bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endoscopic Removal of Displaced Sagittal Intracapsular Condylar Fracture
Authors: Trento Guilherme dos Santos , Gorla Luis Fernando de Oliveira , Rodrigues Marcos Marques , Pereira-Filho Valfrido Antônio 
Published: September 2017

Abstract
Fractures involving the mandibular condyle are among the most common fractures of facial bones and still generate great discussion concerning therapeutic issues. Several factors have influence on the decision of treatment management of these fractures. In some patients, even when there is displacement of fractured fragments, the choice for conservative treatment is made. However, the removal of the condyle fragment may be required. In the oral surgery scope, endoscopy is a procedure used in many areas, and can be helpful to improve the visualization of surgical sites with difficult access. The endoscopic surgery brings benefits to patient such as no scar or minimal scar, lower risk to nerve damage, and decreased of surgical trauma and bleeding. In addition, according to surgeon experience, the surgery may become more dynamic. The aim of this study is to present an endoscopic technique associated with a transoral approach to remove a displaced sagittal intracapsular condyle fragment. Furthermore, to expose the advantages and benefits of this technique as well as the satisfactory results achieved.
Role of M2 Macrophages in Sepsis-Induced Acute Kidney Injury
Authors: Li Xing , Mu Genhua , Song Chunmei , Zhou Liangliang , He Lei , Jin Qin , Lu Zhongqian 
Published: September 2017

ABSTRACT

Background:
Sepsis is a major cause of acute kidney injury (AKI), with high rates of morbidity and mortality. M2 macrophages have been shown to play important roles in the secretion of anti-inflammatory and tissue repair mediators. In this study, we investigate the role of M2 macrophages in sepsis-induced AKI by depleting these cells in vivo through the systemic administration of liposomal clodronate (LC).

Methods:
Male Sprague–Dawley rats were subjected to cecal ligation and puncture (CLP) or sham surgery. Biochemical and histological renal damage was assessed. Macrophage infiltration and M2 macrophage depletion were assessed by immunohistochemistry. RT-PCR was used to investigate the expression of the inducible nitric oxide synthase (iNOS), arginase 1 (Arg-1), and found in inflammatory zone 1 (FIZZ1) mRNAs. Western blots were performed to assay the tissue levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α).

Results:
M2 macrophages were obviously detected 72 h after sepsis-induced AKI. Kidney injury was more severe, renal function was decreased, and blood creatinine and blood urea nitrogen (BUN) levels were higher after M2 macrophage depletion. M2 macrophage depletion significantly inhibited the proliferation of tubular cells. M2 macrophage depletion also downregulated IL-10 expression and increased TNF-α secretion during sepsis-induced AKI.

Conclusions:
M2 macrophages attenuate sepsis-induced AKI, presumably by upregulating IL-10 expression and suppressing TNF-α secretion.
Comparing 3-Dimensional Ultrasound to 3-Dimensional Magnetic Resonance Imaging in the Detection of Levator Ani Defects
Authors: Calderwood Camille S. , Thurmond Amy , Holland Amanda , Osmundsen Blake , Gregory W. Thomas 
Published: September 2017

Objective
The aim of this study was to compare the detection of levator ani defects (LAD) between 3-dimensional (3D) ultrasound (US) and 3D magnetic resonance imaging (MRI).

Methods
This is a secondary analysis of the Pelvic Floor Nerve Injury Following Childbirth Study. Nulliparous women underwent a standardized protocol of pelvic floor evaluations between January 2008 and December 2013, prior to pregnancy (V1) and at 2 points postpartum: 6 weeks (V2) and 6 months (V3). Those women who underwent a high-resolution 3D MRI pelvic floor sequence were selected. Comparisons were made to concomitantly acquired 3D perineal US. Eight tomographic slices were examined in the axial plane, each side independently scored with 0 (no defect) or 1 (defect). A similar tomographic approach was applied to the MRI. For both MRI and US, the right and left sides were each scored. A total score of 0 to 8 was given to each side. A dichotomous variable “complete LAD” was defined. Cohen κ was used as a measurement of agreement of complete LAD between MRI and US. Kendall τ b was used to correlate total scores.

