Jan 07, · 50+ videos Play all Mix - Mas Ricardo - Oxa After-Hours () YouTube DJ Mas Ricardo & DJ Noise -- Remember #2 Trance - Duration: Marc Jäger 46, views. OXA was more active than OXA against oxacillin, cloxacillin, and cefotaxime and had a higher k cat for cefotaxime. Once purified, however, OXA was less efficient (lower k cat /K m than OXA against all the β-lactams tested—even those to which it gave greater resistance than OXACited by: Mar 19, · Klebsiella pneumoniae strains producing extended-spectrum β-lactamases (ESBL) exhibit resistance to antibiotic classes. The production of ESBLs (TEM-1, TEM-2, SHV-1, OXA-1) results in resistance to ampicillin, ticarcillin, piperacillin and cephalosporins. High levels of β-lactamases leads to development of resistance to β-lactamase inhibitors. The present study deals with characterizing.
Kinetic studies. Nucleotide sequence accession number. Table 1. Open in a separate window. Table 2. Genetic support of bla OXA Genetic environment of bla OXA gene. Aktas Z. Chemotherapy 54 — [ PubMed ] [ Google Scholar ]. Aubert D. Benouda A. First detection of oxacillinase-mediated resistance to carbapenems in Klebsiella pneumoniae from Morocco.
Carattoli A. Identification of plasmids by PCR-based replicon typing. Methods 63 — [ PubMed ] [ Google Scholar ]. Agents Chemother. Spread of OXAencoding plasmid in Turkey and beyond. Clinical and Laboratory Standards Institute Performance standards for antimicrobial susceptibility testing. Couture F. Cuzon G. Agents 36 —93 [ PubMed ] [ Google Scholar ]. Docquier J. Girlich D. Goren M. Carbapenem-resistant Escherichia coli and Klebsiella pneumoniae isolates from Turkey with OXAlike carbapenemases and outer membrane protein loss.
Agents 31 — [ PubMed ] [ Google Scholar ]. Jarlier V. Karim A. FEMS Microbiol. Kieser T. Plasmid 12 —36 [ PubMed ] [ Google Scholar ]. Levast M. Matar G. Oxacillinase-mediated resistance to carbapenems in Klebsiella pneumoniae from Lebanon. Moquet O. Nazic H. Further identification of plasmid-mediated quinolone resistance determinant in Enterobacteriaceae in Turkey. Philippon L. Poirel L. Agent Chemother. Emergence of oxacillinase-mediated resistance to imipenem in Klebsiella pneumoniae.
Carbapenem resistance in Acinetobacter baumannii: mechanisms and epidemiology. Carbapenemases: molecular diversity and clinical consequences.
Future Microbiol. Toleman M. Support Center Support Center. These strains were confirmed as being A. Antibiotic susceptiblities of the A. The generation of imipenem-resistant mutants from the imipenem-susceptible A. Briefly, tubes containing antibiotic concentrations that were three doubling dilutions above and three doubling dilutions below the MIC were used. Mutants from the last subculturing tube were inoculated onto drug-free LB plates. Furthermore, in these strains, the outer membrane protein profiles were analyzed together with efflux pump function.
The antibiotics used for the Etest were amikacin, gentamicin, ceftazidime, cefotaxime, cefepime, aztreonam, piperacillin, piperacillin-tazobactam, imipenem, meropenem, ciprofloxacin, and trimethoprim-sulfamethoxazole.
Louis, MO in order to assess efflux pump function. The outer membrane fraction was prepared according to methods described previously by Molloy et al. The supernatant was added to an equal volume of ice-cold 0. The carbonate-treated membranes were collected by ultracentrifugation in a Beckman The protein concentration was determined using the Bradford method 3a. All samples were incubated for 5 min in a boiling water bath before they were subjected to electrophoresis.
The resolved proteins were visualized by silver staining. The procedure for 2-DE was done according to methods described previously by Molloy et al. Isoelectric focusing IEF was conducted for a total of 50, V h. Protein spots were visualized using silver staining. Spot differences were confirmed by three independent experiments. In order to identify specific proteins, tryptic in-gel digestion of the protein spots of interest was followed by tandem mass spectrometry performed as described previously by Kristensen et al.
To obtain the bla OXAlike gene from clinical strains of A. ISAB ab or imipenem-resistant A. These three PCR products were cloned, sequenced, and analyzed using the same procedure as described above for the cloning and sequencing of bla OXA When the cultures had reached an optical density at nm of 0.
