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Muhammed H. Arikan Fatih Eroglu Volkan Eskizeybek Emine Feyza Sukur Mehmet Yildiz Hatice S. Sas 《Materials》2022,15(2)
Aerospace-grade composite parts can be manufactured using Vacuum Bag Only prepregs through an accurate process design. Quality in the desired part can be realized by following process modeling, process optimization, and validation, which strongly depend on a primary and systematic material characterization methodology of the prepreg system and material constitutive behavior. The present study introduces a systematic characterization approach of a Vacuum Bag Only prepreg by covering the relevant material properties in an integrated manner with the process mechanisms of fluid flow, consolidation, and heat transfer. The characterization recipe is practiced under the categories of (i) resin system, (ii) fiber architecture, and (iii) thermal behavior. First, empirical models are successively developed for the cure-kinetics, glass transition temperature, and viscosity for the resin system. Then, the fiber architecture of the uncured prepreg system is identified with X-ray tomography to obtain the air permeability. Finally, the thermal characteristics of the prepreg and its constituents are experimentally characterized by adopting a novel specimen preparation technique for the specific heat capacity and thermal conductivity. Thus, this systematic approach is designed to provide the material data to process modeling with the motivation of a robust and integrated Vacuum Bag Only process design. 相似文献
35.
Abstract – Aim: The aim of this study was to evaluate via a questionnaire the knowledge level of primary school teachers in Ankara, Turkey, regarding dental trauma; to inform them on the subject through a leaflet; and to evaluate the effectiveness of the leaflet by reapplying the questionnaire. Materials and methods: A questionnaire was distributed to 500 teachers in seven randomly selected primary schools. The questionnaire consisted of four different scenarios presented with photographs and a total of eight questions on crown fracture, lateral luxation, root fracture, and avulsion. After responding to the questionnaire, teachers were given a leaflet containing information about traumatic dental injuries and their emergency management. After 1 month, the same questionnaire was distributed, and the responses collected. Results: A total of 450 of 500 teachers responded to the questionnaire. Initial responses indicated the knowledge level of teachers to be quite low. Following the distribution of the information leaflet, the rate of correct answers increased for each of the individual questions, and the total scores for the questionnaire increased significantly (P = 0.0001). Conclusion: There is a clear need to inform teachers about traumatic dental injuries. The use of educational leaflets can be a successful and appropriate means of providing teachers with information. 相似文献
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Effectiveness of the STOPP/START (Screening Tool of Older Persons' potentially inappropriate Prescriptions/Screening Tool to Alert doctors to the Right Treatment) criteria: systematic review and meta‐analysis of randomized controlled studies 下载免费PDF全文
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Amélie Carr?r Laurent Poirel Mesut Yilmaz ?zay Arikan Akan Cilli Feriha Ga?lle Cuzon Ghassan Matar Patrick Honderlick Patrice Nordmann 《Antimicrobial agents and chemotherapy》2010,54(3):1369-1373
Eighteen carbapenem-resistant, OXA-48-positive enterobacterial isolates recovered from Turkey, Lebanon, Egypt, France, and Belgium were analyzed. In most isolates, similar 70-kb plasmids carrying the carbapenemase gene blaOXA-48 were identified. That gene was located within either transposon Tn1999 or transposon Tn1999.2, which was always inserted within the same gene. This work highlights the current plasmid-mediated dissemination of the OXA-48 carbapenemase worldwide.Carbapenem-hydrolyzing β-lactamases belonging to Ambler classes A, B, and D have been reported worldwide among Enterobacteriaceae (22). The extensive spread of Ambler class A carbapenemases of the KPC type highlights that carbapenemases may rapidly become threatening (17). Acquired class D ß-lactamases possessing carbapenemase properties have been reported previously, being identified mainly in Acinetobacter sp. (18, 21) and occasionally in Enterobacteriaceae. The chromosome-encoded oxacillinase OXA-23 was previously described for Proteus mirabilis (4), and the oxacillinase OXA-48 was first identified in a Klebsiella pneumoniae isolate from Turkey (20). Since then, several other OXA-48-producing isolates of various enterobacterial species (Citrobacter freundii and Escherichia coli) have been reported, mainly from Turkey (1, 6, 11, 16) but also from Belgium (8), from Lebanon (15), and more recently from the United Kingdom (14, 23a), India (3a), and Argentina (6a). So far, the blaOXA-48 gene has been found to be plasmid borne and located between two identical insertion sequences, IS1999, forming the composite transposon Tn1999 (3). We have analyzed here the genetic backgrounds associated with the blaOXA-48 gene among Enterobacteriaceae isolates collected from different countries.The study included 18 OXA-48-positive clinical isolates of K. pneumoniae (13 isolates), Enterobacter cloacae (2 isolates), Providencia rettgeri (1 isolate), C. freundii (1 isolate), and E. coli (1 isolate). Isolates were mainly from the Turkish cities Istanbul, Ankara, and Izmir (n = 14) (Table (Table1).1). Among the 13 K. pneumoniae isolates, at least Kp11978 (20) and KpB had been sources of nosocomial outbreaks (6). A single K. pneumoniae isolate (KpBEL) was recovered from Brussels, Belgium (8); another K. pneumoniae isolate (KpL) from Beirut, Lebanon (15); another K. pneumoniae isolate from the Bicêtre Hospital (KpBIC), Paris, France (this study); and another K. pneumoniae isolate from Gizah, Egypt (KpE) (8a). Samples were isolated from blood (KpI1, KpI2, KpB, and Enc1), urine (PR, KpBEL, KpL, Kp11978, and KpBIC), cerebrospinal fluid (Enc2), and catheter (KpE). Isolates from Belgium, France, Egypt, and Lebanon were from patients who did not report recent travel history.
