bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bridging the gap
Authors: Goddard Maria , Kasteridis Panagiotis , Jacobs Rowena , Santos Rita , Mason Anne 
Published: March 2016

Purpose
– The purpose of this paper is to explore the link between one aspect of primary care in England – the annual review by general practitioners for dementia patients – and length of hospital stay (LoS). The annual review should identify the needs of both patients and carers and co-ordinate services across health and social care to address those needs. If this is done well, timely discharge from hospital may be facilitated.

Design/methodology/approach
– The study uses linked national data from 2006/2007 to 2010/2011 on over 36,000 patients, employing sophisticated statistical techniques to isolate the effect of the annual dementia review on LoS.

Findings
– Hospital patients discharged to the community have significantly shorter stays if they are cared for by practices that reviewed a higher percentage of their patients with dementia. However, this effect is small and is not evident for patients discharged to care homes or who died in hospital. Longer LoS is associated with a range of co-morbidities, markers of low availability of social care and with intensive provision of informal care.

Practical implications
– Although the dementia review has only a modest effect on LoS, the components of the review could improve the health and well-being of those with dementia and their carers.

Originality/value
– The study is the first to employ a robust methodology to investigate the impact of the annual dementia review on hospital LoS, an important aspect of the interface between primary and secondary care. There are implications for clinical and financial aspects of health and social care policy.
Option replication and the performance of a market timer
Authors: Hübner Georges 
Published: March 2016

Purpose
– The Treynor and Mazuy framework is a widely used return-based model of market timing. However, existing corrections to the regression intercept can be manipulated through derivatives trading. Because they are conceptually flawed, these corrections produce biased performance measures. This paper aims to get back to Henriksson and Merton’s initial idea of option replication to overcome this issue and adapt the market timing model to various kinds of trading strategies and return-generating processes.

Design/methodology/approach
– This paper proposes a theoretical adjustment based on Merton’s option replication approach adapted to the Treynor and Mazuy specification. The linear and quadratic coefficients of the regression are exploited to assess the cost of the replicating option that yields similar convexity for a passive portfolio. A similar reasoning applies for various timing patterns and in multi-factor models.

Findings
– The proposed framework induces a potential rebalancing risk and involves the delicate issue of choosing the cheapest option. This paper shows that these issues can be overcome for reasonable tolerance levels. The option replication approach is a workable approach for practical applications.

Originality/value
– The adaptation of Merton’s reasoning to the Treynor and Mazuy model has surprisingly never been proposed so far. This paper has the potential to correct for a pervasive bias in the estimation of the performance of a market timer in the context of this very popular quadratic regression setup. Because of the power of the option replication approach, the reasoning is shown to be applicable to multi-factor models, negative timing and market neutral strategies. This paper could fuel empirical studies that would shed new light on the genuine market timing skills of active portfolio managers.
Mergers and acquisitions: a review. Part 1
Authors: Yaghoubi Reza , Yaghoubi Mona , Locke Stuart , Gibb Jenny 
Published: March 2016

Purpose– This paper aims to review the relevant literature on mergers and acquisitions in an attempt to provide a comprehensive account of what we know about mergers and which parts of the puzzle are still incomplete.Design/methodology/approach– This literature review consists of three key sections. The first part of this paper summarises the literature on the cyclical nature of mergers referred to in the literature as merger waves. The second section reviews the causes and consequences of takeovers; it first reviews the causes, or drivers, of acquisitions, while focusing on the fact that acquisitions happen in waves and then reviews the consequences of takeovers, with a predominant focus on the impacts of mergers on the economic performance of acquirers. The third part of the review summarises the theories as well as previous empirical studies on determinants of announcement returns and post-acquisition performance of combined firms.Findings– Merger activity demonstrates a wavy pattern, i.e. mergers are clustered in industries through time. The causes suggested for this fluctuating pattern include industry and economy-level shocks, mis-valuation and managerial herding. Market reaction to announcement of acquisitions is, on average, slightly negative for acquirer stocks and significantly positive for target stocks. The combined abnormal return is positive. These findings have been consistent over several decades of investigation. The prior research also identifies a number of factors that are related to performance of acquisitions. These factors are categorised and reviewed in five different groups: acquirer characteristics, target characteristics, bid characteristics, industry characteristics and macro-environment characteristics.Originality/value– This review illustrates a number of issues. Prior research is heavily biased towards gains to acquirers and factors that affect these gains. It is also biased towards finding sources of value creation through mergers, despite the fact that several theories suggest that mergers can be value-destroying. In fact, value destruction is often attributed to managers’ self-interest (agency problem) and mistakes (hubris). However, the mechanisms through which mergers destroy value are rarely addressed. Aside from that, the possibility of simultaneous creation and destruction of value in acquisitions is not often considered. Finally, after several decades of investigation, a key question is not completely answered yet: “What are the sources of value in mergers and acquisitions?”
The manipulation of LIBOR and related interest rates
Authors: Braml Harald 
Published: March 2016

