bluuebunny/crossref_metadata_2025_split huggingface dataset:
The impact of co‐contaminant SO2, versus salinity and thermodynamic conditions, on residual CO2 trapping during geological storage
Authors: Rasmusson Maria , Rasmusson Kristina , Fagerlund Fritjof , Tsang Yvonne , Niemi Auli 
Published: September 2018

AbstractDuring geological storage in deep saline aquifers, immobilization of CO2 in reservoir rock determines both storage safety and capacity. Assessment of the sensitivity of residual trapping to different parameters (interfacial tension and contact angles) and the storage conditions affecting these is therefore of great importance. One aspect of concern is the presence of co‐contaminants such as SO2 in the injected gas. Using experimentally measured values of interfacial tensions and contact angles, we apply pore‐network modelling (which accounts for pore‐scale mechanisms such as snap‐off, cooperative pore body filling and piston‐type displacement) to a generic sandstone network to quantify the impact of SO2 co‐injection on residual CO2 trapping, and its relative importance as compared to the influences of thermodynamic conditions and salinity. We show that the presence of small amounts of SO2 in the injected CO2 has a notable positive effect on the amount of CO2 becoming residually trapped (∼3% increase at 1 wt% SO2). However, this effect is small compared to that of the brine salinity (∼20% decrease in residually trapped CO2 over the salinity range 0.2 to 5 M NaCl). Still, co‐injection of SO2 could potentially favour the residual trapping of CO2 in reservoir rocks, especially at storage sites with inclined aquifers where the CO2 is set to migrate hydro‐dynamically over long distances. The salinity of the resident brine is of primary importance during storage site selection. Furthermore, sensitivity analysis shows that the advancing contact angle strongly impacts residual CO2 trapping. © 2018 Society of Chemical Industry and John Wiley & Sons, Ltd.
Dedifferentiated spermatic cord liposarcoma with macroscopic ossification
Authors: Ando Takashi , Nakayama Ryo , Mizusawa Takaki , Sakai Takeshi , Otsuka Hiroshi , Katagiri Akiyoshi 
Published: September 2018

IntroductionLiposarcoma is a malignant neoplasm of the adipose tissue, and dedifferentiated liposarcoma is a relatively rare subtype. Liposarcomas are typically located in the lower extremities or retroperitoneum, but dedifferentiated liposarcoma of the spermatic cord is rare and no case of it with macroscopic ossification has been reported in the literature.Case presentationA male presented to our hospital with a painful, palpable, and hard left suprapubic mass, formed over 3 months. The mass was diagnosed as a spermatic cord tumor and was resected using high orchiectomy. Due to the histological diagnosis of dedifferentiated spermatic cord liposarcoma with ossification and positive margins, a second extended resection and adjuvant radiotherapy were performed.ConclusionTo differentiate spermatic cord liposarcoma preoperatively is difficult. There is no gold standard treatment for it, although surgical complete resection with clear microscopic margins would be the most effective treatment.
Multifunctional effects of a modification of SLA titanium implant surface with strontium‐containing nanostructures on immunoinflammatory and osteogenic cell function
Authors: Choi Sung‐Min , Park Jin‐Woo 
Published: September 2018

AbstractThis study investigated the effects of surface modification of clinically available sandblasted/acid‐etched (SLA) titanium oral implants with strontium (Sr)‐containing nanostructures on both early immunoinflammatory macrophage cell functions and osteogenic stem cell functions. The goal was to provide insight for future surface engineering of titanium implants with multifunctional effects, that is, tissue healing capacity at both the nonosteogenic cell centered initial stage and the subsequent osteogenic cell‐governed later stage‐osseointegration process. The Sr‐containing nanostructure was prepared in on the SLA‐type implant surface by wet chemical treatment. The results showed that Sr modification is favorable for early macrophage cell functions and increases osteogenic capacity of the SLA surface. Surface Sr modification notably upregulated regenerative macrophage phenotype expression and anti‐inflammatory cytokine IL10 production while suppressing inflammatory cytokine TNFα. Sr incorporation enhanced certain early cellular events of ST2 stem cells such as early cellular spreading and critical integrin gene expression, which in turn notably increased osteogenic differentiation (osteogenesis‐related phenotype gene expression and osteocalcin production) when combined with the microstructured SLA implant surface. Surface modification of SLA‐type implants with Sr‐containing nanostructures demonstrated the ability to favorably influence early immunoinflammatory macrophage cell functions and the functionality of osteogenesis cells, resulting in an enhanced osseointegration outcome. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 3009–3020, 2018.
Performance comparison of blood collection tubes as liquid biopsy storage system for minimizing cfDNA contamination from genomic DNA
Authors: Zhao Yunlong , Li Yingjie , Chen Ping , Li Shaojun , Luo Jian , Xia Hui 
Published: September 2018

