bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluating the self‐domestication hypothesis of human evolution
Authors: Sánchez‐Villagra Marcelo R. , van Schaik Carel P. 
Published: April 2019

Abstract“Self‐domestication” has been invoked to understand important aspects of human evolution, integrating physiological, behavioral, and morphological information in a novel way. It proposes that selection for reduced aggression on animals undergoing domestication provides a model for selection favoring prosocial behaviors in humans and for a set of seemingly independent features, which arose as a result of developmental correlation. We review the history of the idea and examine patterns of domestication. A lack of empirical studies on evolutionary rates and variation thwarts meaningful comparison with domestication. The neural crest hypothesis for domestication has great explanatory power but it is difficult to test. We suggest a scenario in which the morphological byproducts of domestication can act as an honest signal of reduced xenophobia. Future studies should test if alternative explanations for the features deemed to result from self‐domestication are mutually exclusive and generate data to test predictions of these hypotheses.
A new wall model for slip boundary conditions in dissipative particle dynamics
Authors: Xu Shaofeng , Wang Q. Jane , Wang Jiugen 
Published: April 2019

SummaryDissipative particle dynamics (DPD) for modeling complex flows requires proper boundary conditions to simulate the behavior of a wall‐bounded flow. Although most DPD simulations use the no‐slip boundary condition, slip should be considered for a more complete and realistic description of such flows. The present work suggests a new wall model, via a wall‐particle virtual velocity approach, to impose tunable partial‐slip boundary conditions while structuring a modified reflection mechanism to enforce the no‐slip boundary condition. The new wall model is validated through simulating the planar Poiseuille and Couette flows and implemented to investigate the wall slip status affected by the wall virtual velocity.
American Joint Committee on Cancer eighth edition human papilloma virus positive oropharyngeal cancer staging system: Discordance between clinical and pathological staging systems
Authors: Hall Scott R. , Neel Gregory S. , Chang Brent A. , Howard Brittany E. , Nagel Thomas H. , Lott David G. , Hayden Richard E. , Zhang Nan , Hinni Michael L. 
Published: April 2019

AbstractBackgroundThe American Joint Committee on Cancer (AJCC) eighth edition introduces a staging system specific for human papilloma virus positive oropharyngeal cancer with separate clinical (AJCC 8c) and pathological (AJCC 8p) criteria.MethodsIn this retrospective cohort study, preoperative imaging and pathology reports were used to stage patients based on the AJCC 8c and AJCC 8p criteria, respectively. The primary endpoint was agreement between AJCC 8c and AJCC 8p.ResultsA total of 213 patients met inclusion criteria. Kappa statistics showed poor agreement (κ = 0.3275) between AJCC 8c and AJCC 8p. In total, 30.3% of patient's preoperative AJCC 8c stage changed based on the postoperative pathologic staging (AJCC 8p) with 73.4% of those being upstaged.ConclusionThese data suggest that disagreement exists between AJCC 8c and AJCC 8p, in part due to the separate clinical and pathological staging criteria. This discrepancy should be considered as the new system is implemented.
Trifluoromethyl Derivatives of Benzooxatellurole
Authors: Pietrasiak Ewa , Baxter Amanda F. , Jelier Benson , Santschi Nico , Togni Antonio 
Published: April 2019

AbstractReplacement of the iodine atom in an iodine (III) CF3‐transfer reagent with a Te‐aryl moiety was accomplished in a three‐step synthetic sequence. Three compounds of this type have been prepared, two of which were characterized by X‐ray diffraction. Single crystal structures were also obtained for three related Te(IV) compounds unreported so far (4a, 4b, 6b). Comparison with the iodine (III) analogues indicate a large degree of structural similarity, however these species display an interesting decomposition pathway under thermal conditions. In addition to the expected Te−CF3 bond cleavage, C−F bond cleavage is also observed, unlike in the case of iodine (III) compounds.
RELA promotes hypoxia‐induced angiogenesis in human umbilical vascular endothelial cells via LINC01693/miR‐302d/CXCL12 axis
Authors: Sun Yang , Xiong Xiang , Wang Xiancheng 
Published: April 2019