Purpose
– The “London InterBank Offered Rate” (LIBOR) is one of the most important short-term interest rates with trillions of US dollar in financial products tied to it. Due to recent allegations of manipulation of the LIBOR, this paper aims to investigate the integrity of this rate.

Design/methodology/approach
– The paper analyzes the LIBOR and its rate fixing process using different screens to detect potential manipulative behavior on the macro and micro level. As main frameworks, an interest rate parity approach and the construction of a theoretical LIBOR using Credit Default Swap (CDSs) are applied. A simulation on the potential impact from one through four banks manipulating the LIBOR is performed as well.

Findings
– The results on the macro level show that the LIBOR deviates heavily from other short-term interest rates from mid-2007 onwards, reaching its peak in September 2008 with the collapse of Lehman Brothers. On the micro level, the individual submissions of the panel banks are investigated, finding inconsistencies for Barclays and HSBC. Furthermore, a simulation on the influence from potential manipulation under the current calculation method reveals substantial effects on the LIBOR fixing. Even one bank trying to manipulate the fixing has a strong influence on the rate setting.

Originality/value
– This paper contributes to the academic landscape in that it investigates the LIBOR rate setting process and if irregular behavior can be detected, given the screens used. Due to the findings of conspicuous behavior in the fixing during certain periods, the integrity of the rate setting process is more than questionable.
Delirium recall – an integrative review
Authors: Fuller Valerie 
Published: March 2016

Aims and objectivesThe aim of this article is to review and synthesise the empirical literature on patient recall of delirium episodes and to provide a direction for future research.BackgroundDelirium is a common and costly condition seen in hospitalised and institutionalised patients. Much of the existing literature focuses on delirium detection, risk factors, aetiologies and treatment. Few studies describe the patient experience of delirium recall.DesignA literature search was conducted using the databases of the National Library of Medicine (PubMed/MEDLINE/OVID), the Cumulative Index of Nursing and Allied Health Literature and the American Psychological Association (PsycINFO). Articles were restricted to the English language and from the years 1980–2014.MethodsAn integrative review of 12 selected studies on delirium recall was performed.ResultsThe majority of participants recalled their delirious episodes and during these episodes experienced both perceptual disturbances and psychological distress. Common themes from the qualitative data included incomprehensible experiences, strong emotional feelings and fear.ConclusionDelirium recall is common, is distressing and warrants further investigation. Future studies should employ standardised delirium detection tools and a systematic examination of factors that may predict delirium recall.Relevance to clinical practiceUnderstanding delirium recall may help nurses mitigate the psychological morbidity and distress associated with the phenomenon and generate new theories to improve care.
Plesiomonas shigelloides Revisited
Authors: Janda J. Michael , Abbott Sharon L. , McIver Christopher J. 
Published: March 2016

