bluuebunny/crossref_metadata_2025_split huggingface dataset:
Round versus Anatomical Implants in Primary Cosmetic Breast Augmentation: A Meta-Analysis and Systematic Review
Authors: Cheng Fengrui , Cen Ying , Liu Chuanqi , Liu Ruolin , Pan Cheng , Dai Shuiping 
Published: December 2018

Background:
Choosing implant shape (round or anatomical) is one of the most essential yet controversial decisions in cosmetic breast augmentation. Many surgeons choose implant shape based on personal experience or expert opinion. This is the first systematic review and meta-analysis comparing the aesthetic effect between anatomical and round implants in primary cosmetic breast augmentation.

Methods:
The authors searched the PubMed, MEDLINE, Embase, ScienceDirect, Web of Knowledge, Scopus, and Cochrane Central Register of Controlled Trials databases for studies that compared anatomical and round implants in primary cosmetic breast augmentation. Primary outcomes were postoperative aesthetic effect and correct identification rate of implant shape. Random effects models were used to obtain pooled standardized mean difference and 95 percent confidence intervals.

Results:
One randomized comparative and four observational comparative studies met the inclusion criteria. No aesthetic superiority was found in the anatomical implant group with regard to overall appearance (standardized mean difference, 0.06; 95 percent CI, −0.40 to 0.53), naturalness (standardized mean difference, 0.18; 95 percent CI, −1.51 to 1.15), projection, upper pole contour, and lower pole contour. Pooled correct identification rate of implant shape by plastic surgeons was 52 percent (95 percent CI, 0.46 to 0.58).

Conclusions:
Generally, anatomical implants do not seem to have an aesthetic superiority compared to round implants. Plastic surgeons seemed to be unable to accurately differentiate the two implant shapes in vivo. Further studies should focus on identifying the specific indications for the use of anatomical implants.
Concurrent Joint Hypermobility Syndrome and Spondyloarthropathy
Authors: Shur Natalie F. , Shur Joshua D. , Rennie Winston J. , Moorthy Arumugam 
Published: December 2018

Background
The coexistence of joint hypermobility syndrome (JHS) and spondyloarthropathy (SpA) presents a challenging clinical conundrum due to the contradictory clinical signs that may be present. Classic features such as restricted spinal movement or early morning back stiffness may not be present. Timely diagnosis and appropriate management of these patients are difficult as they tend to have lower scores on validated objective measures.

Methods
We performed a medical records review study to identify patients with both JHS and SpA who had presented to the Leicester Spondyloarthropathy clinic. Patients were diagnosed with axial SpA if they met the Assessment of SpondyloArthritis international Society classification criteria.
1
Their imaging was reviewed by a consultant musculoskeletal radiologist.

Results
Four cases were identified from the patient database (female; average age, 37.5 years). All patients presented with lower back pain or sacroiliac joint pain but preserved spinal movement with a negative Schober's test. Two had a history of symptoms for more than 10 years. All had a Beighton score of greater than 6. Three of the patients were HLA positive, and 3 had a positive family history. All patients thus far have had their symptoms adequately controlled on nonsteroidal anti-inflammatory drugs and physiotherapy.

Conclusions
The coexistence of JHS and SpA is rare but important to recognize. These patients are difficult to diagnose as they may present late because of preserved spinal movements. It is unclear whether the preserved flexibility masks the true extent of disease or whether clinically they represent a less severe disease phenotype.
The Contribution of the Omentum to the Outcome From Sepsis: An Experimental Animal Study
Authors: Wang Andrew W. , Cauvi David M. , Hawisher Dennis , Reyes Tony , Coimbra Raul , Bickler Stephen , De Maio Antonio 
Published: December 2018

