bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rotational variation of the linear polarization of the asteroid (3200) Phaethon as evidence for inhomogeneity in its surface properties
Authors: Borisov G , Devogèle M , Cellino A , Bagnulo S , Christou A , Bendjoya Ph , Rivet J-P , Abe L , Vernet D , Donchev Z , Krugly Yu , Belskaya I , Bonev T , Steeghs D , Galloway D , Dhillon V , O’Brien P , Pollacco D , Poshyachinda S , Ramsay G , Thrane E , Ackley K , Rol E , Ulaczyk K , Cutter R , Dyer M 
Published: July 2018

ABSTRACT
Asteroid (3200) Phaethon is a Near-Earth Apollo asteroid with an unusual orbit that brings it closer to the Sun than any other known asteroid. Its last close approach to the Earth was in 2017 mid-December and the next one will be on 2026 October. Previous rotationally time-resolved spectroscopy of Phaethon showed that its spectral slope is slightly bluish, in agreement with its B/F taxonomic classification, but at some rotational phases, it changes to slightly reddish. Motivated by this result, we performed time-resolved imaging polarimetry of Phaethon during its recent close approach to the Earth. Phaethon has a spin period of 3.604 h, and we found a variation of the linear polarization with rotation. This seems to be a rare case in which such variation is unambiguously found, also a consequence of its fairly large amplitude. Combining this new information with the brightness and colour variation as well as previously reported results from Arecibo radar observations, we conclude that there is no variation of the mineralogy across the surface of Phaeton. However, the observed change in the linear polarization may be related to differences in the thickness of the surface regolith in different areas or local topographic features.
Predictors of Missed Hepatitis C Intake Appointments and Failure to Establish Hepatitis C Care Among Patients Living With HIV
Authors: Cachay Edward R , Hill Lucas , Torriani Francesca , Ballard Craig , Grelotti David , Aquino Abigail , Christopher Mathews W 
Published: July 2018

Abstract

Background
We estimated and characterized the proportion of patients living with HIV (PLWH) who missed hepatitis C (HCV) intake appointments and subsequently failed to establish HCV care.

Methods
Logistic regression analyses were used to identify factors associated with missed HCV intake appointments and failure to establish HCV care among PLWH referred for HCV treatment between January 2014 and December 2017. In addition to demographics, variables included HIV treatment characteristics, type of insurance, liver health status, active alcohol or illicit drug use, unstable housing, and history of a mental health disorder (MHD).

Results
During the study period, 349 new HCV clinic appointments were scheduled for 202 unduplicated patients. Approximately half were nonwhite, and 80% had an undetectable HIV viral load. Drug use (31.7%), heavy alcohol use (32.8%), and MHD (37.8%) were prevalent. Over the 4-year period, 21.9% of PLWH referred for HCV treatment missed their HCV intake appointment. The proportion increased each year, from 17.2% in 2014 to 25.4% in 2017 (P = .021). Sixty-six of the 202 newly referred HCV patients (32.7%) missed their first HCV appointment, and 28 of these (42.4%) failed to establish HCV care. Having a history of MHD, CD4 &lt;200, ongoing drug use, and being nonwhite were independent predictors of missing an intake HCV appointment. The strongest predictor of failure to establish HCV care was having a detectable HIV viral load.

Conclusions
The proportion of PLWH with missed HCV appointments increased over time. HCV elimination among PLWH may require integrated treatment of MHD and substance use.
Epidemiology and Clinical Features of Invasive Fungal Infection in a US Health Care Network
Authors: Webb Brandon J , Ferraro Jeffrey P , Rea Susan , Kaufusi Stephanie , Goodman Bruce E , Spalding James 
Published: July 2018

Abstract

Background
A better understanding of the epidemiology and clinical features of invasive fungal infection (IFI) is integral to improving outcomes. We describe a novel case-finding methodology, reporting incidence, clinical features, and outcomes of IFI in a large US health care network.

Methods
All available records in the Intermountain Healthcare Enterprise Data Warehouse from 2006 to 2015 were queried for clinical data associated with IFI. The resulting data were overlaid in 124 different combinations to identify high-probability IFI cases. The cohort was manually reviewed, and exclusions were applied. European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group Consensus Group definitions were adapted to categorize IFI in a broad patient population. Linear regression was used to model variation in incidence over time.