AbstractHypoxia‐induced angiogenesis plays a critical role in wound healing, which could be disturbed by multifactors. Upon hypoxia stimulation, CXCL12 and its receptor CXCR4 were significantly upregulated in human umbilical vascular endothelial cells (HUVECs); thus, we attempted to investigate the role and mechanism of CXCL12 in HUVEC angiogenesis under hypoxia. Via downloading and analyzing microarray profiles (GSE76743 and GSE116909), we found that LINC01693 was positively correlated with CXCL12 and upregulated by hypoxia in HUVECs, while miR‐302d was downregulated by hypoxia and might target LINC01693 and CXCL12. RELA, a critical transcriptional factor for response to hypoxia, could bind to LINC01693 promoter to activate its transcription, therefore, promoting CXCL12 expression under hypoxia. LINC01693 served as a competing endogenous RNA for miR‐302d to counteract miR‐302d‐mediated CXCL12 suppression via direct targeting. Hypoxia‐induced CXCL12 upregulation and angiogenesis in HUVECs could be significantly suppressed by LINC01693 silence while enhanced by miR‐302d inhibition; the effect of LINC01693 silence could be partially reversed by miR‐302d inhibition. Taken together, RELA promotes the angiogenesis in HUVECs via LINC01693/miR‐302d/CXCL12 axis. We provide a novel mechanism and experimental basis of CXCL12 function in hypoxia‐induced HUVEC angiogenesis.
miR‐199a‐5p promotes proliferation and metastasis and epithelial‐mesenchymal transition through targeting PIAS3 in cervical carcinoma
Authors: Qu Dacheng , Yang Yamei , Huang Xiaoping 
Published: April 2019

AbstractCervical carcinoma is the second most frequent gynecological malignancies in females worldwide. The objective of this study was to investigate the role of miR‐199a‐5p and protein inhibitor of activated signal transducer and activators of transcription 3 (PIAS3) in cervical carcinoma. Quantitative reverse transcription polymerase chain reaction was utilized to detect miR‐199a‐5p and PIAS3 expression in cervical carcinoma tissues and cells. 3‐(4,5‐Dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide Kit, transwell assay were used to explore the biological functions of miR‐199a‐5p in cervical carcinoma. Western blot analysis was applied to determine the expression level of epithelial‐mesenchymal transition (EMT)‐associated proteins and PIAS3 expression. The relationship between miR‐199a‐5p and PIAS3 was verified by luciferase activity reporter assay. We found that miR‐199a‐5p was upregulated in cervical carcinoma tissues and cell lines, and overexpression of miR‐199a‐5p promoted cell proliferation and metastasis in cervical carcinoma. In addition, Western blot analysis indicated that the enforced upregulation of miR‐199a‐5p enhanced mesenchymal markers vimentin and N‐cadherin expressions, whereas reduced epithelial marker E‐cadherin expressions. miR‐199a‐5p directly targeted PIAS3 and negatively regulated PIAS3 level in cervical carcinoma cells. And upregulation of PIAS3 reversed the effects of miR‐199a‐5p in cervical carcinoma. Collectively, our data provide evidence for miR‐199a‐5p function in cervical carcinoma growth, EMT, and metastasis; it may be act as a therapeutic strategy target for patients with cervical carcinoma.
Matrine improves diabetic cardiomyopathy through TGF‐β‐induced protein kinase RNA‐like endoplasmic reticulum kinase signaling pathway
Authors: Hou Huijuan , Zhang Qianqian , Dong Hongwei , Ge Zhiming 
Published: April 2019

AbstractBackgroundMatrine might play a vital role in cardiovascular diseases progression and treatment.ObjectivesWe aimed to explore the protective effects and potential mechanism of matrine against diabetic cardiomyopathy (DCM) in rat model.MethodA rat model of DCM was induced by streptozotocin, which were then divided into two groups and treated with matrine. Inflammatory cytokines were investigated in serum and myocardial cells after matrine administration. The effects of matrine on cardiac reactive oxygen species (ROS) generation, Malondialdehyde (MDA) levels, and Glutathione peroxidase (GPx), PPARγ1 activity were detected in myocardial cells. The protein kinase RNA‐like endoplasmic reticulum kinase (PERK) signal pathway in endoplasmic reticulum stress was studied to elaborated protective effects of matrine in DCM rat by Western blot analysis. Fasting blood glucose and hemodynamic parameters were analyzed after treatment with matrine.ResultsMatrine‐inhibited expression levels of inflammatory cytokines of tumor necrosis factor alpha (TNF‐α) and interleukin 6. Matrine administration decreased ROS generation, MDA, and transforming growth factor beta levels, and Peroxisome proliferator‐activated receptor beta (PPARβ) and Peroxisome proliferator‐activated receptorγ 1 (PPARγ1) activity. Matrine administration also significantly inhibited PERK expression. Endogenic expression of PERK canceled matrine‐induced apoptosis of myocardial cells. Notably, treatment with matrine significantly decreased nonfasting blood glucose levels and improved hemodynamic parameters of DCM rat.ConclusionsMatrine may be a promising agent for the treatment of DCM.
Sema4D/PlexinB1 promotes endothelial differentiation of dental pulp stem cells via activation of AKT and ERK1/2 signaling
Authors: Zou Ting , Jiang Shan , Dissanayaka Waruna Lakmal , Heng Boon Chin , Xu Jianguang , Gong Ting , Huang Xiaojing , Zhang Chengfei 
Published: April 2019

