bluuebunny/crossref_metadata_2025_split huggingface dataset:
Asiaticoside loading into polylactic‐co‐glycolic acid electrospun nanofibers attenuates host inflammatory response and promotes M2 macrophage polarization
Authors: Huang Jia , Zhou Xiaobo , Shen Yanbing , Li Haibo , Zhou Guangdong , Zhang Wenjie , Zhang Yanzhong , Liu Wei 
Published: September 2019

AbstractPolylactic‐co‐glycolic acid (PLGA) is one of the most promising synthetic materials for tissue engineering due to its excellent biocompatibility, good mechanical properties, and tunable biodegradation time. However, the accumulation of PLGA degradative products could cause significant host inflammatory response, a microenvironment favoring tissue fibrosis that is mainly mediated by M1 subtype macrophage. Drug loading is an emerging technology to modify electrospun nanofibers, and asiaticoside (AS) was demonstrated as an anti‐inflammatory drug. This study investigated the potential effect of AS incorporating into PLGA electrospun nanofibers on modulating host inflammatory response. The results showed that AS co‐electrospun with PLGA nanofibers could significantly reduce the infiltration of inflammatory cells at the implantation site as opposed to the site of regular PLGA nanofibers. In particular, immunohistochemistry demonstrated decreased M1 macrophage infiltration whereas increased M2 macrophage infiltration in the implantation site of AS‐PLGA nanofibers when compared to the PLGA implantation site. In vitro study also revealed that culture of human fibroblasts on PLGA nanofibers resulted in significantly enhanced gene expression of inflammatory cytokines when compared to non‐seeded fibroblasts, but these genes were significantly downregulated when seeded on AS‐PLGA. Furthermore, culture of macrophage on AS‐PLGA led to upregulated M2 marker gene expression and downregulated M1 marker gene expression. Collectively, these results indicate that, AS might be an ideal drug for loading into electrospun polymer nanofibers and thus favoring for tissue regeneration via mediating macrophage polarization.
Circular RNA ciRS‐7 inhibits autophagy of ESCC cells by functioning as miR‐1299 sponge to target EGFR signaling
Authors: Meng Lingjiao , Liu Sihua , Ding Pingan , Chang Sheng , Sang Meixiang 
Published: September 2019

AbstractAutophagy is a kind of intracellular degradation pathway which could be regulated by many noncoding RNAs. ciRS‐7, also called CDR1as, is a circular RNA that is relatively well studied at present. In our recent study, we have found that the expression of ciRS‐7 is abnormally increased in the esophageal squamous cell carcinoma (ESCC), and may function as an oncogene to accelerate ESCC progression through sponging miR‐876‐5p. Meanwhile, another study showed that ciRS‐7 is highly expressed in the triple‐negative breast cancer (TNBC) and may function as a competing endogenous RNA of miR‐1299 to maintain the high migration and invasive capacity of TNBC cells. Of interest, in the present work, we observed that ciRS‐7 could inhibit starvation or rapamycin‐induced autophagy of ESCC cells and miR‐1299 promotes starvation or rapamycin‐induced autophagy of ESCC cells. Mechanically, miR‐1299 could directly bind to the 3′‐untranslated region of epidermal growth factor receptor (EGFR) and then affects its downstream Akt‐mTOR pathway in ESCC cells. Consistent with our past findings, ciRS‐7 could also sponge miR‐1299 in ESCC cells. Taken together, this study has shed light on that circular RNA ciRS‐7 inhibits autophagy of ESCC cells by functioning as miR‐1299 sponge to target EGFR signaling.
Bioinformatics prediction and experimental validation of a novel microRNA: hsa‐miR‐B43 within human CDH4 gene with a potential metastasis‐related function in breast cancer
Authors: Rahimi Azadeh , Sedighi Rina , Emadi‐Baygi Modjtaba , Honardoost Mohammad‐Amin , Mowla Seyed‐Javad , Khanahmad Hossein , Nikpour Parvaneh 
Published: September 2019

