bluuebunny/crossref_metadata_2025_split huggingface dataset:
Parallels in the sequential organization of birdsong and human speech
Authors: Sainburg Tim , Theilman Brad , Thielk Marvin , Gentner Timothy Q. 
Published: August 2019

AbstractHuman speech possesses a rich hierarchical structure that allows for meaning to be altered by words spaced far apart in time. Conversely, the sequential structure of nonhuman communication is thought to follow non-hierarchical Markovian dynamics operating over only short distances. Here, we show that human speech and birdsong share a similar sequential structure indicative of both hierarchical and Markovian organization. We analyze the sequential dynamics of song from multiple songbird species and speech from multiple languages by modeling the information content of signals as a function of the sequential distance between vocal elements. Across short sequence-distances, an exponential decay dominates the information in speech and birdsong, consistent with underlying Markovian processes. At longer sequence-distances, the decay in information follows a power law, consistent with underlying hierarchical processes. Thus, the sequential organization of acoustic elements in two learned vocal communication signals (speech and birdsong) shows functionally equivalent dynamics, governed by similar processes.
(Pro)renin receptor contributes to renal mitochondria dysfunction, apoptosis and fibrosis in diabetic mice
Authors: Li Caixia , Matavelli Luis C. , Akhtar Safia , Siragy Helmy M. 
Published: August 2019

AbstractRecently we demonstrated that increased renal (Pro)renin receptor (PRR) expression in diabetes contributes to development of diabetic kidney disease. However, the exact mechanisms involving PRR activity and diabetic kidney dysfunction are unknown. We hypothesized that PRR is localized in renal mitochondria and contributes to renal fibrosis and apoptosis through oxidative stress-induced mitochondria dysfunction. Controls and streptozotocin-induced diabetic C57BL/6 mice were injected with scramble shRNA and PRR shRNA and followed for a period of eight weeks. At the end of study, diabetic mice showed increased expressions of PRR and NOX4 in both total kidney tissue and renal mitochondria fraction. In addition, renal mitochondria of diabetic mice showed reduced protein expression and activity of SOD2 and ATP production and increased UCP2 expression. In diabetic kidney, there was upregulation in the expressions of caspase3, phos-Foxo3a, phos-NF-κB, fibronectin, and collagen IV and reduced expressions of Sirt1 and total-FOXO3a. Renal immunostaining revealed increased deposition of PRR, collagen and fibronectin in diabetic kidney. In diabetic mice, PRR knockdown decreased urine albumin to creatinine ratio and the renal expressions of PRR, NOX4, UCP2, caspase3, phos-FOXO3a, phos-NF-κB, collagen, and fibronectin, while increased the renal mitochondria expression and activity of SOD2, ATP production, and the renal expressions of Sirt1 and total-FOXO3a. In conclusion, increased expression of PRR localized in renal mitochondria and diabetic kidney induced mitochondria dysfunction, and enhanced renal apoptosis and fibrosis in diabetes by upregulation of mitochondria NOX4/SOD2/UCP2 signaling pathway.
Assessment of intracardiac and extracardiac anomalies associated with coarctation of aorta and interrupted aortic arch using dual-source computed tomography
Authors: Zhao Qin , Wang Jin , Yang Zhi-gang , Shi Ke , Diao Kai-yue , Huang Shan , Shen Meng-ting , Guo Ying-kun 
Published: August 2019

