bluuebunny/crossref_metadata_2025_split huggingface dataset:
MHD boundary layer flow of SWCNT‐water and MWCNT‐water nanofluid over a vertical cone with heat generation/absorption
Authors: Reddy Y. Raja Obula , Reddy M. Suryanarayana , Reddy P. Sudarsana 
Published: October 2018

AbstractThe analysis is carried out to investigate the magneto hydro dynamics (MHD) boundary layer flow, heat and mass transfer characteristics of two carbon nanotubes, namely, single‐wall carbon nanotubes (SWCNTs) and multiwall carbon nanotubes (MWCNTs), with water as the base fluid by taking thermal radiation and chemical reaction into consideration. Suitable similarity conversions are employed to reduce nonlinear partial differential equations into the system of ordinary differential equations, and these equations together with boundary conditions are solved numerically using the finite element method. Velocity, temperature, and concentration distributions as well as skin friction coefficient, Nusselt number, and Sherwood number for diverse values of influencing parameters are examined in detail, and the results are displayed graphically and in tabular form. It is found that the rate of heat transfer is remarkably higher in water‐based MWCNTs than the SWCNTs as the value of the nanoparticle volume fraction parameter rises in the boundary layer regime.
Optimizing C2C12 myoblast differentiation using polycaprolactone–polypyrrole copolymer scaffolds
Authors: Browe Daniel , Freeman Joseph 
Published: October 2018

AbstractAdvancements in tissue engineering and biomaterial development have the potential to provide a scalable solution to the problem of large‐volume skeletal muscle defects. Previous research on the development of scaffolds for skeletal muscle regeneration has focused on strategies for increasing conductivity, which has improved satellite cell attachment and differentiation. However, these strategies usually increase scaffold stiffness, which some studies suggest may be detrimental to myoblast development. In this study, the polymers polypyrrole (PPy) and polycaprolactone (PCL) were synthesized together into a copolymer (PPy–PCL) designed to increase scaffold conductivity without significantly influencing stiffness. Different scaffold groups were fabricated via electrospinning, characterized, and assessed for their suitability for myoblast proliferation and differentiation. The groups included an aligned and random iteration of pure PCL, 10% PPy–PCL, 20% PPy–PCL, and 40% PPy–PCL. Only the 40% PPy–PCL group had a measureable conductivity, and the addition of PPy–PCL had no significant effect on the stiffness of the scaffolds. The PPy–PCL copolymer significantly increased the attachment of C2C12 myoblasts as compared to pure PCL scaffolds, but the concentration of PPy–PCL did not significantly alter cell attachment. In addition, scaffolds with PPy–PCL promoted myoblast differentiation to a greater extent than scaffolds made of PCL as measured by fusion index and number of nuclei per myotube. Aligned scaffolds were superior to random scaffolds in almost all measures. These results suggest that conductivity may not be the key factor in improving skeletal muscle scaffolds. Instead, cell attachment and aligned guidance cues may have a greater impact on myoblast differentiation. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 220–231, 2019.
Synergistic antitumor effects of rhein and doxorubicin in hepatocellular carcinoma cells
Authors: Wu Li , Liu Xiao , Cao Ke Xin , Ni Zi hui , Li Wei Dong , Chen Zhi Peng 
Published: October 2018

AbstractThe aim of this study was to investigate the synergistic antitumor activity of rhein and doxorubicin (DOX) and to elucidate the underlying mechanisms in hepatocellular SMMC‐7721 and HepG2 cells. Cell growth curves, caspase‐3 activity, and intracellular DOX accumulation were observed using an IncuCyte real‐time video imaging system. Combination index was used to calculate synergistic potential of rhein and DOX. Cell apoptosis was detected by the Annexin V‐FITC/PI apoptosis kit. Lactate dehydrogenase and adenosine triphosphate (ATP) levels were assessed using an assay kit. Oxygen consumption rates (OCR) and extracellular acidification rates were assessed by the Seahorse XFe96 Extracellular Flux Analyzer. Mitochondrial inner membrane potential (ΔΨm) was monitored with JC‐1 fluorescence. Western blot analysis was used to detect the level of P‐glycoprotein. Synergistic antiproliferative and proapoptotic effects were exerted by the combination of rhein at 10 μM and DOX at 2 μM in SMMC‐7721 and HepG2 cells. Rhein could influenced the accumulation of DOX in both cells, which was associated with remarkably decreased mitochondrial energy metabolism and ATP levels. Rhein could reduce ΔΨm in both cells. mPTP, opener atractyloside (ATR) could accelerate the loss of ΔΨm, and further suppress the OCR induced by rhein. In contrast, the mPTP blocker cyclosporin A (Cs A) inhibited the loss of ΔΨm and the OCR induced by rhein. Our data indicate that a decline in mitochondrial energy metabolism was responsible for the synergistic antitumor effects of rhein and DOX in hepatocellular carcinoma cells. Reduction of ΔΨm and opening of mPTP inhibited the exchange of ATP/adenosine diphosphate between mitochondrial matrix and cytoplasm is the important mechanism.
Expression and the potential functions of TRIM32 in lung cancer tumorigenesis
Authors: Yin Hongmei , Li Zhen , Chen Jia , Hu Xiaobo 
Published: October 2018