BackgroundThe ratio of target cfDNA in total plasma is low. The abundant gDNA background resulting from blood cell lysis caused by improper operation has become a major obstacle to accurately measure cfDNA. In this study, we investigated the storage capacity of three blood cell collection tubes (BCTs) in the prevention of genomic DNA contamination caused by white blood cell rupture and evaluated their performance when they were utilized combining with highly sensitive mutation detection technology.MethodsBlood samples were drawn from six healthy blood donors and stored in three types of BCTs (BD K2‐EDTA tube, Roche tube, and Streck tube). Plasma samples were isolated at specific time points (day 0, day 3, day 7, and day 14) for content analysis.ResultsRoche BCT was more capable for preventing cfDNA contamination caused by white blood cell disruption within 14 days, comparing with BD K2‐EDTA tube and Streck tube. Severe white blood cell lysis and gDNA contamination were found in the BD tube. The impacts of Roche and Streck tubes on the quantity and complexity of next‐generation sequencing (NGS) libraries did not differ significantly within 3 days, satisfying most of our daily demands. In addition, the rupture of WBC was not synchronized with hemolysis in BCTs.ConclusionThis study showed that capacities of blood collection tubes differed considerably in preservation of blood samples. Therefore, suitable blood collection devices should be selected to minimize gDNA contamination and to standardize blood samples processing for achieving more accurate and reliable clinical analysis of cfDNA.
The prognostic and therapeutic values of long noncoding RNA PANDAR in colorectal cancer
Authors: Rivandi Mahdi , Pasdar Alireza , Hamzezadeh Leila , Tajbakhsh Amir , Seifi Sima , Moetamani‐Ahmadi Mehrdad , Ferns Gordon A. , Avan Amir 
Published: September 2018

AbstractLong noncoding RNAs (lncRNAs) consist of 200 nucleotide sequences that play essential roles in different processes, including cell proliferation, and differentiation. There is evidence showing that the dysregulation of lncRNAs promoter of CDKN1A antisense DNA damage‐activated RNA (PANDAR) leads to the development and progression in several cancers including colorectal cancer, via p53‐dependent manner. This suggests that these lncRNAs may be of value as prognostic indices and a therapeutic target, as a high expression of lncRNAs PANDAR is associated with poor prognosis. Furthermore, modulating lncRNAs PANDAR has been reported to induce apoptosis and inhibit the tumor growth through modulation of cell cycle and epithelial‐mesenchymal transition (EMT) pathway. The aim of the current review was to provide an overview of the prognostic and therapeutic values of lncRNAs PANDAR in colorectal cancer
HNF6 promotes tumor growth in colorectal cancer and enhances liver metastasis in mouse model
Authors: Jiang Kai , Jiao Yurong , Liu Yue , Fu Dongliang , Geng Haitao , Chen Liubo , Chen Haiyan , Shen Xiangfeng , Sun Lifeng , Ding Kefeng 
Published: September 2018

AbstractHepatocyte nuclear factor 6 (HNF6), as a transcription factor, has been reported to be involved in cell proliferation, carcinogenesis, and tumor metastasis. Here, we demonstrated the role of HNF6 in tumor growth and liver metastasis in colorectal cancer (CRC). Through bioinformatics and clinical samples analysis, we found HNF6 messenger RNA was upregulated both in CRC primary sites and liver metastases, and its high expression indicated poor survival in CRC patients. In vitro studies confirmed that HNF6 promoted cell proliferation and colony formation. What is more, in mouse models, the xenografts grew significantly faster and liver metastasis rate was nearly 45% higher in mice injected with HNF6‐overexpressing cells. Further mechanism exploration showed that HNF6 expression affected cell adhesion and conferred resistance to anoikis in CRC cells. Taken together, HNF6 expression was upregulated in CRC and closely correlated with poor survival. HNF6 promoted CRC cell proliferation and tumor growth, and may contribute to liver metastasis via conferring cell resistance to anoikis.
Protective effect of extractive and biotechnological chondroitin in insulin amyloid and advanced glycation end product‐induced toxicity
Authors: Iannuzzi Clara , Borriello Margherita , D’Agostino Antonella , Cimini Donatella , Schiraldi Chiara , Sirangelo Ivana 
Published: September 2018