ABSTRACT
The omentum is a large mesenchymal fibro-fatty tissue with remarkable healing capability. It is also rich in immune cells, including macrophages and lymphocytes, within particular structures named milky spots. Clinical observations indicate a high incidence of peritonitis after the removal of the omentum suggesting that it may play a role in sepsis. To test this possibility, male CD-1 mice underwent simultaneous omentectomy and cecal ligation and puncture (CLP), omentectomy-sham operation and CLP alone, and mortality was documented within 72 h post the insults. A significant increase in mortality was observed in mice subjected to omentectomy and CLP in comparison with CLP alone. Mortality was correlated with an increase in cytokine gene expression within the lung after omentectomy and CLP as opposed to CLP alone. However, no differences in bacterial load were observed within the peritoneum or blood between groups. To test the long-term effect of omentectomy, mice were subjected to omentum removal or sham operation, allowed to recover from surgery for 14 or 28 days, and then both were subjected to CLP. In these cases, no differences in mortality were observed between the groups suggesting that the lack of omentum triggers a compensatory mechanism. Finally, omentectomy and sham operation altered the composition of peritoneal immune cells with the disappearance of F4/80high macrophages and the appearance of a new population of F4/80low macrophages within 1 or 14 days post-surgery. The F4/80high positive cells reappeared after 28 days following the procedures. All of these observations suggest that the omentum plays an early role in the outcome from sepsis.
Communication involving special populations: older adults with cancer
Authors: Adelman Ronald D. , Greene Michele G. , Phongtankuel Veerawat , Silva Milagros D. 
Published: December 2018

Purpose of review
Cancer has a high incidence and death rate among older adults. The objective of this article is to summarize current literature about communication between older adults and medical professionals in cancer care. Our article addresses four categories related to communication: first, ageism; second, screening; third, treatment; and fourth, end of life (EoL) care.

Recent findings
Current literature suggests that cancer treatment for older patients may be influenced by ageist biases. Older patients prefer that clinicians incorporate health status to individualize screening decisions although some patients don’t consider life expectancy to be an important factor in screening. Patients often agree with the oncologists’ treatment recommendations but want to be involved in the decision-making process. Lastly, work is being conducted to associate quality communication of EoL issues with hospital performance measures.

Summary
Patients are at risk of age-based disparities in cancer screening, treatment, and EoL care. Older adults are not a homogenous group and all elderly cancer patients need to have an individualized approach to care. Medical professionals must understand patients’ goals and values and involve them in shared decision-making and preparation for EoL.
Pediatric emergency department readiness among US trauma hospitals
Authors: Remick Katherine , Gaines Barbara , Ely Michael , Richards Rachel , Fendya Diana , Edgerton Elizabeth A. 
Published: December 2018

BACKGROUND
Pediatric readiness among US emergency departments is not universal. Trauma hospitals adhere to standards that may support day-to-day readiness for children.

METHODS
In 2013 4,146 emergency departments participated in the NPRP to assess compliance with the 2009 Guidelines to Care for Children in the Emergency Department. Probabilistic linkage (90%) to the 2009 American Hospital Association survey found 1,247 self-identified trauma hospitals (levels 1, 2, 3, 4). Relationship between trauma hospital level and weighted pediatric readiness score (WPRS) on a 100-point scale was performed; significance was assessed using a Kruskal-Wallis test and pediatric readiness elements using χ2. Adjusted relative risks were calculated using modified Poisson regression, controlling for pediatric volume, hospital configuration, and geography.

RESULTS
The overall WPRS among all trauma hospitals (1,247) was 71.8. Among those not self-identified as a children's hospital or emergency department approved for pediatrics (EDAP) (1088), Level 1 and 2 trauma hospitals had higher WPRS than level 3 and 4 trauma hospitals, 83.5 and 71.8, respectively versus 64.9 and 62.6. Yet, compared with EDAP trauma hospitals (median 90.5), level 1 general trauma hospitals were less likely to have critical pediatric-specific elements. Common gaps among general trauma hospitals included presence of interfacility transfer agreements for children, measurement of pediatric weights solely in kilograms, quality improvement processes with pediatric-specific metrics, and disaster plans that include pediatric-specific needs.

CONCLUSION
Self-identified trauma hospital level may not translate to pediatric readiness in emergency departments. Across all levels of general non-EDAP, nonchildren's trauma hospitals, gaps in pediatric readiness exist. Nonchildren's hospital EDs (i.e., EDAPs) can be prepared to meet the emergency needs of all children and trauma hospital designation should incorporate these core elements of pediatric readiness.