AbstractTo evaluate the value of dual-source computed tomography (DSCT) compared with transthoracic echocardiography (TTE) in assessing intracardiac and extracardiac anomalies in patients with coarctation of aorta (CoA) and interrupted aortic arch (IAA). Seventy-five patients (63 with CoA and 12 with IAA) who received preoperative DSCT and TTE were retrospectively studied. Intracardiac and extracardiac anomalies were recorded and compared by DSCT and TTE, in reference to surgical or cardiac catheterization findings. A total of 155 associated anomalies were finally found. Collateral circulation (56, 74.70%), patent ductus arteriosus (PDA; 41, 54.67%) were the most common anomalies. PDA, aortopulmonary window, and collateral circulation were more frequently present in patients with IAA than those with CoA (100% vs. 46.03%, 16.67% vs. 0%, and 100% vs. 69.84%, respectively, all p < 0.05). DSCT was superior to TTE in assessing associated extracardiac-vascular anomalies (sensitivity: 100% vs. 39.81%; specificity: 100% vs. 100%; positive predictive value: 100% vs. 100%; negative predictive value: 100% vs. 76.06%). Extracardiac-vascular anomalies, including collateral circulation and PDA, were the most common anomalies in patients with IAA and CoA. Compared with TTE, DSCT is more reliable in providing an overall preoperative evaluation of morphological features and extracardiac anomalies for surgical planning.
VEGF mediates fat embolism-induced acute lung injury via VEGF receptor 2 and the MAPK cascade
Authors: Lin Chin-Kuo , Lin Yu-Hao , Huang Tai-Chun , Shi Chung-Sheng , Yang Cheng-Ta , Yang Yi-Ling 
Published: August 2019

AbstractFat embolism (FE) is a lethal medical emergency often caused by fracture of long bones and amputation of limbs. Vascular endothelial growth factor (VEGF) promotes angiogenesis and increases vascular permeability. We tested the hypothesis that VEGF plays a critical role in FE-induced acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Fat tissues were collected from male Sprague-Dawley rats, and animal oil was extracted and mixed with water to form fatty micelles. The micelles were then injected into the tail vein to produce FE and ALI in rats. Lung weight gain was measured as the index of pulmonary edema. The expression of pulmonary VEGF was evaluated by real-time PCR and western blot analysis. Inducible nitric oxide synthase (iNOS) and phosphorylation of mitogen-activated protein kinase (MAPK) were determined by western blot analyses. Interleukin-1β (IL-1β) was quantified by ELISAs. Hematoxylin and eosin staining was used to evaluate the pathological damage of ALI. In this study, we found that animal oil-induced FE significantly increased pulmonary VEGF expression and MAPK phosphorylation. We also evaluated the inflammatory response after FE and found that iNOS and IL-1β significantly increased after FE. Systemic administration of SU-1498, an antagonist of VEGF receptor 2 (VEGFR-2), significantly attenuated the FE-induced inflammatory response and histological damage. This study suggested that VEGF is involved in FE-induced ARDS via the VEGFR-2 and MAPK cascades, which induce IL-1β release and iNOS upregulation. Blockade of could be used to treat FE-induced pulmonary damage.
Involvement of the P2X7 receptor in the migration and metastasis of tamoxifen-resistant breast cancer: effects on small extracellular vesicles production
Authors: Park Miso , Kim Jieun , Phuong Nguyen T. T. , Park Jung Gyu , Park Jin-Hee , Kim Yong-Chul , Baek Moon Chang , Lim Sung Chul , Kang Keon Wook 
Published: August 2019

AbstractTamoxifen (TAM) is the standard anti-hormonal therapy for estrogen receptor-positive breast cancer. However, long-term TAM therapy can make acquisition of TAM resistance and there are still no solutions to treat TAM-resistant breast cancer. In this study, we found that protein and mRNA expression of the P2X purinoreceptor 7 (P2X7) was higher in tamoxifen resistant MCF-7 (TAMR-MCF-7) cells than in control MCF-7 cells. P2X7 inhibition potently inhibited the migration of TAMR-MCF-7 cells and the liver metastasis burden of TAMR-MCF-7 cells in the spleen-liver metastasis experiment. However, the P2X7 antagonist did not affect protein expression of matrix metalloproteinase (MMP)-2, MMP-9, and epithelial-mesenchymal transition markers. Here our data indicate a link between small extracellular vesicles (sEV) and P2X7, and suggest a new mechanism of metastasis in TAM-resistant breast cancer cells through P2X7 receptors. The migration of TAMR-MCF-7 cells was increased in a concentration-dependent manner by purified sEV treatment. The number of secreted sEVs and the protein levels of CD63 in TAMR-MCF-7 cells were decreased by the P2X7 antagonist, showing that P2X7 influences the production of sEV. Our results suggest that inhibiting the P2X7 could be considered for metastasis prevention in TAM-resistant cancer patients.
Exploring the initiation of fiber fuse
Authors: Xiao Qirong , Tian Jiading , Yan Ping , Li Dan , Gong Mali 
Published: August 2019