Results
On the right side, 80 (90%) of 89 pairs were in agreement (concordant in the diagnosis or not of a “defect”). On the left side, 72 (81%) of 89 pairs were in agreement. Correlations (Cohen κ) of complete LAD were 0.65 (P < 0.001) on the right and 0.37 (P < 0.001) on the left. Correlations of total scores were 0.47 (P < 0.001) on the right and 0.41 (P < 0.001) on the left.

Conclusions
Moderate agreement was found between 3D US and 3D MRI LAD detection. More LADs and discordance were seen on the left.
When the Lyon(ized chromosome) roars: ongoing expression from an inactive X chromosome
Authors: Carrel Laura , Brown Carolyn J. 
Published: September 2017

A tribute to Mary Lyon was held in October 2016. Many remarked about Lyon's foresight regarding many intricacies of the X-chromosome inactivation process. One such example is that a year after her original 1961 hypothesis she proposed that genes with Y homologues should escape from X inactivation to achieve dosage compensation between males and females. Fifty-five years later we have learned many details about these escapees that we attempt to summarize in this review, with a particular focus on recent findings. We now know that escapees are not rare, particularly on the human X, and that most lack functionally equivalent Y homologues, leading to their increasingly recognized role in sexually dimorphic traits. Newer sequencing technologies have expanded profiling of primary tissues that will better enable connections to sex-biased disorders as well as provide additional insights into the X-inactivation process. Chromosome organization, nuclear location and chromatin environments distinguish escapees from other X-inactivated genes. Nevertheless, several big questions remain, including what dictates their distinct epigenetic environment, the underlying basis of species differences in escapee regulation, how different classes of escapees are distinguished, and the roles that local sequences and chromosome ultrastructure play in escapee regulation.This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
Mechanistic insights in X-chromosome inactivation
Authors: Lu Zhipeng , Carter Ava C. , Chang Howard Y. 
Published: September 2017

X-chromosome inactivation (XCI) is a critical epigenetic mechanism for balancing gene dosage between XY males and XX females in eutherian mammals. A long non-coding RNA (lncRNA), XIST, and its associated proteins orchestrate this multi-step process, resulting in the inheritable silencing of one of the two X-chromosomes in females. The XIST RNA is large and complex, exemplifying the unique challenges associated with the structural and functional analysis of lncRNAs. Recent technological advances in the analysis of macromolecular structure and interactions have enabled us to systematically dissect the XIST ribonucleoprotein complex, which is larger than the ribosome, and its place of action, the inactive X-chromosome. These studies shed light on key mechanisms of XCI, such as XIST coating of the X-chromosome, recruitment of DNA, RNA and histone modification enzymes, and compaction and compartmentalization of the inactive X. Here, we summarize recent studies on XCI, highlight the critical contributions of new technologies and propose a unifying model for XIST function in XCI where modular domains serve as the structural and functional units in both lncRNA–protein complexes and DNA–protein complexes in chromatin.This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
XISTRNA: a window into the broader role of RNA in nuclear chromosome architecture
Authors: Creamer K. M. , Lawrence J. B. 
Published: September 2017

XISTRNA triggers the transformation of an active X chromosome into a condensed, inactive Barr body and therefore provides a unique window into transitions of higher-order chromosome architecture. Despite recent progress, howXISTRNA localizes and interacts with the X chromosome remains poorly understood. Genetic engineering ofXISTinto a trisomic autosome demonstrates remarkable capacity ofXISTRNA to localize and comprehensively silence that autosome. Thus,XISTdoes not require X chromosome-specific sequences but operates on mechanisms available genome-wide. Prior results suggestedXISTlocalization is controlled by attachment to the insoluble nuclear scaffold. Our recent work affirms that scaffold attachment factor A (SAF-A) is involved in anchoringXIST, but argues against the view that SAF-A provides a unimolecular bridge between RNA and the chromosome. Rather, we suggest that a complex meshwork of architectural proteins interact withXISTRNA. Parallel work studying the territory of actively transcribed chromosomes suggests that repeat-rich RNA ‘coats’ euchromatin and may impact chromosome architecture in a manner opposite ofXIST. A model is discussed whereby RNA may not just recruit histone modifications, but more directly impact higher-order chromatin condensation via interaction with architectural proteins of the nucleus.This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
Regulation of X-chromosome dosage compensation in human: mechanisms and model systems
Authors: Sahakyan Anna , Plath Kathrin , Rougeulle Claire 
Published: September 2017

