bluuebunny/crossref_metadata_2025_split huggingface dataset:
Urdu Translation of Friendship Scale: Evidence for the Validity and Measurement Invariance Across Gender
Authors: Khan Anam , Adil Adnan 
Published: June 2020

AbstractSocial isolation is a state of nearly-absolute lack of interaction between an individual and society. The Friendship Scale (Hawthorne, 2006) is a measure of social isolation that needed to be translated in the Urdu language for its validation for the Pakistani population owing to its brevity and sound psychometric properties. For the Urdu translation, the standard back-translation procedure was adopted, and the cross-language validation of the translated version was undertaken on a purposive sample of (N= 60) older adults with a minimum age of 60 years. The test-retest reliability of one week for the Urdu-English and English-Urdu version was .95 and .97, respectively. In an independent purposive sample of older adults (N= 500; men = 263 and women = 237) from Lahore and Sargodha districts, the CFA of the Friendship Scale revealed a single factor solution with six indicators, which demonstrated configural, metric, and scalar invariance across both genders and comparable latent mean scores of men and women. The Friendship Scale demonstrated a significant positive relationship with depression and non-significant association with the assimilation, which provided evidence for the convergent and discriminant validities, respectively. Furthermore, evidence of the concurrent validity was established as the older adults whose spouses had died scored significantly higher on the Friendship scale as compared to their counterparts who were living with their spouses. These pieces of evidence suggest that the Urdu version of the Friendship scale is a reliable and valid measure of flourishing for both genders.
Genetic and epigenetic profiling of BRCA1/2 in ovarian tumors reveals additive diagnostic yield and evidence of a genomic BRCA1/2 DNA methylation signature
Authors: Aref-Eshghi Erfan , McGee Jacob D. , Pedro Victor P. , Kerkhof Jennifer , Stuart Alan , Ainsworth Peter J. , Lin Hanxin , Volodarsky Michael , McLachlin Catherine Meg , Sadikovic Bekim 
Published: June 2020

AbstractPoly-ADP-ribose-polymerase inhibitor (PARPi) treatment is indicated for advanced-stage ovarian tumors with BRCA1/2 deficiency. The “BRCAness” status is thought to be attributed to a tumor phenotype associated with a specific epigenomic DNA methylation profile. Here, we examined the diagnostic impact of combined BRCA1/2 sequence, copy number, and promoter DNA methylation analysis, and evaluated whether genomic DNA methylation patterns can predict the BRCAness in ovarian tumors. DNA sequencing of 172 human tissue samples of advanced-stage ovarian adenocarcinoma identified 36 samples with a clinically significant tier 1/2 sequence variants (point mutations and in/dels) and 9 samples with a CNV causing a loss of function in BRCA1/2. DNA methylation analysis of the promoter of BRCA1/2 identified promoter hypermethylation of BRCA1 in two mutation-negative samples. Computational modeling of genome-wide methylation markers, measured using Infinium EPIC arrays, resulted in a total accuracy of 0.75, sensitivity: 0.83, specificity: 0.64, positive predictive value: 0.76, negative predictive value: 0.74, and area under the receiver’s operating curve (AUC): 0.77, in classifying tumors harboring a BRCA1/2 defect from the rest. These findings indicate that the assessment of CNV and promoter DNA methylation in BRCA1/2 increases the cumulative diagnostic yield by 10%, compared with the 20% yield achieved by sequence variant analysis alone. Genomic DNA methylation data can partially predict BRCAness in ovarian tumors; however, further investigation in expanded BRCA1/2 cohorts is needed, and the effect of other double strand DNA repair gene defects in these tumors warrants further investigations.
SARS-CoV-2 infection and overactivation of Nlrp3 inflammasome as a trigger of cytokine “storm” and risk factor for damage of hematopoietic stem cells
Authors: Ratajczak Mariusz Z. , Kucia Magda 
Published: June 2020

AbstractThe scientific community faces an unexpected and urgent challenge related to the SARS-CoV-2 pandemic and is investigating the role of receptors involved in entry of this virus into cells as well as pathomechanisms leading to a cytokine “storm,” which in many cases ends in severe acute respiratory syndrome, fulminant myocarditis and kidney injury. An important question is if it may also damage hematopoietic stem progenitor cells?
MeCP2 facilitates breast cancer growth via promoting ubiquitination-mediated P53 degradation by inhibiting RPL5/RPL11 transcription
Authors: Tong DongDong , Zhang Jing , Wang XiaoFei , Li Qian , Liu Li Ying , Yang Juan , Guo Bo , Ni Lei , Zhao LingYu , Huang Chen 
Published: June 2020