Results
A total of 3374 IFI episodes occurred in 3154 patients. The mean incidence was 27.2 cases/100 000 patients per year, and there was a mean annual increase of 0.24 cases/100 000 patients (P = .21). Candidiasis was the most common (55%). Dimorphic fungi, primarily Coccidioides spp., comprised 25.1% of cases, followed by Aspergillus spp. (8.9%). The median age was 55 years, and pediatric cases accounted for 13%; 26.1% of patients were on immunosuppression, 14.9% had autoimmunity or immunodeficiency, 13.3% had active malignancy, and 5.9% were transplant recipients. Lymphopenia preceded IFI in 22.1% of patients. Hospital admission occurred in 76.2%. The median length of stay was 16 days. All-cause mortality was 17.0% at 42 days and 28.8% at 1 year. Forty-two-day mortality was highest in Aspergillus spp. (27.5%), 20.5% for Candida, and lowest for dimorphic fungi (7.5%).

Conclusions
In this population, IFI was not uncommon, affected a broad spectrum of patients, and was associated with high crude mortality.
Adenovirus Type 21 Outbreak Among Lung Transplant Patients at a Large Tertiary Care Hospital
Authors: Philo Sarah E , Anderson Benjamin D , Costa Sylvia F , Henshaw Nancy , Lewis Sarah S , Reynolds John M , Jayakumar Jayanthi , Su Yvonne C F , Gray Gregory C 
Published: July 2018

Abstract
Here we summarize an April 2016, 7-patient cluster of human adenovirus (HAdV) infections in a cardiothoracic surgery intensive care unit. We show that the patients were infected with a single HAdV21b type. Rapid HAdV typing diagnostics and effective antiviral interventions are needed for immunocompromised patients suffering from HAdV infections.
Anatomic Nuances of the Ophthalmic Artery Origin from a Ventral Viewpoint: Considerations and Implications for Endoscopic Endonasal Surgery
Authors: Naudy Cristian A , Yanez-Siller Juan C , Mesquita Filho Paulo M , Gomez G. Matias , Otto Bradley A , Carrau Ricardo L , Prevedello Daniel M 
Published: July 2018

Abstract

BACKGROUND
The origin of the ophthalmic artery is within the surgical field of endoscopic endonasal approaches (EEAs) to the suprasellar and parasellar regions. However, its anatomy from the endoscopic point-of-view has not been adequately elucidated.

OBJECTIVE
To highlight the anatomy of the ophthalmic artery origin from an endoscopic endonasal perspective.

METHODS
The origin of the ophthalmic artery was studied bilaterally under endoscopic visualization, after performing transplanum/transtubercular EEAs in 17 cadaveric specimens (34 arteries). Anatomic relationships relevant to surgery were evaluated. To complement the cadaveric findings, the ophthalmic artery origin was reviewed in 200 “normal” angiographic studies.

RESULTS
On the right side, 70.6% of ophthalmic arteries emerged from the superior aspect, while 17.6% and 11.8% emerged from the superomedial and superolateral aspects of the intradural internal carotid artery, respectively. On the left, 76.5%, 17.6%, and 5.9% of ophthalmic arteries emerged from the superior, superomedial, and superolateral aspects of the internal carotid, respectively. Similar findings were observed on angiography. All ophthalmic arteries emerged at the level of the medial opticocarotid recess. Overall, 47%, 26.5%, and 26.5% of ophthalmic arteries (right and left) were inferolateral, inferior, and inferomedial to the intracranial optic nerve segment, respectively. On both sides, the intracranial length of the ophthalmic artery ranged from 1.5 to 4.5 mm (mean: 2.90 ± standard deviation of 0.74 mm).

