bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improving the Care of Elderly Adults Undergoing Surgery in Michigan
Authors: Sheetz Kyle H. , Guy Karen , Allison James H. , Barnhart Kara A. , Hawken Scott R. , Hayden Emily L. , Starr Jordan B. , Terjimanian Michael N. , Waits Seth A. , Mullard Andrew J. , Krapohl Greta , Ghaferi Amir A. , Campbell Darrell A. , Englesbe Michael J. 
Published: January 2014

ObjectivesTo determine whether failure to rescue, as a driver of mortality, can be used to identify which hospitals attenuate the specific risks inherent to elderly adults undergoing surgery.DesignRetrospective cohort study.SettingState‐wide surgical collaborative in Michigan.ParticipantsOlder adults undergoing major general or vascular surgery between 2006 and 2011 (N = 24,216).MeasurementsThirty‐four hospitals were ranked according to risk‐adjusted 30‐day mortality and grouped into tertiles. Within each tertile, rates of major complications and failure to rescue were calculated, stratifying outcomes according to age (<75 vs ≥75). Next, differences in failure‐to‐rescue rates between age groups within each hospital were calculated.ResultsFailure‐to‐rescue rates were more than two times as high in elderly adults as in younger individuals in each tertile of hospital mortality (26.0% vs 10.3% at high‐mortality hospitals, P < .001). Within hospitals, the average difference in failure‐to‐rescue rates was 12.5%. Nine centers performed better than expected, and three performed worse than expected, with the largest differences exceeding 25%.ConclusionAlthough elderly adults experience higher failure‐to‐rescue rates, this does not account for hospitals' overall capacity to rescue individuals from complications. Comparing rates of younger and elderly adults within hospitals may identify centers where efforts toward complication rescue favor, or are customized for, elderly adults. These centers should be studied as part of the collaborative's effort to address the disparate outcomes that elderly adults in Michigan experience.
Quick and Easy Is Not without Cost: Implications of Poorly Performing Nutrition Screening Tools in Hip Fracture
Authors: Bell Jack J. , Bauer Judith D. , Capra Sandra , Pulle Ranjeev C. 
Published: January 2014

ObjectivesTo evaluate the performance of commonly applied nutrition screening tools and measures and to consider the potential costs of undiagnosed malnutrition in a case‐based reimbursement funding environment.DesignA diagnostic accuracy study to compare a variety of nutrition screening techniques against primary, secondary, and comparative measures of nutritional status.SettingPublic metropolitan hospital orthogeriatric unit.ParticipantsIndividuals with acute hip fracture admitted to the orthogeriatric unit; 150 prospective, consecutively admitted individuals were considered, with eight exclusions, yielding a sample size of 142 participants.MeasurementsScreens included the Mini Nutritional Assessment—Short Form, Malnutrition Screening Tool, Malnutrition Universal Screening Tool, Nutrition Risk Screen 2002, anthropometric measures, and albumin. Malnutrition was diagnosed using International Statistical Classification of Diseases and Health Related Problems, Tenth Edition, Australian Modification (ICD‐10‐AM) criteria. Healthcare coders costed malnutrition‐related diagnostic related groups and cost‐weight changes for individual participants.ResultsMalnutrition prevalence was 48%. Screening tools had only slight to moderate agreement with ICD‐10‐AM diagnosis of malnutrition, and none of the screening tools tested met the a priori requirement of 80% sensitivity and 60% specificity. The estimated cost effect of poor screening tool sensitivity on a 16‐bed hip fracture unit ranged from AUS$46,506 to AUS$228,896 per year.ConclusionPoor screening tool sensitivity leads to undiagnosed malnutrition; tools that are quick and easy to apply are not without cost. Routine nutrition assessment should replace nutrition risk screening in hip fracture settings with a high prevalence of malnutrition reliant on case‐mix funding. Further pragmatic studies are urgently required to determine whether findings apply to other elderly inpatient populations with endemic malnutrition, comorbidities, and cognitive impairment.
Sarcopenic Obesity and Risk of Cardiovascular Disease and Mortality: A Population‐Based Cohort Study of Older Men
Authors: Atkins Janice L. , Whincup Peter H. , Morris Richard W. , Lennon Lucy T. , Papacosta Olia , Wannamethee S. Goya 
Published: January 2014

