bluuebunny/crossref_metadata_2025_split huggingface dataset:
An integrated approach to understanding the depositional environment and organic matter enrichment factor in Carboniferous source rocks, Junggar Basin, NW China
Authors: Tao Huifei , Qiu Zhen , Ji Hongjie , Qiu Junli , Allen Mark B. 
Published: December 2018

Multiple indicators (trace fossils, trace metals, and δ13Corg) are used to assess the depositional environments and controls on organic carbon accumulation in the Lower Carboniferous Nanmingshui Formation, Junggar Basin, NW China. The majority of trace fossils belong to the Nereites ichnofacies, representing low energy, oxygen‐poor, and relatively quiet bottom water environments. However, the shallow water trace fossil Planolites also appears in the strata, possibly reflecting variations in the bottom water oxygen contents of the turbidite succession. Redox proxies Th/U, V/Sc, and V/(V + Ni) reveal variable redox conditions; most of the samples are in the range from suboxic to anoxic depositional conditions. Ni and Cu show a positive correlation with TOC, but U and V have no correlation with TOC, also suggesting the redox conditions were mainly suboxic. The P/Al and Cu/Al ratios of all samples are higher than those of Post‐Archean Australian Shales (PAAS), and about two‐thirds of the samples' Ba/Al and Ni/Al ratios are close to or higher than PAAS, suggesting the Early Carboniferous Junggar Basin had relatively high palaeo‐productivity levels. δ13Corg values average − 23.75‰, reflecting a mixture of terrestrial organic and marine organic matter. The indexes of Ba/Al, Cu/Al, Ni/Al, and δ13Corg show good positive correlations with TOC, indicating the palaeo‐productivity played an important role for the organic matter accumulation. On the other hand, the TOC correlates inversely with redox proxies (Th/U, V/Sc, and V/(V + Ni)), suggesting the preservation conditions (anoxia) are not the control factor of organic matters accumulation. Using these multiple approaches, our results indicate that productivity was the primary factor controlling organic matter accumulation.
Investigation of platelet‐rich plasma in increasing proliferation and migration of endometrial mesenchymal stem cells and improving pregnancy outcome of patients with thin endometrium
Authors: Wang Xiaohan , Liu Ling , Mou Shanmao , Zhao Huishan , Fang Jianye , Xiang Yanjie , Zhao Tong , Sha Tongye , Ding Jie , Hao Cuifang 
Published: December 2018

AbstractBackgroundPlatelet‐rich plasma (PRP) contains abundant growth factors and is gradually used in the field of reproduction. A thin endometrium is recognized as a critical factor in embryo implantation failure. Endometrial mesenchymal stem cells (EnMSCs), which were isolated from human menstrual blood, are highly proliferative and show multiple differentiation capacity. The current study was to investigate the effect of PRP on the proliferation and migration of EnMSCs, and the effectiveness of PRP in the treatment of patients with thin endometrium.Materials and MethodsEnMSCs were treated with PRP in vitro, followed by measuring cell proliferation, migration, and adhesion by using CCK8, scratch, and adhesion test, respectively. Twenty patients undergoing in vitro fertilization (IVF) with refractory thin endometrium history were given PRP by infusion into the uterine cavity after the treatment of hormone replacement therapy (HRT).ResultsAll components of PRP significantly stimulated the growth, migration, and adhesion of EnMSCs when compared with the negative control. Cell proliferation and migration were induced by PRP in a dose‐dependent manner with maximum proliferation at a 2% PRP dose. The clinical data showed that successful endometrial expansion and pregnancy were discovered in 12 patients after PRP infusion, and the pregnancy rate increased to 60%.ConclusionIntrauterine PRP infusion represents a new way for female patients with thin endometrium with poor response. This study lays the foundations for the potential treatment of thin endometrium with PRP in vivo.
Asymmetric dimethylarginine targets MAPK pathway to regulate insulin resistance in liver by activating inflammation factors
Authors: Huang Shan , Xu Yong , Peng Wen‐Fang , Cheng Jie , Li Hui‐Hua , Shen Li‐Sha , Xia Li‐Li 
Published: December 2018