Open in a separate windowaclav. acid, clavulanic acid.bKp, K. pneumoniae; Enc, E. cloacae; CF, C. freundii; PR, P. rettgeri; Ec, E. coli.Antibiotic susceptibility of the isolates was determined by the disk diffusion method (7). MICs of β-lactams were determined using Etest strips (AB bioMérieux, Solna, Sweden). All isolates were resistant to penicillins. Fourteen of the 18 isolates were resistant to carbapenems according to the CLSI guidelines (Table (Table1)1) (7). The four remaining isolates (KpBIC, KpE, Enc1, and Enc2) exhibited MICs of carbapenems remaining in the intermediate or in the susceptible range. Resistance to broad-spectrum cephalosporins was observed for most of the isolates. However, isolates Kp3A, Kp7A, KpBEL, KpL, and KpBIC remained susceptible to broad-spectrum cephalosporins (Table (Table1).1). All isolates were resistant to fluoroquinolones, except isolates Kp6A, Enc1, and Enc2. All isolates were resistant to aminoglycosides and sulfamethoxazole, except isolate CF, which remained susceptible to the latter antibiotic.Carbapenemase- and extended-spectrum-β-lactamase (ESBL)-encoding genes were identified by PCR experiments using previously designed primers (6, 8), followed by sequencing. Additional ESBL production was detected by synergy tests as described previously (12). Positive results for ESBL production were observed for isolates EcA, Enc1, Enc2, Kp4A, Kp5A, Kp6A, KpI-1, KpI-2, and KpE. Several ESBL determinants were identified, including CTX-M-15, SHV-5, SHV-2a, TEM-101, TEM-150, and VEB-1 (Table (Table11).Isolates belonging to the same species (13 K. pneumoniae isolates or two E. cloacae isolates) were compared by pulsed-field gel electrophoresis (PFGE) as described previously (6). Ten pulsotypes were identified among the 13 K. pneumoniae isolates. The two K. pneumoniae isolates from Izmir were clonally related, and the three K. pneumoniae isolates from Ankara (Kp4A, Kp5A, and Kp6A) shared very similar PFGE patterns. The two E. cloacae isolates recovered from Istanbul were not clonally related (Fig. (Fig.11).Open in a separate windowFIG. 1.Pulsed-field gel electrophoresis patterns of the 13 OXA-48-producing K. pneumoniae isolates and the two OXA-48-producing E. cloacae isolates. (A) Lane 1, Kp3A; lane 2, Kp4A; lane 3, Kp5A; lane 4, Kp6A; lane 5, Kp7A; lane 6, KpI-1; lane 7, KpI-2; lane 8, unrelated K. pneumoniae isolate (included as a comparative strain); lane 9, Enc1; lane 10, Enc2; lane 11, unrelated E. cloacae isolate (included as a comparative strain); lane M, molecular size marker. (B) Lane 1, Kp3A; lane 2, Kp11978; lane 3, Kp4A; lane 4, Kp7A; lane 5, KpI-1; lane 6, KpL; lane 7, KpB; lane 8, KpBEL; lane 9, KpE; lane 10, KpBIC; lane M, molecular size marker.Transferability of the blaOXA-48 gene was studied by conjugation experiments as described previously (6). When conjugation experiments failed, plasmid DNA extract was used for transformation as described previously (20). Transformants were selected on LB agar containing ticarcillin (50 μg/ml). Transconjugants and transformants with decreased susceptibility to carbapenems were obtained for all isolates (Table (Table1),1), and MICs for the transconjugants/transformants remained in the susceptible range. The E. coli transformant obtained from the P. rettgeri isolate exhibited reduced susceptibility to carbapenems associated with resistance to cefotaxime and ceftazidime.Plasmids were analyzed by using the Kieser technique (13). A 70-kb plasmid was identified in all transconjugants/transformants (data not shown). However, a 150-kb plasmid was identified in the blaOXA-48-positive transformant obtained with the PR isolate. The blaOXA-48 and blaTEM-101 genes were codetected on the same 150-kb plasmid, as confirmed by Southern blot hybridization as described previously (20) (data not shown), explaining the resistance to all β-lactams of the PR isolate and its transformant (Table (Table1).1). Plasmid restriction profiles were compared as described