The concentrations and the quality of the RNA in each sample were determined by measuring their absorbance at nm. The detection of A. Briefly, the reaction mixtures contained ng total RNA and appropriate amounts of reagents and primers.
Antibiotic susceptibility testing revealed that the 23 clinical A. The outer membrane proteins from 23 clinical strains of A. Based on the pulsed-field gel electrophoresis banding pattern using ApaI restriction enzyme digestion see Fig. The levels of expression of two spots, spots 1 and 2 near pI 7. These two spots from the 2-DE were cut out, washed, reduced, alkylated, digested in gel with trypsin, extracted from the gel, and subjected to peptide mass fingerprinting by tandem mass spectrometry.
The results revealed that these two spots were made up of peptides in reasonable agreement with predicted values for an OXAlike carbapenemase, with a relative molecular mass Overexpression of a kDa outer membrane protein band in imipenem-resistant clinical strains of A.
Lanes 1 to 9, ISAB ATCCab3, ab4, ab8, ab12, ab20, ab, ab, and ab, respectively; lanes 11 to 24, IRAB abh9, abh11, abh13, abh14, abh17, abh18, abh20, abh26, abh29,abh36, abh37, abh39, ab, and ab, respectively; lane 25, IIAB ab; and lane 10, molecular mass markers. The molecular masses of three protein markers are indicated in the left margin.
The arrows indicate the kDa protein band. The molecular masses of six protein markers are indicated in the left margin. The protein spots that were significantly changed are indicated by arrows.
These primers were designed based on an alignment of the nucleotide sequences of bla OXA and its closely related variants. The corresponding strain is indicated at the left of each line. Numbers on the top of each three-line group indicate the relative posi tions within the open reading frame.
Identity is indicated below the alignment by an asterisk. The bla OXA or bla OXAlike gene is present in all clinical strains tested, and therefore, we determined whether there were differences in gene expression at the mRNA level across the various A. As shown in Fig. This approach showed that the relative mRNA levels had increased by 5. Quantification of the transcript levels of the bla OXA genes from different clinical strains of A.
B Relative expression n -fold determined from data in A. The relative expression n -fold was measured against the expression level of ISAB strain ab3. The 17.12.1994 - OXA After Hours of the 16S rRNA gene was used as the internal control. Each bar represents the average value of three independent experiments, and the error bars represent the standard deviations. The three 1. Furthermore, a 1.
Lanes 3 to 10, ISAB strains ab3, ab4, ab8, ab12, ab20, 17.12.1994 - OXA After Hours, ab, ab, and ab; lane 11, IIAB strain ab; lanes 12 to 25, IRAB strain ab, ab, abh9, abh11, abh13, abh14, abh17, abh18, abh20, abh26, abh29,abh36, abh37, and abh Lane C represents a negative control no A.
Lane M represents DNA size markers, with molecular masses in kilodaltons indicated by the arrows in the left margin. The arrow in the right margin indicates a 1. The dashed areas represent the terminal inverted repeat sequences of IS Aba1. Susceptibilities of these three recombinant strains to imipenem were determined by Etest. Furthermore, 17.12.1994 - OXA After Hours resistance to imipenem increased by 7.
However, resistance to meropenem was not affected when the bla OXA gene from either strain ab or ab was introduced into E. Thus, the increased imipenem resistance effect of the OXA carbapenemase occurs not only in 17.12.1994 - OXA After Hours.
Effect of the introduction of the bla OXA gene from A. A TOP10 only. The imipenem susceptibility tests were determined by Etest. The expression of OXA carbapenemase was induced by the addition of 0.
The MICs are indicated by arrows. Multistep resistance selection with imipenem from two clinical strains of A. There are few studies that have examined drug resistance mediated by an efflux pump s.
They include the efflux system AdeABC, which has been identified as mediating multidrug resistance, and the efflux system AbeM, which has been suggested to be involved in drug resistance 1721 This result agrees with recent reports that have demonstrated that an OXAlike oxacillinase naturally occurs in A.
Like with another OXA class D beta-lactamase 8it may be possible to explain the resistance because a high level of OXA carbapenemase is able to convert the enzyme from a monomeric to a dimeric form; this form is more active in the bacterial periplasm. This would confer imipenem resistance to A. Like other recent reports, the up-regulation seems to have resulted from the presence of an upstream insertion sequence, IS Aba1 Fig.
Similar regulation by IS Aba1 has also been found for A. The successful expression in E. We also identified a C-to-G change at nucleotide positionwhich resulted in a leucine-to-valine change at amino acid residue of the OXA or OXAlike carbapenemase in several IRAB strains tested data not shown. However, the elevation of resistance in E. Thus, the cloned OXA enzyme from either strain shows carbapenemase activity that is able to confer reduced susceptibility to imipenem but not to meropenem.