AbstractMethyl-CpG-binding protein 2 (MeCP2) facilitates the carcinogenesis and progression of several types of cancer. However, its role in breast cancer and the relevant molecular mechanism remain largely unclear. In this study, analysis of the Cancer Genome Atlas (TCGA) data that MeCP2 expression was significantly upregulated in breast cancer tissues, and high MeCP2 expression was correlated with poor overall survival. Knockdown of MeCP2 inhibited breast cancer cell proliferation and G1–S cell cycle transition and migration as well as induced cell apoptosis in vitro. Moreover, MeCP2 knockdown suppressed cancer cell growth in vivo. Investigation of the molecular mechanism showed that MeCP2 repressed RPL11 and RPL5 transcription by binding to their promoter regions. TCGA data revealed significantly lower RPL11 and RPL5 expression in breast cancer tissues; additionally, overexpression of RPL11/RPL5 significantly suppressed breast cancer cell proliferation and G1–S cell cycle transition and induced apoptosis in vitro. Furthermore, RPL11 and RPL5 suppressed ubiquitination-mediated P53 degradation through direct binding to MDM2. This study demonstrates that MeCP2 promotes breast cancer cell proliferation and inhibits apoptosis through suppressing RPL11 and RPL5 transcription by binding to their promoter regions.
Potential utilization of terrestrially derived dissolved organic matter by aquatic microbial communities in saline lakes
Authors: Yang Jian , Jiang Hongchen , Liu Wen , Huang Liuqin , Huang Jianrong , Wang Beichen , Dong Hailiang , Chu Rosalie K , Tolic Nikola 
Published: June 2020

AbstractLakes receive large amounts of terrestrially derived dissolved organic matter (tDOM). However, little is known about how aquatic microbial communities interact with tDOM in lakes. Here, by performing microcosm experiments we investigated how microbial community responded to tDOM influx in six Tibetan lakes of different salinities (ranging from 1 to 358 g/l). In response to tDOM addition, microbial biomass increased while dissolved organic carbon (DOC) decreased. The amount of DOC decrease did not show any significant correlation with salinity. However, salinity influenced tDOM transformation, i.e., microbial communities from higher salinity lakes exhibited a stronger ability to utilize tDOM of high carbon numbers than those from lower salinity. Abundant taxa and copiotrophs were actively involved in tDOM transformation, suggesting their vital roles in lacustrine carbon cycle. Network analysis indicated that 66 operational taxonomic units (OTUs, affiliated with Alphaproteobacteria, Actinobacteria, Bacteroidia, Bacilli, Gammaproteobacteria, Halobacteria, Planctomycetacia, Rhodothermia, and Verrucomicrobiae) were associated with degradation of CHO compounds, while four bacterial OTUs (affiliated with Actinobacteria, Alphaproteobacteria, Bacteroidia and Gammaproteobacteria) were highly associated with the degradation of CHOS compounds. Network analysis further revealed that tDOM transformation may be a synergestic process, involving cooperation among multiple species. In summary, our study provides new insights into a microbial role in transforming tDOM in saline lakes and has important implications for understanding the carbon cycle in aquatic environments.
Exosomal miR-130b-3p targets SIK1 to inhibit medulloblastoma tumorigenesis
Authors: Huang Saihua , Xue Ping , Han Xiao , Zhang Caiyan , Yang Lan , Liu Lijuan , Wang Xiang , Li Hao , Fu Jinrong , Zhou Yufeng 
Published: June 2020

AbstractExosomes are an important carrier for cell communication. miRNAs in exosomes are potential biomarkers and therapeutic targets in different types of cancer. However, the role of exosomal miRNAs in medulloblastoma (MB) patients is largely unknown. In this study, we reported that there was a higher level of miR-130b-3p in exosomes derived from MB patient plasma compared with exosomes from healthy control plasma. Exosomes from MB patient plasma could transfer miR-130b-3p to an MB cell line and played suppressor roles for cell proliferation. miR-130b-3p suppressed MB tumorigenesis by targeting a previously unknown target, serine/threonine-protein kinase 1 (SIK1), through the p53 signaling pathways. In addition, we found an unreported role of SIK1 in promoting MB tumor growth and an SIK1 inhibitor could inhibit MB cell proliferation. This research provides new insight into the molecular mechanism of MB and may provide a new therapeutic strategy for MB treatment.
Point-wise correlations between 10-2 Humphrey visual field and OCT data in open angle glaucoma
Authors: Cirafici Paola , Maiello Guido , Ancona Chiara , Masala Alessandro , Traverso Carlo Enrico , Iester Michele 
Published: June 2020

Abstract
Purpose
Optical Coherence Tomography (OCT) is a powerful instrument for helping clinicians detect and monitor glaucoma. The aim of this study was to provide a detailed mapping of the relationships between visual field (VF) sensitivities and measures of retinal structure provided by a commercial Spectral Domain (SD)-OCT system (RTvue-100 Optovue).