previously (10) (data not shown), and very similar restriction patterns (suggesting highly related structures) were obtained for all of the 70-kb plasmids but not for the 150-kb plasmid pPR.PCR mapping was used to assess the presence of insertion sequence IS1999 upstream of the blaOXA-48 gene, to confirm the presence of transposon Tn1999, and to identify the transposon insertion site for all of the OXA-48-positive isolates (3, 20). In all isolates, the blaOXA-48 gene was flanked by two copies of IS1999, as described previously (3). The prototype IS1999 located at the left extremity of transposon Tn1999 was identified in isolates Kp3A, Kp4A, Kp5A, Kp6A, Kp7A, CF, PR, Enc1, and Enc2. Insertion of IS1R into IS1999 as described for KpB (6) and giving rise to Tn1999.2 was identified for isolates EcA, KpBIC, KpI, KpL, KpBEL, and KpE (Fig. (Fig.2).2). In isolate Kp11978, transposon Tn1999 had been identified to be inserted into the tir gene, being functionally homologous to the F3 gene encoding the factor F involved in the plasmid replicative machinery (23). By use of a primer located upstream of Tn1999 inserted into the tir gene, insertion of Tn1999 at the same target site was evidenced in all of the blaOXA-48-positive plasmids except for the pPR plasmid (Fig. (Fig.2).2). Inverse PCR performed as described previously (3) was used for identifying the blaOXA-48-surrounding structures in isolate PR. Sequencing of the obtained amplicons indicated that Tn1999 had targeted a gene encoding a phosphoadenosine phosphosulfate reductase (ΔPPR).Open in a separate windowFIG. 2.Genetic environments of the blaOXA-48-carrying plasmids identified among the 18 OXA-48-positive Enterobacteriaceae isolates. (A) Structure described for pA-1, p3A, p4A, p5A, p6A, p7A, pCF, pEnc1, and pEnc2. (B) Structure of the 150-kb pPR plasmid. (C) Structure described for pBb, pI, pL, pBEL, pEcA, pBIC, and pE.Attempts to identify the incompatibility group of the 70-kb OXA-48-positive plasmids failed using a PCR-based replicon typing method as described previously (5). Since rep genes are often located close to the hot spots for resistance gene integration, cloning experiments were performed to study these plasmids further. A gene encoding phage replication protein P (RepP) was identified upstream of the blaOXA-48 gene. Primers specific for the repP gene were designed (RepPA, 5′-AATGGTTAACTTTGACTGTG-3′; RepPB, 5′-GCACGATTTAGAGGTCTAC-3′), and positive results were obtained for all 70-kb plasmids. Association of the repP gene with the blaOXA-48 gene on the 70-kb plasmid was confirmed by hybridization with a specific RepP probe (data not shown). However, the repP gene could not be detected on the 150-kb plasmid identified from isolate PR. Our study showed the spread of a blaOXA-48-carrying plasmid among different enterobacterial species, being identified first in Turkey and later in other European countries and in the Middle East. The present work indicates that dissemination of the blaOXA-48 gene is not driven by the dissemination of a single K. pneumoniae clone. Since the blaOXA-48-carrying plasmid confers by itself a low level of resistance to carbapenems, clinical laboratory detection of OXA-48-producing strains may be difficult. Since the reservoir of blaOXA-48 has been identified in the waterborne Gram-negative organism Shewanella oneidensis (19), it is likely that the process leading to the dissemination of this gene may be the consequence of a wide interspecies exchange. In addition, since plasmids belonging to the RepP group have been described among Pseudomonas sp., phytopathogenic Xanthomonas sp., and samples from soils and sludges (2, 9, 24), it may be hypothesized that the blaOXA-48 gene could also be identified in those species. This work underlines that besides class B (VIM and IMP) and class A (KPC) carbapenemases, the class D carbapenemase OXA-48 type might contribute significantly to carbapenem resistance in Enterobacteriaceae. 相似文献
TABLE 1.
