bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimizing detergent concentration and processing time to balance the decellularization efficiency and properties of bioprosthetic heart valves
Authors: Luo Yu , Lou Dong , Ma Lie , Gao Changyou 
Published: May 2019

AbstractDecellularization treatment has been widely used to decrease the potential immunogenicity and improve the anticalcification properties of bio‐derived materials, which may be utilized as an alternative method for the preparation of bioprosthetic heart valves. However, the excessive decellularization treatments will deteriarate the properties of heart valves. Among the decellularizaton parameters, detergent concentration and processing time are considered as those of the most key factors. Therefore, it should be meaningful to balance the decellularization efficiency and properties of bioprosthetic heart valves by optimizing the detergent concentration and processing time. In this study, three groups of the decellularized heart valves treated by sodium deoxycholate (SD) with different concentration and processing time were investigated through histological, biochemical, and mechanical analysis. Similar decellularization efficiency can be concluded through histological staining, DNA and α‐Gal quantification results. Extracellular matrix contents quantification and tensile test results revealed that there is no obvious difference among the three decellularized heart valves. in vitro cytotoxicity assay showed that the remnant detergent is not enough to cause cell death, which indicated that the decellularized porcine aortic heart valves may be suitable for further in vivo research. In conclusion, Triton X‐100/SD may be a suitable protocol used for heart valves decellularization. And it is feasible to vary the detergent processing time by changing the detergent concentration without compromising the decellularization efficiency.
Retracted: Long noncoding RNA MEG3 is a tumor suppressor in choriocarcinoma by upregulation of microRNA‐211
Authors: Ji Li , Li Xue 
Published: May 2019

AbstractTumor suppressor long noncoding RNA maternally expressed gene 3 (lncRNA MEG3) exists in various cancers. Nonetheless, the functions of lncRNA MEG3 in choriocarcinoma (CC) are still not well studied. We explored the effects of lncRNA MEG3 on human CC JEG‐3 and BeWo cells. lncRNA MEG3 was overexpressed, and the effects of lncRNA MEG3 on cell viability, proliferation, apoptosis, migration, and invasion were assessed by the cell counting kit‐8 assay, western blot analysis, flow cytometry (plus western blot analysis), and transwell assay (plus western blot analysis), respectively. Then, the expression level of miR‐211 was detected by real‐time quantitative polymerase chain reaction. After that, the effects of dysregulated microRNA‐211 (miR‐211) with overexpressing lncRNA MEG3 on JEG‐3 cells and BeWo cells were testified. Western blot analysis was used to study the involvements of the signaling pathways in the lncRNA MEG3‐associated modulation. We found that lncRNA MEG3 upregulation reduced cell viability, inhibited proliferation, migration and invasion, and promoted apoptosis. Expression of miR‐211 was upregulated after lncRNA MEG3 overexpression. Effects of lncRNA MEG3 overexpression were augmented by miR‐211 overexpression, while they were declined by miR‐211 silencing. Phosphorylated levels of PI3K, AKT, and AMP‐activated protein kinase (AMPK) were decreased by lncRNA MEG3 overexpression via regulation of miR‐211. To sum up, lncRNA MEG3 could repress proliferation, migration and invasion, and promote apoptosis of JEG‐3 and BeWo cells through upregulating miR‐211. The PI3K/AKT and AMPK pathways were inhibited by lncRNA MEG3 overexpression via regulation of miR‐211.
Exosomes from human adipose‐derived stem cells promote sciatic nerve regeneration via optimizing Schwann cell function
Authors: Chen Jing , Ren Sen , Duscher Dominik , Kang Yu , Liu Yutian , Wang Cheng , Yuan Meng , Guo Guojun , Xiong Hewei , Zhan Peng , Wang Yang , Machens Hans‐Günther , Chen Zhenbing 
Published: May 2019

AbstractHuman adipose‐derived stem cells (ASCs) have a potential for the treatment of peripheral nerve injury. Recent studies demonstrated that stem cells can mediate therapeutic effect by secreting exosomes. We aimed to investigate the effect of human ASCs derived exosomes (ASC‐Exos) on peripheral nerve regeneration in vitro and in vivo. Our results showed after being internalized by Schwann cells (SCs), ASC‐Exos significantly promoted SC proliferation, migration, myelination, and secretion of neurotrophic factors by upregulating corresponding genes in vitro. We next evaluated the efficacy of ASC‐Exo therapy in a rat sciatic nerve transection model with a 10‐mm gap. Axon regeneration, myelination, and restoration of denervation muscle atrophy in ASC‐Exos treated group was significantly improved compared to vehicle control. This study demonstrates that ASC‐Exos effectively promote peripheral nerve regeneration via optimizing SC function and thereby represent a novel therapeutic strategy for regenerative medicine and nerve tissue engineering.
Prediction of pregnancy complications by second‐trimester uterine artery Doppler assessment in monochorionic twins
Authors: Masini Giulia , Tordini Chiara , Pietrosante Annamaria , Gaini Claudia , Di Tommaso Mariarosaria , Pasquini Lucia 
Published: May 2019