AbstractInducing of dental pulp stem cells (DPSCs) into endothelial cells (ECs) to prevascularize pulp tissue constructs may offer a novel and viable approach for enhancing pulp regeneration. However, there are numerous challenges in current methods for the acquisition of sufficient translational ECs. It was known that Sema4D/PlexinB1 signaling exerts profound effects on enhancing vascular endothelial growth factor (VEGF) secretion and angiogenesis. Whether Sema4D/PlexinB1 could regulate endothelial differentiation of DPSCs is not yet investigated. In this study, when DPSCs were treated with Sema4D (2 μg/mL), ECs‐specific (VEGFR1, VEGFR2, CD31, and vWF), and angiogenic genes and proteins were significantly upregulated. The induced ECs exhibited similar endothelial vessel formation ability to that of human umbilical vein endothelial cells (HUVECs). Furthermore, phosphorylation of AKT increased dramatically within 5 minutes (from 0.93 to 21.8), while p‐ERK1/2 was moderately elevated (from 0.94 to 2.65). In summary, our results demonstrated that Sema4D/PlexinB1 signaling induces endothelial differentiation of DPSCs. The interactions of Sema4D, VEGF, ANGPTL4, ANG1, and HIF‐1α may play a crucial role in mediating the differentiation process.
MicroRNA‐181a regulates the activation of the NLRP3 inflammatory pathway by targeting MEK1 in THP‐1 macrophages stimulated by ox‐LDL
Authors: Song Jinyang , Yang Shaonan , Yin Ruihua , Xiao Qi , Ma Aijun , Pan Xudong 
Published: April 2019

AbstractAtherosclerosis (AS) is a chronic inflammatory disease that is characterized by the deposition of lipids in the vascular wall and the formation of foam cells. Macrophages play a critical role in the development of this chronic inflammation. An increasing amount of research shows that microRNAs affect many steps of inflammation. The goal of our study was to investigate the regulatory effect of miR‐181a on the NLRP3 inflammasome pathway and explore its possible mechanism. Compared with the control group, the expression of miR‐181a was downregulated in the carotid tissue of AS group mice, while the expression of MEK1 and NLRP3‐related proteins was upregulated significantly. In vitro, when THP‐1 macrophages were stimulated with oxidized low‐density lipoprotein (ox‐LDL), the expression of miR‐181a was decreased, the MEK/ERK/NF‐κB inflammatory pathways were activated and the expression of NLRP3 inflammasome‐related proteins was upregulated. Exogenous overexpression of miR‐181a downregulated the activation of the MEK/ERK/NF‐κB pathway and decreased the expression of NLRP3 inflammasome‐related proteins (such as NLRP3, caspase‐1, interleukin‐18 [IL‐18], IL‐1β, etc). Exogenous miR‐181a knockdown showed the opposite results to those of overexpression group. A luciferase reporter assay proved that miR‐181a inhibited the expression of MEK1 by binding to its 3′‐untranslated region. When we knocked down miR‐181a and then treated cells with U0126 before ox‐LDL stimulation, we found that U0126 reversed the increased activation of the MEK/ERK/NF‐κB pathway and upregulation of NLRP3 inflammasome‐related proteins (NLRP3, caspase‐1, IL‐18, IL‐1β) that resulted from miR‐181a knockdown. Our study suggests that miR‐181a regulates the activation of the NLRP3 inflammatory pathway by altering the activity of the MEK/ERK/NF‐κB pathway via targeting of MEK1.
Homeobox D10, a tumor suppressor, inhibits the proliferation and migration of esophageal squamous cell carcinoma
Authors: Zhang Jin , Liu Shiyuan , Zhang Danjie , Ma Zhenchuan , Sun Liangzhang 
Published: April 2019