MICs of β-lactams for the 18 isolates of Enterobacteriaceae and their transconjugants and/or transformants (pOXA-48) E. coli J53 and E. coli TOP10β-Lactam(s)a | MIC (μg/ml) of β-lactam forb: | MIC (μg/ml) of β-lactam forb: | ||||||||||||||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Kp11978 (Istanbul; OXA-48, SHV-2a, TEM-1) | E. coli J53(pA-1) | KpB (Istanbul; OXA-48, CTX-M-15) | E. coli J53(pBb) | Kp3A (Ankara; OXA-48) | E. coli J53(p3A) | Kp4A (Ankara; OXA-48, CTX- M-15), Kp5A (Ankara; OXA-48, SHV-5), Kp6A (Ankara; OXA-48, TEM-150) | E. coli J53(p4A, p5A, p6A) | Kp7A (Ankara; OXA-48) | E. coli J53(p7A) | KpI-1 and KpI-2 (Izmir; OXA- 48, CTX-M-15) | E. coli J53(pI-1, pI-2) | KpBIC (Paris; OXA-48) | E. coli TOP10(pBIC) | KpE (Gizah; OXA-48, CTX-M-15) | E. coli J53(pE) | KpBEL (Brussels; OXA-48) | E. coli J53(pBEL) | KpL (Beirut; OXA-48) | E. coli J53(pL) | PR (Izmir; OXA-48, TEM-101) | E. coli TOP10(pPR) | Enc1 (Istanbul; OXA-48, SHV-5) | E. coli J53(pEnc1) | Enc2 (Istanbul; OXA-48, SHV-2a) | E. coli J53(pEnc2) | CF (Istanbul; OXA-48, VEB-1) | E. coli J53(pCF) | EcA (Ankara; OXA-48, TEM-150) | E. coli J53(pEcA) | E. coli J53 | E. coli TOP10 | |
Imipenem | 64 | 2 | 16 | 0.5 | >32 | 0.75 | >32 | 0.38 | >32 | 0.75 | 24 | 0.5 | 0.5 | 0.5 | 2 | 2 | 0.75 | 0.75 | >16 | 4 | >32 | 1.5 | 0.5 | 0.5 | 0.75 | 0.75 | >32 | 0.75 | 24 | 0.75 | 0.06 | 0.06 |
Ertapenem | 64 | 0.19 | >32 | 0.25 | >32 | 0.25 | >32 | 0.12 | >32 | 0.19 | 24 | 0.25 | 2 | 0.5 | 3 | 3 | 4 | 2 | >16 | 4 | >32 | 0.75 | 0.5 | 0.125 | 0.75 | 0.19 | >32 | 0.25 | >32 | 0.25 | 0.06 | 0.06 |
Meropenem | 64 | 0.25 | 32 | 0.12 | >32 | 0.12 | >32 | 0.094 | >32 | 0.12 | 16 | 0.094 | 0.5 | 0.5 | 2 | 2 | 0.5 | 0.5 | >16 | 0,19 | >32 | 0.25 | 0.5 | 0.094 | 0.75 | 0.12 | >32 | 0.12 | 24 | 0.19 | 0.06 | 0.06 |
Amoxicillin | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | >256 | >256 | >256 | >256 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | 4 | 4 |
Amoxicillin + clav. acid | >512 | 128 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | >256 | >256 | >256 | >256 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | 4 | 4 |
Ticarcillin | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | >256 | >256 | >256 | >256 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | 2 | 4 |
Ticarcillin + clav. acid | >512 | 128 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | >256 | >256 | >256 | >256 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | >256 | 2 | 4 |
Piperacillin | >512 | 8 | >512 | >512 | >512 | 512 | >512 | >512 | >512 | >512 | >512 | 512 | >512 | >512 | >512 | 512 | >256 | 128 | 96 | 64 | >256 | 128 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | 128 | 1 | 2 |
Piperacillin + tazobactam | 512 | 4 | >512 | >512 | >512 | 512 | >512 | >512 | >512 | >512 | >512 | 512 | >512 | >512 | >512 | 512 | >256 | 128 | 96 | 64 | >256 | 128 | >512 | >512 | >512 | >512 | >512 | >512 | >256 | 128 | 1 | 2 |