AbstractTRIM32 is a member of the tripartite motif (TRIM) family, which has been associated with tumorigenesis. However, its expression and potential functional role(s) in lung cancer progression have not been fully understood. To evaluate the relationship between the expression of TRIM32 and the prognosis of patients with lung cancer, an independent data set (The Human Protein Atlas website) was introduced. The expression and function analysis of TRIM32 in lung cancer cell lines were also performed by using cell counting kit‐8, flow cytometry, transwell, real‐time polymerase chain reaction and Western blot analysis. Our data showed that TRIM32 was overexpressed in lung cancer tissues and cell lines and was associated with a poor prognosis. TRIM32 silencing inhibited cell proliferation, migration, invasion, adhesion, and the activation of janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling. The results showed knockdown of TRIM32 in NCI‐H446 cells also inhibited cell growth in nude mice in the xenograft model. Additionally, TRIM32 overexpression promoted lung cancer cell proliferation and motility and mediated the expression of Bax, Bcl‐2, cleaved caspase‐3, matrix metalloproteinase‐2 (MMP‐2) and MMP‐9 were inhibited by JAK2/STAT3 signaling inhibitor (AG490). Taken together, our findings suggest that TRIM32 may regulate lung cancer cell proliferation, apoptosis, and motility through activating the JAK2/STAT3‐signaling pathway and may be a novel and promising target for lung cancer.
Therapeutic potential of RAS prenylation pharmacological inhibitors in the treatment of breast cancer, recent progress, and prospective
Authors: Soleimani Atena , Amirinejad Mostafa , Rahsepar Sara , Vazirian Fatemeh , Bahrami Afsane , Ferns Gordon A. , Khazaei Majid , Avan Amir , Hassanian Seyed Mahdi 
Published: October 2018

AbstractBreast cancer is one of the most prevalent malignancies among women around the world. RAS proteins require posttranslational modifications, including protein prenylation for proper membrane localization and signaling. Regulation of RAS signaling via specific and novel pharmacological inhibitors is a potentially novel therapeutic approach in breast cancer therapy. This review summarizes the recent knowledge about the clinical value of RAS prenylation pharmacological inhibitors in breast cancer treatment.
Identification of a universal 6‐lncRNA prognostic signature for three pathologic subtypes of renal cell carcinoma
Authors: Zuo Shuguang , Wang Liping , Wen Yuqing , Dai Gongpeng 
Published: October 2018

AbstractRenal cell carcinoma (RCC) is the most common adult renal epithelial cancer susceptible to metastasis and patients with irresectable RCC always have a poor prognosis. Long noncoding RNAs (lncRNAs) have recently been documented as having critical roles in the etiology of RCC. Nevertheless, the prognostic significance of lncRNA‐based signature for outcome prediction in patients with RCC has not been well investigated. Therefore, it is essential to identify a lncRNA‐based signature for predicting RCC prognosis. In the current study, we comprehensively analyzed the RNA sequencing data of the three main pathological subtypes of RCC (kidney renal clear cell carcinoma [KIRC], kidney renal papillary cell carcinoma [KIRP], and kidney chromophobe carcinoma [KICH]) from The Cancer Genome Atlas (TCGA) database, and identified a 6‐lncRNA prognostic signature with the help of a step‐wise multivariate Cox regression model. The 6‐lncRNA signature stratified the patients into low‐ and high‐risk groups with significantly different prognosis. Multivariate Cox regression analysis showed that predictive value of the 6‐lncRNA signature was independent of other clinical or pathological factors in the entire cohort and in each cohort of RCC subtypes. In addition, the three independent prognostic clinical factors (including age, pathologic stage III, and stage IV) was also stratified into low‐ and high‐risk groups basis on the risk score, and the stratification analyses demonstrated that the high‐risk score was a poor prognostic factor. In conclusion, these findings indicate that the 6‐lncRNA signature is a novel prognostic biomarker for all three subtypes of RCC, and can increase the accuracy of predicting overall survival.
Tumor microenvironment: Interactions and therapy
Authors: Najafi Masoud , Goradel Nasser Hashemi , Farhood Bagher , Salehi Eniseh , Solhjoo Somaye , Toolee Heidar , Kharazinejad Ebrahim , Mortezaee Keywan 
Published: October 2018