SUMMARY

After many years in the family
Vibrionaceae
, the genus
Plesiomonas
, represented by a single species,
P. shigelloides
, currently resides in the family
Enterobacteriaceae
, although its most appropriate phylogenetic position may yet to be determined. Common environmental reservoirs for plesiomonads include freshwater ecosystems and estuaries and inhabitants of these aquatic environs. Long suspected as being an etiologic agent of bacterial gastroenteritis, convincing evidence supporting this conclusion has accumulated over the past 2 decades in the form of a series of foodborne outbreaks solely or partially attributable to
P. shigelloides
. The prevalence of
P. shigelloides
enteritis varies considerably, with higher rates reported from Southeast Asia and Africa and lower numbers from North America and Europe. Reasons for these differences may include hygiene conditions, dietary habits, regional occupations, or other unknown factors. Other human illnesses caused by
P. shigelloides
include septicemia and central nervous system disease, eye infections, and a variety of miscellaneous ailments. For years, recognizable virulence factors potentially associated with
P. shigelloides
pathogenicity were lacking; however, several good candidates now have been reported, including a cytotoxic hemolysin, iron acquisition systems, and lipopolysaccharide. While
P. shigelloides
is easy to identify biochemically, it is often overlooked in stool samples due to its smaller colony size or relatively low prevalence in gastrointestinal samples. However, one FDA-approved PCR-based culture-independent diagnostic test system to detect multiple enteropathogens (FilmArray) includes
P. shigelloides
on its panel. Plesiomonads produce β-lactamases but are typically susceptible to many first-line antimicrobial agents, including quinolones and carbapenems.
In Vitro
Antimicrobial Susceptibility of Staphylococcus pseudintermedius Isolates of Human and Animal Origin
Authors: Humphries Romney M. , Wu Max T. , Westblade Lars F. , Robertson Amy E. , Burnham Carey-Ann D. , Wallace Meghan A. , Burd Eileen M. , Lawhon Sara , Hindler Janet A. 
Published: March 2016

ABSTRACT

MIC results for 115
Staphylococcus intermedius
group isolates are presented. Of these, 33% were methicillin resistant, among which 51.4% were susceptible to doxycycline, 29.7% to clindamycin, and 21.6% to trimethoprim-sulfamethoxazole. All of the isolates were susceptible to ceftaroline, daptomycin, linezolid, nitrofurantoin, quinupristin-dalfopristin, rifampin, tigecycline, and vancomycin. Of all the isolates, 82.6%, 67.8%, and 23.5% were susceptible to ciprofloxacin, erythromycin, and penicillin, respectively. No isolates harbored
mupA
or
qacA
/
B
genes, which suggested a lack of resistance to mupirocin or chlorhexidine.
Human Papillomavirus E2 Regulates SRSF3 (SRp20) To Promote Capsid Protein Expression in Infected Differentiated Keratinocytes
Authors: Klymenko T. , Hernandez-Lopez H. , MacDonald A. I. , Bodily J. M. , Graham S. V. 
Published: March 2016

ABSTRACT

The human papillomavirus (HPV) life cycle is tightly linked to differentiation of the infected epithelial cell, suggesting a sophisticated interplay between host cell metabolism and virus replication. Previously, we demonstrated in differentiated keratinocytes
in vitro
and
in vivo
that HPV type 16 (HPV16) infection caused increased levels of the cellular SR splicing factors (SRSFs) SRSF1 (ASF/SF2), SRSF2 (SC35), and SRSF3 (SRp20). Moreover, the viral E2 transcription and replication factor that is expressed at high levels in differentiating keratinocytes could bind and control activity of the SRSF1 gene promoter. Here, we show that the E2 proteins of HPV16 and HPV31 control the expression of SRSFs 1, 2, and 3 in a differentiation-dependent manner. E2 has the greatest transactivation effect on expression of SRSF3. Small interfering RNA depletion experiments in two different models of the HPV16 life cycle (W12E and NIKS16) and one model of the HPV31 life cycle (CIN612-9E) revealed that only SRSF3 contributed significantly to regulation of late events in the virus life cycle. Increased levels of SRSF3 are required for L1 mRNA and capsid protein expression. Capsid protein expression was regulated specifically by SRSF3 and appeared independent of other SRSFs. Taken together, these data suggest a significant role of the HPV E2 protein in regulating late events in the HPV life cycle through transcriptional regulation of SRSF3 expression.

IMPORTANCE
Human papillomavirus replication is accomplished in concert with differentiation of the infected epithelium. Virus capsid protein expression is confined to the upper epithelial layers so as to avoid immune detection. In this study, we demonstrate that the viral E2 transcription factor activates the promoter of the cellular SRSF3 RNA processing factor. SRSF3 is required for expression of the E4
^
L1 mRNA and so controls expression of the HPV L1 capsid protein. Thus, we reveal a new dimension of virus-host interaction crucial for production of infectious virus. SRSF proteins are known drug targets. Therefore, this study provides an excellent basis for developing strategies to regulate capsid protein production in the infected epithelium and the production of new virions.
Comparative Analysis of HIV-1 and Murine Leukemia Virus Three-Dimensional Nuclear Distributions
Authors: Quercioli Valentina , Di Primio Cristina , Casini Antonio , Mulder Lubbertus C. F. , Vranckx Lenard S. , Borrenberghs Doortje , Gijsbers Rik , Debyser Zeger , Cereseto Anna 
Published: March 2016