AbstractEsophageal squamous cell carcinoma (ESCC) is one of the most common types of esophageal cancer, which is the sixth leading cause of cancer death globally. Homeobox D10 (HOXD10) is a member of the homeobox (HOX) gene family and has been reported to act as a tumor suppressor. However, the potential role of HOXD10 in ESCC has not been reported. Thus, the aim of this study was to examine the expression and function of HOXD10 in ESCC. The expressions of HOXD10 in human ESCC tissues and cell lines were detected by quantitative reverse transcription polymerase chain reaction and Western blot. The HOXD10 overexpressing cell lines were established, then CCK‐8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. The expression of EMT‐related proteins and signaling pathway‐related proteins were detected by Western blot. Our results showed that HOXD10 is lowly expressed in ESCC tissues as well as in ESCC cell lines. Ectopic overexpression of HOXD10 inhibited cell proliferation, migration, and invasion of ESCC cells (P < 0.05). HOXD10 overexpression repressed the epithelial‐mesenchymal transition (EMT) process in ESCC cells. Besides, HOXD10 overexpression suppressed the activation of PI3K/AKT/mTOR signaling pathway. PI3K/Akt agonist, insulin‐like growth factor‐1, reversed the inhibitory effects of HOXD10 on cell proliferation and migration in ESCC cells. Additional in vivo study proved that ectopic expression of HOXD10 caused an obvious inhibitory effect on the tumor growth. These findings indicated that overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. Thus, targeting HOXD10 may be considered as a therapeutic strategy for ESCC treatment.
LncRNA AC096664.3/PPAR‐γ/ABCG1‐dependent signal transduction pathway contributes to the regulation of cholesterol homeostasis
Authors: Xu Bang‐Ming , Xiao Lei , Kang Chun‐Min , Ding Li , Guo Feng‐Xia , Li Pan , Lu Zhi‐Feng , Wu Qian , Xu Yuan‐Jun , Bai Huan‐Lan , Tang Jun‐Yi , Zheng Lei , Hu Yan‐Wei , Wang Qian 
Published: April 2019

AbstractAtherosclerosis is a complex inflammatory disease that involves disrupted cellular cholesterol levels and formation of foam cells. Studies about long noncoding RNA (lncRNA) have revealed its function in the development of atherosclerosis, by mediating reverse cholesterol transport and formation of foam cells. In this study, we found that oxidized low‐density lipoprotein (ox‐LDL) markedly decreased lncRNA AC096664.3 in vascular smooth muscle cells (VSMCs) and THP‐1 macrophages. We also found that ox‐LDL reduced ATP‐binding cassette (ABC) G1 through inhibiting lncRNA AC096664.3 in VSMCs. Further experiments showed that the downregulation of lncRNA AC096664.3 reduced ABCG1 expression through inhibiting the expression of peroxisome proliferator–activated receptor‐γ (PPAR‐γ) and that ox‐LDL reduced ABCG1 expression through inhibiting the expression of PPAR‐γ. Furthermore, we discovered that ox‐LDL inhibited ABCG1 via the lncRNA AC096664.3/PPAR‐γ/ABCG1 pathway, which led to an increase in total and free cholesterol in VMSCs. Thus, we confirmed that ox‐LDL induces cholesterol accumulation via the lncRNA AC096664.3/PPAR‐γ/ABCG1 pathway in VSMCs, indicating a promising novel therapy in protecting against atherosclerosis.
Inhibition of the chimeric DnaJ‐PKAc enzyme by endogenous inhibitor proteins
Authors: Averill April M. , Rehman Hibba tul , Charles Joseph W. , Dinh Timothy A. , Danyal Karamatullah , Verschraegen Claire F. , Stein Gary S. , Dostmann Wolfgang R. , Ramsey Jon E. 
Published: April 2019

AbstractThe chimeric DnaJ‐PKAc enzymeresulting from an approximately 400‐kb deletion of chromosome 19 is a primary contributor to the oncogenic transformation that occurs in fibrolamellar hepatocellular carcinoma, also called fibrolamellar carcinoma (FLC). This oncogenic deletion juxtaposes exon 1 of the DNAJB1 heat shock protein gene with exon 2 of the PRKACA gene encoding the protein kinase A catalytic subunit, resulting in DnaJ‐PKAc fusion under the transcriptional control of the DNAJB1 promoter. The expression of DnaJ‐PKAc is approximately 10 times that of wild‐type (wt) PKAc catalytic subunits, causing elevated and dysregulated kinase activity that contributes to oncogenic transformation. In normal cells, PKAc activity is regulated by a group of endogenous proteins, termed protein kinase inhibitors (PKI) that competitively inhibit PKAc and assist with the nuclear export of the enzyme. Currently, it is scarcely known whether interactions with PKI are perturbed in DnaJ‐PKAc. In this report, we survey existing data sets to assess the expression levels of the various PKI isoforms that exist in humans to identify those that are candidates to encounter DnaJ‐PKAc in both normal liver and FLC tumors. We then compare inhibition profiles of wtPKAc and DnaJ‐PKAc against PKI and demonstrate that extensive structural homology in the active site clefts of the two enzymes confers similar kinase activities and inhibition by full‐length PKI and PKI‐derived peptides.
The effects of acupuncture and electroacupuncture on Parkinson's disease: Current status and future perspectives for molecular mechanisms
Authors: Tamtaji Omid Reza , Naderi Taheri Mojtaba , Notghi Fahimeh , Alipoor Reza , Bouzari Reihanesadat , Asemi Zatollah 
Published: April 2019