AbstractTumor microenvironment (TME) is a host for a complex network of heterogeneous stromal cells with overlapping or opposing functions depending on the dominant signals within this milieu. Reciprocal paracrine interactions between cancer cells with cells within the tumor stroma often reshape the TME in favor of the promotion of tumor. These complex interactions require more sophisticated approaches for cancer therapy, and, therefore, advancing knowledge about dominant drivers of cancer within the TME is critical for designing therapeutic schemes. This review will provide knowledge about TME architecture, multiple signaling, and cross communications between cells within this milieu, and its targeting for immunotherapy of cancer.
Tubulin–Na+,K+‐ATPase interaction: Involvement in enzymatic regulation and cellular function
Authors: Santander Veronica S. , Campetelli Alexis N. , Monesterolo Noelia E. , Rivelli Juan F. , Nigra Ayelen D. , Arce Carlos A. , Casale César H. 
Published: October 2018

AbstractA new function for tubulin was described by our laboratory: acetylated tubulin forms a complex with Na+,K
+‐ATPase (NKA) and inhibits its activity. This process was shown to be a regulatory factor of physiological importance in cultured cells, human erythrocytes, and several rat tissues. Formation of the acetylated tubulin–NKA complex is reversible. We demonstrated that in cultured cells, high concentrations of glucose induce translocation of acetylated tubulin from cytoplasm to plasma membrane with a consequent inhibition of NKA activity. This effect is reversed by adding glutamate, which is coctransported to the cell with Na
+. Another posttranslational modification of tubulin, detyrosinated tubulin, is also involved in the regulation of NKA activity: it enhances the NKA inhibition induced by acetylated tubulin. Manipulation of the content of these modifications of tubulin could work as a new strategy to maintain homeostasis of Na
+ and K
+, and to regulate a variety of functions in which NKA is involved, such as osmotic fragility and deformability of human erythrocytes. The results summarized in this review show that the interaction between tubulin and NKA plays an important role in cellular physiology, both in the regulation of Na
+/K
+ homeostasis and in the rheological properties of the cells, which is mechanically different from other roles reported up to now.
VEGF‐C attenuates renal damage in salt‐sensitive hypertension
Authors: Beaini Shadia , Saliba Youakim , Hajal Joelle , Smayra Viviane , Bakhos Jules‐Joel , Joubran Najat , Chelala Dania , Fares Nassim 
Published: October 2018

AbstractSalt‐sensitive hypertension is a major risk factor for renal impairment leading to chronic kidney disease. High‐salt diet leads to hypertonic skin interstitial volume retention enhancing the activation of the tonicity‐responsive enhancer‐binding protein (TonEBP) within macrophages leading to vascular endothelial growth factor C (VEGF‐C) secretion and NOS3 modulation. This promotes skin lymphangiogenesis and blood pressure regulation. Whether VEGF‐C administration enhances renal and skin lymphangiogenesis and attenuates renal damage in salt‐sensitive hypertension remains to be elucidated. Hypertension was induced in BALB/c mice by a high‐salt diet. VEGF‐C was administered subcutaneously to high‐salt‐treated mice as well as control animals. Analyses of kidney injury, inflammation, fibrosis, and biochemical markers were performed in vivo. VEGF‐C reduced plasma inflammatory markers in salt‐treated mice. In addition, VEGF‐C exhibited a renal anti‐inflammatory effect with the induction of macrophage M2 phenotype, followed by reductions in interstitial fibrosis. Antioxidant enzymes within the kidney as well as urinary RNA/DNA damage markers were all revelatory of abolished oxidative stress under VEGF‐C. Furthermore, VEGF‐C decreased the urinary albumin/creatinine ratio and blood pressure as well as glomerular and tubular damages. These improvements were associated with enhanced TonEBP, NOS3, and lymphangiogenesis within the kidney and skin. Our data show that VEGF‐C administration plays a major role in preserving renal histology and reducing blood pressure. VEGF‐C might constitute an interesting potential therapeutic target for improving renal remodeling in salt‐sensitive hypertension.
Allicin attenuates calcium oxalate crystal deposition in the rat kidney by regulating gap junction function
Authors: Lai Yongchang , Liang Xiongfa , Zhong Fangling , Wu Weizhou , Zeng Tao , Huang Jian , Duan Xiaolu , Li Shujue , Zeng Guohua , Wu Wenqi 
Published: October 2018