AbstractAs a class of short noncoding RNAs, microRNAs (miRNAs) play a key role in the modulation of gene expression. Although, the regulatory roles of currently identified miRNAs in various cancer types including breast cancer have been well documented, there are many as yet undiscovered miRNAs. The aim of the current study was to bioinformatically reanalyze a list of 189 potentially new miRNAs introduced in a previously published paper (PMID: 21346806) and experimentally explore the existence and function of a candidate one: hsa‐miR‐B43 in breast cancer cells. The sequences of 189 potential miRNAs were re‐checked in the miRbase database. Genomic location and conservation of them were assessed with the University of California Santa Cruz (UCSC) genome browser. SSC profiler, RNAfold, miRNAFold, MiPred, and FOMmiR bioinformatics tools were furthermore utilized to explore potential hairpin structures and differentiate real miRNA precursors from pseudo ones. hsa‐miR‐B43 was finally selected as one of the best candidates for laboratory verification. The expression and function of hsa‐miR‐B43 were examined by real‐time polymerase chain reaction, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide, and wound‐healing assays. DIANA‐microT, RNAhybrid and Enrichr tools were used to predict the miRNA target genes and for further enrichment analysis. We could detect the exogenous and endogenous expression of hsa‐miR‐B43, as a real novel miRNA, in cancer cell lines. Gene Ontology enrichment, pathway analysis and wound‐healing assay results furthermore confirmed that a metastasis‐related function may be assigned to hsa‐miR‐B43. Our results introduced hsa‐miR‐B43, as a novel functional miRNA, which might play a role in the metastatic process. Further studies will be necessary to completely survey the existence and function of hsa‐miR‐B43 in other cancer types.
Circulating microRNA expression profiling and bioinformatics analysis of patients with coronary artery disease by RNA sequencing
Authors: Zhong Zhixiong , Zhong Wei , Zhang Qifeng , Zhang Qunji , Yu Zhikang , Wu Heming 
Published: September 2019

AbstractBackgroundMicroRNAs play a vital role in coronary artery disease. Abnormal expression of microRNAs has been found to be associated with the occurrence of CAD.MethodsWe identified significantly differentially expressed microRNAs in plasma between 40 patients with CAD and 10 controls with NCA using RNA sequencing. The differentially expressed microRNAs were analyzed for Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment.ResultsFifty cDNA libraries were constructed and sequenced, and a total of 1871.82 M raw reads were obtained, and 2135 microRNAs were found. Compared to the expressed microRNAs of NCA controls, 159 microRNAs were differentially expressed in CAD patients, including 119 upregulated microRNAs and 40 downregulated microRNAs. The top 10 upregulated miRNAs were miR‐144‐3p, miR‐34a‐5p, miR‐15b‐3p, miR‐22‐3p, miR‐29b‐3p, miR‐1270, miR‐6891‐5p, miR‐106a‐5p, miR‐15b‐5p, and hsa‐miR‐499b‐3p. The top ten downregulated miRNAs were miR‐4437, miR‐6842‐3p, miR‐4664‐3p, miR‐671‐3p, miR‐219a‐1‐3p, miR‐7848‐3p, miR‐664a‐3p, miR‐1284, miR‐361‐3p, and miR‐6780a‐5p. The target genes of differentially expressed microRNAs were related to many basic biological terms, such as biological process, cellular component, and molecular function. According to the KEGG pathway analysis, the most enriched pathways of the differentially expressed microRNAs were endocytosis, focal adhesion, axon guidance, and so on. Furthermore, six upregulated and two downregulated microRNAs were detected by qRT‐PCR (Quantitative Real‐time PCR) and ROC analysis for diagnosing CAD.ConclusionThe results suggest that the expression levels of some microRNAs may play a vital role in the physiological and pathological course of CAD. Our study may provide useful information for the diagnosis and treatment of CAD.
Involvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells
Authors: Huang Wenhui , Huang Cheng , Ding Huanyu , Luo Jianfang , Liu Yuan , Fan Ruixin , Xiao Fei , Fan Xiaoping , Jiang Zhisheng 
Published: September 2019

AbstractAimThe current study aimed to examine miR‐145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs).MethodsThe concentration of circulating miR‐145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR‐145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR‐145, involved in the TGF‐β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR‐145 mimics or inhibitors was conducted. Finally, the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively.ResultsThe amounts of miR‐145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P < .05). miR‐145 was mostly located in VSMCs. Proliferation and apoptosis of VSMCs were significantly induced in vitro by the downregulation of miR‐145. Also, miR‐145 modulated SMAD3 expression.ConclusionsmiR‐145 was found to be downregulated in patients with AD, which induced the proliferation, migration, and apoptosis of VSMCs by targeting SMAD3. This suggested the involvement of miR‐145 in the pathogenesis of AD.
Understanding of evidence‐based mental health care and the perceived importance of scientific information in a sample of U.S. adults
Authors: Mora Ringle Vanesa A. , Walsh Lucia M. , Maxwell Colleen A. , Smith Ashley M. , Grossman Rebecca A. , Becker Sara J. , Jensen‐Doss Amanda 
Published: September 2019