Methods
Sixty-three eyes of open angle glaucoma patients (17 males, 16 females, and mean age 71 ± 7.5 years) were included in this retrospective, observational clinical study. Thickness values for superior and inferior retina, as well as average values, were recorded for the full retina, the outer retina, the ganglion cell complex, and the peripapillary retinal nerve fiber layer (RNFL). RNFL thickness was further evaluated along eight separate sectors (temporal lower, temporal upper, superior temporal, superior nasal, nasal upper, nasal lower, inferior nasal, and inferior temporal). Point-wise correlations were then computed between each of these OCT measures and the visual sensitivities at all VF locations assessed via Humphrey 10-2 and 24-2 perimetry. Lastly, OCT data were fit to VF data to predict glaucoma stage.

Results
The relationship between retinal thickness and visual sensitivities reflects the known topography of the retina. Spatial correlation patterns between visual sensitivities and RNFL thickness along different sectors broadly agree with previously hypothesized structure–function maps, yet suggest that structure–function maps still require more precise characterizations. Given these relationships, we find that OCT data can predict glaucoma stage.

Conclusion
Ganglion cell complex and RNFL thickness measurements are highlighted as the most promising candidate metrics for glaucoma detection and monitoring.
The TSPO-NOX1 axis controls phagocyte-triggered pathological angiogenesis in the eye
Authors: Wolf Anne , Herb Marc , Schramm Michael , Langmann Thomas 
Published: June 2020

AbstractAberrant immune responses including reactive phagocytes are implicated in the etiology of age-related macular degeneration (AMD), a major cause of blindness in the elderly. The translocator protein (18 kDa) (TSPO) is described as a biomarker for reactive gliosis, but its biological functions in retinal diseases remain elusive. Here, we report that tamoxifen-induced conditional deletion of TSPO in resident microglia using Cx3cr1CreERT2:TSPOfl/fl mice or targeting the protein with the synthetic ligand XBD173 prevents reactivity of phagocytes in the laser-induced mouse model of neovascular AMD. Concomitantly, the subsequent neoangiogenesis and vascular leakage are prevented by TSPO knockout or XBD173 treatment. Using different NADPH oxidase-deficient mice, we show that TSPO is a key regulator of NOX1-dependent neurotoxic ROS production in the retina. These data define a distinct role for TSPO in retinal phagocyte reactivity and highlight the protein as a drug target for immunomodulatory and antioxidant therapies for AMD.
The central amygdala recruits mesocorticolimbic circuitry for pursuit of reward or pain
Authors: Warlow Shelley M. , Naffziger Erin E. , Berridge Kent C. 
Published: June 2020

AbstractHow do brain mechanisms create maladaptive attractions? Here intense maladaptive attractions are created in laboratory rats by pairing optogenetic channelrhodopsin (ChR2) stimulation of central nucleus of amygdala (CeA) in rats with encountering either sucrose, cocaine, or a painful shock-delivering object. We find that pairings make the respective rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks. CeA-induced maladaptive attractions, even to the painful shock-rod, recruit mesocorticolimbic incentive-related circuitry. Shock-associated cues also gain positive incentive value and are pursued. Yet the motivational effects of paired CeA stimulation can be reversed to negative valence in a Pavlovian fear learning situation, where CeA ChR2 pairing increases defensive reactions. Finally, CeA ChR2 valence can be switched to neutral by pairing with innocuous stimuli. These results reveal valence plasticity and multiple modes for motivation via mesocorticolimbic circuitry under the control of CeA activation.
Magnetic and electronic phase transitions probed by nanomechanical resonators
Authors: Šiškins Makars , Lee Martin , Mañas-Valero Samuel , Coronado Eugenio , Blanter Yaroslav M. , van der Zant Herre S. J. , Steeneken Peter G. 
Published: June 2020