AbstractGlycosaminoglycans are extracellular matrix components related to several biological functions and diseases. Chondroitin sulfate is a sulphated glycosaminoglycan synthesized as part of proteoglycan molecules. They are frequently associated with amyloid deposits and possess an active role in amyloid fibril formation. Recently, a neuroprotective effect of extracellular matrix components against amyloid toxicity and oxidative stress has been reported. Advanced glycation end products (AGEs), the end products of the glycation reaction, have been linked to amyloid‐based neurodegenerative disease as associated with oxidative stress and inflammation. In this study we have analyzed the effect of chondroitin sulfate isolated from different species, in comparison with a new biotechnological unsulfated chondroitin, in the amyloid aggregation process of insulin, as well as the ability to prevent the formation of AGEs and related toxicity. The results have showed a determining role of chondroitin sulfate groups in modulating insulin amyloid aggregation. In addition, both sulfated and unsulfated chondroitins have shown protective properties against amyloid and AGEs‐induced toxicity. These data are very relevant as a protective effect of these glycosaminoglycans in the AGE‐induced toxicity was never observed before. Moreover, considering the issues related to the purity and safety of chondroitin from natural sources, this study suggests a new potential application for the biotechnological chondroitin.
Retinal pigment epithelium‐derived transforming growth factor‐β2 inhibits the angiogenic response of endothelial cells by decreasing vascular endothelial growth factor receptor‐2 expression
Authors: Jeong Han‐Seok , Yun Jang‐Hyuk , Lee Da‐Hye , Lee Eun Hui , Cho Chung‐Hyun 
Published: September 2018

AbstractTransforming growth factor‐β (TGF‐β) is a multifunctional cytokine that is known to modulate various aspects of endothelial cell (EC) biology. Retinal pigment epithelium (RPE) is important for regulating angiogenesis of choriocapillaris and one of the main cell sources of TGF‐β secretion, particularly TGF‐β2. However, it is largely unclear whether and how TGF‐β2 affects angiogenic responses of ECs. In the current study, we demonstrated that TGF‐β2 reduces vascular endothelial growth factor receptor‐2 (VEGFR‐2) expression in ECs and thereby inhibits vascular endothelial growth factor (VEGF) signaling and VEGF‐induced angiogenic responses such as EC migration and tube formation. We also demonstrated that the reduction of VEGFR‐2 expression by TGF‐β2 is due to the suppression of JNK signaling. In coculture of RPE cells and ECs, RPE cells decreased VEGFR‐2 levels in ECs and EC migration. In addition, we showed that TGF‐β2 derived from RPE cells is involved in the reduction of VEGFR‐2 expression and inhibition of EC migration. These results suggest that TGF‐β2 plays an important role in inhibiting the angiogenic responses of ECs during the interaction between RPE cells and ECs and that angiogenic responses of ECs may be amplified by a decrease in TGF‐β2 expression in RPE cells under pathologic conditions.
Sevoflurane anesthesia represses neurogenesis of hippocampus neural stem cells via regulating microRNA‐183‐mediated NR4A2 in newborn rats
Authors: Shao Chang‐Zhong , Xia Kun‐Peng 
Published: September 2018

AbstractSevoflurane has been commonly utilized in nonobstetric surgeries in pregnant women, and its impacts on fetal brain are still not completely known. Ectopic NR4A2 expression has been reported to be related with familial Parkinson disease, and through dual luciferase we found that
NR4A2 is a target gene of microRNA‐183 (miR‐183). We proposed a hypothesis that miR‐183 may participate in the process by targeting
NR4A2 in neurons after sevoflurane anesthesia. To verify the effect of sevoflurane on hippocampal neural stem cells (NSCs) proliferation and differentiation, we conducted EdU assay and immunofluorescence staining. Next, for better understanding of the impact of miR‐183, we altered the miR‐183 expression using mimic and inhibitor. Meanwhile, the targeting relationship between miR‐183 and
NR4A2 was validated by a bioinformatics website and dual‐luciferase reporter gene assay. Finally, expressions of miR‐184,
NR4A2, SRY (sex‐determining region Y)‐box 2 (Sox2), and brain‐derived neurotrophic factor (BDNF) were determined and evaluated by reverse transcription quantitative polymerase chain reaction and western blot analysis. First, sevoflurane was determined a crucial factor in biological behaviors of hippocampal NSCs. Moreover, upregulated miR‐183 expression by mimic inhibited the proliferation and differentiation of NSCs. Sevoflurane negatively regulated
NR4A2 and Sox2 expressions but positively regulated miR‐183 and BDNF expressions. Our findings revealed the underlying novel mechanism by which sevoflurane inhibits hippocampal NSC proliferation and differentiation through interaction with miR‐183 and
NR4A2. The study provides reliable reference for safe application of sevoflurane anesthesia in neonates.
Exosomes and microRNAs: New potential therapeutic candidates in Alzheimer disease therapy
Authors: Iranifar Elmira , Seresht Banafsheh Mirzaei , Momeni Fatemeh , Fadaei Elyas , Mehr Maysam Havasi , Ebrahimi Zahra , Rahmati Majid , Kharazinejad Ebrahim , Mirzaei Hamed 
Published: September 2018