AbstractWe report an investigation of conditions for the initiation of fiber fuse (IFF), a kind of catastrophic damage that troubles all kinds of optical fibers, in silica-based optical fibers. The fibers of different chemical compositions were processed and tested in controlled conditions without mechanical damages before the IFF. For all the fibers of IFF, the same correlation between the critical temperatures and the optical powers transmitted therein was revealed for the first time. The fibers of different chemical compositions exhibited different resistances to the IFF under the threshold powers for propagation of fiber fuses. The results offered promise for predicting fiber fuses in optical fiber systems, which could facilitate avoiding catastrophic losses. They could direct the optimization of fiber production technologies for suppressing the damages, as well as open a new path towards controlled utilization of fiber fuse in in-fiber microstructure fabrication.
OsCAldOMT1 is a bifunctional O-methyltransferase involved in the biosynthesis of tricin-lignins in rice cell walls
Authors: Lam Pui Ying , Tobimatsu Yuki , Matsumoto Naoyuki , Suzuki Shiro , Lan Wu , Takeda Yuri , Yamamura Masaomi , Sakamoto Masahiro , Ralph John , Lo Clive , Umezawa Toshiaki 
Published: August 2019

AbstractLignin is a phenylpropanoid polymer produced in the secondary cell walls of vascular plants. Although most eudicot and gymnosperm species generate lignins solely via polymerization of p-hydroxycinnamyl alcohols (monolignols), grasses additionally use a flavone, tricin, as a natural lignin monomer to generate tricin-incorporated lignin polymers in cell walls. We previously found that disruption of a rice 5-HYDROXYCONIFERALDEHYDE O-METHYLTRANSFERASE (OsCAldOMT1) reduced extractable tricin-type metabolites in rice vegetative tissues. This same enzyme has also been implicated in the biosynthesis of sinapyl alcohol, a monolignol that constitutes syringyl lignin polymer units. Here, we further demonstrate through in-depth cell wall structural analyses that OsCAldOMT1-deficient rice plants produce altered lignins largely depleted in both syringyl and tricin units. We also show that recombinant OsCAldOMT1 displayed comparable substrate specificities towards both 5-hydroxyconiferaldehyde and selgin intermediates in the monolignol and tricin biosynthetic pathways, respectively. These data establish OsCAldOMT1 as a bifunctional O-methyltransferase predominantly involved in the two parallel metabolic pathways both dedicated to the biosynthesis of tricin-lignins in rice cell walls. Given that cell wall digestibility was greatly enhanced in the OsCAldOMT1-deficient rice plants, genetic manipulation of CAldOMTs conserved in grasses may serve as a potent strategy to improve biorefinery applications of grass biomass.
TGR(mREN2)27 rats develop non-alcoholic fatty liver disease-associated portal hypertension responsive to modulations of Janus-kinase 2 and Mas receptor
Authors: Klein Sabine , Kleine Carola-Ellen , Pieper Andrea , Granzow Michaela , Gautsch Sebastian , Himmit Mimoun , Kahrmann Katharina , Schierwagen Robert , Uschner Frank Erhard , Magdaleno Fernando , Naoum Maria Eleni , Kristiansen Glen , Walther Thomas , Bader Michael , Sauerbruch Tilman , Trebicka Jonel 
Published: August 2019