AbstractObjectivesThis online survey sought to qualitatively ascertain the extent to which a sample of U.S. adults understood the concept of evidence‐based mental health care (EBMHC). Additional goals included assessing the perceived importance of scientific information in EBMHC, and examining whether understanding EBMHC and science values varied as a function of participant factors.MethodParticipants (N = 221) defined EBMHC and rated the importance of scientific information. Open‐ended EBMHC definitions were content‐coded, and binomial logistic and linear regressions examined predictors of accurately defining EBMHC and of the perceived importance of scientific information.ResultsParticipants endorsed seven definitions of EBMHC, and only 20% defined it accurately. Having greater knowledge about mental health conditions was associated with understanding EBMHC and with the higher perceived importance of scientific information. Greater help‐seeking efficacy also predicted higher perceived importance of scientific information.ConclusionsResults support customized strategies to promote basic EBMHC education among U.S. adults.
TGF‐β/SMAD4 signaling pathway activates the HAS2–HA system to regulate granulosa cell state
Authors: Li Xinyu , Du Xing , Yao Wang , Pan Zengxiang , Li Qifa 
Published: September 2019

AbstractBoth TGF‐β/SMAD4 signaling pathway and HAS2–HA system have been shown to control granulosa cell (GC) state in mammalian ovary. However, the regulatory relationship between TGF‐β/SMAD4 signaling pathway and HA system in GCs is not well known. Here, we report that the TGF‐β/SMAD4 signaling pathway activates the HAS2–HA system by binding directly to the HAS2 promoter, ultimately controlling the GC state via the CD44–Caspase3 axis. SMAD4‐induced HAS2 expression, HAS2‐driven HA secretion, and HAS2‐mediated GC state (proliferation and apoptosis) by interacting directly with the promoter region of the HAS2 gene. The CD44–Caspase3 axis, located downstream of the HAS2–HA system, was also activated by SMAD4 and the TGF‐β/SMAD4 signaling pathway. However, there was no feedback regulation of the TGF‐β/SMAD4 signaling pathway by the HAS2–HA system in GCs. In addition, we found that miRNA‐26b attenuated HAS2 expression via SMAD4‐dependent and ‐independent mechanisms. Our findings provide compelling evidence that HAS2 is a direct transcriptional target of SMAD4. They also reveal a novel mechanism by which the TGF‐β/SMAD4 signaling pathway controls the GC state and alters the structural components of GCs in porcine ovaries.
MicroRNA‐26b inhibits oligodendrocyte precursor cell differentiation by targeting adrenomedullin in spinal cord injury
Authors: Cheng Li , Wang Chongchong , Yao Fei , Li Ziyu , Liu Wei , Jing Juehua 
Published: September 2019

AbstractOligodendrocyte precursor cells (OPCs) serve as a reservoir of newborn oligodendrocytes (OLs) in pathological and homeostatic conditions. After spinal cord injury (SCI), OPCs are activated to generate myelinating OLs, contributing to remyelination and functional recovery; however, the underlying molecular mechanisms remain unclear. Here, microRNA‐26b (miR‐26b) expression in the spinal cord tissues of SCI rats was examined by real‐time polymerase chain reaction analysis. The influences of miR‐26b on locomotor recovery following SCI were assessed utilizing Basso, Beattie, and Bresnahan (BBB) scores. The effects of miR‐26b on OPC differentiation were explored using immunofluorescence and western blot analyses in vitro and in vivo. The potential targets that are modulated by miR‐26b were identified by bioinformatics, luciferase reporter assays, and western blot analyses. The effects of adrenomedullin (ADM) on OPC differentiation were explored in vitro using immunofluorescence and western blot analyses. We demonstrated that miR‐26b was significantly downregulated after SCI. BBB scores showed that miR‐26b exacerbated the locomotor function deficits induced by SCI. In vitro, miR‐26b inhibited the differentiation of primary rat OPCs. In vivo, miR‐26b suppressed OPC differentiation in SCI rats. Bioinformatics analyses and experimental detection revealed that miR‐26b directly targeted ADM in OPCs. In addition, knockdown of ADM suppressed the differentiation of primary rat OPCs. Our study provides evidence that ADM may mediate miR‐26b‐inhibited OPC differentiation in SCI.
Sodium polyacrylate inhibits fermentative hydrogen production from waste diaper‐like material
Authors: Sotelo‐Navarro Perla X , Poggi‐Varaldo Héctor M , Turpin‐Marion Sylvie J , Rinderknecht Seijas Noemi F 
Published: September 2019