AbstractExosomes are biological nanocarriers which could be involved in a variety of basic physiological events. They exert their effects via targeting their cargos (i.e., DNAs, messenger RNAs, microRNAs [miRNAs], and proteins) to host cells, which led to change behaviors of recipient cells. One of the important aspects of exosomes is the roles of them in disease conditions. Increasing evidence indicated that exosomes are one of the main players in Alzheimer’s disease (AD) pathogenesis. Hence, it seems that these nanocarriers could be used as diagnostic and therapeutic biomarkers in AD treatment. Another important player in AD pathogenesis is miRNA. MiRNAs are short noncoding RNAs which exert their effects as epigenetic regulators. These molecules involved in different stages of AD. Therefore, miRNAs could be used as prognostic, diagnostic, and therapeutic biomarkers in AD. Here, we summarized various roles of exosomes and application of them in AD pathogenesis. Moreover, we highlighted the utilization of miRNAs as a therapeutic option in AD therapy.
Nicotinamide phosphoribosyl transferase regulates cell growth via the Sirt1/P53 signaling pathway and is a prognosis marker in colorectal cancer
Authors: Pan Jing‐hua , Zhou Hong , Zhu Sheng‐Bin , Huang Jin‐Lian , Zhao Xiao‐Xu , Ding Hui , Qin Li , Pan Yun‐Long 
Published: September 2018

AbstractColorectal cancer (CRC) is the third most common malignancy, and the metabolic properties of CRC cells include enhanced aerobic glycolysis (the Warburg effect). Nicotinamide phosphoribosyl transferase (NAMPT) is one of the crucial enzymes that regulate the activity of nicotinamide adenine dinucleodinucleotide dependent enzymes. Targeting NAMPT is a potential method of CRC therapy. Nevertheless, the underlying clinical implications and regulatory mechanisms of NAMPT in CRC remain unclear. In this study, we showed that NAMPT protein expression was increased in subjects with rectal localization compared with those with colon localization, and NAMPT was a poor prognostic marker for the overall survival rate in patients with CRC. In addition, the NAMPT inhibitor FK866 or lentivirus‐mediated silencing induced CRC cell growth inhibition. Mechanistically, NAMPT regulated Sirt1 and P53 expression and induced G0/G1 cell cycle arrest, along with the upregulation of downstream p21 and downregulation of cyclin D1, cyclin E1, and cyclin E2 expression. FK866 administration or knockdown of NAMPT induced CRC cell apoptosis via upregulation of caspase‐3. In conclusion, NAMPT regulated Sirt1/P53 signaling during CRC cell growth and warrants further investigation for clinical administration in CRC.
Potential therapeutic effects of curcumin in gastric cancer
Authors: Barati Nastaran , Momtazi‐Borojeni Amir A. , Majeed Muhammed , Sahebkar Amirhossein 
Published: September 2018

AbstractDespite recent advancements in understanding of the biology of gastric cancer, treatment of patients with advanced gastric cancer remains a major problem. Among different type of phytochemicals, curcumin, a welltable ‐known phytochemical, has been shown to be a promising cancer chemopreventive agent. Pharmacokinetics, safety, and efficacy of curcumin have been evaluated in several clinical trials against numerous diseases, and for the treatment of human cancer. In the present review, we have collected in vitro and in vivo investigations and studied the chemosensitizing and anticancer effects of curcumin against the gastric cancer cells. In summary, curcumin has been found to have efficient chemosensitizing effect and also inhibits viability, proliferation, and migration of gastric cancer cells mainly via cell cycle arrest and induction of apoptosis by both mitochondrial‐dependent and ‐independent pathways.
Muscarinic M5 receptors trigger acetylcholine‐induced Ca2+ signals and nitric oxide release in human brain microvascular endothelial cells
Authors: Zuccolo Estella , Laforenza Umberto , Negri Sharon , Botta Laura , Berra‐Romani Roberto , Faris Pawan , Scarpellino Giorgia , Forcaia Greta , Pellavio Giorgia , Sancini Giulio , Moccia Francesco 
Published: September 2018