CONCLUSION
Awareness of the endoscopic nuances of the ophthalmic artery origin is paramount to minimize the risk of sight-threatening neurovascular injury during EEAs to the suprasellar and parasellar regions.
Cloning, gene regulation, and neuronal proliferation functions of novel N‐terminal–truncated carboxypeptidase E/neurotrophic factor‐αl variants in embryonic mouse brain
Authors: Xiao Lan , Yang Xuyu , Sharma Vinay Kumar , Loh Y. Peng 
Published: July 2018

ABSTRACTCarboxypeptidase E (CPE), an exopeptidase involved in proneuropeptide processing, is also a neurotrophic factor, named neurotrophic factor‐α1 (NF‐α1) and has important roles in neuroprotection, stem cell differentiation, and neurite outgrowth, independent of enzymatic activity. Additionally, an N‐terminal–truncated CPE/NF‐α1 variant, (CPE/NF‐α1)‐ΔN, proposed from bioinformatic analysis of GenBank (National Center for Biotechnology Information, Bethesda, MD, USA) DNA sequences and encoding a 40‐kDa protein, has been found to be exclusively expressed in embryonic neurons. To investigate the function of (CPEZNF‐α1)‐ΔN in neurodevelopment, we first cloned (CPEZNF‐α1)‐ΔN transcripts from an embryonic mouse brain. A rapid amplification of cDNA ends assay, DNA sequencing, and Northern blot revealed 1.9‐ and 1.73‐kb transcripts, which encoded 47‐ and 40‐kDa (CPE/NF‐α1)‐ΔN proteins, respectively. Those proteins were expressed in embryonic mouse brain. Expression of the 2 (CPE/NF‐α1)‐ΔN mRNAs surged at embryonic d 10.5, correlating with the time of neurogenesis in the developing brain and also at postnatal d 1. HT22 cells, a mouse hippocampal cell line, transduced with 40 kDa (CPE/NF‐α1)‐ΔN up‐regulated expression of genes involved in embryonic neurodevelopment: insulin‐like growth factor binding protein 2 (IGFBP2), death‐associated protein 1, and ephrin A1, which regulate proliferation, programmed cell death, and neuronal migration, respectively. HT22 cells and embryonic cortical neurons overexpressing 40 kDa (CPE/NF‐α1)‐ΔN exhibited enhanced proliferation, which was inhibited by IGFBP2 short interfering RNA treatment. Thus, 40 kDa (CPE/NF‐α1)‐ΔN has an important, enzymatically independent role in the regulation of genes critical for neurodevelopment.—Xiao, L., Yang, X., Sharma, V. K., Loh, Y. P. Cloning, gene regulation, and neuronal proliferation functions of novel N‐terminal–truncated carboxypeptidase E/neurotrophic factor‐α1 variants in embryonic mouse brain. FASEB J. 33, 808–820 (2019). www.fasebj.org
Juvenile hormone–dependent Kazal‐type serine protease inhibitor Greglin safeguards insect vitellogenesis and egg production
Authors: Guo Wei , Wu Zhongxia , Yang Libin , Cai Zhaokui , Zhao Lianfeng , Zhou Shutang 
Published: July 2018

ABSTRACTIn addition to preventing insect metamorphosis, juvenile hormone (JH) is known to stimulate aspects of insect reproduction. However, the molecular mechanisms of JH action in insect reproduction remain largely unknown. By reanalyzing the transcriptomic data from adults and other developmental stages of the migratory locust Locusta migratoria, we identified a gene coding for Kazal‐type protease inhibitor, previously named Greglin. Greglin is specifically expressed in adult females and most abundant in the fat body and ovaries. Interestingly, Greglin is among the top 3 of highly expressed genes in adult female locusts, after 2 vitellogenin (Vg) genes. Greglin is induced by JH and expressed at remarkably high levels in the vitellogenic stage. Knockdown of Greglin in adult female locusts results in accelerated degradation of serine protease substrate and significantly reduced levels of Greglin protein in hemolymph and ovaries. The consequent phenotypes include blocked oocyte maturation, arrested ovarian growth and shrunken follicular epithelium, as well as declines in egg number and hatchability. The data provide the first evidence, to our knowledge, that JH‐dependent Greglin is involved in locust vitellogenesis and oocyte maturation likely by protecting vitellogenesis and other forms of yolk precursors from proteolysis. The result offers new insights into the regulation of JH and function of protease inhibitors in insect vitellogenesis, oocyte maturation and fecundity.—Guo, W., Wu, Z., Yang, L., Cai, Z., Zhao, L., Zhou, S. Juvenile hormone–dependent Kazal‐type serine protease inhibitor Greglin safeguards insect vitellogenesis and egg production. FASEB J. 33, 917–927 (2019). www.fasebj.org
Sexually dimorphic gene expression and transcriptome evolution provides mixed evidence for a fast-Z effect inHeliconius
Authors: Pinharanda A , Rousselle M , Martin SH , Hanly JJ , Davey JW , Kumar S , Galtier N , Jiggins CD 
Published: July 2018

