bluuebunny/crossref_metadata_2025_split huggingface dataset:
Parallel group ICA+ICA: Joint estimation of linked functional network variability and structural covariation with application to schizophrenia
Authors: Qi Shile , Sui Jing , Chen Jiayu , Liu Jingyu , Jiang Rongtao , Silva Rogers , Iraji Armin , Damaraju Eswar , Salman Mustafa , Lin Dongdong , Fu Zening , Zhi Dongmei , Turner Jessica A. , Bustillo Juan , Ford Judith M. , Mathalon Daniel H. , Voyvodic James , McEwen Sarah , Preda Adrian , Belger Aysenil , Potkin Steven G. , Mueller Bryon A. , Adali Tulay , Calhoun Vince D. 
Published: May 2019

AbstractThere is growing evidence that rather than using a single brain imaging modality to study its association with physiological or symptomatic features, the field is paying more attention to fusion of multimodal information. However, most current multimodal fusion approaches that incorporate functional magnetic resonance imaging (fMRI) are restricted to second‐level 3D features, rather than the original 4D fMRI data. This trade‐off is that the valuable temporal information is not utilized during the fusion step. Here we are motivated to propose a novel approach called “parallel group ICA+ICA” that incorporates temporal fMRI information from group independent component analysis (GICA) into a parallel independent component analysis (ICA) framework, aiming to enable direct fusion of first‐level fMRI features with other modalities (e.g., structural MRI), which thus can detect linked functional network variability and structural covariations. Simulation results show that the proposed method yields accurate intermodality linkage detection regardless of whether it is strong or weak. When applied to real data, we identified one pair of significantly associated fMRI‐sMRI components that show group difference between schizophrenia and controls in both modalities, and this linkage can be replicated in an independent cohort. Finally, multiple cognitive domain scores can be predicted by the features identified in the linked component pair by our proposed method. We also show these multimodal brain features can predict multiple cognitive scores in an independent cohort. Overall, results demonstrate the ability of parallel GICA+ICA to estimate joint information from 4D and 3D data without discarding much of the available information up front, and the potential for using this approach to identify imaging biomarkers to study brain disorders.
Dynamic talent management capabilities and organizational agility—A qualitative exploration
Authors: Harsch Katharina , Festing Marion 
Published: May 2019

AbstractToday's business environment is becoming increasingly dynamic, and the concept of agility is gaining attention in the corporate world and in academia. The objective of our research is to explain how talent management (TM) can shape talents as key human resources, according to company‐specific agility needs, and thus contribute to gaining competitive advantage in dynamic firm environments. We approach this task by viewing it from the perspective of dynamic capabilities. A total of 24 semistructured interviews were conducted with senior TM professionals working in German companies differing in terms of size, age, structure, industry, and ownership. As a result, we identified three different types of dynamic TM capabilities promoting organizational agility to various extents. By rooting our qualitative study in the research fields of TM and agility in the under‐researched theoretical realm of dynamic capabilities, we contribute to the theoretical as well as the empirical discussion by addressing the specific challenges of an increasingly dynamic environment. As a result, we provide a contextualized viewpoint from which to explain the process inherent in dynamic TM capabilities that continuously shape talent and organizational agility.
Understanding Spatial Relationships in Admission Competition
Authors: Williams David S. 
Published: May 2019

AbstractOne of the most critical functions on campus is enrollment management. As budgets become tighter and institutions rely more heavily on tuition, the competition to “make the class” intensifies. How can institutional research help inform strategic planning in such a market? This paper will discuss the way that institutional researchers can use exploratory spatial data analysis (ESDA) to help enrollment management professionals and senior campus leadership better understand how their institutional selectivity may be related to neighboring competitors. By knowing this information, campuses can make strategic decisions with respect to their enrollment management policies and procedures.
Gender-Affirming Hormone Treatment Decreases Bone Turnover in Transwomen and Older Transmen
Authors: Vlot Mariska C , Wiepjes Chantal M , de Jongh Renate T , T’Sjoen Guy , Heijboer Annemieke C , den Heijer Martin 
Published: May 2019