AbstractPurposeWe aimed to investigate whether transabdominal uterine artery (UtA) pulsatility index (PI) differs between monochorionic (MC) diamniotic and dichorionic (DC) twins and is useful to predict pregnancy complications.MethodsA total of 406 uncomplicated twin pregnancies (94 MC, 312 DC) were examined at 22+0‐24+6 weeks and compared for demographic characteristics, mean UtA PI, presence of notch, development of preeclampsia, fetal growth restriction (FGR), placental abruption, intrauterine fetal death and preterm delivery. Mann‐Whitney and Fisher's exact tests were performed for continuous and categorical variables, respectively. Sensitivity, specificity, positive predictive value, negative predictive value, and likelihood ratio were calculated for mean PI >95th percentile, presence of notch, and presence of either elevated PI or notch.ResultsMedian mean UtA PI was 0.68 in DC and 0.75 in MC pregnancies (P = .005). Bilateral notches were observed in one MC pregnancy; unilateral notch was seen in 8 DC (2.6%) and 5 MC diamniotic (5.3%) pregnancies. FGR occurred more frequently in DC twin pregnancies, while intrauterine fetal death in MC. Overall, the sensitivity of the parameters tested was low. Pregnancies with both PI above 95th percentile and presence of notch were all associated with complications, particularly FGR.ConclusionMC pregnancies have higher mean UtA PI. UtA screening in twins shows lower performances than in singletons for the detection of complications.
Observational study of the microcirculation in patients with liver cirrhosis
Authors: Wythe Stephen , Davies Thomas W , O'Beirne James , Martin Daniel , Gilbert‐Kawai Edward 
Published: May 2019

Background and AimLiver cirrhosis is associated with widespread microcirculatory dysfunction and hemodynamic derangement, which may play a role in the pathogenesis of multiple organ failure. Little is known, however, about the progression of microvascular alterations as the severity of liver disease worsens. Therefore, our aim is to quantify the peripheral systemic microcirculatory changes associated with increasing severity of liver cirrhosis.MethodsForty patients with liver cirrhosis were studied and divided into groups based on Child‐Pugh classes A (n = 9), B (n = 18), and C (n = 13) for comparison. Incident dark field imaging was used to evaluate the sublingual microcirculation and near‐infrared spectroscopy at the thenar eminence to assess microvascular reactivity and function.ResultsThere was no difference in microcirculatory flow index (P = 0.655), heterogeneity index (P = 0.702), or vessel density (P = 0.923) between the different Child‐Pugh groups. Microvascular reactivity did not change as the severity of liver disease worsened.ConclusionsThis study showed no association between peripheral systemic microcirculatory alterations and the severity of liver disease. Further research with larger study cohorts are needed to clarify the relationship between microcirculatory abnormalities and disease progression and to establish if the peripheral microcirculation is affected by the pathophysiology of worsening cirrhosis.
Breast Cancer Brain Metastasis Response to Radiation After Microbubble Oxygen Delivery in a Murine Model
Authors: Delaney Lauren J. , Ciraku Lorela , Oeffinger Brian E. , Wessner Corinne E. , Liu Ji‐Bin , Li Jingzhi , Nam Kibo , Forsberg Flemming , Leeper Dennis B. , O'Kane Patrick , Wheatley Margaret A. , Reginato Mauricio J. , Eisenbrey John R. 
Published: May 2019