This suggests that this beta-lactamase has hydrolytic activity specific to imipenem. This is supported by a previous result where the OXA carbapenemase a member of OXA family was shown to confer low levels of imipenem resistance to E.
Therefore, it is necessary to sequence more clinical strains 17.12.1994 - OXA After Hours determine the importance of the leucine-to-valine change at amino acid residue in IRAB strains isolated from Taiwan. If confirmed, the role of amino acid residue in carbapenemase activity would then need to be further studied because residue is not among the various known conserved motifs that have been predicted by multiple sequence alignment for class D beta-lactamase Furthermore, no changes in gene expression were detected either.
This suggests that this intrinsic gene is not induced by exposure to imipenem but that resistance is affected mainly by the presence of IS Aba1 upstream. In addition, there were no differences in the outer membrane protein profiles. However, we could not exclude the hypothesis that decreased drug permeability was associated with imipenem resistance, and this resistance mechanism is found quite often as a drug resistance mechanism in bacteria.
This suggests that an efflux mechanism is possibly involved in the imipenem and meropenem resistance of these selected mutants of A. Also, the results of this study confirm that this naturally occurring beta-lactamase plays an important role in A. Thus, it is necessary to identify the efflux pump sother than AdeB and AbeM, that may be affected and which, as a result, may be correlated with imipenem resistance in our clinical strains of A.
We also thank Ya-Luen Chen for assistance with preparation of manuscript. National Center for Biotechnology InformationU. Journal List Antimicrob Agents Chemother v. Antimicrob Agents Chemother. Published online Aug Wensi S. Author information Article notes Copyright and License information Disclaimer. Phone: Fax: E-mail: wt. This article has been cited by other articles in PMC. Associated Data Supplementary Materials [Supplemental material]. Abstract We investigated the mechanisms involved in imipenem resistance in 23 clinical strains of Acinetobacter baumannii.
TABLE 1. Open in a separate window. Multistep selection resistance. Antibiotics for susceptibility testing. Preparation of bacterial outer membrane. Peptide sequencing and protein identification. Plasmin plays a major role in halting the clotting process.
Normally, bleeding should be controlled by the time plasmin begins its fibrinolytic work. If it is not, the consequences can be significant. As early aspathologists noted that the last blood exiting from fatal gunshot wounds did not clot. The role of antifibrinolytics, like tranexamic acid, is to temporarily halt clot breakdown until bleeding can be surgically controlled and the patient adequately resuscitated. CRASH-2 studied a 20, trauma patients in hospitals across 40 countries.
When TXA was given within the first hour from time of injury, death due to hemorrhage reduced by one third. When give between one and three hours from injury, death rates dropped by one fifth.
Curiously, when given beyond the third hour, there was a 40 percent increase in hemorrhagic deaths. There were no differences in stroke, DVT deep venous thrombosis or PE pulmonary embolism between the two groups. The number needed to treat to save one life NNT was a rather high 67, considering the whole cohort only half of which actually required blood transfusion.
TXA also did not affect the transfusions actually needed between the two groups. Some of the findings, coupled with the study design, wide variability in trauma care between countries, many of them poor and underdeveloped, raise numerous questions and concerns about the study design and data collection. Regardless, the mere size of the study certainly suggested that TXA might have a prehospital role in reducing hemorrhagic mortality in trauma patients.
The TXA group had 6. They also had a higher incidence of blood clots, specifically DVT and PE but when adjusted for injury severity, this difference disappeared. The NNT was 7. Some of the limitations of MATTERs were its retrospective design, no standard protocol or dosing, no lab testing for fibrinolysis and no data on the timing of TXA administration.
The study did speak very strongly to the benefits of TXA in resuscitating severe battlefield injuries with hemorrhage. The PATCH Pre-hospital Anti-fibrinolytics for Traumatic Coagulopathy and Haemorrhage trial, currently under 17.12.1994 - OXA After Hours in Australia and New Zealand will specifically address some of the civilian and prehospital TXA administration questions and more closely examine long term patient outcomes. Tranexamic acid has multiple generic forms in the U.
Tablets come in milligram strength. A diluted mixture may be stored for up to 4 hours at room temperature, according to the manufacturer. IV TXA is compatible with dextrose, saline, electrolytes, amino acid, dextran and heparin solutions. It is incompatible with solutions containing penicillin. TXA crosses the blood-brain barrier, penetrates the eye and results in cerebrospinal fluid concentrations roughly 10 percent of plasma levels. Seizures have been reported from TXA, as have visual defects consisting of color blindness and visual loss.