ABSTRACT
Sex steroids play a key role in bone turnover and preserving BMD; hence, gender-affirming hormone treatment (HT) in transgender people affects bone metabolism. Most studies have looked into the effect of HT on changes in BMD; however, they do not provide insights into changes in bone metabolism caused by HT. This study investigated changes in bone turnover markers (BTMs) and sclerostin, as well as their correlations with change in BMD in transwomen and transmen during the first year of HT. Transwomen received estradiol and antiandrogens; transmen received testosterone. Sclerostin; P1NP; alkaline phosphatase (ALP); CTx; and BMD of the total hip, the femoral neck, and the lumbar spine were evaluated at baseline and after 1 year of HT. There were 121 transwomen (median age 30 years, interquartile range [IQR] 24 to 41 years) and 132 transmen (median age 24 years, IQR 21 to 33 years) included in the study. In transwomen, ALP decreased in 19% (95% CI, –21 to–16), CTx in 11% (95% CI, –18 to–4), and sclerostin in 8% (95%CI, –13 to–4) of study participants after 1 year of HT. In contrast, in transmen P1NP, ALP, and sclerostin increased in 33% (95% CI, 24 to 42), 16% (95% CI, 12 to 20), and 15% (95% CI, 10 to 20) of study participants, respectively, after 1 year of HT. No age differences were seen in transwomen, whereas in transmen aged ≥50 years a decrease in all BTMs was found in contrast with the other age groups. These transmen had low estrogen concentration at the start of HT based on their postmenopausal state before the start of HT; their estradiol concentrations increased during testosterone treatment. Changes in BTMs and BMD were weakly correlated (correlation coefficient all &lt;0.30). To conclude, 1 year of HT resulted in decreased bone turnover in transwomen and older transmen, whereas it increased in younger transmen. The decrease in bone resorption in older transmen shows the importance of estrogen as a key regulator of bone turnover. © 2019 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc.
Comparison of cord blood CD34 + stem cell expansion in coculture with mesenchymal stem cells overexpressing SDF‐1 and soluble /membrane isoforms of SCF
Authors: Ajami Mansoureh , Soleimani Masoud , Abroun Saeid , Atashi Amir 
Published: May 2019

AbstractAimUmbilical cord blood hematopoietic stem cells (UCB HSCs) have been considered for the treatment of hematological malignancies due to their noninvasive collection, greater capacity of expansion, and remarkable tolerance for HLA mismatch in transplantation. On the other hand, the most considerable limitation of these cells is their inadequate amount of CD34 + HSCs which leads to delayed engraftment. The aim of this study was the expansion of CD34 + HSCs by coculturing with mesenchymal stem cells (MSCs) overexpressing stromal cell‐derived factor‐1, soluble and membrane isoforms of stem cell factor (sSCF/mSCF). Keeping structure and function of overexpressed cytokines by MSCs was expected which could beneficially affect the CD34 + HSC expansion.MethodsMSCs and CD34 + HSCs were isolated from UCB mononuclear cells. UCB MSCs were nucleofected with one or more of sSCF, mSCF, and SDF‐1 expression vectors. Isolated CD34 + HSCs were then cocultured with nucleofected MSCs in 10 groups in culture medium containing TPO and Flt3L with or without SCF (3F or 2F groups). Then the CD34 + HSCs numeration, clonogenic capacity, and transcriptional levels of well‐known HSCs regulatory and stemness genes (CXCR4, HOXB4, BMI1, and SALL4) were assessed following coculture with modified MSCs.ResultsCD34 + HSCs which expanded on MSCs overexpressing mSCF/sSCF/SDF‐1 in the 3F group showed the most significant increase in the expansion (4.73 ± 0.26 fold), clonogenic capacity (5.3 ± 0.25 fold) and also transcriptional levels of CXCR4, HOXB4, and BMI1 (3.49 ± 0.13, 9.49 ± 0.78, and 11.6 ± 0.9 fold), respectively (
P < 0.05).ConclusionOverexpression of SCF and SDF‐1 by UCB MSCs in coculture system has efficient effect on UCB HSCs expansion. Furthermore nucleofected MSC overexpressing either sSCF/mSCF or mSCF/ sSCF /SDF‐1 could substitute the rhu SCF in HSC expansion culture medium.
Downregulation of microRNA‐155 stimulates sevoflurane‐mediated cardioprotection against myocardial ischemia/reperfusion injury by binding to SIRT1 in mice
Authors: Huang Guirong , Hao Fengguan , Hu Xueyan 
Published: May 2019