AbstractBACKGROUNDThe inhibitory effect of a moisture‐absorbent sodium polyacrylate (SPA), that is commonly used in disposable diapers, on the bio‐hydrogen (H2) generation from waste diaper‐like material (WDM) was assessed in dark fermentation studies. Three types of treatments were evaluated in batch bioreactors at 37 °C: mixture of bond paper and filter paper (WDM, no SPA), SPA alone (only SPA or control), and WDM spiked with SPA [paper plus sodium polyacrylate hydrogel (WDM‐SPA)]. The WDM simulated the cellulosic fraction of diaper composition.RESULTSThe units with only SPA did not produce H2. The WDM‐SPA units exhibited H2production 25% lower than those of bioreactors loaded with only WDM but no SPA. Cumulative H2 production was 0.03, 4.22 and 5.50 mmolH2 gTS–1 for the SPA, WDM‐SPA and WDM reactors, respectively (0.04, 5.90 and 8.77 mmolH2 gVS–1; 0.89, 132.19 and 196.45 NmLH2 gVS–1). BioH2 generation was related to predominance of the fermentation route that produces 1 mol L–1 of butyric acid (HBu) plus 2 mol L–1 H2 in the WDM and WDM‐SPA units, as suggested by the ratio A:B (acetic: butyric acids; A:B < 0.79 mg HAc‐COD mg HBu‐COD–1 in both cases).CONCLUSIONIt seems that this is the first documented result on the inhibitory effect of SPA on the bioH2 fermentation of cellulosic wastes. However, further research should be carried out at different levels of SPA to determine, for instance, the half‐inhibition value of SPA, that is, the concentration of SPA that would cause a 50% drop in H2 generation of the non‐SPA treatment. © 2019 Society of Chemical Industry
Franz Joseph Gall's non‐cortical faculties and their organs
Authors: Eling Paul , Finger Stanley 
Published: September 2019

AbstractFranz Joseph Gall (1758–1828) is remembered for his claims that behavior results from a large number of independent mental faculties, and that these faculties are associated with cortical organs. Apart from the 26 faculties he localized in the cerebrum, he also recognized one faculty (reproductive drive) in the cerebellum. This picture, however, is based on Gall's presentations in his well‐known later works, his four volume Anatomie et Physiologie. These books reflect the outcomes of Gall's thinking. They were steered by the observations and feedback he received in Vienna and while presenting his theories in the German states and neighboring countries between 1805 and 1807. Examining his lists before what he published in Paris shows how his faculties were changing. Notably, and as shown here, he had previously included several faculties associated with brainstem structures, in addition to the cerebellum, which he would continue to associate with some reproductive behaviors.
Th17 cell pathogenicity and plasticity in rheumatoid arthritis
Authors: Yang Pei , Qian Fei-Ya , Zhang Ming-Fei , Xu A-Lan , Wang Xiang , Jiang Bao-Ping , Zhou Ling-Ling 
Published: September 2019

AbstractCD4+ Th cells play an important role in the development of rheumatoid arthritis (RA) by regulating adaptive immune response. As major subsets of CD4+ Th cells, Th17 cells can produce a large number of hallmark cytokines such as IL-17A and IL-17F, which participate in host defense and immune homeostasis. However, increasing researches have shown that Th17 cells are unstable and exhibit a certain degree of plasticity, which aggravates their pathogenicity. Furthermore, the plasticity and pathogenicity of Th17 cells are closely related with the disease activity in RA. In this paper, the characteristics including phenotype, differentiation, plasticity, and pathogenicity of Th17 cells in RA will be systematically summarized. This will contribute to clarify the immunologic mechanism of RA and further provide a novel strategy for the clinical treatment of autoimmune diseases.
Are the costs worth the benefits? Shared perception and the aggregation of organizational climate ratings
Authors: Kessler Stacey R. 
Published: September 2019