AbstractPrevalence of non-alcoholic fatty liver disease (NAFLD) is increasing. Resulting fibrosis and portal hypertension, as a possible secondary event, may necessitate treatment. Overexpression of mouse renin in the transgenic rat model, TGR(mREN2)27, leads to spontaneous development of NAFLD. Therefore, we used TGR(mREN2)27 rats as a model of NAFLD where we hypothesized increased susceptibility and investigated fibrosis and portal hypertension and associated pathways. 12-week old TGR(mREN2)27 rats received either cholestatic (BDL) or toxic injury (CCl4 inhalation). Portal and systemic hemodynamic assessments were performed using microsphere technique with and without injection of the Janus-Kinase 2 (JAK2) inhibitor AG490 or the non-peptidic Ang(1-7) agonist, AVE0991. The extent of liver fibrosis was assessed in TGR(mREN2)27 and wild-type rats using standard techniques. Protein and mRNA levels of profibrotic, renin-angiotensin system components were assessed in liver and primary hepatic stellate cells (HSC) and hepatocytes. TGR(mREN2)27 rats developed spontaneous, but mild fibrosis and portal hypertension due to the activation of the JAK2/Arhgef1/ROCK pathway. AG490 decreased migration of HSC and portal pressure in isolated liver perfusions and in vivo. Fibrosis or portal hypertension after cholestatic (BDL) or toxic injury (CCl4) was not aggravated in TGR(mREN2)27 rats, probably due to decreased mouse renin expression in hepatocytes. Interestingly, portal hypertension was even blunted in TGR(mREN2)27 rats (with or without additional injury) by AVE0991. TGR(mREN2)27 rats are a suitable model of spontaneous liver fibrosis and portal hypertension but not with increased susceptibility to liver damage. After additional injury, the animals can be used to evaluate novel therapeutic strategies targeting Mas.
Opposing roles of endothelial and leukocyte-expressed IL-7Rα in the regulation of psoriasis-like skin inflammation
Authors: Vranova Martina , Friess Mona C. , Haghayegh Jahromi Neda , Collado-Diaz Victor , Vallone Angela , Hagedorn Olivia , Jadhav Maria , Willrodt Ann-Helen , Polomska Anna , Leroux Jean-Christophe , Proulx Steven T. , Halin Cornelia 
Published: August 2019

AbstractThe interleukin 7 receptor alpha chain (IL-7Rα) is predominately expressed by lymphocytes, and activation by its ligand IL-7 supports the development and maintenance of T cells and boosts T-cell mediated immunity. We recently reported that lymphatic endothelial cells (LECs) in dermal lymphatics also express IL-7 and its receptor chains (IL-7Rα and CD132) and that IL-7 supports lymphatic drainage. This suggested that activation of IL-7Rα signaling in lymphatics could exert inflammation-resolving activity, by promoting the clearance of excess tissue fluid. Here we investigated how the potentially opposing effects of IL-7Rα signaling in immune cells and in the lymphatic vasculature would affect the development and progression of psoriasis-like skin inflammation. We found that during acute and chronic skin inflammation mice with an endothelial-specific deletion of IL-7Rα (IL-7RαΔEC mice) developed more edema compared to control mice, as a consequence of impaired lymphatic drainage. However, systemic treatment of wild-type mice with IL-7 exacerbated edema and immune cell infiltration in spite of increasing lymphatic drainage, whereas treatment with IL-7Rα blocking antibody ameliorated inflammatory symptoms. These data identify IL-7Rα signaling as a new pathway in psoriasis-like skin inflammation and show that its pro-inflammatory effects on the immune compartment override its anti-inflammatory, drainage-enhancing effects on the endothelium.
Crowdsourcing punishment: Individuals reference group preferences to inform their own punitive decisions
Authors: Son Jae-Young , Bhandari Apoorva , FeldmanHall Oriel 
Published: August 2019