The human blastocyst forms 5 days after one of the smallest human cells (the sperm) fertilizes one of the largest human cells (the egg). Depending on the sex-chromosome contribution from the sperm, the resulting embryo will either be female, with two X chromosomes (XX), or male, with an X and a Y chromosome (XY). In early development, one of the major differences between XX female and XY male embryos is the conserved process of X-chromosome inactivation (XCI), which compensates gene expression of the two female X chromosomes to match the dosage of the single X chromosome of males. Most of our understanding of the pre-XCI state and XCI establishment is based on mouse studies, but recent evidence from human pre-implantation embryo research suggests that many of the molecular steps defined in the mouse are not conserved in human. Here, we will discuss recent advances in understanding the control of X-chromosome dosage compensation in early human embryonic development and compare it to that of the mouse.
This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
What makes the maternal X chromosome resistant to undergoing imprinted X inactivation?
Authors: Sado Takashi 
Published: September 2017

In the mouse, while either X chromosome is chosen for inactivation in a random fashion in the embryonic tissue, the paternally derived X chromosome is preferentially inactivated in the extraembryonic tissues. It has been shown that the maternal X chromosome is imprinted so as not to undergo inactivation in the extraembryonic tissues. X-linked noncodingXistRNA becomes upregulated on the X chromosome that is to be inactivated. An antisense noncoding RNA,Tsix, which occurs at theXistlocus and has been shown to negatively regulateXistexpression in cis, is imprinted to be expressed from the maternal X in the extraembryonic tissues. AlthoughTsixappears to be responsible for the imprint laid on the maternal X, those who disagree with this idea would point out the fact thatTsixhas not yet been expressed from the maternal X whenXistbecomes upregulated on the paternal but not the maternal X at the onset of imprinted X-inactivation in preimplantation embryos. Recent studies have demonstrated, however, that there is a prominent difference in the chromatin structure at theXistlocus depending on the parental origin, which I suggest might account for the repression of maternalXistin the absence of maternalTsixat the preimplantation stages.This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
Sensory neuropathy-causing mutations in ATL3 cause aberrant ER membrane tethering
Authors: Krols Michiel , Detry Sammy , Asselbergh Bob , Almeida-Souza Leonardo , Kremer Anna , Lippens Saskia , Rycke Riet de , Winter Vicky De , Müller Franz-Josef , Kurth Ingo , McMahon Harvey T. , Savvides Savvas N. , Timmerman Vincent , Janssens Sophie 
Published: September 2017

SUMMARYThe ER is a complex network of sheets and tubules that is continuously being remodeled. The relevance of this membrane dynamics is underscored by the fact that mutations in Atlastins (ATL), the ER fusion proteins in mammals, cause neurodegeneration. How defects in this process disrupt neuronal homeostasis is largely unknown. Here we show by EM volume reconstruction of transfected cells, neurons and patient fibroblasts that the HSAN-causing ATL3 mutants promote aberrant ER tethering hallmarked by bundles of laterally attached ER tubules.In vitro, these mutants cause excessive liposome tethering, recapitulating the results in cells. Moreover, ATL3 variants retain their dimerization-dependent GTPase activity, but are unable to promote membrane fusion, suggesting a defect on an intermediate step of the ATL3 functional cycle. Our data therefore show that the effects of ATL3 mutations on ER network organization stretch beyond a loss of fusion, shedding a new light on neuropathies caused by atlastin defects.
Dual-trait pleiotropic analysis in highly stratified natural populations using genome-wide association summary statistics
Authors: Feng Xiao , Zan Yanjun , Ning Zheng , Xu Weilin , Wan Qianhui , Zeng Dongyu , Zeng Ziyi , Liu Yang , Shen Xia 
Published: September 2017