AbstractThe reduced dimensionality of two-dimensional (2D) materials results in characteristic types of magnetically and electronically ordered phases. However, only few methods are available to study this order, in particular in ultrathin insulating antiferromagnets that couple weakly to magnetic and electronic probes. Here, we demonstrate that phase transitions in thin membranes of 2D antiferromagnetic FePS3, MnPS3 and NiPS3 can be probed mechanically via the temperature-dependent resonance frequency and quality factor. The observed relation between mechanical motion and antiferromagnetic order is shown to be mediated by the specific heat and reveals a strong dependence of the Néel temperature of FePS3 on electrostatically induced strain. The methodology is not restricted to magnetic order, as we demonstrate by probing an electronic charge-density-wave phase in 2H-TaS2. It thus offers the potential to characterize phase transitions in a wide variety of materials, including those that are antiferromagnetic, insulating or so thin that conventional bulk characterization methods become unsuitable.
Improving the safety of human pluripotent stem cell therapies using genome-edited orthogonal safeguards
Authors: Martin Renata M. , Fowler Jonas L. , Cromer M. Kyle , Lesch Benjamin J. , Ponce Ezequiel , Uchida Nobuko , Nishimura Toshinobu , Porteus Matthew H. , Loh Kyle M. 
Published: June 2020

AbstractDespite their rapidly-expanding therapeutic potential, human pluripotent stem cell (hPSC)-derived cell therapies continue to have serious safety risks. Transplantation of hPSC-derived cell populations into preclinical models has generated teratomas (tumors arising from undifferentiated hPSCs), unwanted tissues, and other types of adverse events. Mitigating these risks is important to increase the safety of such therapies. Here we use genome editing to engineer a general platform to improve the safety of future hPSC-derived cell transplantation therapies. Specifically, we develop hPSC lines bearing two drug-inducible safeguards, which have distinct functionalities and address separate safety concerns. In vitro administration of one small molecule depletes undifferentiated hPSCs >106-fold, thus preventing teratoma formation in vivo. Administration of a second small molecule kills all hPSC-derived cell-types, thus providing an option to eliminate the entire hPSC-derived cell product in vivo if adverse events arise. These orthogonal safety switches address major safety concerns with pluripotent cell-derived therapies.
Triggering typical nemaline myopathy with compound heterozygous nebulin mutations reveals myofilament structural changes as pathomechanism
Authors: Lindqvist Johan , Ma Weikang , Li Frank , Hernandez Yaeren , Kolb Justin , Kiss Balazs , Tonino Paola , van der Pijl Robbert , Karimi Esmat , Gong Henry , Strom Josh , Hourani Zaynab , Smith John E. , Ottenheijm Coen , Irving Thomas , Granzier Henk 
Published: June 2020

AbstractNebulin is a giant protein that winds around the actin filaments in the skeletal muscle sarcomere. Compound-heterozygous mutations in the nebulin gene (NEB) cause typical nemaline myopathy (NM), a muscle disorder characterized by muscle weakness with limited treatment options. We created a mouse model with a missense mutation p.Ser6366Ile and a deletion of NEB exon 55, the Compound-Het model that resembles typical NM. We show that Compound-Het mice are growth-retarded and have muscle weakness. Muscles have a reduced myofibrillar fractional-area and sarcomeres are disorganized, contain rod bodies, and have longer thin filaments. In contrast to nebulin-based severe NM where haplo-insufficiency is the disease driver, Compound-Het mice express normal amounts of nebulin. X-ray diffraction revealed that the actin filament is twisted with a larger radius, that tropomyosin and troponin behavior is altered, and that the myofilament spacing is increased. The unique disease mechanism of nebulin-based typical NM reveals novel therapeutic targets.
Controls on surface water carbonate chemistry along North American ocean margins
Authors: Cai Wei-Jun , Xu Yuan-Yuan , Feely Richard A. , Wanninkhof Rik , Jönsson Bror , Alin Simone R. , Barbero Leticia , Cross Jessica N. , Azetsu-Scott Kumiko , Fassbender Andrea J. , Carter Brendan R. , Jiang Li-Qing , Pepin Pierre , Chen Baoshan , Hussain Najid , Reimer Janet J. , Xue Liang , Salisbury Joseph E. , Hernández-Ayón José Martín , Langdon Chris , Li Qian , Sutton Adrienne J. , Chen Chen-Tung A. , Gledhill Dwight K. 
Published: June 2020