AbstractObjectiveThe inhaled sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (I/R) injury. However, the relative mechanisms of sevoflurane‐mediated cardioprotection remain largely unknown. This study intends to explore the effect of miR‐155 on the sevoflurane‐mediated cardioprotection by regulating Sirtuin 1 (SIRT1) in mouse models of myocardial I/R.MethodsLeft anterior descending coronary artery ligation was used to induce models of myocardial I/R in mice. The I/R mice were treated with sevoflurane, sevoflurane + mimics negative control (NC) or sevoflurane + miR‐155 mimics. The expression of microRNA‐155 (miR‐155) and SIRT1 was examined by quantitative real‐time polymerase chain reaction and Western blot assay. Then cardiac functions and hemodynamic alterations were evaluated. Evans blue‐2,3,5‐triphenyltetrazolium chloride and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling assay staining methods were adopted to evaluate infarct size and cardiomyocyte apoptosis, respectively.ResultsIn the I/R mice, miR‐155 was expressed at a high level and SIRT1 at a low level. SIRT1 was confirmed to be a target gene of miR‐155. The treatment of sevoflurane could reduce miR‐155 expression and increased SIRT1 expression in the myocardial tissues, under which conditions, cardiac functions were promoted, accompanied by reduced infarct size and inhibited cardiomyocyte apoptosis. In response to miR‐155 upregulation, the sevoflurane‐treated I/R mice showed reduced cardiac functions, and increased infarct size and cardiomyocyte apoptosis.ConclusionThe findings obtained in this study provide evidence suggesting that miR‐155 targets and negatively regulates SIRT1 expression, a mechanism by which the protection of sevoflurane is inhibited against myocardial I/R in mice.
uNK cell‐derived TGF‐β1 regulates the long noncoding RNA MEG3 to control vascular smooth muscle cell migration and apoptosis in spiral artery remodeling
Authors: Liu Weifang , Luo Minglian , Zou Li , Liu Xiaoxia , Wang Rongli , Tao Hui , Wu Di , Zhang Wen , Luo Qingqing , Zhao Yin 
Published: May 2019

AbstractSuccessful pregnancy depends on correct spiral artery (SpA) remodeling, and thus, on normal patterns of the vascular smooth muscle cell (VSMC) apoptosis and migration. Uterine natural killer (uNK) cells‐derived transforming growth factor β1 (TGF‐β1) is known to mediate the separation of VSMC layers via as yet unknown mechanisms. Likewise, the long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor that has been shown to regulate cancer cell apoptosis and migration; however, its role in VSMC loss is unclear. Thus, the aim of the present study was to assess the effects of uNK‐derived TGF‐β1 and MEG3 on VSMC function during SpA. Analyses were conducted to assess the effects of downregulating MEG3 expression, and/or administering treatments to increase or block TGF‐β1 signaling on VSMC survival and behavior. The results of these analyses showed that treating the VSMC with uNK cell‐derived supernatant or recombinant human TGF‐β1 promoted MEG3 and matrix metalloprotease 2 expression and VSMC apoptosis and migration, and suppressed VSMC proliferation. Conversely, MEG3 silencing promoted VSMC proliferation and inhibited VSMC apoptosis and migration. Notably, TGF‐β1 signaling induction had no significant effect on the proliferation, apoptosis, nor migration of the MEG3‐silenced VSMC. Together, these findings suggest that MEG3 is regulated by uNK‐derived TGF‐β1, and itself mediates VSMC apoptosis and migration; thus, it may be an important positive regulator of VSMCs separation during maternal SpA remodeling.
LncRNA PAPAS promotes oral squamous cell carcinoma by upregulating transforming growth factor‐β1
Authors: Zhang Panpan , Liu Ying , Li Chong , Zhang Li , Liu Qing , Jiang Tao 
Published: May 2019