ObjectivesTo examine associations between sarcopenia, obesity, and sarcopenic obesity and risk of cardiovascular disease (CVD) and all‐cause mortality in older men.DesignProspective cohort study.SettingBritish Regional Heart Study.ParticipantsMen aged 60–79 years (n = 4,252).MeasurementsBaseline waist circumference (WC) and midarm muscle circumference (MAMC) measurements were used to classify participants into four groups: sarcopenic, obese, sarcopenic obese, or optimal WC and MAMC. The cohort was followed for a mean of 11.3 years for CVD and all‐cause mortality. Cox regression analyses assessed associations between sarcopenic obesity groups and all‐cause mortality, CVD mortality, CVD events, and coronary heart disease (CHD) events.ResultsThere were 1,314 deaths, 518 CVD deaths, 852 CVD events, and 458 CHD events during follow‐up. All‐cause mortality risk was significantly greater in sarcopenic (HR = 1.41, 95% CI = 1.22–1.63) and obese (HR = 1.21, 95% CI = 1.03–1.42) men than in the optimal reference group, with the highest risk in sarcopenic obese (HR = 1.72, 95% CI = 1.35–2.18), after adjustment for lifestyle characteristics. Risk of CVD mortality was significantly greater in sarcopenic and obese but not sarcopenic obese men. No association was seen between sarcopenic obesity groups and CHD or CVD events.ConclusionSarcopenia and central adiposity were associated with greater cardiovascular mortality and all‐cause mortality. Sarcopenic obese men had the highest risk of all‐cause mortality but not CVD mortality. Efforts to promote healthy aging should focus on preventing obesity and maintaining muscle mass.
Chronic sazetidine‐A maintains anxiolytic effects and slower weight gain following chronic nicotine without maintaining increased density of nicotinic receptors in rodent brain
Authors: Hussmann G. Patrick , DeDominicis Kristen E. , Turner Jill R. , Yasuda Robert P. , Klehm Jacquelyn , Forcelli Patrick A. , Xiao Yingxian , Richardson Janell R. , Sahibzada Niaz , Wolfe Barry B. , Lindstrom Jon , Blendy Julie A. , Kellar Kenneth J. 
Published: January 2014

AbstractChronic nicotine administration increases the density of brain α4β2* nicotinic acetylcholine receptors (nAChRs), which may contribute to nicotine addiction by exacerbating withdrawal symptoms associated with smoking cessation. Varenicline, a smoking cessation drug, also increases these receptors in rodent brain. The maintenance of this increase by varenicline as well as nicotine replacement may contribute to the high rate of relapse during the first year after smoking cessation. Recently, we found that sazetidine‐A (saz‐A), a potent partial agonist that desensitizes α4β2* nAChRs, does not increase the density of these receptors in brain at doses that decrease nicotine self‐administration, increase attention in rats, and produce anxiolytic effects in mice. Here, we investigated whether chronic saz‐A and varenicline maintain the density of nAChRs after their up‐regulation by nicotine. In addition, we examined the effects of these drugs on a measure of anxiety in mice and weight gain in rats. After increasing nAChRs in the rodent brain with chronic nicotine, replacing nicotine with chronic varenicline maintained the increased nAChR binding, as well as the α4β2 subunit proteins measured by western blots. In contrast, replacing nicotine treatments with chronic saz‐A resulted in the return of the density of nAChRs to the levels seen in saline controls. Nicotine, saz‐A and varenicline each demonstrated anxiolytic effects in mice, but only saz‐A and nicotine attenuated the gain of weight over a 6‐week period in rats. These findings suggest that apart from its modest anxiolytic and weight control effects, saz‐A, or drugs like it, may be useful in achieving long‐term abstinence from smoking.
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Chronic treatment with nicotine increases brain α4β2 nicotinic receptors, which may be related to nicotine addiction. When nicotine is replaced by varenicline, this receptor increase is maintained; in contrast, when nicotine is replaced by sazetidine‐A the receptors return to baseline levels. The doses of drugs used here are anxiolytic and slow gain of body weight compared to saline controls.
Refining rare weed trait syndromes along arable intensification gradients
Authors: Pinke Gyula , Gunton Richard M. 
Published: January 2014