LEVEL OF EVIDENCE
Care management, level III.
Tranexamic acid suppresses the release of mitochondrial DAMPs and reduces lung inflammation in a murine burn model
Authors: Carter Damien Wilson , Prudovsky Igor , Kacer Doreen , Soul Tee , Kumpel Chloe , Pyburn Kathleen , Palmeri Monica , Kramer Robert , Rappold Joseph 
Published: December 2018

BACKGROUND
Severe burn injuries are known to initiate a profound systemic inflammatory response (SIRS) that may lead to burn shock and other SIRS-related complications. Damage-associated molecular patterns (DAMPs) are important early signaling molecules that initiate SIRS after burn injury. Previous work in a rodent model has shown that application of a topical immune modulator (p38MAPK inhibitor) applied directly to the burn wound decreases cytokine expression, reduces pulmonary inflammation and edema. Our group has demonstrated that tranexamic acid (TXA)—in addition to its use as an antifibrinolytic—has cell protective in vitro effects. We hypothesized that administration of TXA after burn injury would attenuate DAMP release and reduce lung inflammation.

METHODS
C57/BL6 male mice underwent a 40% Total Body Surface Area (TBSA) scald burn. Sham animals underwent the same procedure in room temperature water. One treatment group received the topical application of p38MAPK inhibitor after burn injury. The other treatment group received an intraperitoneal administration of TXA after burn injury. Animals were sacrificed at 5 hours. Plasma was collected by cardiac puncture. MtDNA levels in plasma were determined by quantitative Polymerase Chain Reaction (qPCR). Syndecan-1 levels in plasma were measured by ELISA. Lungs were harvested, fixed, and paraffin-embedded. Sections of lungs were stained for antigen to detect macrophages.

RESULTS
Topical p38MAPK inhibitor and TXA significantly attenuated mtDNA release. Both TXA and the topical p38MAPK inhibitor reduced lung inflammation as represented by decreased macrophage infiltration. Syndecan-1 levels showed no difference between burn and treatment groups.

CONCLUSION
Both p38 MAPK inhibitor and TXA demonstrated the ability to attenuate burn-induced DAMP release and lung inflammation. Beyond its role as an antifibrinolytic, TXA may have significant anti-inflammatory effects pertinent to burn resuscitation. Further study is required; however, TXA may be a useful adjunct in burn resuscitation.
Interactions of immediate and long-term action regulation in the course and complications of bipolar disorder
Authors: Lijffijt Marijn , O'Brien Brittany , Salas Ramiro , Mathew Sanjay J. , Swann Alan C. 
Published: December 2018

Immediate and long-term mechanisms interact in the regulation of action. We will examine neurobiology and practical clinical consequences of these interactions. Long-term regulation of immediate behavioural control is based on analogous responses to highly rewarding or stressful stimuli: (i) impulsivity is a failure of the balance between activation and inhibition in the immediate regulation of action. (ii) Sensitization is a persistently exaggerated behavioural or physiological response to highly salient stimuli, such as addictive stimuli or inescapable stress. Sensitization can generalize across classes of stimuli. (iii) Impulsivity, possibly related to poor modulation of catecholaminergic and glutamatergic functions, may facilitate development of long-term sensitized responses to stressful or addictive stimuli. In turn, impulsivity is prominent in sensitized behaviour. (iv) While impulsivity and sensitization are general components of behaviour, their interactions are prominent in the course of bipolar disorder, emphasizing roles of substance-use, recurrent course and stressors. (v) Suicide is a complex and severe behaviour that exemplifies the manner in which impulsivity facilitates behavioural sensitization and is, in turn, increased by it, leading to inherently unpredictable behaviour. (vi) Interactions between impulsivity and sensitization can provide targets for complementary preventive and treatment strategies for severe immediate and long-term behavioural disorders. Progress along these lines will be facilitated by predictors of susceptibility to behavioural sensitization.This article is part of the theme issue ‘Risk taking and impulsive behaviour: fundamental discoveries, theoretical perspectives and clinical implications’.
Why has evolution not selected for perfect self-control?
Authors: Hayden Benjamin Y. 
Published: December 2018