AbstractInsulin resistance is associated with impaired glucose uptake and altered protein kinase B (Akt) signaling. Previous studies have suggested asymmetric dimethylarginine (ADMA) and inflammation are two distinguish factors that correlate with insulin resistance (IR). How ADMA and inflammation factors interact and synchronize in the regulation of IR in liver remain to be elucidated. In this study, we systematically investigated whether ADMA is involved in IR using primary hepatocytes, if yes, by via which molecular mechanism. Our results demonstrated that ADMA inhibits insulin sensitivity in a concentration‐dependent manner by activating inflammation factors tumor necrosis factor (TNF)‐α, interleukin (IL)‐1, and IL‐6 in primary hepatocytes. Further analysis revealed that mitogen‐activated protein kinase (MAPK) signaling pathway act downstream of ADMA and inflammation factors, and inhibition of MAPK pathway rescued the IR. Furthermore, metformin effects has been found which could reverse ADMA‐induced IR by suppressing MAPK signaling pathway. To our knowledge, we, for the first time, unveiled the complicated regulatory network and interactions among ADMA, inflammation, and MAPK signaling pathway, which advanced current research on the development and regulation of IR in liver. This study also certainly provided novel insights on comprehensive diagonistics roles of ADMA as a potential biomarker.
Shared KEGG pathways of icariin‐targeted genes and osteoarthritis
Authors: Liu Yi , Mi Bobin , Lv Huijuan , Liu Jing , Xiong Yuan , Hu Liangcong , Xue Hang , Panayi Adriana C. , Liu Guohui , Zhou Wu 
Published: December 2018

AbstractThe beneficial effects of icariin in the management of many diseases, such as chronic renal failure and heart failure, are well known. Icariin has also been shown to ameliorate osteoarthritis (OA) symptoms; however, the underlying mechanisms remain unclear. In this study, a bioinformatics analysis was performed to investigate the KEGG pathways of icariin‐targeted genes involved in OA. Our study suggests that icariin plays a role in OA by regulating inflammatory cytokine production, insulin resistance, and cell survival through modulation of the NF‐κB, MAPK, and Akt signaling pathways. Importantly, IKBKB, NFKBIA, MAPK8, MAPK9, and MAPK10 may be the hub genes affected by icariin when providing its beneficial effects on OA. In addition, we found that icariin decreases proinflammatory factors and inhibits chondrocyte apoptosis through suppression of the NF‐κB pathway. Our study highlights a set of KEGG pathways that could explain the molecular mechanism of icariin's action on OA, suggesting that icariin could be considered as a promising therapeutic option for OA.
Plant DNases are potent therapeutic agents against Echis carinatus venom‐induced tissue necrosis in mice
Authors: Rudresha Gotravalli V. , Urs Amog P. , Manjuprasanna Vaddarahally N. , Suvilesh Kanve N. , Sharanappa Puttappa , Vishwanath Bannikuppe S. 
Published: December 2018

AbstractEchis carinatus envenomation leads to severe tissue necrosis at the bitten site by releasing DNA from immune cells that blocks the blood flow. An earlier report has shown that exogenous DNase 1 offers protection against such severe local tissue necrosis. Tricosanthus tricuspidata is a medicinal plant and the paste prepared from its leaves has been used extensively for the treatment of snakebite‐induced tissue necrosis. Most studies including reports from our laboratory focused on plant secondary metabolite as therapeutic molecules against snakebite envenomation. However, the involvement of hydrolytic enzymes including DNase in treating snake venom‐induced tissue necrosis has not been addressed. Several folk medicinal plants used against snakebite treatment showed the presence of DNase activity and found to be rich in T. tricuspidata. Further, purified T. tricuspidata DNase showed a single sharp peak in reversed‐phase high‐performance liquid chromatography (RP‐HPLC) with an apparent molecular mass of 17 kDa. T. tricuspidata DNase exhibited potent DNA degrading activity performed using agarose gel electrophoresis, spectrophotometric assay, and DNA zymography. In addition, purified DNase from T. tricuspidata was able to neutralize E. carinatus venom‐induced mouse tail tissue necrosis and normalized elevated serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels 30 minutes post venom injection. T. tricuspidata DNase was also able to reverse E. carinatus venom‐induced histopathological changes and collagen depletion in mice tail tissue. All these observed pharmacological actions of T. tricuspidata DNase were inhibited by sodium fluoride (NaF). This study provides scientific validation of the traditional use of T. tricuspidata leaf paste in the healing of snakebite‐induced tissue necrosis and might be exploited to treat snake venom‐induced local toxicity.
ClC‐3 chloride channels are involved in estradiol regulation of bone formation by MC3T3‐E1 osteoblasts
Authors: Deng Zhiqin , Li Wencui , Xu Jianying , Yu Meishen , Li Duan , Tan Qiuchan , Wang Daping , Chen Lixin , Wang Liwei 
Published: December 2018