AbstractJustice systems delegate punishment decisions to groups in the belief that the aggregation of individuals’ preferences facilitates judiciousness. However, group dynamics may also lead individuals to relinquish moral responsibility by conforming to the majority’s preference for punishment. Across five experiments (N = 399), we find Victims and Jurors tasked with restoring justice become increasingly punitive (by as much as 40%) as groups express a desire to punish, with every additional punisher augmenting an individual’s punishment rates. This influence is so potent that knowing about a past group’s preference continues swaying decisions even when they cannot affect present outcomes. Using computational models of decision-making, we test long-standing theories of how groups influence choice. We find groups induce conformity by making individuals less cautious and more impulsive, and by amplifying the value of punishment. However, compared to Victims, Jurors are more sensitive to moral violation severity and less readily swayed by the group. Conformity to a group’s punitive preference also extends to weightier moral violations such as assault and theft. Our results demonstrate that groups can powerfully shift an individual’s punitive preference across a variety of contexts, while additionally revealing the cognitive mechanisms by which social influence alters moral values.
Temporal attention causes systematic biases in visual confidence
Authors: Recht Samuel , Mamassian Pascal , de Gardelle Vincent 
Published: August 2019

AbstractTemporal attention enhances the perceptual representation of a stimulus at a particular point in time. The number of possible attentional episodes in a given period is limited, but whether observers’ confidence reflects such limitations is still unclear. To investigate this issue, we adapted an “Attentional Blink” paradigm, presenting observers with a rapid visual stream of letters containing two targets cued for subsequent perceptual reports and confidence judgments. We found three main results. First, when two targets fell within the same attentional episode, the second target underwent a strong under-confidence bias. In other words, confidence neglected that a single attentional episode can benefit to both targets. Second, despite this initial bias, confidence was strongly correlated with response probability. Third, as confidence was yoked to the evidence used in perceptual reports, it remains blind to delays in response selection for the second target. Notably, the second target was often mistaken with a later item associated with higher confidence. These results suggest that confidence does not perfectly evaluate the limits of temporal attention in challenging situations.
Cancer Testis Antigen Promotes Triple Negative Breast Cancer Metastasis and is Traceable in the Circulating Extracellular Vesicles
Authors: Kannan Anbarasu , Philley Julie V. , Hertweck Kate L. , Ndetan Harrison , Singh Karan P. , Sivakumar Subramaniam , Wells Robert B. , Vadlamudi Ratna K. , Dasgupta Santanu 
Published: August 2019

AbstractTriple negative breast cancer (TNBC) has poor survival, exhibits rapid metastases, lacks targeted therapies and reliable prognostic markers. Here, we examined metastasis promoting role of cancer testis antigen SPANXB1 in TNBC and its utility as a therapeutic target and prognostic biomarker. Expression pattern of SPANXB1 was determined using matched primary cancer, lymph node metastatic tissues and circulating small extracellular vesicles (sEVs). cDNA microarray analysis of TNBC cells stably integrated with a metastasis suppressor SH3GL2 identified SPANXB1 as a potential target gene. TNBC cells overexpressing SH3GL2 exhibited decreased levels of both SPANXB1 mRNA and protein. Silencing of SPANXB1 reduced migration, invasion and reactive oxygen species production of TNBC cells. SPANXB1 depletion augmented SH3GL2 expression and decreased RAC-1, FAK, A-Actinin and Vinculin expression. Phenotypic and molecular changes were reversed upon SPANXB1 re-expression. SPANXB1 overexpressing breast cancer cells with an enhanced SPANXB1:SH3GL2 ratio achieved pulmonary metastasis within 5 weeks, whereas controls cells failed to do so. Altered expression of SPANXB1 was detected in the sEVs of SPANXB1 transduced cells. Exclusive expression of SPANXB1 was traceable in circulating sEVs, which was associated with TNBC progression. SPANXB1 represents a novel and ideal therapeutic target for blocking TNBC metastases due to its unique expression pattern and may function as an EV based prognostic marker to improve TNBC survival. Uniquely restricted expression of SPANXB1 in TNBCs, makes it an ideal candidate for targeted therapeutics and prognostication.
In Utero Gene Therapy (IUGT) Using GLOBE Lentiviral Vector Phenotypically Corrects the Heterozygous Humanised Mouse Model and Its Progress Can Be Monitored Using MRI Techniques
Authors: Shangaris Panicos , Loukogeorgakis Stavros P. , Subramaniam Sindhu , Flouri Christina , Jackson Laurence H. , Wang Wei , Blundell Michael P. , Liu Shanrun , Eaton Simon , Bakhamis Nahla , Ramachandra Durrgah Latchumi , Maghsoudlou Panayiotis , Urbani Luca , Waddington Simon N. , Eddaoudi Ayad , Archer Joy , Antoniou Michael N. , Stuckey Daniel J. , Schmidt Manfred , Thrasher Adrian J. , Ryan Thomas M. , De Coppi Paolo , David Anna L. 
Published: August 2019