AbstractSex chromosomes have different evolutionary properties as compared to the autosomes due to their hemizygous nature. In particular, recessive mutations are more readily exposed to selection, which can lead to faster rates of molecular evolution. Here, we report patterns of gene expression and molecular evolution in the sex chromosomes of a group of tropical butterflies. We first improved the completeness of theHeliconius melpomenereference annotation, a neotropical butterfly with a ZW sex determination system. Then we sequenced RNA from male and female whole abdomens and female ovary and gut tissue to identify sex and tissue specific gene expression profiles inH. melpomene. Using these expression profiles we compare sequence divergence and polymorphism, the strength of positive and negative selection and rates of adaptive evolution for Z and autosomal genes between two species ofHeliconiusbutterflies,H. melpomeneandH. erato.We show that the rate of adaptive substitutions is higher for Z as compared to autosomal genes, but contrary to expectation it is also higher for male as compared to female biased genes. There is therefore mixed evidence that hemizygosity influences the rate of adaptive substitutions. Additionally, we find no significant increase in the rate of adaptive evolution or purifying selection on genes expressed in ovary tissue, a heterogametic specific tissue. Together our results provide limited support for fast-Z evolution. This contributes to a growing body of literature from other ZW systems that also provide mixed evidence for a fast-Z effect.
Considerations for imaging thick, low contrast, and beam sensitive samples with liquid cell transmission electron microscopy
Authors: Moser Trevor H. , Shokuhfar Tolou , Evans James E. 
Published: July 2018

AbstractTransmission electron microscopy of whole cells is hindered by the inherently large thickness and low atomic contrast intrinsic of cellular material. Liquid cell transmission electron microscopy allows samples to remain in their native hydrated state and may permit visualizing cellular dynamics in-situ. However, imaging biological cells with this approach remains challenging and identifying an optimal imaging regime using empirical data would help foster new advancements in the field. Recent questions about the role of the electron beam inducing morphological changes or damaging cellular structure and function necessitates further investigation of electron beam-cell interactions, but is complicated by variability in imaging techniques used across various studies currently present in literature. The necessity for using low electron fluxes for imaging biological samples requires finding an imaging strategy which produces the strongest contrast and signal to noise ratio for the electron flux used. Here, we experimentally measure and evaluate signal to noise ratios and damage mechanisms between liquid and cryogenic samples for cells using multiple electron imaging modalities all on the same instrument and with equivalent beam parameters to standardize the comparison. We also discuss considerations for optimal electron microscopy imaging conditions for future studies on whole cells within liquid environments.
Modeling the MYC-driven normal-to-tumour switch in breast cancer
Authors: Lourenco Corey , Kalkat Manpreet , Houlahan Kathleen E. , Melo Jason De , Longo Joseph , Done Susan J. , Boutros Paul C. , Penn Linda Z. 
Published: July 2018

ABSTRACTThe potent MYC oncoprotein is deregulated in many human cancers, including breast carcinoma, and is associated with aggressive disease. To understand the mechanisms and vulnerabilities of MYC-driven breast cancer, we have generated anin vivomodel that mimics human disease in response to MYC deregulation. MCF10A cells ectopically expressing a common breast cancer mutation in the PI3 kinase pathway (PIK3CAH1047R) lead to the development of organized acinar structures in mice. However, expressing both PIK3CAH1047Rand deregulated-MYC lead to the development of invasive ductal carcinoma, thus creating a model in which a MYC-dependent normal-to-tumour switch occursin vivo. These MYC-driven tumors exhibit classic hallmarks of human breast cancer at both the pathological and molecular levels. Moreover, tumour growth is dependent upon sustained deregulated MYC expression, further demonstrating addiction to this potent oncogene and regulator of gene transcription. We therefore provide a MYC-dependent human model of breast cancer which can be assayed forin vivotumour initiation, proliferation, and transformation from normal breast acini into invasive breast carcinoma. Taken together, we anticipate that this novel MYC-driven transformation model will be a useful research tool to both better understand MYC’s oncogenic function and identify therapeutic vulnerabilities.Conflict of interest statementThe authors declare no potential conflicts of interest.
Effect ofde novotranscriptome assembly on transcript quantification
Authors: Hsieh Ping-Han , Oyang Yen-Jen , Chen Chien-Yu 
Published: July 2018

