prepared by a precipitation-oxidation method. The structure of the CO sensor is composed of a polysilicon resistor and a sensing film. The sensor, which is of a resistive type, changes its resistance when the sensing film adsorbs or desorbs CO gas. The readout circuit is used to convert the sensor resistance into the voltage output. The post-processing of the sensor includes etching the sacrificial layers and coating the sensing film. The advantages of the sensor include room temperature operation, short response/recovery times and easy post-processing. Experimental results show that the sensitivity of the CO sensor is about 0.19 mV/ppm, and the response and recovery times are 23 s and 34 s for 200 ppm CO, respectively.[[incitationindex]]SCI[[booktype]]電子

Manufacture of a Polyaniline Nanofiber Ammonia Sensor Integrated with a Readout Circuit Using the CMOS-MEMS Technique

This study presents the fabrication of a polyaniline nanofiber ammonia sensor integrated with a readout circuit on a chip using the commercial 0.35 μm complementary metal oxide semiconductor (CMOS) process and a post-process. The micro ammonia sensor consists of a sensing resistor and an ammonia sensing film. Polyaniline prepared by a chemical polymerization method was adopted as the ammonia sensing film. The fabrication of the ammonia sensor needs a post-process to etch the sacrificial layers and to expose the sensing resistor, and then the ammonia sensing film is coated on the sensing resistor. The ammonia sensor, which is of resistive type, changes its resistance when the sensing film adsorbs or desorbs ammonia gas. A readout circuit is employed to convert the resistance of the ammonia sensor into the voltage output. Experimental results show that the sensitivity of the ammonia sensor is about 0.88 mV/ppm at room temperature