AbstractQuestionHow does the conservation (rarity) value of arable weed communities differ along intensification gradients? Which functional traits best distinguish the weed communities of more and less extensively managed fields? Can the same traits predict the rarity of individual weed species?LocationHungary.MethodsUsing relevé data from 60 cereal and 70 stubble fields, together with weed trait data, we characterized community responses to arable intensification using functional trait analyses based on trait‐convergence and trait‐divergence assembly patterns. We also examined how well the broad‐scale rarity status of species predicts their occurrence along intensification gradients, and how it maps onto our functional classifications describing intensification responses.ResultsThe response of weeds to intensification in cereal fields was best described by a functional classification based on species' flowering duration, maximum height and seed weight: weeds of extensively managed fields have short flowering seasons (2–5 mo) and particularly large or small seeds. The highest proportions of rare species also happen to be found in these groups. The rarest weeds among these species tend to be late‐winter and early‐summer annuals, while the rare species of stubble fields tend to be broad‐leaved with low nitrogen requirements, small seeds and short height. Stubble fields showed a decline in weed cover with increasing application of fertilizer and distance from the field edge, but we could detect no strong associations of management factors with trait composition, perhaps because the intensification gradient across these fields was shorter.ConclusionsMany rare Hungarian weeds are associated with traditional extensive farming practices. They are particularly characterized by short, midsummer flowering periods and by preference for low nitrogen levels, but a range of trait syndromes must be considered to understand their ecology and conservation. Analyses based on trait‐divergence patterns, rather than trait‐convergence patterns, provide better insights into the functional composition of weed communities, emphasizing the importance of disruptive filters in weed community assembly and the need for improved methods to detect such effects.
Frequency and Sequelae of Retained Implanted Cardiac Device Material Post Heart Transplantation
Authors: MARTIN ANDREW , VOSS JAMIE , SHANNON DUNCAN , RUYGROK PETER , LEVER NIGEL 
Published: January 2014

BackgroundCardiac implantable electronic devices (CIEDs) have now become common therapeutic adjuncts for patients prior to orthotopic heart transplantation (OHT). Removal of the generator and the intracardiac components occurs at time of transplantation but removal of the intravascular portion of leads may be unsuccessful without specialized extraction equipment.MethodsWe performed a retrospective audit of chest radiographs and clinical records of patients undergoing OHT at Green Lane and Auckland City Hospitals between 2002 and 2012.ResultsAt the time of transplant surgery, 56 of 100 patients had a CIED in situ. Hardware was retained postoperatively in 22 (39%), and the CIED had been in situ for 47 (interquartile range [IQR] 16–68) months for these cases, compared to 14 (IQR 3–24) months in those without. In two (9%) patients, the device generator was electively explanted during the week following OHT. There were no subsequent procedures undertaken to remove retained lead fragments. One (4%) had lead fragment embolization, one (4%) had endoluminal fragment migration, and one (4%) had lead fragment erosion into the mediastinum; all were asymptomatic and without adverse clinical sequelae. There was no infection associated with this hardware. The presence of retained lead fragments was not associated with additional mortality.ConclusionsRetained lead fragments following OHT occur commonly, without adverse clinical events for this cohort; however, the long‐term clinical implications remain uncertain. Complete removal of all CIED hardware should be attempted at the time of OHT, and when this is not possible leads should be left in a state that facilitates their removal at a later date if required.
An Epistemic Case for Empathy
Authors: Steinberg Justin 
Published: January 2014

AbstractMuch recent work on empathy assumes that one cannot give non‐question‐begging reasons for empathizing with others. In this article I argue that there are epistemic reasons for cultivating empathy. After sketching a brief general account of empathy, I proceed to argue that empathic information is user‐friendly, fostering the achievement of widely held cognitive goals. It can also contribute to social knowledge and the satisfaction of democratic ideals. The upshot of my analysis is that there are strong, but defeasible, epistemic reasons for empathizing with others.
Inhibition of mutant BRAF splice variant signaling by next‐generation, selective RAF inhibitors
Authors: Basile Kevin J. , Le Kaitlyn , Hartsough Edward J. , Aplin Andrew E. 
Published: January 2014