Cephalotin | >512 | 0.5 | >512 | 16 | >512 | 16 | >512 | 16 | >512 | 16 | >512 | 16 | >512 | 16 | >512 | 16 | 16 | 16 | 32 | 8 | >512 | 16 | >512 | 16 | >512 | 16 | >512 | >512 | >512 | 16 | 4 | 4 |
Cefotaxime | 64 | 0.06 | >512 | 0.5 | 1 | 0.5 | 64 | 0.12 | 0.5 | 0.5 | 64 | 0.12 | 0.5 | 0.5 | 64 | 0.12 | 0.12 | 0.12 | 1.5 | 0.25 | 64 | 32 | >512 | 0.25 | 512 | 0.25 | 64 | 0.12 | 64 | 0.12 | 0.06 | 0.06 |
Ceftazidime | 512 | 0.12 | >512 | 1 | 0.25 | 0.25 | 512 | 0.12 | 0.12 | 0.12 | 512 | 0.12 | 0.12 | 0.12 | 512 | 0.12 | 1 | 0.75 | 0.75 | 0.75 | 512 | 512 | >512 | 0.75 | 32 | 0.75 | 512 | 0.75 | 512 | 0.75 | 0.06 | 0.06 |
Cefepime | 32 | 0.06 | >512 | <0.5 | 0.5 | 0.12 | 32 | 0.12 | 0.5 | 0.5 | 32 | 0.12 | 0.5 | 0.5 | 32 | 0.12 | 0.12 | 0.12 | 0.12 | 0.06 | 32 | 0.5 | 4 | 0.12 | 32 | 0.12 | 32 | 0.12 | 32 | 0.12 | 0.03 | 0.06 |
Aztreonam | 512 | 0.06 | >512 | <0.12 | 0.06 | 0.06 | 512 | 0.06 | 0.06 | 0.06 | 512 | 0.06 | 0.06 | 0.06 | 512 | 0.06 | 0.06 | 0.06 | 0.06 | 0.06 | 512 | 0.06 | >512 | 0.06 | 512 | 0.06 | 512 | 0.06 | 512 | 0.06 | 0.03 | 0.06 |
Cefoxitin | 128 | 2 | 128 | 4 | 2 | 2 | 128 | 2 | 128 | 2 | 128 | 2 | 128 | 2 | 128 | 2 | 2 | 2 | 8 | 2 | 128 | 4 | >512 | 2 | 512 | 2 | 128 | 2 | 128 | 2 | 2 | 4 |
39.
Phylogenetic analysis of human G9P[8] rotavirus strains circulating in Jiangsu,China between 2010 and 2016 下载免费PDF全文
Cheng Xu MD Jianguang Fu DC Jing Ai MD Jun Zhang MD Cheng Liu BD Xiang Huo MD Changjun Bao MD Yefei Zhu DM 《Journal of medical virology》2018,90(9):1461-1470
Rotavirus A (RVA) is the leading cause of acute viral gastroenteritis in children under 5 years of age worldwide. G9P[8] is a common RVA genotype that has been persistently prevalent in Jiangsu, China. To determine the genetic diversity of G9P[8] RVAs, 7 representative G9P[8] strains collected from Suzhou Children’s Hospital between 2010 and 2016 (named JS2010‐JS2016) were analyzed through whole‐genome sequencing. All evaluated strains showed the Wa‐like constellation G9‐P[8]‐I1‐R1‐C1‐M1‐A1‐N1‐T1‐E1‐H1. Furthermore, phylogenetic analysis revealed that the VP7 genes of all strains clustered into lineage G9‐III and G9‐VI. With the exception of strain JS2012 (P[8]‐4), the VP4 sequences of all strains belonged to the P[8]‐3 lineage. Sequencing further revealed that amino acid substitutions were present in the antigenic regions of the VP7 and VP4 genes of all strains. Moreover, there were multiple substitutions in antigenic sites I and II of the nonstructural protein 4 (NSP4) genes, whereas the other NSP genes were relatively conserved. In conclusion, our phylogenetic analysis of these 7 G9P[8] strains suggests that RVA varied across regions and time. Therefore, our findings suggest that continued surveillance is necessary to explore the molecular evolutionary characteristics of RVA for better prevention and treatment of acute viral gastroenteritis. 相似文献
40.
Mendilcioglu I Bilgen T Arikan Y Keser I Simsek M Timuragaoglu A 《Archives of gynecology and obstetrics》2011,284(4):837-841