AbstractSyntheses of carbonate chemistry spatial patterns are important for predicting ocean acidification impacts, but are lacking in coastal oceans. Here, we show that along the North American Atlantic and Gulf coasts the meridional distributions of dissolved inorganic carbon (DIC) and carbonate mineral saturation state (Ω) are controlled by partial equilibrium with the atmosphere resulting in relatively low DIC and high Ω in warm southern waters and the opposite in cold northern waters. However, pH and the partial pressure of CO2 (pCO2) do not exhibit a simple spatial pattern and are controlled by local physical and net biological processes which impede equilibrium with the atmosphere. Along the Pacific coast, upwelling brings subsurface waters with low Ω and pH to the surface where net biological production works to raise their values. Different temperature sensitivities of carbonate properties and different timescales of influencing processes lead to contrasting property distributions within and among margins.
Machine learning uncovers cell identity regulator by histone code
Authors: Xia Bo , Zhao Dongyu , Wang Guangyu , Zhang Min , Lv Jie , Tomoiaga Alin S. , Li Yanqiang , Wang Xin , Meng Shu , Cooke John P. , Cao Qi , Zhang Lili , Chen Kaifu 
Published: June 2020

AbstractConversion between cell types, e.g., by induced expression of master transcription factors, holds great promise for cellular therapy. Our ability to manipulate cell identity is constrained by incomplete information on cell identity genes (CIGs) and their expression regulation. Here, we develop CEFCIG, an artificial intelligent framework to uncover CIGs and further define their master regulators. On the basis of machine learning, CEFCIG reveals unique histone codes for transcriptional regulation of reported CIGs, and utilizes these codes to predict CIGs and their master regulators with high accuracy. Applying CEFCIG to 1,005 epigenetic profiles, our analysis uncovers the landscape of regulation network for identity genes in individual cell or tissue types. Together, this work provides insights into cell identity regulation, and delivers a powerful technique to facilitate regenerative medicine.
Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly
Authors: Li Yuying , Yuan Jie , Chen Fengyuan , Zhang Suyang , Zhao Yu , Chen Xiaona , Lu Leina , Zhou Liang , Chu Ching Yan , Sun Hao , Wang Huating 
Published: June 2020

AbstractThe functional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage. Here we identifySAM(Sugt1 asssociated muscle) lncRNA that is enriched in the proliferating myoblasts. Global deletion ofSAMhas no overt effect on mice but impairs adult muscle regeneration following acute damage; it also exacerbates the chronic injury-induced dystrophic phenotype in mdx mice. Consistently, inducible deletion ofSAMin SCs leads to deficiency in muscle regeneration. Further examination reveals thatSAMloss results in a cell-autonomous defect in the proliferative expansion of myoblasts. Mechanistically, we findSAMinteracts and stabilizes Sugt1, a co-chaperon protein key to kinetochore assembly during cell division. Loss ofSAMor Sugt1 both disrupts kinetochore assembly in mitotic cells due to the mislocalization of two components: Dsn1 and Hec1. Altogether, our findings identifySAMas a regulator of SC proliferation through facilitating Sugt1 mediated kinetochore assembly during cell division.
Implanting Ni-O-VOx sites into Cu-doped Ni for low-overpotential alkaline hydrogen evolution
Authors: Li Yibing , Tan Xin , Hocking Rosalie K. , Bo Xin , Ren Hangjuan , Johannessen Bernt , Smith Sean C. , Zhao Chuan 
Published: June 2020

AbstractNickel-based catalysts are most commonly used in industrial alkaline water electrolysis. However, it remains a great challenge to address the sluggish reaction kinetics and severe deactivation problems of hydrogen evolution reaction (HER). Here, we show a Cu-doped Ni catalyst implanted with Ni-O-VOx sites (Ni(Cu)VOx) for alkaline HER. The optimal Ni(Cu)VOx electrode exhibits a near-zero onset overpotential and low overpotential of 21 mV to deliver –10 mA cm−2, which is comparable to benchmark Pt/C catalyst. Evidence for the formation of Ni-O-VOx sites in Ni(Cu)VOx is established by systematic X-ray absorption spectroscopy studies. The VOx can cause a substantial dampening of Ni lattice and create an enlarged electrochemically active surface area. First-principles calculations support that the Ni-O-VOx sites are superactive and can promote the charge redistribution from Ni to VOx, which greatly weakens the H-adsorption and H2release free energy over Ni. This endows the Ni(Cu)VOx electrode high HER activity and long-term durability.