AbstractRenal calculus is a global common urological disease that is closely related to crystal adhesion and renal tubular epithelial cell impairment. Gap junctions (GJs) and their components (connexins and Cxs) are involved in various pathophysiology processes, but their roles in renal calculi progression are not well defined. Our previous RNA microarray analysis suggests that GJs are one of the key predicted pathways involved in the renal calcium oxalate (CaOx) crystal rat model. In the current study, we found that the Cx43 and Cx32 expression and the GJ function decreased significantly after stimulation with CaOx or sodium oxalate (NaOx) in NRK‐52E, MDCK, and HK‐2 cells, and Cx43 expression also decreased in renal tissues in renal CaOx crystal model rats. Inhibition of Cx43 in NRK‐52E cells by small interference RNA significantly increased the CD44 and androgen receptor expression, and the adhesion between CaOx crystals and cells, which were consistent with the function of GJ inhibitors. On the other hand, after GJ function and Cx43 expression were increased by allicin, diallyl disulfide, or diallyl trisulfide, the impairment of NRK‐52E cells by NaOx or other GJ inhibitors and the adhesion between CaOx crystals and renal cells decreased significantly. Furthermore, allicin also increased Cx43 expression and inhibited crystal deposition in rat kidneys. Taken together, our results provide a basis that GJs and Cx43 may participate in renal CaOx stone progression and that allicin, together with its analogues, could be potential drugs for renal calculus precaution.
Myostatin induces tumor necrosis factor‐α expression in rheumatoid arthritis synovial fibroblasts through the PI3K–Akt signaling pathway
Authors: Su Chen‐Ming , Hu Sung‐Lin , Sun Yi , Zhao Jin , Dai Chengqian , Wang Lihong , Xu Guohong , Tang Chih‐Hsin 
Published: October 2018

AbstractIn rheumatoid arthritis (RA), a chronic inflammatory disease, loss of muscle mass is an important contributor to the loss of muscle strength in RA patients. Myostatin, a myokine involved in the process of muscle hypertrophy and myogenesis, enhances osteoclast differentiation and inflammation. Here, we investigated the mechanisms of myostatin in RA synovial inflammation. We found a positive correlation between myostatin and tumor necrosis factor‐α (TNF‐α), a well‐known proinflammatory cytokine, in RA synovial tissue. Our in vitro results also showed that myostatin dose‐dependently induced TNF‐α expression through the phosphatidylinositol 3‐kinase (PI3K)–Akt–AP‐1 signaling pathway. Myostatin treatment of human MH7A cells stimulated AP‐1‐induced luciferase activity and activation of the c‐Jun binding site on the TNF‐α promoter. Our results indicated that myostatin increases TNF‐α expression via the PI3K–Akt–AP‐1 signaling pathway in human RA synovial fibroblasts. Myostatin appears to be a promising target in RA therapy.
Interaction between mesenchymal stromal cell‐derived extracellular vesicles and immune cells by distinct protein content
Authors: Mardpour Soura , Hamidieh Amir Ali , Taleahmad Sara , Sharifzad Farzaneh , Taghikhani Adeleh , Baharvand Hossein 
Published: October 2018