AbstractEvidence has been reported by us and others supporting the important roles of chloride channels in a number of osteoblast cell functions. The ClC‐3 chloride channel is activated by estradiol binding to estrogen receptor alpha on the cell membranes of osteoblasts. However, the functions of these chloride channels in estrogen regulation of osteoblast metabolism remain unclear. In the present study, the roles of chloride channels in estrogen regulation of osteoblasts were investigated in the osteoblastic cell line MC3T3‐E1. Estrogen 17β‐estradiol enhanced collagen I protein expression, alkaline phosphatase activity, and mineralization were inhibited, by chloride channel blockers. Estradiol promoted ClC‐3 chloride channel protein expression. Silencing of ClC‐3 chloride channel expression prevented the elevation of osteodifferentiation in osteoblasts, which were regulated by estrogen. These data suggest that estrogen can regulate bone formation by activating ClC‐3 chloride channels and the activation of ClC‐3 chloride channels can enhance the osteodifferentiation in osteoblasts.
miR‐452 promotes cell metastasis and the epithelial to mesenchymal by targeting SOX7 in clear‐cell renal‐cell carcinoma
Authors: Liu Feng , Guo Lihua , Xin Guangda , Wang Zhixin 
Published: December 2018

AbstractClear‐cell renal‐cell carcinoma (ccRCC) is the most common renal cell carcinoma (RCC), representing 75%‐80% of the cases of RCC, and characterized by a high recurrence rate and poor prognosis. miR‐452 acts as a tumor promoter in several tumors, including ccRCC. The purpose of this study was to determine the role of miR‐452 in ccRCC. miR‐452 and SOX7 messenger RNA and protein levels were calculated by quantitative reverse transcription polymerase chain reaction and Western blot analysis. MTT and Transwell assays were utilized to measure proliferative and invasive abilities. The Kaplan‐Meier method was used to evaluate the association between the expression of miR‐452 or SOX7 and the overall survival of ccRCC patients. Our results showed that miR‐452 was overexpressed in ccRCC tissues and cells, and upregulation of miR‐452 predicted a poor 5‐year survival in ccRCC patients. In contrast, expression of SOX7 was low and downregulation of SOX7 predicted poor prognosis in ccRCC. In addition, miR‐452 promoted cell proliferation, invasion, and the EMT, while SOX7 reversed the function of miR‐452 on cell proliferation and invasion in 786‐O cells. In conclusion, miR‐452 was shown to inhibit cell proliferation, invasion, and the EMT through SOX7 in ccRCC, and the newly identified miR‐452/SOX7 axis provided novel insight into the pathogenesis of ccRCC.
microRNAs‐107 inhibited autophagy, proliferation, and migration of breast cancer cells by targeting HMGB1
Authors: Ai Hongyan , Zhou Wei , Wang Zeqiang , Qiong Guo , Chen Zhouxi , Deng Shungang 
Published: December 2018

AbstractPurposeTo investigate the effects of microRNAs‐107 (miR‐107) on autophagy, proliferation, and migration of breast cancer cells and its mechanism by targeting high mobility group protein B1 (HMGB1).MethodsReal‐time polymerase chain reaction assay was used to detect the expression of miR‐107 in breast cancer and its cell lines. In MDA‐MB‐231 and MDA‐MB‐453 breast cancer cells, the expression of p62, Beclin1 protein, and the changes of cell proliferation and migration after overexpression of m miR‐107 were detected by Western blotting, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide, and transwell assays. Target Scan online prediction, dual luciferase reporter gene, and Western blot were used to verify the targeting relationship between miR‐107 and HMGB1. The effects of silencing HMGB1 expression on p62, Beclin1 protein expression, cell proliferation, and migration ability were detected. The transfected MDA‐MB‐453 cells were inoculated into the right axilla of the nude mice, the tumor volume and weight were weighed, and the expression of miR‐107, HMGB1, p62, and Beclin1 in the tumor were detected.ResultsThe expression of miR‐107 was downregulated in breast cancer tissues and cell lines (P < 0.01). The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after overexpressing miR‐107 in MDA‐MB‐231 and MDA‐MB‐453 cells. The results of TargetScan online prediction, dual luciferase reporter gene, and Western blot showed that miR‐107 could regulate HMGB1 expression. The expression of p62 protein was upregulated (P < 0.01), while Beclin1 protein was downregulated (P < 0.01) and cell proliferation and migration ability were decreased (P < 0.01) after silencing HMGB1 in MDA‐MB‐231 and MDA‐MB‐453 cells. The results of xenograft experiments showed that miR‐107 could delay tumor growth and inhibit autophagy.ConclusionmiR‐107 could inhibit cell autophagy, proliferation, and migration of breast cancer cells by targeting HMGB1.
Human RNF113A participates of pre‐mRNA splicing in vitro
Authors: Gatti da Silva Guilherme H. , Jurica Melissa S. , Chagas da Cunha Julia P. , Oliveira Carla C. , Coltri Patricia P. 
Published: December 2018

