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Extended spectrum β-lactamases (ESBL)-producing Escherichia coli have been found in healthy individuals in Indonesia and Vietnam. The ISEcp1-bla CTX-M transposition unit of ESBL-producing bacterial isolates has been considered responsible for the production of CTX-M type ESBL and is important for the dissemination of bla CTX-M . This study aimed to characterize the upstream genetic structure (UGS) of E. coli isolates possessing bla CTX-M-1 group and/or bla CTX-M-9 group genes obtained from healthy individuals in Indonesia and Vietnam. A total of 501 CTX-M type ESBL-producing E. coli isolates possessing bla CTX-M-1 group and/or bla CTX-M-9 group genes were obtained from healthy individuals of the two countries in 2018. UGSs of the ISEcp1-bla CTX-M transposition unit of the 501 ESBL-producing E. coli isolates were amplified by barcode-adaptor-ligation-mediated PCR and analyzed using the Nanopore sequencer. The obtained sequence information was used to classify the UGSs of the ISEcp1-bla CTX-M transposition unit. From the 501 ESBL-producing E. coli isolates, 502 UGSs were obtained, which were classified into 85 UGS types based on the sequence. ISEcp1 of 359 (71.5%) of the 502 UGSs was disrupted by gene insertion, and ISEcp1-bla CTX-M transposition unit of most (87.1%) of the determined UGSs was confirmed as plasmidic. Only 6 (7.1%) of the 85 UGS types were common to both countries. Our results indicated that many different UGSs of ISEcp1-bla CTX-M transposition units were detected in Indonesia and Vietnam; hence, we suggest that structurally different kinds of plasmids harboring bla CTX-M were separately distributed in the two countries. This article is protected by copyright. All rights reserved.

Prior studies on chief executive officer (CEO) compensation focus mainly on large firms. This paper aims to suggest new factors associated with CEO compensation for small, homogeneous firms, specifically, Australian early‐stage mining exploration entities (MEEs). We document a set of predictors of CEO compensation proxying for economic performance, including geological prospectivity components of the exploration and evaluation (E&E) asset account and proceeds from equity raisings that enhances survival probabilities. We find positive associations between these predictors and CEO remuneration. In terms of CEO pay mix, we find that E&E asset acquisitions and equity proceeds are both positively associated with the proportion of option value in CEO total compensation. This suggests MEEs allocate their cash resources to investment opportunities, rather than CEO compensation. Overall, these findings, coupled with a significant and positive pay‐performance relation, provide evidence supporting efficient compensation practices in the MEE context.

This literature review aimed to provide a narrative review of evidence on validity of clinical and microbial indicators of infection and to gain insights into the diagnosis of infection in chronic leg ulcers (CLUs). A search was conducted in Cinahl, Medline, the Cochrane Library databases, Embase, Web of Science, ScienceDirect, Pubmed, PsycINFO, ProQuest dissertations, and Google Scholar from January 1990 to July 2017. The inclusion criteria were original studies, systematic reviews, and consensus documents focused on "infection" in CLUs, English language, clinical and community settings, and human. The reviewed studies were inconsistent in criteria for infection between investigated wound types and lack of specificity regarding wound types. There were few studies investigating the criteria for diagnosis of infection in leg ulcers. The identification of leg ulcer infection still remains problematic and relies on out-of-date and not uniform evidence. Literature in this area was mostly limited to level III and IV evidence based on The Australian National Health and Medical Research Council Levels of Evidence, or expert opinion. This literature review showed seven clinical signs and symptoms that could be diagnostic for infection in CLUs, including: new, increased, or altered ulcer pain; malodour; increased ulcer area; wound breakdown, delayed or non-healing; and erythema and increased local temperature, whilst the microbial indicators used to diagnose infected leg ulcers were varied and regarded as less important.

© 2017 International Council of Nurses Aim: To identify the practice patterns of the Australian registered nurse workforce according to position title and to map these disparate titles across all jurisdictions of the country. Introduction: Effective nursing workforce planning can contribute to improved patient care and increased effectiveness and efficiency of healthcare systems. Background: The prevailing approach to nursing workforce planning focuses on number of nursing staff needed in relation to the number of patients. The level of expertise and skill mix of registered nurses as a variable in workforce planning is rarely considered. Methods: A national cross-sectional electronic survey of registered nurses in Australia was conducted using the validated Advanced Practice Role Delineation tool developed from the Strong Model of Advanced Practice. The study involved a sample of 5599 registered nurses. Results: Sixty-six nursing position titles nationally were mapped using cluster analysis technique and gave rise to seven clusters of equivalent Australian jurisdictional nursing position titles and practice profiles. Discussion: Effective workforce policy and planning is reliant upon access to reliable evidence. This research is an international first in that it has provided comprehensive knowledge of the clinical level and practice profiles of a national nursing workforce. Implications for nursing policy: Effective, patient-centred workforce planning must consider both the numerical and expertise mix of a nursing workforce. This research provides Australian health service and policy planners with evidence-base knowledge of the nursing workforce. Internationally, this research establishes a platform from which to develop validated tools and established processes to support replication of this research.

Maternal death is one of the highest causes of global mortality. Governments have long used regulation to improve maternal health but concurrent fiscal-decentralisation reforms can undermine clinical performance. This article focuses on public Vietnamese hospitals to explore how regulatory compliance is pursued in decentralised health facilities, since Vietnam has seen increasing autonomisation of public hospitals in the last decade while simultaneously experiencing marked reductions in the maternal mortality ratio. Our analysis suggests that autonomisation has allowed regional regulatory regimes to emerge and that regulatory compliance must compete with other priorities. Compliance can therefore be rethought as a negotiation having implications for how government and maternal health advocates persuade self-sufficient hospitals to take on wider health-system goals.

B lymphocytes partially contribute to autoimmune type 1 diabetes (T1D) as a subset of APC with a preferential ability to trigger pathogenic CD4 T cells. We hypothesized that this resulted from the unique ability of B lymphocytes to take up pancreatic beta cell proteins through Ig mediated capture. T1D was significantly delayed, but not prevented, in a NOD stock in which the B lymphocyte Ig repertoire was strongly restricted because of the allelic exclusion induced by transgenic Ig molecules specific for the disease irrelevant hen egg lysozyme (HEL) protein (NOD.IgHEL mice). However, introducing the Ig(mu)null mutation to eliminate the small residual numbers of non-transgenic B lymphocytes in the NOD.IgHEL stock strongly suppressed T1D to the same low levels that characterize B lymphocyte deficient NOD.Ig(mu)null mice. In contrast to standard NOD mice, both the NOD.IgHEL.Ig(mu)null and NOD.Ig(mu)null stocks were unable to generate T cell responses against the candidate diabetes autoantigen, glutamic acid decarboxylase. These results indicate that Ig-mediated capture of beta cell autoantigens accounts for why B lymphocytes have a greater capacity than other APC subtypes to trigger diabetogenic T cells. Hence, defects in B lymphocyte, as well as T lymphocyte, tolerance induction mechanisms may contribute to T1D in NOD mice.