Cardiac surgery studies suggest that moderate to high TXA doses significantly increase the risk of seizures. Visual defects, when reported, occurred in patients treated with TXA for several days or longer. Obviously, an antifibrinolytic agent such as TXA can result in clots. Venous and arterial blood clots thromboembolic events including DVT, PE and cerebral thrombosis stroke have been reported. Caution should be exercised when considering TXA for patients with a history of thrombotic events or a familial history of thrombosis.
As mentioned previously, dose adjustments are necessary in patients with renal impairment. Gastrointestinal side effects are the most commonly reported by patients receiving TXA and occur in 30 percent of people given more than 6 grams daily of TXA.
Other side effects are relatively rare less than 1 percent. Dizziness has been reported and is likely dose related or, in the case of intravenous administration, related to the speed of administration. Currently, there are only a handful of drugs reported to interact with tranexamic acid. Of these, three are worth noting for prehospital and emergency medicine providers.
Patients taking estrogens or progestins may have enhanced thrombogenic effects with TXA. Patients taking oral tretinoin, a chemotherapy agent used to treat leukemia may also have enhanced effects from TXA.
Note that tretinoin is also used as a topical cream for treatment of acne; it is the systemic oral form that interacts with TXA. Tranexamic acid in trauma: How should we use it? J Trauma Acute Care Surg. Ausset S, Glassberg E.
Oxa Andreasstrasse 70 CH Zürich Switzerland Tel: +41 (0)1 60 33 Fax: +41 (0)1 12 65 Mail: [email protected] The OXA β-lactamases were among the earliest β-lactamases detected; however, these molecular class D β-lactamases were originally relatively rare and always plasmid mediated. They had a substrate profile limited to the penicillins, but some became able to confer resistance to cephalosporins. From the s onwards, isolates of Acinetobacter baumannii that were resistant to the carbapenems. Explore releases from DJ Jumpin' Jack at Discogs. Shop for Vinyl, CDs and more from DJ Jumpin' Jack at the Discogs Marketplace.
LETTER. Reports of carbapenemase-producing Enterobacteriaceae (CPE) have increased dramatically in the past decade. OXA was first described in Turkey in , and outbreaks of OXAproducing Enterobacteriaceae have since been reported worldwide, including Ireland (3, 12, 16). Escherichia coli O25b:H4-ST is a very successful uropathogenic clonal group, and its close association with the.
OXA differed from OXA by a 4-amino-acid deletion (corresponding to Arg, Ile, Glu, and Pro in OXA, DBL numbering), corresponding to a lack of 12 nucleotides in the bla OXA gene (Fig. 1). In addition, it had a single amino acid substitution (Ser to Asp) at position DBL Dec 10, · Salary: Regular rate = Salary divided by the number of hours the salary is intended to compensate. If the regular hours are less than Add regular rate for each hour up to 40, then pay time and a half for hours over If the regular hours = Pay time and a half for hours over Exempt from Overtime in Oregon.
In Europe, OXAtype-producing Enterobacteriaceae (including variants OXA, OXA, OXA, OXA, OXA, OXA, OXA, OXA, OXA, etc.) have been found in many countries, often due to imports from endemic regions, and their regional spread was reported, for example, in Spain, France, Belgium, the UK, and Ireland (Poirel et.
LETTER. Reports of carbapenemase-producing Enterobacteriaceae (CPE) have increased dramatically in the past decade. OXA was first described in Turkey in , and outbreaks of OXAproducing Enterobacteriaceae have since been reported worldwide, including Ireland (3, 12, 16). Escherichia coli O25b:H4-ST is a very successful uropathogenic clonal group, and its close association with the. In Europe, OXAtype-producing Enterobacteriaceae (including variants OXA, OXA, OXA, OXA, OXA, OXA, OXA, OXA, OXA, etc.) have been found in many countries, often due to imports from endemic regions, and their regional spread was reported, for example, in Spain, France, Belgium, the UK, and Ireland (Poirel et.
Aug 27, · After the orientation was determined, ISAb-F3 (Table (Table2), 2), based on the 3′-end sequence of ISAba1, and OXA/IS-R were used with PCR to obtain a complete copy of the ISAba1 gene and part of the adjacent bla OXA /bla OXAlike gene from imipenem-intermediate A. baumannii (IIAB) ab, IRAB ab, and IRAB abh9.
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