AbstractBasal forebrain neurons control cerebral blood flow (CBF) by releasing acetylcholine (Ach), which binds to endothelial muscarinic receptors to induce nitric (NO) release and vasodilation in intraparenchymal arterioles. Nevertheless, the mechanism whereby Ach stimulates human brain microvascular endothelial cells to produce NO is still unknown. Herein, we sought to assess whether Ach stimulates NO production in a Ca2+‐dependent manner in hCMEC/D3 cells, a widespread model of human brain microvascular endothelial cells. Ach induced a dose‐dependent increase in intracellular Ca2+ concentration ([Ca2+]i) that was prevented by the genetic blockade of M5 muscarinic receptors (M5‐mAchRs), which was the only mAchR isoform coupled to phospholipase Cβ (PLCβ) present in hCMEC/D3 cells. A comprehensive real‐time polymerase chain reaction analysis revealed the expression of the transcripts encoding for type 3 inositol‐1,4,5‐trisphosphate receptors (InsP3R3), two‐pore channels 1 and 2 (TPC1–2), Stim2, Orai1–3. Pharmacological manipulation showed that the Ca2+ response to Ach was mediated by InsP3R3, TPC1–2, and store‐operated Ca2+ entry (SOCE). Ach‐induced NO release, in turn, was inhibited in cells deficient of M5‐mAchRs. Likewise, Ach failed to increase NO levels in the presence of l‐NAME, a selective NOS inhibitor, or BAPTA, a membrane‐permeant intracellular Ca2+ buffer. Moreover, the pharmacological blockade of the Ca2+ response to Ach also inhibited the accompanying NO production. These data demonstrate for the first time that synaptically released Ach may trigger NO release in human brain microvascular endothelial cells by stimulating a Ca2+ signal via M5‐mAchRs.
Stat3 activation is critical for pluripotency maintenance
Authors: Zhang Yan , Wang Dan , Xu Jia , Wang Yuebing , Ma Fengxia , Li Zongjin , Liu Na 
Published: September 2018

AbstractSignal transducer and activator of transcription 3 (Stat3) is a cytoplasmic transcription with many important functions, including regulation of cell proliferation, differentiation, survival, angiogenesis, and immune response. Besides, it plays critical roles in regulating the pluripotency. With the ability of self‐renewal and differentiation, embryonic stem (ES) cells provide an unlimited source for cell transplantation. ES cells can maintain its undifferentiated state with leukemia inhibitory factor, the role which is achieved by the activation of the Stat3 pathway. Moreover, Stat3 activation is necessary for the naïve state maintenance of the ES cells and somatic stem cells reprogramming. This study presents an overview of the critical roles of Stat3 activation in the pluripotency maintenance of ES cells, somatic cell reprogramming, and naïve‐primed pluripotent states conversion of ES cells.
Nanostructured lipid carriers containing rapamycin for prevention of corneal fibroblasts proliferation and haze propagation after burn injuries: In vitro and in vivo
Authors: Zahir‐Jouzdani Forouhe , Khonsari Fatemeh , Soleimani Masoud , Mahbod Mirgholamreza , Arefian Ehsan , Heydari Mostafa , Shahhosseini Saeed , Dinarvand Rassoul , Atyabi Fatemeh 
Published: September 2018

AbstractChemical burns are a major cause of corneal haze and blindness. Corticosteroids are commonly used after corneal burns to attenuate the severity of the inflammation‐related fibrosis. While research efforts have been aimed toward application of novel therapeutics. In the current study, a novel drug delivery system based nanostructured lipid carriers (NLCs) were designed to treat corneal alkaline burn injury. Rapamycin, a potent inhibitor of mammalian target of rapamycin pathway, was loaded in NLCs (rapa‐NLCs), and the NLCs were characterized. Cell viability assay, cellular uptake of NLCs, and in vitro evaluation of the fibrotic/angiogenic genes suppression by rapa‐NLCs were carried out on human isolated corneal fibroblasts. Immunohistochemistry (IHC) assays were also performed after treatment of murine model of corneal alkaline burn with rapa‐NLCs. According to the results, rapamycin was efficiently loaded in NLCs. NLCs could enhance coumarin‐6 fibroblast uptake by 1.5 times. Rapa‐NLCs efficiently downregulated platelet‐derived growth factor and transforming growth factor beta genes in vitro. Furthermore, proliferation of fibroblasts, a major cause of corneal haze after injury, reduced. IHC staining of treated cornea with alpha‐smooth muscle actin and CD34
+ antibodies showed efficient prevention of myofibroblasts differentiation and angiogenesis, respectively. In conclusion, ocular delivery of rapamycin using NLCs after corneal injury may be considered as a promising antifibrotic/angiogenic treatment approach to preserve patient eyesight.