AbstractAmong the progressive neurodegenerative disorders, Parkinson's disease (PD) is the second most common. Different factors have critical role in pathophysiology of PD such as apoptosis pathways, inflammatory cytokines, oxidative stress, and neurotransmitters and its receptors abnormalities. Acupuncture and electroacupuncture were considered as nondrug therapies for PD. Although numerous studies has been conducted for assessing the mechanism underlying electroacupuncture and acupuncture, various principal aspects of these treatment procedures remain not well‐known. There have also been few investigations on the molecular mechanism of acupuncture and electroacupuncture therapy effects in PD. This review evaluates the effects of electroacupuncture and acupuncture on the molecular mechanism in PD.
Decreased accumulation of superoxide dismutase 2 within mitochondria in the yeast model of Shwachman‐Diamond syndrome
Authors: Jensen Laran T. , Phyu The , Jain Ayushi , Kaewwanna Chonlada , Jensen Amornrat Naranuntarat 
Published: April 2019

AbstractMutations in the human SBDS gene is the most common cause of Shwachman‐Diamond syndrome (SDS). The SBDS protein participates in ribosome biogenesis; however, effects beyond reduced translation efficiency are thought to be involved in SDS progression. Impaired mitochondrial function has been reported for cells lacking either SBDS or Sdo1p, the Saccharomyces cerevisiae SBDS ortholog. To better understand how the loss of SBDS/Sdo1p leads to mitochondria damage, we utilized the S. cerevisiae model of SDS. Yeast deleted for SDO1 show increased oxidative damage to mitochondrial proteins and a marked decrease in protein levels and activity of mitochondrial superoxide dismutase 2 (Sod2p), a key enzyme involved in defense against oxidants. Immature forms of Sod2p are observed in sdo1∆ cells suggesting a defect in proteolysis of the presequence. Yeast deleted for CYM1, encoding a presequence protease, display a similar reduction in Sod2p activity as sdo1∆ cells, as well as elevated oxidative damage, to mitochondrial proteins. Sod2p protein levels and activity are largely restored in a por1∆ sdo1∆ strain, lacking the major mitochondrial voltage‐dependent anion channel. Together these results indicate that mitochondrial insufficiency in sdo1∆ cells may be linked to the accumulation of immature presequence containing proteins and this effect is a consequence, at least in part, from loss of counter‐regulation of Por1p by Sdo1p.
Long noncoding RNA NEAT1 suppresses sorafenib sensitivity of hepatocellular carcinoma cells via regulating miR‐335–c‐Met
Authors: Chen Shuwei , Xia Xinhu 
Published: April 2019

AbstractObjectivesTo investigate the role of long noncoding RNA (lncRNA) nuclear‐enriched abundant transcript 1 (NEAT1) in regulating sorafenib (Sora) sensitivity of hepatocellular carcinoma (HCC) cells and possible signaling pathways.MethodsHCC cell lines and tumor tissue were quantified for NEAT1 expression by quantitative polymerase chain reaction (qPCR). Following shRNA (short hairpin RNA) knockdown of NEAT1, cell viability, apoptosis, and related protein expression were measured after drug treatment. The downstream target of NEAT1, including miR‐335 and c‐Met was studied using a combination of luciferase binding assay, gene knockdown/overexpression, western blot analysis, and cell viability/apoptosis assay. Cancer cells with NEAT1 knockdown were transplanted onto nude mice for in vivo tumorigenesis assay.ResultsSilencing of NEAT1 in HCC cells facilitated Sora sensitivity by enhancing drug‐induced apoptosis, and led to smaller tumor size on nude mice. Mechanistic study suggested that miR‐335 was negatively regulated by NEAT1, and miR‐335 further suppressed c‐Met–Akt pathway, whose activation caused drug resistance of HCC cells. The knockdown of miR‐335, or overexpression of c‐Met, all remarkably abolished the proapoptotic effect of NEAT1 knockdown in HCC cells.ConclusionlncRNA NEAT1 mediates Sora resistance of HCC cells by suppressing miR‐335 expression, and disinhibition on c‐Met–Akt signaling pathway. Our results provide potency of NEAT1 as the biomarker for drug resistant HCC and possible treating targets.