ABSTRACT
Recent advances in fluorescence microscopy allow three-dimensional analysis of HIV-1 preintegration complexes in the nuclei of infected cells. To extend this investigation to gammaretroviruses, we engineered a fluorescent Moloney murine leukemia virus (MLV) system consisting of MLV-integrase fused to enhanced green fluorescent protein (MLV-IN-EGFP). A comparative analysis of lentiviral (HIV-1) and gammaretroviral (MLV) fluorescent complexes in the nuclei of infected cells revealed their different spatial distributions. This research tool has the potential to achieve new insight into the nuclear biology of these retroviruses.
Why is there variation in the practice of evidence-based medicine in primary care? A qualitative study
Authors: Hisham Ranita , Ng Chirk Jenn , Liew Su May , Hamzah Nurazira , Ho Gah Juan 
Published: March 2016

ObjectiveTo explore the factors, including barriers and facilitators, influencing the practice of evidence-based medicine (EBM) across various primary care settings in Malaysia based on the doctors’ views and experiences.Research designThe qualitative study was used to answer the research question. 37 primary care physicians participated in six focus group discussions and six individual in-depth interviews. A semistructured topic guide was used to facilitate both the interviews and focus groups, which were audio recorded, transcribed verbatim, checked and analysed using a thematic approach.Participants37 primary care doctors including medical officers, family medicine specialists, primary care lecturers and general practitioners with different working experiences and in different settings.SettingThe study was conducted across three primary care settings—an academic primary care practice, private and public health clinics in Klang Valley, Malaysia.ResultsThe doctors in this study were aware of the importance of EBM but seldom practised it. Three main factors influenced the implementation of EBM in the doctors’ daily practice. First, there was a lack of knowledge and skills in searching for and applying evidence. Second, workplace culture influenced doctors’ practice of EBM. Third, some doctors considered EBM as a threat to good clinical practice. They were concerned that rigid application of evidence compromised personalised patient care and felt that EBM did not consider the importance of clinical experience.ConclusionsDespite being aware of and having a positive attitude towards EBM, doctors in this study seldom practised EBM in their routine clinical practice. Besides commonly cited barriers such as having a heavy workload and lack of training, workplace ‘EBM culture’ had an important influence on the doctors’ behaviour. Strategies targeting barriers at the practice level should be considered when implementing EBM in primary care.
The Error-Prone DNA Polymerase κ Promotes Temozolomide Resistance in Glioblastoma through Rad17-Dependent Activation of ATR-Chk1 Signaling
Authors: Peng Chenghao , Chen Zhengxin , Wang Shuai , Wang Hong-Wei , Qiu Wenjin , Zhao Lin , Xu Ran , Luo Hui , Chen Yuanyuan , Chen Dan , You Yongping , Liu Ning , Wang Huibo 
Published: March 2016

Abstract
The acquisition of drug resistance is a persistent clinical problem limiting the successful treatment of human cancers, including glioblastoma (GBM). However, the molecular mechanisms by which initially chemoresponsive tumors develop therapeutic resistance remain poorly understood. In this study, we report that Pol κ, an error-prone polymerase that participates in translesion DNA synthesis, was significantly upregulated in GBM cell lines and tumor tissues following temozolomide treatment. Overexpression of Pol κ in temozolomide-sensitive GBM cells conferred resistance to temozolomide, whereas its inhibition markedly sensitized resistant cells to temozolomide in vitro and in orthotopic xenograft mouse models. Mechanistically, depletion of Pol κ disrupted homologous recombination (HR)-mediated repair and restart of stalled replication forks, impaired the activation of ATR-Chk1 signaling, and delayed cell-cycle re-entry and progression. Further investigation of the relationship between Pol κ and temozolomide revealed that Pol κ inactivation facilitated temozolomide-induced Rad17 ubiquitination and proteasomal degradation, subsequently silencing ATR-Chk1 signaling and leading to defective HR repair and the reversal of temozolomide resistance. Moreover, overexpression of Rad17 in Pol κ-depleted GBM cells restored HR efficiency, promoted the clearance of temozolomide-induced DNA breaks, and desensitized cells to the cytotoxic effects of temozolomide observed in the absence of Pol κ. Finally, we found that Pol κ overexpression correlated with poor prognosis in GBM patients undergoing temozolomide therapy. Collectively, our findings identify a potential mechanism by which GBM cells develop resistance to temozolomide and suggest that targeting the DNA damage tolerance pathway may be beneficial for overcoming resistance. Cancer Res; 76(8); 2340–53. ©2016 AACR.
Impact of Improved Glycemic Control on Cardiac Function in Type 2 Diabetes Mellitus
Authors: Leung Melissa , Wong Vincent W. , Hudson Malcolm , Leung Dominic Y. 
Published: March 2016