AbstractIn utero gene therapy (IUGT) to the fetal hematopoietic compartment could be used to treat congenital blood disorders such as β-thalassemia. A humanised mouse model of β-thalassemia was used, in which heterozygous animals are anaemic with splenomegaly and extramedullary hematopoiesis. Intrahepatic in utero injections of a β globin-expressing lentiviral vector (GLOBE), were performed in fetuses at E13.5 of gestation. We analysed animals at 12 and 32 weeks of age, for vector copy number in bone marrow, peripheral blood liver and spleen and we performed integration site analysis. Compared to noninjected heterozygous animals IUGT normalised blood haemoglobin levels and spleen weight. Integration site analysis showed polyclonality. The left ventricular ejection fraction measured using magnetic resonance imaging (MRI) in treated heterozygous animals was similar to that of normal non-β-thalassemic mice but significantly higher than untreated heterozygous thalassemia mice suggesting that IUGT ameliorated poor cardiac function. GLOBE LV-mediated IUGT normalised the haematological and anatomical phenotype in a heterozygous humanised model of β-thalassemia.
Vitamin D reverts resistance to the mTOR inhibitor everolimus in hepatocellular carcinoma through the activation of a miR-375/oncogenes circuit
Authors: Provvisiero Donatella Paola , Negri Mariarosaria , de Angelis Cristina , Di Gennaro Gilda , Patalano Roberta , Simeoli Chiara , Papa Fortuna , Ferrigno Rosario , Auriemma Renata Simona , De Martino Maria Cristina , Colao Annamaria , Pivonello Rosario , Pivonello Claudia 
Published: August 2019

AbstractPrimary or acquired resistant mechanisms prevent the employment of individualized therapy with target drugs like the mTOR inhibitor everolimus (EVE) in hepatocellular carcinoma (HCC). The current study evaluated the effect of 1,25(OH)2Vitamin D (VitD) treatment on EVE sensitivity in established models of HCC cell lines resistant to everolimus (EveR). DNA content and colony formation assays, which measure the proliferative index, revealed that VitD pre-treatment re-sensitizes EveR cells to EVE treatment. The evaluation of epithelial and mesenchymal markers by western blot and immunofluorescence showed that VitD restored an epithelial phenotype in EveR cells, in which prolonged EVE treatment induced transition to mesenchymal phenotype. Moreover, VitD treatment prompted hepatic miRNAs regulation, evaluated by liver miRNA finder qPCR array. In particular, miR-375 expression was up-regulated by VitD in EveR cells, in which miR-375 was down-regulated compared to parental cells, with consequent inhibition of oncogenes involved in drug resistance and epithelial-mesenchymal transition (EMT) such as MTDH, YAP-1 and c-MYC. In conclusion, the results of the current study demonstrated that VitD can re-sensitize HCC cells resistant to EVE treatment triggering miR-375 up-regulation and consequently down-regulating several oncogenes responsible of EMT and drug resistance.