Self-control refers to the ability to deliberately reject tempting options and instead select ones that produce greater long-term benefits. Although some apparent failures of self-control are, on closer inspection, reward maximizing, at least some self-control failures are clearly disadvantageous and non-strategic. The existence of poor self-control presents an important evolutionary puzzle because there is no obvious reason why good self-control should be more costly than poor self-control. After all, a rock is infinitely patient. I propose that self-control failures result from cases in which well-learned (and thus routinized) decision-making strategies yield suboptimal choices. These mappings persist in the decision-makers’ repertoire because they result from learning processes that are adaptive in the broader context, either on the timescale of learning or of evolution. Self-control, then, is a form of cognitive control and the subjective feeling of effort likely reflects the true costs of cognitive control. Poor self-control, in this view, is ultimately a result of bounded optimality.
This article is part of the theme issue ‘Risk taking and impulsive behaviour: fundamental discoveries, theoretical perspectives and clinical implications.
Three gaps and what they may mean for risk preference
Authors: Hertwig Ralph , Wulff Dirk U. , Mata Rui 
Published: December 2018

Risk preference is one of the most important building blocks of choice theories in the behavioural sciences. In economics, it is often conceptualized as preferences concerning the variance of monetary payoffs, whereas in psychology, risk preference is often thought to capture the propensity to engage in behaviour with the potential for loss or harm. Both concepts are associated with distinct measurement traditions: economics has traditionally relied on behavioural measures, while psychology has often relied on self-reports. We review three important gaps that have emerged from work stemming from these two measurement traditions: first, a description–experience gap which suggests that behavioural measures do not speak with one voice and can give very different views on an individual's appetite for risk; second, a behaviour–self-report gap which suggests that different self-report measures, but not behavioural measures, show a high degree of convergent validity; and, third, a temporal stability gap which suggests that self-reports, but not behavioural measures, show considerable temporal stability across periods of years. Risk preference, when measured through self-reports—but not behavioural tests—appears as a moderately stable psychological trait with both general and domain-specific components. We argue that future work needs to address the gaps that have emerged from the two measurement traditions and test their differential predictive validity for important economic, health and well-being outcomes.This article is part of the theme issue ‘Risk taking and impulsive behaviour: fundamental discoveries, theoretical perspectives and clinical implications’.
Neural circuitry and mechanisms of waiting impulsivity: relevance to addiction
Authors: Dalley Jeffrey W. , Ersche Karen D. 
Published: December 2018

Impatience—the failure to wait or tolerate delayed rewards (e.g. food, drug and monetary incentives)—is a common behavioural tendency in humans. However, when rigidly and rapidly expressed with limited regard for future, often negative consequences, impatient or impulsive actions underlie and confer susceptibility for such diverse brain disorders as drug addiction, attention-deficit hyperactivity disorder (ADHD) and major depressive disorder. Consequently, ‘waiting’ impulsivity has emerged as a candidate endophenotype to inform translational research on underlying neurobiological mechanisms and biomarker discovery for many of the so-called impulse-control disorders. Indeed, as reviewed in this article, this research enterprise has revealed a number of unexpected targets and mechanisms for intervention. However, in the context of drug addiction, impulsive decisions that maximize short-term gains (e.g. acute drug consumption) over longer-term punishment (e.g. unemployment, homelessness, personal harm) defines one aspect of impulsivity, which may or may not be related to rapid, unrestrained actions over shorter timescales. We discuss the relevance of this distinction in impulsivity subtypes for drug addiction with reference to translational research in humans and other animals.
This article is part of the theme issue ‘Risk taking and impulsive behaviour: fundamental discoveries, theoretical perspectives and clinical implications’.
Epstein-Barr virus reprograms human B-lymphocytes immediately in the pre-latent phase of infection
Authors: Mrozek-Gorska Paulina , Buschle Alexander , Pich Dagmar , Schwarzmayr Thomas , Fechtner Ron , Scialdone Antonio , Hammerschmidt Wolfgang 
Published: December 2018