SummaryA definitional component of organizational climate is the focus on employees' shared perceptions of the focal climate domain. To operationalize the notion of sharedness, researchers typically aggregate employees' domain‐specific climate perceptions to a higher level and justify this aggregation using quantitative indices of agreement. In the current paper, I argue that although accounting for sharedness among employees can provide some valuable insight, our overreliance on sharedness obscures some of the very organizational phenomena of interest. I discuss this issue by focusing on four costs of making unfounded assumptions regarding sharedness: (a) Aggregation assumes individual differences are a function of random error; (b) aggregation assumes that social situations are uniform across employees; (c) aggregation assumes that the unit of analysis is clear‐cut; and (d) aggregation assumes the group mean is meaningful. I argue that researchers carefully need to weigh the costs of violating these assumptions against the expected benefits of aggregating employees' climate perceptions, recognizing that sometimes employees' perceptions (i.e., psychological climate) might provide greater insight into phenomena of interest. Although I discuss these costs within the context of organizational climate research, these arguments apply to other research areas where individual perceptions are aggregated (e.g., research on leadership and teams).
Projected changes in mid–high‐latitude Eurasian climate during boreal spring in a 1.5 and 2°C warmer world
Authors: Chen Shangfeng , Wu Renguang , Chen Wen , Song Linye 
Published: September 2019

AbstractThis study examines projected changes in surface air temperature (SAT) and precipitation over mid–high latitudes of Eurasia during boreal spring in a 1.5/2°C warmer world (relative to pre‐industrial level) using historical, RCP4.5 and RCP8.5 simulations from 16 climate models of the Coupled Model Intercomparison Project Phase 5. Results show that spatial patterns of spring SAT and precipitation changes over Eurasia in the 1.5/2°C warmer world relative to the current climate (1979–2005) are similar between the two RCPs, but with a slightly larger amplitude in the RCP8.5. Spring SAT warmings over Eurasia are faster than the global annual mean. Amplitudes of the spring Eurasian SAT warmings are larger over higher latitudes. An additional 0.5°C global warming leads to extra spring Eurasian SAT warmings, with the magnitude larger than 0.5°C. Changes in the spring maximum temperature are comparable to the mean temperature changes both in the 1.5 and 2°C warming targets. Significant increases in the mean and extreme precipitation are only seen over parts of Eurasia. An additional 0.5°C global warming does not lead to obvious changes in the mean and extreme spring precipitation. Further analyses show that there are large uncertainties in the projected changes in the inter‐annual variability of the Eurasian spring SAT and precipitation.
Effect of Aging on the Macrophage Response to Titanium Particles
Authors: Jämsen Eemeli , Pajarinen Jukka , Lin Tzu‐hua , Lo Chi‐Wen , Nabeshima Akira , Lu Laura , Nathan Karthik , Eklund Kari K. , Yao Zhenyu , Goodman Stuart B. 
Published: September 2019

ABSTRACTMacrophage‐mediated inflammatory reaction to implant wear particles drives bone loss around total joint replacements (TJR). Although most TJR recipients are elderly, studies linking wear particle‐activated macrophages and peri‐implant osteolysis have not taken into account the multiple effects that aging has on the innate immune system and, in particular, on macrophages. To address this, we compared the wear particle responses of bone marrow macrophages obtained from young (2‐month) and aged (18‐month) mice. Macrophages were polarized to M0, M1, or M2 phenotypes in vitro, challenged with titanium particles, and their inflammatory response was characterized at multiple time points by quantitative reverse‐transcription polymerase chain reaction and enzyme‐linked immunosorbent assay. In addition, age‐dependent changes in activation of transcription factor nuclear factor‐κB were analyzed by a lentiviral vector‐based luciferase reporter system. The particle stimulation experiment was further repeated using human primary macrophages isolated from blood donors of different ages. We found that the pro‐inflammatory responses were generally higher in macrophages obtained from young mice, but differences between the age groups remained small and of uncertain biological significance. Noteworthily, M2 polarization effectively suppressed the particle‐induced inflammation in both young and aged macrophages. These results suggest that aging of the innate immune system per se plays no significant role in the response of macrophages to titanium particles, whereas induction of M2 polarization appears a promising strategy to limit macrophage‐mediated inflammation regardless of age. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:405‐416, 2020