AbstractGenome-wide association analysis is a powerful tool to identify genomic loci underlying complex traits. However, the application in natural populations comes with challenges, especially power loss due to population stratification. Here, we introduce a bivariate analysis approach to a GWAS dataset ofArabidopsis thaliana. We demonstrate the efficiency of double-phenotype analysisto uncover hidden genetic loci masked by population structure via a series of simulations. In real data analysis, acommon allele, strongly confounded with population structure, is discovered to be associated with late flowering and slow maturation of the plant. The discovered genetic effect on flowering time is further replicated in independent datasets. Using Mendelian randomization analysis based on summary statistics from our GWAS and expression QTL scans, we predicted and replicated a candidate geneAT1G11560that potentially causes this association. Further analysis indicates that this locusis co-selected with flowering-time-related genes. The discovered pleiotropic genotypephenotype map provides new insights into understanding the genetic correlation of complex traits.
Lactose crystallisation in concentrated whey: the influence of vat type
Authors: Simeão Moisés , DA Silva Cleuber R , Stephani Rodrigo , de Oliveira Luiz Fernando C , Schuck Pierre , de Carvalho Antônio F , Perrone Ítalo T 
Published: September 2017

This work aimed to describe the rate of lactose crystallisation in concentrated whey carried out using two different crystallisers, utilising central or lateral stirring. The lactose crystallisation rate differed between treatments, showing high values with use of the central stirrer. Under the experimental conditions, after 4 h of crystallisation, in neither of the vats was 70% lactose crystallisation achieved. With the standardised conditions applied in this study, with soluble solids, time, and stirring and rate cooling being constant, it was possible to verify the influence of the vat type on the rate of lactose crystallisation.
Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma
Authors: Li Shicheng , Sun Xiao , Miao Shuncheng , Liu Jia , Jiao Wenjie 
Published: September 2017

BackgroundCigarette smoking is one of the greatest preventable risk factors for developing cancer, and most cases of lung squamous cell carcinoma (lung SCC) are associated with smoking. The pathogenesis mechanism of tumor progress is unclear. This study aimed to identify biomarkers in smoking‐related lung cancer, including protein‐coding gene, long noncoding RNA, and transcription factors.MethodsWe selected and obtained messenger RNA microarray datasets and clinical data from the Gene Expression Omnibus database to identify gene expression altered by cigarette smoking. Integrated bioinformatic analysis was used to clarify biological functions of the identified genes, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, the construction of a protein–protein interaction network, transcription factor, and statistical analyses. Subsequent quantitative real‐time PCR was utilized to verify these bioinformatic analyses.ResultsFive hundred and ninety‐eight differentially expressed genes and 21 long noncoding RNA were identified in smoking‐related lung SCC. GO and KEGG pathway analysis showed that identified genes were enriched in the cancer‐related functions and pathways. The protein–protein interaction network revealed seven hub genes identified in lung SCC. Several transcription factors and their binding sites were predicted. The results of real‐time quantitative PCR revealed that AURKA and BIRC5 were significantly upregulated and LINC00094 was downregulated in the tumor tissues of smoking patients. Further statistical analysis indicated that dysregulation of AURKA, BIRC5, and LINC00094 indicated poor prognosis in lung SCC.ConclusionProtein‐coding genes AURKA, BIRC5, and LINC00094 could be biomarkers or therapeutic targets for smoking‐related lung SCC.
Alternative Markers of Performance in Simulation: Where We Are and Where We Need To Go
Authors: Willemsen‐Dunlap Ann M. , Binstadt Emily S. , Nguyen Michael C. , Elliott Nicole C. , Cheney Alan R. , Stevens Ronald H. , Dooley‐Hash Suzanne 
Published: September 2017

AbstractThis article on alternative markers of performance in simulation is the product of a session held during the 2017 Academic Emergency Medicine Consensus Conference “Catalyzing System Change Through Health Care Simulation: Systems, Competency, and Outcomes.” There is a dearth of research on the use of performance markers other than checklists, holistic ratings, and behaviorally anchored rating scales in the simulation environment. Through literature review, group discussion, and consultation with experts prior to the conference, the working group defined five topics for discussion: 1) establishing a working definition for alternative markers of performance, 2) defining goals for using alternative performance markers, 3) implications for measurement when using alternative markers, identifying practical concerns related to the use of alternative performance markers, and 5) identifying potential for alternative markers of performance to validate simulation scenarios. Five research propositions also emerged and are summarized.
Primary thromboprophylaxis (PTP) in ambulatory patients with lung cancer receiving chemotherapy: A systematic review and meta‐analysis of randomized controlled trials (RCTs)
Authors: Thein Kyaw Zin , Yeung Sai‐Ching J. , Oo Thein Hlaing 
Published: September 2017