AbstractMesenchymal stromal cells (MSCs) can effectively contribute to tissue regeneration inside the inflammatory microenvironment mostly through modulating immune responses. MSC‐derived extracellular vesicles (MSC‐EVs) display immunoregulatory functions similar to parent cells. Interactions between MSC‐EVs and immune cells make them an ideal therapeutic candidate for infectious, inflammatory, and autoimmune diseases. These properties of MSC‐EVs have encouraged researchers to perform extensive studies on multiple factors that mediate MSC‐EVs immunomodulatory effects. Investigation of proteins involved in the complex interplay of MSC‐EVs and immune cells may help us to better understand their functions. Here, we performed a comprehensive proteomic analysis of MSC‐EVs that was previously reported by ExoCarta database. A total of 938 proteins were identified as MSC‐EV proteome using quantitative proteomics techniques. Kyoto Encyclopedia of Genes and Genomes analysis demonstrates that ECM–receptor interaction, focal adhesion, and disease‐specific pathways are enriched in MSC‐EVs. By detail analysis of proteins presence in immune system process, we found that expression of some cytokines, chemokines, and chemokine receptors such as IL10, HGF, LIF, CCL2, VEGFC, and CCL20, which leads to migration of MSC‐EVs to injured sites, suppression of inflammation and promotion of regeneration in inflammatory and autoimmune diseases. Also, some chemoattractant proteins such as CXCL2, CXCL8, CXCL16, DEFA1, HERC5, and IFITM2 were found in MSC‐EV proteome. They may actively recruit immune cells to the proximity of MSC or MSC‐EVs, may result in boosting immune response under specific circumstances, and may have protective role in infectious diseases. In this review, we summarize available information about immunomodulation of MSC‐EVs with particular emphasis on their proteomics analysis.
Stromal‐induced downregulation of miR‐1247 promotes prostate cancer malignancy
Authors: Taddei Maria Letizia , Cavallini Lorenzo , Ramazzotti Matteo , Comito Giuseppina , Pietrovito Laura , Morandi Andrea , Giannoni Elisa , Raugei Giovanni , Chiarugi Paola 
Published: October 2018

AbstractCancer progression is strictly dependent on the relationship between tumor cells and the surrounding stroma, which supports cancer malignancy promoting several crucial steps of tumor progression, including the execution of the epithelial to mesenchymal transition (EMT) associated with enhancement in cell invasion, resistance to both anoikis and chemotherapeutic treatments. Recently it has been highlighted the central role of microRNAs (miRNAs) as regulators of tumor progression. Notably, in several tumors a strong deregulation of miRNAs is observed, supporting proliferation, invasion, and metabolic reprogramming of tumor cells. Here we demonstrated that cancer‐associated fibroblasts induce a downregulation of miR‐1247 in prostate cancer (PCa) cells. We proved that miR‐1247 repression is functional for the achievement of EMT and increased cell invasion as well as stemness traits. These phenomena contribute to promote the metastatic potential of PCa cells as demonstrated by increased lung colonization in in vivo experiments. Moreover, as a consequence of miR‐1247 downregulation, we observed a correlated increased expression level of neuropilin‐1, a miR‐1247 target involved as a coreceptor in the epidermal growth factor receptor signaling. Taken together, our data highlight miR‐1247 as a potential target for molecular therapies aimed to block the progression and diffusion of PCa.
Adipose‐derived stem cells‐conditioned medium improved osteogenic differentiation of induced pluripotent stem cells when grown on polycaprolactone nanofibers
Authors: Soleimanifar Fatemeh , Hosseini Fatemeh Sadat , Atabati Hadi , Behdari Asma , Kabiri Ladan , Enderami Seyed Ehsan , Khani Mohammad‐Mehdi , Ardeshirylajimi Abdolreza , Saburi Ehsan 
Published: October 2018

AbstractConsidering that the common osteogenic growth factors cannot be transplanted with stem cells to the patients, many studies are underway to find a replacement for these factors. Recently, it has been determined that mesenchymal stem cell (MSC)‐derived conditioned medium (CM) contains effective factors in the bone formation process. In the current study, the synergistic effect of adipose‐derived MSC’s CM, and polycaprolactone (PCL) scaffold was investigated on the osteogenic differentiation potential of human induced pluripotent stem cells (iPSCs). After scaffold fabrication by electrospinning and characterization by scanning electron microscopy, iPSCs proliferation in the presence of CM, PCL, and both was evaluated using 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide. Then, iPSCs osteogenic differentiation was investigated while cultured on tissue culture plate and PCL under CM compared with the osteogenic medium using alizarin red staining, calcium content, alkaline phosphatase activity and gene and protein expression analysis. Proliferation rate of the iPSCs was increased while cultured under CM and its effect was synergistically enhanced by culture on PCL. Evaluation of the osteogenic markers was showed CM alone could induce osteogenic differentiation into the iPSCs and this potential was significantly increased while combined with PCL nanofibrous scaffold. According to the results, it was demonstrated that CM has an osteogenic induction property almost the same of the common osteogenic medium and it can also be used potentially with stem cells when transplant to the patients. CM can also help by prolonging cell survival at the site of the defect as well as accelerating healing process.