AbstractPre‐messenger RNA (mRNA) splicing is an essential step in the control of eukaryotic gene expression. During splicing, the introns are removed from the gene transcripts as the exons are ligated to create mature mRNA sequences. Splicing is performed by the spliceosome, which is a macromolecular complex composed of five small nuclear RNAs (snRNAs) and more than 100 proteins. Except for the core snRNP proteins, most spliceosome proteins are transiently associated and presumably involved with the regulation of spliceosome activity. In this study, we explored the association and participation of the human protein RNF113A in splicing. The addition of excess recombinant RNF113A to in vitro splicing reactions results in splicing inhibition. In whole‐cell lysates, RNF113A co‐immunoprecipitated with U2, U4, and U6 snRNAs, which are components of the tri‐snRNP, and with proteins PRP19 and BRR2. When HeLa cells were CRISPR‐edited to reduce the RNF113A levels, the in vitro splicing efficiency was severely affected. Consistently, the splicing activity was partially restored after the addition of the recombinant GST‐RNF113A. On the basis on these results, we propose a model in which RNF113A associates with the spliceosome by interacting with PRP19, promoting essential rearrangements that lead to splicing.
microRNA‐193a‐5p inhibits migration of human HT‐29 colon cancer cells via suppression of metastasis pathway
Authors: Shirafkan Naghmeh , Shomali Navid , Kazemi Tohid , Shanehbandi Dariush , Ghasabi Mehri , Baghbani Elham , Ganji Maziar , Khaze Vahid , Mansoori Behzad , Baradaran Behzad 
Published: December 2018

AbstractPurposeAltered expression of microRNAs (miRNAs) is indicated strongly in colorectal cancer (CRC). This study aims to evaluate the inhibitory role of miR‐193a‐5p on epithelial‐mesenchymal transition markers in CRC lines. The cellular effects and potential mechanisms of
miR‐193a‐5p were also examined.MethodsQuantitative reverse‐transcription polymerase chain reaction (RT‐PCR) was performed to determine the expression of miR‐193a‐5p in three CRC cell lines (HCT‐116, SW‐480, and HT‐29) and its impact on metastasis‐related genes (
vimentin and
CXCR4) before and after mimic transfection. Of those, the cell line with the highest changes was selected for the next upcoming experiments such as wound‐healing assay, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT), and annexin‐V staining tests.ResultsOur results revealed that miR‐193a‐5p was significantly downregulated in three CRC cell lines and that HT‐29 displayed the most decrease (
P < 0.0001). The restoration of
miR‐193a‐5p in human HT‐29 cell line inhibited cell migration. But,
miR‐193a‐5p transfection did not affect cell viability and had no significant effect on apoptosis induction. Also, the quantitative RT‐PCR analysis of
miR‐193a‐5p mimic transfected cells revealed a significant increase in
miR‐193a‐5p messenger RNA (mRNA) expression level (
P < 0.0001) with reduction of
vimentin and
CXCR4 mRNA expression levels in HT‐29 cell line (
P < 0.01 and < 0.05, respectively).ConclusionOur results indicated that miR‐193a‐5p acts as a tumor suppressor miRNA and its downregulation plays an important role in metastasis via upregulation of metastasis‐related genes in CRC. Therefore, it can be considered as a potential therapeutic target for applying in CRC management in the future.
Lecithin soybean phospholipid nano‐transfersomes as potential carriers for transdermal delivery of the human growth hormone
Authors: Kateh Shamshiri Maryam , Momtazi‐Borojeni Amir Abbas , Khodabandeh Shahraky Mahvash , Rahimi Fatemeh 
Published: December 2018