ObjectivesHypoxic cancer cells have been shown to be more resistant to radiation therapy than normoxic cells. Hence, this study investigated whether ultrasound (US)‐induced rupture of oxygen‐carrying microbubbles (MBs) would enhance the response of breast cancer metastases to radiation.MethodsNude mice (n = 15) received stereotactic injections of brain‐seeking MDA‐MB‐231 breast cancer cells into the right hemisphere. Animals were randomly assigned into 1 of 5 treatment groups: no intervention, 10 Gy radiation using a small‐animal radiation research platform, nitrogen‐carrying MBs combined with US‐mediated MB rupture immediately before 10 Gy radiation, oxygen‐carrying MBs immediately before 10 Gy radiation, and oxygen‐carrying MBs with US‐mediated MB rupture immediately before 10 Gy radiation. Tumor progression was monitored with 3‐dimensional US, and overall survival was noted.ResultsAll groups except those treated with oxygen‐carrying MB rupture and radiation had continued rapid tumor growth after treatment. Tumors treated with radiation alone showed a mean increase in volume ± SD of 337% ± 214% during the week after treatment. Tumors treated with oxygen‐carrying MBs and radiation without MB rupture showed an increase in volume of 383% ± 226%. Tumors treated with radiation immediately after rupture of oxygen‐carrying MBs showed an increase in volume of only 41% ± 1% (P = 0.045), and this group also showed a 1 week increase in survival time.ConclusionsAdding US‐ruptured oxygen‐carrying MBs to radiation therapy appears to delay tumor progression and improve survival in a murine model of metastatic breast cancer.
Contextual role of E2F1 in suppression of melanoma cell motility and invasiveness
Authors: Meng Peng , Bedolla Roble G. , Yun Huiyoung , Fitzpatrick James E. , Kumar Addanki P. , Ghosh Rita 
Published: May 2019

AbstractThe general transcription factor E2F1 reportedly functions in a protumorigenic manner in several cancer models. We show that the genetic context of cancer cells influence E2F1's role to impede the protumorigenic role. Thirty to fifty percent of melanoma patients carry mutant BRAF with about 90% of mutant BRAF melanomas being V600E mutation. Tissue microarrays from melanoma patients were used to establish an association between E2F1 and BRAFV600E. We show for the first time that low E2F1 levels in BRAFV600E melanomas are associated with lymph node metastasis. Genetic manipulation of E2F1 in BRAFV600E and BRAFwt cells were used to determine its role in malignant melanoma progression by examining effects on migration and invasion. E2F1‐mediated negative regulation of myosin light chain kinase (MYLK) increased migration and invasion in BRAFV600E cells by phosphorylating myosin light chain and increased stress fiber formation. We show that E2F1 inhibits extracellular signal‐regulated kinase (ERK) activation in BRAFV600E cells and provide evidence for a negative feedback loop between E2F1 and ERK in these cells. This study shows for the first time that E2F1 has a cancer protective role in oncogenic BRAF‐activated melanoma cells and that loss of E2F1 can allow disease progression through a novel mechanism of E2F1‐mediated MYLK regulation. This study has implications for oncogenic BRAF‐activated tumors and resistance to targeted oncogenic BRAF therapy.
Association study between matrix metalloproteinase‐3 gene (MMP3) polymorphisms and ankylosing spondylitis susceptibility
Authors: Zhu Yong , Li Shunan , Huang Zhi , Xing Wenhua , Li Feng , Da Yifeng , Xue Jianmin , Li Manglai , Sun Ke , Jia Haiyu , Yang Xuejun 
Published: May 2019

AbstractBackgroundAnkylosing spondylitis (AS) is the second most common cause of inflammatory arthritis worldwide affecting the axial skeleton. Single nucleotide polymorphisms (SNPs) of matrix metalloproteinase‐3 (MMP3) in the development of AS has few been investigated in Chinese population.MethodsA total of 362 patients with AS and 362 healthy controls were enrolled in the study. Five SNPs in MMP3 genotypes were identified by Agena MassARRAY. Chi‐squared tests and genetic model were used to evaluate associations.Resultsrs522616 had a significant risk of AS development compared to those with the TT genotype (p = 0.008). By multiple logistic regression models analysis, in codominant model, rs522616 CT genotypes also had a 1.44‐fold risk (95% CI = 1.06–1.96, p = 0.008) for AS development compared to those with TT genotypes. In recessive model, the CC genotypes was a significantly reduced AS risk for individuals with TT/CT genotype (OR = 0.64; 95% CI = 0.41–0.99, p = 0.040).ConclusionThe present study suggests that MMP3 rs522616 polymorphism is associated with AS susceptibility and MMP3 might be a potential diagnostic biomarker for AS. Further independent studies with larger cohorts are warranted to validate our findings in different populations.
Precise CCM1 gene correction and inactivation in patient‐derived endothelial cells: Modeling Knudson's two‐hit hypothesis in vitro
Authors: Spiegler Stefanie , Rath Matthias , Much Christiane D. , Sendtner Barbara S. , Felbor Ute 
Published: May 2019

