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Abstract LGAD detectors on 300 μ m thick high resistivity p-type substrates were proposed for the first time by IMB-CNM-CSIC. They are customized Avalanche Photodiodes (APD) to obtain a high electric field region confined close to the reversed junction. Therefore, only electrons generated by an incident particle passing through the detector and drifting to the n+ contact, start the impact ionization process. Thus, the collected charge is multiplied. The basic difference between APDs and LGADs is the gain. LGADs have a moderate gain in order to avoid the inherent problems due to high multiplication: cross talk and high noise. In that way, the detector signal can be kept high without increasing the noise. These devices have been successfully fabricated and extensively characterized, before and after irradiation. Unfortunately, neutron and proton radiation cause the degradation of the gain and the creation of bulk traps, degrading the timing resolution. One way to reduce the radiation induced degradation is to minimize the substrate thickness, thus improving the timing resolution of LGAD detectors. Two technology approaches have been contemplated: the use of SOI (Silicon on insulator) substrates and Silicon to Silicon bonding substrates, both with a very thin active silicon layer of 50 μ m. As a consequence, drifting distances of generated electrons and holes are significantly reduced, resulting in a decrease in the number of electrons and holes trapped by radiation induced bulk defects. A new family of thin detectors, produced in 2 × 2 arrays prototypes, for the ATLAS experiment High Granularity Timing Detector (HGTD) is proposed. These detectors are suitable for timing applications with time resolution in the range of 30 ps at 20 °C. Optimization of the LGAD structures for the HGTD experiment and the detector experimental performances are presented and discussed. [ABSTRACT FROM AUTHOR]

Clinically significant NDM-1-producing Acinetobacter schindleri has not yet been described in the literature. We report the first case of bacteraemia due to an A. schindleri strain harbouring bla NDM-1 recovered from an immunocompromised patient. Our report reinforces the fact that NDM-1 can easily be acquired by Acinetobacter species. [ABSTRACT FROM AUTHOR]

This study investigated the mechanisms involved in reduced susceptibility to amoxycillin–clavulanic acid and the prevalence of enzymes compatible with inhibitor-resistant TEM (IRT) β-lactamases produced by Escherichia coli isolates from patients in north-eastern Spain. The resistance mechanisms of 158 strains showing resistance or intermediate resistance to amoxycillin–clavulanic acid among 1122 ampicillin-resistant clinical isolates of E. coli were assessed on the basis of their β-lactam resistance phenotypes. β-Lactamases produced by strains showing resistant phenotypes suggestive of inhibitor-resistant penicillinase production were characterised by their isoelectric point. Specific activity and the concentration of clavulanic acid required to inhibit β-lactamase activity by 50% (IC50) were determined in strains harbouring enzymes that focused at pI 5.2 or 5.4 in order to achieve presumptive identification of IRT β-lactamases. Resistance phenotypes were consistent with overproduction of TEM-1, TEM-2 or SHV-1 β-lactamases in 56 strains, with AmpC cephalosporinase hyperproduction in 46 strains, and with production of inhibitor-resistant penicillinases in 49 strains. Of the latter isolates, 17 produced moderately high or high levels of enzymes co-focusing with TEM-1, 17 produced enzymes co-focusing with OXA-1 ( n = 12) or with PSE-1 ( n = 5), either alone or in association with TEM-1, while only 15 produced enzymes with a phenotype characteristic of IRT β-lactamases. It was concluded that resistance to amoxycillin–clavulanic acid in E. coli isolates from this area was mainly associated with presumptive overproduction of TEM-1, TEM-2 or SHV-1 β-lactamases (46%) or of AmpC cephalosporinase (29%), while the occurrence of enzymes categorised as IRT β-lactamases was unusual (9.5%). [ABSTRACT FROM AUTHOR]

Abstract Ochrobactrum anthropi, a rare human pathogen, has been isolated predominantly from patients with catheter-related bacteraemia and rarely from other infections. In 2016, six cases of pseudo-bacteraemia caused by carbapenem-resistant O. anthropi isolates were recovered from an Argentinian hospital. The resistant phenotype exposed by the isolates caught our attention and led to an extensive epidemiologic investigation. Here we describe the characterization of a carbapenem-resistant O. anthropi outbreak whose probable cause was by contaminated collection tubes. The genome analysis of one strain revealed the presence of various resistant determinants. Among them, a metal-dependent hydrolase of the β-lactamase superfamily I, phnP, was found. Lately the recovery of unusual multidrug-resistant pathogens in the clinical setting has increased, thus emphasizing the need to implement standardized infection control practice and epidemiologic investigation to identify the real cause of hospital outbreaks. [ABSTRACT FROM AUTHOR]