AbstractEpstein-Barr virus (EBV) is a human tumor virus and a model of herpesviral latency. The virus efficiently infects resting human B-lymphocytes and induces their continuous proliferation in vitro, which mimics certain aspects of EBV’s oncogenic potential in vivo. This seminal finding was made 50 years ago, but how EBV activates primary human B-lymphocytes and how lymphoblastoid cell lines (LCLs) evolve from the EBV-infected lymphocytes is uncertain. We conducted a systematic time-resolved longitudinal study of cellular functions and transcriptional profiles of newly infected naïve primary B-lymphocytes. EBV reprograms these human cells comprehensively and globally. Rapid and extensive transcriptional changes occur within 24 hours of infection and precede any metabolic and phenotypic changes. Within the next 48 hours, the virus activates the cells, changes their phenotypes with respect to cell size, RNA and protein content and induces metabolic pathways to cope with the increased demand for energy, supporting an efficient cell cycle entry on day three post infection. The transcriptional program that EBV initiates consists of three waves of clearly discernable clusters of cellular genes that peak on day one, two, or three and regulate RNA synthesis, metabolic pathways and cell division, respectively. Upon the onset of cell doublings on day four the cellular transcriptome appears to be completely reprogrammed to support the activated and proliferating cell, but three additional clusters of EBV regulated genes adjust the infected immune cells to fine-tune cell signaling, migration, and immune response pathways, eventually. Our study reveals that more than 98 % of the 13,000 expressed genes in B-lymphocytes are regulated upon infection demonstrating that EBV governs the entire biology of its target cell.
Somatic LINE-1 retrotransposition in cortical neurons and non-brain tissues of Rett patients and healthy individuals
Authors: Zhao Boxun , Wu Qixi , Ye Adam Yongxin , Guo Jing , Zheng Xianing , Yang Xiaoxu , Yan Linlin , Liu Qing-Rong , Hyde Thomas M. , Wei Liping , Huang August Yue 
Published: December 2018

AbstractMounting evidence supports that LINE-1 (L1) retrotransposition can occur postzygotically in healthy and diseased human tissues, contributing to genomic mosaicism in the brain and other somatic tissues of an individual. However, the genomic distribution of somatic L1Hs (Human-specific LINE-1) insertions and their potential impact on carrier cells remain unclear. Here, using a PCR-based targeted bulk sequencing approach, we profiled 9,181 somatic insertions from 20 postmortem tissues from five Rett patients and their matched healthy controls. We identified and validated somatic L1Hs insertions in both cortical neurons and non-brain tissues. In Rett patients, somatic insertions were significantly depleted in exons—mainly contributed by long genes—than healthy controls, implying that cells carryingMECP2mutations might be defenseless against a second exonic L1Hs insertion. We observed a significant increase of somatic L1Hs insertions in the brain compared with non-brain tissues from the same individual. Compared to germline insertions, somatic insertions were less sense-depleted to transcripts, indicating that they underwent weaker selective pressure on the orientation of insertion. Our observations demonstrate that somatic L1Hs insertions contribute to genomic diversity and MECP2 dysfunction alters their genomic patterns in Rett patients.Author SummaryHuman-specific LINE-1 (L1Hs) is the most active autonomous retrotransposon family in the human genome. Mounting evidence supports that L1Hs retrotransposition occurs postzygotically in the human brain cells, contributing to neuronal genomic diversity, but the extent of L1Hs-driven mosaicism in the brain is debated. In this study, we profiled genome-wide L1Hs insertions among 20 postmortem tissues from Rett patients and matched controls. We identified and validated somatic L1Hs insertions in both cortical neurons and non-brain tissues, with a higher jumping activity in the brain. We further found that MECP2 dysfunction might alter the genomic pattern of somatic L1Hs in Rett patients.
Combinatorial Control through Allostery
Authors: Galstyan Vahe , Funk Luke , Einav Tal , Phillips Rob 
Published: December 2018

AbstractMany instances of cellular signaling and transcriptional regulation involve switch-like molecular responses to the presence or absence of input ligands. To understand how these responses come about and how they can be harnessed, we develop a statistical mechanical model to characterize the types of Boolean logic that can arise from allosteric molecules following the Monod-Wyman-Changeux (MWC) model. Building upon previous work, we show how an allosteric molecule regulated by two inputs can elicit AND, OR, NAND and NOR responses, but is unable to realize XOR or XNOR gates. Next, we demonstrate the ability of an MWC molecule to perform ratiometric sensing - a response behavior where activity depends monotonically on the ratio of ligand concentrations. We then extend our analysis to more general schemes of combinatorial control involving either additional binding sites for the two ligands or an additional third ligand and show how these additions can cause a switch in the logic behavior of the molecule. Overall, our results demonstrate the wide variety of control schemes that biological systems can implement using simple mechanisms.