AbstractPAPAS is a recently identified long noncoding RNA (lncRNA) with inhibitory effects on ribosomal RNA synthesis. We studied the role of PAPAS in oral squamous cell carcinoma (OSCC). In the present study we showed that plasma PAPAS and transforming growth factor β1 (TGF‐β1) were both upregulated in patients with OSCC, and were positively correlated only in patients with OSCC. Plasma levels of PAPAS were not significantly affected by AJCC stages and upregulation of PAPAS distinguished stage I OSCC patients from healthy controls. High plasma levels of PAPAS were followed by low overall survival rate. PAPAS overexpression led to upregulation of TGF‐β1 in OSCC cells, while TGF‐β1 treatment failed to significantly affect PAPAS. PAPAS overexpression and exogenous TGF‐β1 treatment led to promoted invasion and migration of OSCC cells. In addition, TGF‐β inhibitor attenuated the effects of PAPAS overexpression. Therefore, lncRNA PAPAS may promote OSCC by upregulating TGF‐β1.
Phase‐shifted pentafluorobutane nanoparticles for ultrasound imaging and ultrasound‐mediated hypoxia modulation
Authors: Chen Wei‐Jian , Zhang Hua , Zeng Xue‐Yi , Chen Long , Fang Gui‐Ting , Cai Huai‐Hong , Zhong Xing 
Published: May 2019

AbstractThe integration of ultrasound (US) contrast enhancement with oxygen‐loading nanoagents provide the synergistic strategy for simultaneously US imaging and hypoxic microenvironment modulation. Herein, we synthesize pentafluorobutane (PFB)‐loading methoxy poly(ethylene glycol)‐b‐poly(l‐lactide) (PLLA) nanoparticle as the novel US‐contrast‐enhanced agent and demonstrate that PFB@PLLA effectively loads oxygen. We characterize the nanosize, phase‐transformation property and oxygen‐loading amount of PFB@PLLA and investigate the effectiveness of these nanoagents in US‐contrast‐enhanced imaging. The PFB@PLLA displays a perfect temperature‐responsive phase‐transition property and its liquid‐to‐gas phase transition temperature is 45°C, which produces microbubbles in the targeted regions. Moreover, PFB@PLLA loads high amount of oxygen and US‐triggering PFB@PLLA reoxygenation effectively inhibits the expression of hypoxia‐related proteins (HIF‐1α and CAIX), reduces lactate secretion and glycolysis, which modulates hypoxic microenvironment and inhibits cancer cell migration and invasion in vitro. This study demonstrates that the US contrast‐enhanced activity of PFB@PLLAs and the promising utility of oxygen‐loading nanoagents to improve hypoxic microenvironment.
LncRNA SOX2‐OT regulates proliferation and metastasis of nasopharyngeal carcinoma cells through miR‐146b‐5p/HNRNPA2B1 pathway
Authors: Zhang Enqin , Li Xueping 
Published: May 2019