AbstractBackgroundThe CRISPR/Cas9 system has opened new perspectives to study the molecular basis of cerebral cavernous malformations (CCMs) in personalized disease models. However, precise genome editing in endothelial and other hard‐to‐transfect cells remains challenging.MethodsIn a proof‐of‐principle study, we first isolated blood outgrowth endothelial cells (BOECs) from a CCM1 mutation carrier with multiple CCMs. In a CRISPR/Cas9 gene correction approach, a high‐fidelity Cas9 variant was then transfected into patient‐derived BOECs using a ribonucleoprotein complex and a single‐strand DNA oligonucleotide. In addition, patient‐specific CCM1 knockout clones were expanded after CRISPR/Cas9 gene inactivation.ResultsDeep sequencing demonstrated correction of the mutant allele in nearly 33% of all cells whereas no CRISPR/Cas9‐induced mutations in predicted off‐target loci were identified. Corrected BOECs could be cultured in cell mixtures but demonstrated impaired clonal survival. In contrast, CCM1‐deficient BOECs displayed increased resistance to stress‐induced apoptotic cell death and could be clonally expanded to high passages. When cultured together, CCM1‐deficient BOECs largely replaced corrected as well as heterozygous BOECs.ConclusionWe here demonstrate that a non‐viral CRISPR/Cas9 approach can not only be used for gene knockout but also for precise gene correction in hard‐to‐transfect endothelial cells (ECs). Comparing patient‐derived isogenic CCM1+/+, CCM1+/−, and CCM1−/− ECs, we show that the inactivation of the second allele results in clonal evolution of ECs lacking CCM1 which likely reflects the initiation phase of CCM genesis.
Structural neuroimaging in mild traumatic brain injury: A chronic effects of neurotrauma consortium study
Authors: Bigler Erin D. , Abildskov Tracy J. , Eggleston Barry , Taylor Brian A. , Tate David F. , Petrie Jo Ann , Newsome Mary R. , Scheibel Randall S. , Levin Harvey , Walker William C. , Goodrich‐Hunsaker Naomi , Tustison Nicholas J. , Stone James R. , Mayer Andrew R. , Duncan Timothy D. , York Gerry E. , Wilde Elisabeth A. 
Published: May 2019

AbstractObjectivesThe chronic effects of neurotrauma consortium (CENC) observational study is a multisite investigation designed to examine the long‐term longitudinal effects of mild traumatic brain injury (mTBI). All participants in this initial CENC cohort had a history of deployment in Operation Enduring Freedom (Afghanistan), Operation Iraqi Freedom (Iraq), and/or their follow‐on conflicts (Operation Freedom's Sentinel). All participants undergo extensive medical, neuropsychological, and neuroimaging assessments and either meet criteria for any lifetime mTBI or not. These assessments are integrated into six CENC core studies—Biorepository, Biostatistics, Data and Study Management, Neuroimaging, and Neuropathology.MethodsThe current study outlines the quantitative neuroimaging methods managed by the Neuroimaging Core using FreeSurfer automated software for image quantification.ResultsAt this writing, 319 participants from the CENC observational study have completed all baseline assessments including the imaging protocol and tertiary data quality assurance procedures.Conclusions/DiscussionThe preliminary findings of this initial cohort are reported to describe how the Neuroimaging Core manages neuroimaging quantification for CENC studies.
The belonging model of trust
Authors: Knapp Joshua R. , Sprinkle Therese A. , Urick Michael J. , Delaney‐Klinger Kelly A. 
Published: May 2019

AbstractAlthough we know that high‐quality employee–organization relationships are beneficial, these relationships are complex and not fully understood, especially among employees of nonprofit organizations. In particular, we know little about how these employees perceive trust, which may overlook an important contributor to effective management. We begin to address this issue by testing a new theoretical model that conceptualizes perceived insider status, psychological ownership, and organizational identification as foundations for the perception of justice and subsequent trust. Our results indicate that psychological ownership and perceived insider status relate to trust through procedural and interpersonal justice. These results contrast those typically found in for‐profit contexts in that organizational identification did not predict justice and that distributive and informational justice did not predict trust.
Proteomics Analysis of Avian Eggshell Matrix Proteins: Toward New Advances on Biomineralization
Authors: Gautron Joël 
Published: May 2019