SummaryVemurafenib and dabrafenib block MEK‐ERK1/2 signaling and cause tumor regression in the majority of advanced‐stage BRAFV600E melanoma patients; however, acquired resistance and paradoxical signaling have driven efforts for more potent and selective RAF inhibitors. Next‐generation RAF inhibitors, such as PLX7904 (PB04), effectively inhibit RAF signaling in BRAFV600E melanoma cells without paradoxical effects in wild‐type cells. Furthermore, PLX7904 blocks the growth of vemurafenib‐resistant BRAFV600E cells that express mutant NRAS. Acquired resistance to vemurafenib and dabrafenib is also frequently driven by expression of mutation BRAF splice variants; thus, we tested the effects of PLX7904 and its clinical analog, PLX8394 (PB03), in BRAFV600E splice variant‐mediated vemurafenib‐resistant cells. We show that paradox‐breaker RAF inhibitors potently block MEK‐ERK1/2 signaling, G1/S cell cycle events, survival and growth of vemurafenib/PLX4720‐resistant cells harboring distinct BRAFV600E splice variants. These data support the further investigation of paradox‐breaker RAF inhibitors as a second‐line treatment option for patients failing on vemurafenib or dabrafenib.
Demographic and Socioeconomic Status, Child Support Grant, and Teenage Pregnancy among Blacks in South Africa
Authors: Udjo Eric O. 
Published: January 2014

While the evidence is internationally inconclusive, social protection systems have been blamed for various perverse incentives or unintended consequences. This article explores one particular case in point. The South African Constitution and the Social Assistance Act of 2004 provide a child support grant (CSG) to low‐income single parents/caregivers. There is nevertheless concern regarding possible perverse incentives of the grant, sparking debate that it may encourage teenage pregnancy. Several studies have examined the validity of the claim, yet methodological weaknesses cast doubt on their conclusions. This article examines the probability of being pregnant with another child among black teenagers receiving the CSG in South Africa compared with black teenagers who are not recipients. Results indicate that black teenagers aged 15‐18 years receiving the grant have significantly lower odds of being pregnant with another child compared with their peers who do not receive the grant, controlling for demographic and socioeconomic factors.Related Articles
Flavin, Patrick, Alexander Pacek, and Benjamin Radcliff. 2011. “.” Politics & Policy 39 (): 251‐269. http://onlinelibrary.wiley.com/doi/10.1111/j.1747‐1346.2011.00290.x/abstract

Coan, James. 2008. “.” Politics & Policy 36 (): 806‐833. http://onlinelibrary.wiley.com/doi/10.1111/j.1747‐1346.2008.00136.x/abstract

Luccisano, Lucy, and Amy Romagnoli. 2007. “” Politics & Policy 35 (): 716‐751. http://onlinelibrary.wiley.com/doi/10.1111/j.1747‐1346.2007.00082.x/abstract
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Polymorphisms in a disintegrin and metalloprotease 33 gene and the risk of chronic obstructive pulmonary disease: A meta‐analysis
Authors: Zhang Rui , Li He , Zhao Haiming , Chen Wangyue , Cheng Deyun 
Published: January 2014

AbstractA number of polymorphisms in a disintegrin and metalloprotease 33 (ADAM33) gene have been implicated in susceptibility to chronic obstructive pulmonary disease (COPD). However, results to date have been inconclusive. We conducted meta‐analyses to investigate the associations between multiple polymorphisms in ADAM33 gene and COPD susceptibility. PubMed, Embase and Chinese databases (Wanfang and China National Knowledge Infrastructure) were searched for eligible case‐control studies. We extracted data and used meta‐analysis to calculate pooled odds ratios with 95% confidence intervals to evaluate the strength of associations. Twelve studies containing six ADAM33 polymorphisms (F+1, S1, S2, T1, V4 and Q‐1) were identified, which involved 2630 cases and 4376 controls. ADAM33 S1 polymorphism showed stable and significant associations with COPD risks among the Chinese and smoking populations, and Q‐1 polymorphism showed stable and significant associations with COPD risks among the overall populations. In subgroup analyses, T1 and Q‐1 polymorphisms were significantly associated with COPD risks among the Chinese and smoking populations, and among the Chinese, Caucasians and smoking populations, respectively. However, none of the significant results was stable in sensitivity analyses. With respect to F+1, S2 or V4 polymorphism, there was no evidence of any significant association with COPD risks in either the overall or the subgroup analysis. The results of this meta‐analysis indicate that ADAM33 S1 polymorphism is a risk factor for COPD among the Chinese and smoking populations, and that Q‐1 polymorphism is a risk factor for COPD among the overall populations.
Training Mode’s Influence on the Relationships between Training-Load Models During Basketball Conditioning
Authors: Scanlan Aaron T. , Wen Neal , Tucker Patrick S. , Borges Nattai R. , Dalbo Vincent J. 
Published: January 2014