AbstractPharmaceutical molecules such as peptides and proteins are usually injected into the body. Numerous efforts have been made to find new noninvasive ways to administer these peptides. In this study, highly flexible vesicles (transfersomes [TFs]) were designed as a new modern transdermal drug delivery system for systemic drug administration through the skin, which had also been evaluated in vitro. In this study, two growth hormone‐loaded TF formulations were prepared, using soybean lecithin and two different surfactants; F1_sodium deoxycholate and F
2_sodium lauryl sulfate. Thereafter, the amount of skin penetration by the two formulas was assessed using the Franz diffusion cell system. TF formulations were evaluated for size, zeta potential and in vitro skin penetration across the rat skin. Results indicated that vesicle formulations were stable for 4 weeks and their mean sizes were 241.33 ± 17 and 171 ± 12.12 nm in the F
1 and F
2 formulation, respectively. After application to rat skin, transport of the human growth hormone (hGH) released from the TF formulations was found to be higher than that of the hGH alone. Maximum amounts of transdermal hormone delivery were estimated to be 489.54 ± 8.301  and 248.46 ± 4.019 ng·cm−2 , for F
1 and F
2, respectively. The results demonstrate the capability of the TF‐containing growth hormone in transdermal delivery and superiority of the F
1 to F
2 TFs.
Cold exposure induces nuclear translocation of CRTC3 in brown adipose tissue
Authors: Xu Ziye , Liu Jiaqi , You Wenjing , Wang Yizhen , Shan Tizhong 
Published: December 2018

AbstractIn mammals, cold stress activates the cAMP‐protein kinase A (PKA) signaling pathway, increases brown adipose tissue (BAT) activity, and induces thermogenesis to maintain body temperature. The cAMP responsive element binding protein (CREB)‐regulated transcription coactivator 3 (CRTC3) plays important role in adipose development and energy metabolism. However, the effect of cold exposure on the intracellular localization of CRTC3 in BAT is unclear. Here, we report that cold‐treated mice have higher expression of uncoupling protein 1 (UCP1) in adipose tissues and lower body weights and fat masses. Notably, cold exposure results in the nuclear translocation of CRTC3 in BAT. Moreover, forskolin (FSK), the activator of PKA pathway, induces the nuclear translocation of CRTC3 in brown adipocytes. At the molecular level, cold exposure and FSK treatment decrease liver kinase B1 (Lkb1) expression in brown adipocytes, which is related to the nuclear localization of CRTC3. These results demonstrate that the localization of CRTC3 involves in regulating cold‐induced upregulation of UCP1 in BAT and provide useful information for understanding the molecular regulation of BAT thermogenesis induced by a cold environment.
Clinical significance of long noncoding RNA VIM‐AS1 and CTBP1‐AS2 expression in type 2 diabetes
Authors: Erfanian Omidvar Maryam , Ghaedi Hamid , Kazerouni Faranak , kalbasi Saeid , Shanaki Mehrnoosh , Miraalamy Ghasem , Zare Ali , Rahimipour Ali 
Published: December 2018

AbstractBackground/AimsThe risk of type 2 diabetes (T2D) is determined by a combination of genetic and environmental factors. Multiple studies have proposed that long noncoding RNAs (lncRNAs) are crucial molecules in regulating several biological processes and complex diseases. The study was aimed at investigating the association between the expression levels of lncRNA VIM‐AS1, lncRNA CTBP1‐AS2, and T2D susceptibility.MethodslncRNA VIM‐AS1 and lncRNA CTBP1‐AS2 in the peripheral blood mononuclear cell (PBMC) of 100 healthy individuals and 100 T2D patients were collected for Quantitative Real‐Time RT‐PCR analysis. A logistic regression was performed to understand whether the likelihood of T2D can be predicted based on the expression levels of lncRNA VIM‐AS1 and lncRNA CTBP1‐AS2. Receiver operating characteristic (ROC) analysis was also performed to determine the statistical analysis of VIM‐AS1 and CTBP1‐AS2 levels in 200 samples.ResultsOur results display that decreased levels of VIM‐AS1 and CTBP1‐AS2 in PBMC were associated with diabetes in Iranian population. The logistic regression revealed that Systolic blood pressure (SBP), low‐density lipoprotein cholesterol (LDL‐C), Fasting blood glucose (FBG) and CTBP1‐AS2 are substantial predictors of T2D. The ROC analysis of CTBP1‐AS2 revealed the area under the ROC curve (AUC) of 0.68 with a sensitivity of 58.7% and specificity of 75.3% in distinguishing nondiabetic from diabetic subjects. The ROC analysis of VIM‐AS1 determined AUC of 0.63 with a sensitivity of 56.1% and specificity of 68.37% in distinguishing the two diagnostic groups.ConclusionlncRNA VIM‐AS1 and lncRNA CTBP1‐AS2 expression levels are associated with T2D susceptibility.