Background—
Patients with type 2 diabetes mellitus are at risk of heart failure. Specific therapeutic interventions for diabetic heart disease are still elusive. We aimed to examine the impact of improved glycemic control on left ventricular (LV) function in these patients.

Methods and Results—

A total of 105 subjects with type 2 diabetes mellitus (aged 54±10 years) and poor glycemic control received optimization of treatment for blood glucose, blood pressure, and cholesterol to recommended targets for 12 months. LV systolic and diastolic function, measured by LV global longitudinal strain (GLS) and septal e′ velocities, were compared before and after optimization. At baseline, patients had impaired LV systolic (GLS −14.9±3.2%) and diastolic function (e′ 6.2±1.7 cm/s). After 12 months, glycated hemoglobin (HbA1c) decreased from 10.3±2.4% to 8.3±2.0%, which was associated with significant relative improvement in GLS of 21% and septal e′ of 24%. There was a progressively greater improvement in GLS as patients achieved a lower final HbA1c. Patients achieving an HbA1c of <7.0% had the largest improvement. The 15 patients whose HbA1c worsened experienced a decline in GLS. Patients who improved their HbA1c by ≥1.0% had a significantly higher relative improvement in e′ than those who did not (32% versus 8%;
P
=0.003). Baseline GLS, decrease in body mass index, and treatment with metformin were additional independent predictors of GLS improvement.

Conclusions—
Improvements in glycemic control over a 12-month period led to improvements in LV systolic and diastolic function. This may have long-term prognostic implications.
Sample Size in Clinical Cardioprotection Trials Using Myocardial Salvage Index, Infarct Size, or Biochemical Markers as Endpoint
Authors: Engblom Henrik , Heiberg Einar , Erlinge David , Jensen Svend Eggert , Nordrehaug Jan Erik , Dubois‐Randé Jean‐Luc , Halvorsen Sigrun , Hoffmann Pavel , Koul Sasha , Carlsson Marcus , Atar Dan , Arheden Håkan 
Published: March 2016

Background

Cardiac magnetic resonance (
CMR
) can quantify myocardial infarct (
MI
) size and myocardium at risk (MaR), enabling assessment of myocardial salvage index (
MSI
). We assessed how
MSI
impacts the number of patients needed to reach statistical power in relation to
MI
size alone and levels of biochemical markers in clinical cardioprotection trials and how scan day affect sample size.

Methods and Results

Controls (n=90) from the recent
CHILL
‐
MI
and
MITOCARE
trials were included.
MI
size, MaR, and
MSI
were assessed from
CMR
. High‐sensitivity troponin T (hsTnT) and creatine kinase isoenzyme
MB
(
CKMB
) levels were assessed in
CHILL
‐
MI
patients (n=50). Utilizing distribution of these variables, 100 000 clinical trials were simulated for calculation of sample size required to reach sufficient power. For a treatment effect of 25% decrease in outcome variables, 50 patients were required in each arm using
MSI
compared to 93, 98, 120, 141, and 143 for
MI
size alone, hsTnT (area under the curve [
AUC
] and peak), and
CKMB
(
AUC
and peak) in order to reach a power of 90%. If average
CMR
scan day between treatment and control arms differed by 1 day, sample size needs to be increased by 54% (77 vs 50) to avoid scan day bias masking a treatment effect of 25%.

Conclusion

Sample size in cardioprotection trials can be reduced 46% to 65% without compromising statistical power when using
MSI
by
CMR
as an outcome variable instead of
MI
size alone or biochemical markers. It is essential to ensure lack of bias in scan day between treatment and control arms to avoid compromising statistical power.