Purpose:To compare perceptual and physiological training-load responses during various basketball training modes.Methods:Eight semiprofessional male basketball players (age 26.3 ± 6.7 y, height 188.1 ± 6.2 cm, body mass 92.0 ± 13.8 kg) were monitored across a 10-wk period in the preparatory phase of their training plan. Player session ratings of perceived exertion (sRPE) and heart-rate (HR) responses were gathered across base, specific, and tactical/game-play training modes. Pearson correlations were used to determine the relationships between the sRPE model and 2 HR-based models: the training impulse (TRIMP) and summated HR zones (SHRZ). One-way ANOVAs were used to compare training loads between training modes for each model.Results:Stronger relationships between perceptual and physiological models were evident during base (sRPE-TRIMP r = .53, P < .05; sRPE-SHRZ r = .75, P < .05) and tactical/game-play conditioning (sRPE-TRIMP r = .60, P < .05; sRPE-SHRZ r = .63; P < .05) than during specific conditioning (sRPE-TRIMP r = .38, P < .05; sRPE-SHRZ r = .52; P < .05). Furthermore, the sRPE model detected greater increases (126–429 AU) in training load than the TRIMP (15–65 AU) and SHRZ models (27–170 AU) transitioning between training modes.Conclusions:While the training-load models were significantly correlated during each training mode, weaker relationships were observed during specific conditioning. Comparisons suggest that the HR-based models were less effective in detecting periodized increases in training load, particularly during court-based, intermittent, multidirectional drills. The practical benefits and sensitivity of the sRPE model support its use across different basketball training modes.
Epidermal Growth Factor Receptor-PI3K Signaling Controls Cofilin Activity To Facilitate Herpes Simplex Virus 1 Entry into Neuronal Cells
Authors: Zheng Kai , Xiang Yangfei , Wang Xiao , Wang Qiaoli , Zhong Meigong , Wang Shaoxiang , Wang Xiaoyan , Fan Jianglin , Kitazato Kaio , Wang Yifei 
Published: January 2014

ABSTRACT
Herpes simplex virus type 1 (HSV-1) establishes latency in neurons and can cause severe disseminated infection with neurological impairment and high mortality. This neurodegeneration is thought to be tightly associated with virus-induced cytoskeleton disruption. Currently, the regulation pattern of the actin cytoskeleton and the involved molecular mechanisms during HSV-1 entry into neurons remain unclear. Here, we demonstrate that the entry of HSV-1 into neuronal cells induces biphasic remodeling of the actin cytoskeleton and an initial inactivation followed by the subsequent activation of cofilin, a member of the actin depolymerizing factor family that is critical for actin reorganization. The disruption of F-actin dynamics or the modulation of cofilin activity by mutation, knockdown, or overexpression affects HSV-1 entry efficacy and virus-mediated cell ruffle formation. Binding of the HSV-1 envelope initiates the epidermal growth factor receptor (EGFR)-phosphatidylinositide 3-kinase (PI3K) signaling pathway, which leads to virus-induced early cofilin phosphorylation and F-actin polymerization. Moreover, the extracellular signal-regulated kinase (ERK) kinase and Rho-associated, coiled-coil-containing protein kinase 1 (ROCK) are recruited as downstream mediators of the HSV-1-induced cofilin inactivation pathway. Inhibitors specific for those kinases significantly reduce the virus infectivity without affecting virus binding to the target cells. Additionally, lipid rafts are clustered to promote EGFR-associated signaling cascade transduction. We propose that HSV-1 hijacks cofilin to initiate infection. These results could promote a better understanding of the pathogenesis of HSV-1-induced neurological diseases.

IMPORTANCE
The actin cytoskeleton is involved in many crucial cellular processes and acts as an obstacle to pathogen entry into host cells. Because HSV-1 establishes lifelong latency in neurons and because neuronal cytoskeletal disruption is thought to be the main cause of HSV-1-induced neurodegeneration, understanding the F-actin remodeling pattern by HSV-1 infection and the molecular interactions that facilitate HSV-1 entry into neurons is important. In this study, we showed that HSV-1 infection induces the rearrangement of the cytoskeleton as well as the initial inactivation and subsequent activation of cofilin. Then, we determined that activation of the EGFR-PI3K-Erk1/2 signaling pathway inactivates cofilin and promotes F-actin polymerization. We postulate that by regulating actin cytoskeleton dynamics, cofilin biphasic activation could represent the specific cellular machinery usurped by pathogen infection, and these results will greatly contribute to the understanding of HSV-1-induced early and complex changes in host cells that are closely linked to HSV-1 pathogenesis.