AbstractBackgroundCorrect quantification of transcript expression is essential to understand the functional products of the genome in different physiological conditions and developmental stages. Recently, the development of high-throughput RNA sequencing (RNA-Seq) allows the researchers to perform transcriptome analysis for the organisms without the reference genome and transcriptome. For such projects,de novotranscriptome assembly must be carried out prior to quantification. However, a large number of erroneous contigs produced by the assemblers might result in unreliable estimation on the abundance of transcripts. In this regard, this study comprehensively investigates how assembly quality affects the performance of quantification for RNA-Seq analysis based onde novotranscriptome assembly.ResultsSeveral important factors that might seriously affect the accuracy of the RNA-Seq analysis were thoroughly discussed. First, we found that the assemblers perform comparatively well for the transcriptomes with lower biological complexity. Second, we examined the over-extended and incomplete contigs, and then demonstrated that assembly completeness has a strong impact on the estimation of contig abundance. Lastly, we investigated the behavior of the quantifiers with respect to sequence ambiguity which might be originally present in the transcriptome or accidentally produced by assemblers. The results suggest that the quantifiers often over-estimate the expression of family-collapse contigs and under-estimate the expression of duplicated contigs. For organisms without reference transcriptome, it remained challenging to detect the inaccurate abundance estimation on family-collapse contigs. On the contrary, we observed that the situation of under-estimation on duplicated contigs can be warned through analyzing the read distribution of the duplicated contigs.ConclusionsIn summary, we explicated the behavior of quantifiers when erroneous contigs are present and we outlined the potential problems that the assemblers might cause for the downstream analysis of RNA-Seq. We anticipate the analytic results conducted in this study provides valuable insights for future development of transcriptome assembly and quantification.Availabilitywe proposed an open-source Python based package QuantEval that builds connected components for the assembled contigs based on sequence similarity and evaluates the quantification results for each connected component. The package can be downloaded fromhttps://github.com/dn070017/QuantEval.
Developmental fidelity imposed by the RGL-1 “Balanced Switch” mediating opposing signals
Authors: Shin Hanna , Braendle Christian , Monahan Kimberly B. , Kaplan Rebecca E.W. , Zand Tanya P. , Mote F. Sefakor , Craig DeSean R. , Peters Eldon , Reiner David J. 
Published: July 2018

AbstractThe sixC. elegansvulval precursor cells (VPCs) are induced to form the 30-30-20-Γ-20-3° pattern of cell fates with high fidelity. In response to EGF signal, the LET-60/Ras-LIN-45/Raf-MEK-2/MEK-MPK-1/ERK canonical MAP kinase cascade is necessary to induce 1° fate and synthesis of DSL ligands. In turn, LIN-12/Notch signal is necessary to induce neighboring cells to become 2°. We previously showed that, in response to lower dose of EGF signal, the modulatory LET-60/Ras-RGL-1/RalGEF-RAL-1/Ral signal promotes 2° fate in support of LIN-12. In this study we identify two key differences between RGL-1 and RAL-1 functions. First, deletion of RGL-1 confers no overt developmental defects, while previous studies showed RAL-1 to be essential for viability and fertility. From this observation we hypothesize that the developmentally essential functions of RAL-1 are independent of upstream activation. Second, RGL-1 plays opposing and genetically separable roles in VPC fate patterning. RGL-1 promotes 2° fate via canonical GEF-dependent activation of RAL-1 and 1° fate via a non-canonical GEF-independent activity. Our genetic epistasis experiments are consistent with RGL-1 functioning in the modulatory 1°-promoting AGE-1/PI3-Kinase-PDK-1-AKT-1 cascade. Additionally, animals without RGL-1 experience 15-fold higher rates of VPC patterning errors compared to the wild type. Yet VPC patterning in RGL-1 deletion mutants is not more sensitive to environmental perturbations. We propose that RGL-1 functions as a “Balanced Switch” that orchestrates opposing 1°- and 2°-promoting modulatory cascades to decrease inappropriate fate decisions. We speculate that such switches are broadly conserved but mostly masked by paralog redundancy or essential genes.