AbstractEggs are widely consumed all over the world. The eggshell is its protective barrier whose original function is to protect the embryo during development. Avian eggshells are made of calcium carbonate with a small amount of organic matrix (proteins and proteoglycans). During eggshell formation, the mineral precursors interact with matrix proteins to regulate the calcification of this highly resistant biomineral. In order to better characterize the functions of matrix proteins in eggshell biominerals, many proteomics studies have been performed during the last 15 years. The chicken eggshell is the main model studied in birds, but there is a need for comparative approaches in order to determine whether there is a general protein toolkits associated with calcitic biomineralization, and to determine its components. The study by Zhu et al., reported in article number 1900011, volume 19, issue 11, is a major step forward as it is the first shell proteomics survey performed on duck. Thus, it will contribute to improved knowledge of the eggshell mineralization process and will provide new insight for shell quality improvement and to guide biomimetic efforts in material sciences.
Controlled processing of polymer nanoribbons: Enabling microhelix transformations
Authors: Choudhary Satyan , Crosby Alfred J. 
Published: May 2019

ABSTRACTFlow‐coated, two‐dimensional polymer ribbon structures undergo a shape‐transformation into a three‐dimensional helix upon their release into a solution. Driven by surface forces and due to geometric asymmetry, the helix radius and spring constant depend upon the ribbon cross‐section dimensions, surface energy, and material elastic modulus. Such spring‐like microhelices offer multiple functionalities combined with mechanical stretching and shape recovery. Fabricating such microhelices requires a sequence of processing steps, beginning with flow‐coating of ribbons on a substrate, followed by etching of a “scum layer” to allow for an independent release into a solution, upon which shape‐transformation occurs. During the deposition‐etch‐release sequence, various control parameters influence the nanoribbon size and geometry, hence the helix properties. The experimental study presented here focuses on the influence of meniscus height, substrate velocity, substrate surface energy, and etch time on nanoribbon size (height and width), scum layer thickness, and helix radius. The results show that meniscus height and contact angle dictate flux toward the meniscus edge and volume available for spatial assembly, allowing control over the aspect ratio of ribbons. We vary the aspect ratio by two orders of magnitude, while maintaining geometric asymmetry needed for helix shape‐transformation. We provide robust scaling for the nanoribbon size and geometry and report the advantages and disadvantages of different parameters, in the control of polymer nanoribbon and helix fabrication. © 2019 Wiley Periodicals, Inc. J. Polym. Sci., Part B: Polym. Phys. 2019, 57, 1270–1278
l‐α‐Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK‐dependent pathway
Authors: Robertson‐Gray Olivia J. , Walsh Sarah K. , Ryberg Erik , Jönsson‐Rylander Ann‐Cathrine , Lipina Christopher , Wainwright Cherry L. 
Published: May 2019

AbstractThe phospholipid l‐α‐lysophosphatidylinositol (LPI), an endogenous ligand for GPR55, is elevated in patients with acute coronary syndrome, and a GPR55 antagonist cannabidiol (CBD) reduces experimental ischemia/reperfusion (I/R) injury. While LPI activates multiple signaling pathways, little is known about which ones are important in cardiomyocytes. In this study we explored whether activation of the Rho kinase/ROCK/p38 MAPK pathway is responsible for LPI‐induced extension of I/R injury. Using a high‐throughput screening method (dynamic mass redistribution; DMR), mouse‐ and human‐induced pluripotent stem cell (iPSC) cardiomyocytes exposed to LPI were shown to exhibit a rapid, sustained, and concentration‐dependent (1 nmol L−1‐30 μmol L−1) cellular response. Y‐27632 (ROCK inhibitor; 10 & 50 μmol L−1) and CBD (1 μmol L−1) both abolished the DMR response to LPI (10 μmol L−1). In murine iPSC cardiomyocytes, LPI‐induced ROCK and p38 MAPK phosphorylation, both of which were prevented by Y‐27632 and CBD, but did not induce JNK activation or cleavage of caspase‐3. In hearts isolated from wild type (WT) mice subjected to 30 minutes global I/R, LPI (10 μmol L−1) administered via the coronary circulation increased infarct size when applied prior to ischemia onset, but not when given at the time of reperfusion. The exacerbation of tissue injury by LPI was not seen in hearts from GPR55−/− mice or in the presence of Y‐27632, confirming that injury is mediated via the GPR55/ROCK/p38 MAPK pathway. These findings suggest that raised levels of LPI in the vicinity of a developing infarct may worsen the outcome of AMI.