AbstractBackgroundThromboembolism (TE) is a leading cause of death in cancer patients. Primary thromboprophylaxis (PTP) in ambulatory cancer patients receiving chemotherapy has been debated and considered to potentially improve survival by reducing TE occurrence.ObjectiveWe conducted a systematic review and meta‐analysis of randomized controlled trials (RCTs) in ambulatory lung cancer (LC) patients on chemotherapy to determine the benefit and risk of PTP with low‐molecular‐weight heparins (LMWHs).MethodA literature search using MEDLINE and EMBASE databases was performed through June 2016. RCTs with venous thromboembolism (VTE) reduction as primary or secondary endpoints were included. Mantel–Haenszel method was used to estimate the pooled event risk ratio as well as pooled absolute risk difference with 95% confidence interval (CI).ResultA total of 4315 LC patients from six studies were available for analysis. PTP lasted for 4 to 6 months. The venous thromboembolism (VTE) incidence was 4.0% and 7.9% in LMWH and control groups, respectively (risk ratio, 0.510 (95% CI, 0.397–0.654, P < 0.001). The absolute risk difference in VTE was −0.039 (95% CI, −0.053 to −0.025, P < 0.001), with an estimated number needed to treat (NNT) of 25 to prevent one VTE event. The pooled risk ratio for major bleeding was 1.468 (95% CI, 0.785–2.746, P = 0.229). The pooled risk ratio for overall survival was statistically nonsignificant at 1.020 (95% CI, 0.938–1.109, P = 0.648).ConclusionRoutine PTP for ambulatory LC patients receiving chemotherapy is not recommended and further studies are necessary to define a subset of ambulatory LC patients receiving chemotherapy who may benefit from PTP.
Distinct peripheral vs mucosal T‐cell phenotypes in chlamydia‐infected women
Authors: Ogendi Brian M. O. , Bakshi Rakesh K. , Sabbaj Steffanie , Brown LaDraka' , Lee Jeannette Y. , Kapil Richa , Geisler William M. 
Published: September 2017

ProblemDifferences in circulating (peripheral) and mucosal T‐cell phenotypes in chlamydia‐infected women remain largely unknown.Method of studyThirteen paired mononuclear cell specimens from blood and cervicovaginal lavages collected from chlamydia‐infected women were stained and analyzed using ten‐color cell surface flow cytometry for T‐cell distribution, activation status, homing, and T helper (Th)‐associated chemokine receptors (CKRs).ResultsA higher proportion of genital mucosal T‐cells were activated (CD38+HLA‐DR+) and expressed CCR5 and Th1‐associated CKR CXCR3+CCR5+ compared to peripheral T‐cells, but a lower proportion of mucosal T‐cells expressed homing CKR CCR7, Th‐2 associated CKR CCR4, and CXCR3+CCR4+ for both T‐cell subsets.ConclusionT‐cell phenotypes differed in the peripheral vs genital mucosa compartments in chlamydia‐infected women. As chlamydia infects mucosal epithelial cells, the finding of a higher frequency of activated T‐cells and Th‐1 phenotypes in the mucosa likely reflects an adaptive immune response to infection.
Informing Aerial Total Counts with Demographic Models: Population Growth of Serengeti Elephants Not Explained Purely by Demography
Authors: Morrison Thomas A. , Estes Anna B. , Mduma Simon A.R. , Maliti Honori T. , Frederick Howard , Kija Hamza , Mwita Machoke , Sinclair A.R.E. , Kohi Edward M. 
Published: September 2017

AbstractConservation management is strongly shaped by the interpretation of population trends. In the Serengeti ecosystem, Tanzania, aerial total counts indicate a striking increase in elephant abundance compared to all previous censuses. We developed a simple age‐structured population model to guide interpretation of this reported increase, focusing on three possible causes: (1) in situ population growth, (2) immigration from Kenya, and (3) differences in counting methodologies over time. No single cause, nor the combination of two causes, adequately explained the observed population growth. Under the assumptions of maximum in situ growth and detection bias of 12.7% in previous censuses, conservative estimates of immigration from Kenya were between 250 and 1,450 individuals. Our results highlight the value of considering demography when drawing conclusions about the causes of population trends. The issues we illustrate apply to other species that have undergone dramatic changes in abundance, as well as many elephant populations.