AbstractNasopharyngeal carcinoma (NPC) is an aggressive malignancy with a high mortality on account of its frequent metastasis and poor prognosis. An extensive body of investigations has proven that long noncoding RNAs are implicated in a variety of biological processes. Although SOX2‐OT has been reported to play an oncogenic role in osteosarcoma, the mechanism of SOX2‐OT‐driven NPC progression is still obscure. The aim of this study was to elucidate the biological function of SOX2‐OT and the related possible mechanism in NPC. In our study, SOX2‐OT was notably elevated in NPC samples and cells. Further, a high expression level of SOX2‐OT was correlated with poor clinical outcomes of NPC. Results from loss‐of‐function experiments suggested that knockdown of SOX2‐OT repressed cell proliferation, arrested cell cycle, facilitated cell apoptosis, and inhibited cell metastasis of NPC. To further investigate the molecular mechanism of SOX2‐OT, miR‐146b‐5p was found to directly bind to SOX2‐OT, which mediated the role of SOX2‐OT in NPC tumorigenesis. In addition, HNRNPA2B1 was a target of miR‐146b‐5p and SOX2‐OT modulated the expression of HNRNPA2B1 through competitively binding to miR‐146b‐5p. At last, we discovered that SOX2‐OT regulated NPC progression by targeting miR‐146b‐5p/HNRNPA2B1 pathway, which may provide more innovative targets for the treatment of patients with NPC.
A natural product enhances apoptosis via mitochondria/caspase‐mediated pathway in HeLa cells
Authors: Fan Yangyang , Zhang Yang , Liu Yutian , Xu Wenping , Yang Yun , Hao Youwu , Tao Liming 
Published: May 2019

AbstractCervical cancer is the fourth most lethal human malignancy and the leading cause of death among females around the world. Many antitumor agents have microbial origins. 5′‐epi‐SPA‐6952A is a new 24‐membered macrolide isolated from the cultured broth of Streptomyces diastatochromogenes. Therefore, we studied the activity and molecular mechanism of 5′‐epi‐SPA‐6952A in human cervical carcinoma HeLa cell. The results showed that 5′‐epi‐SPA‐6952A significantly inhibited cell proliferation and migration. In addition, 5′‐epi‐SPA‐6952A obviously increased the production of intracellular reactive oxygen species and DNA damage in HeLa cells. Moreover, nuclear shrinkage of cells, decrease in mitochondrial membrane potential, and upregulation of Bax/Bcl‐2 ratio resulted in the release of cytochrome c, and activation of caspase‐9/3 was observed in HeLa cells treated with 5′‐epi‐SPA‐6952A, which means it enhanced the intrinsic mitochondrial apoptosis. Besides, DNA‐damage associated proteins poly (ADP‐ribose) polymerase (PARP) and p53 were also studied, and the expressions of cleaved‐PARP and p53 were drastically increased in HeLa cells treated with 5′‐epi‐SPA‐6952A. Furthermore, we confirmed that 5′‐epi‐SPA‐6952A affected the survival of HeLa cells by blocking cell cycle progression in the G1 phase. Taken together, the results shows that 5′‐epi‐SPA‐6952A significantly inhibited HeLa cells proliferation via intrinsic mitochondrial apoptosis, cell cycle arrest, and blocking cell migration.
LncRNA NOC2L‐4.1 functions as a tumor oncogene in cervical cancer progression by regulating the miR‐630/YAP1 pathway
Authors: Wang Qingwei , Ding Jin , Nan Guo , Lyu Yuanyuan , Ni Guantai 
Published: May 2019

AbstractLong noncoding RNA (lncRNA) is a new class of noncoding RNA playing an indispensable role in different diseases by regulating miRNA. Our previous studies have suggested that miR‐630 was decreased in patients with cervical cancer. Recently, studies have shown that lncRNA NOC2L‐4.1 was abnormally expressed in patients with cervical cancer and can target miR‐630. Therefore, we wanted to identify the integrated relationship between lncRNA NOC2L‐4.1 and miR‐630 in the pathological processes regarding cervical cancer either in vitro or in vivo. Quantitative reverse transcription‐polymerase chain reaction detection shows that compared with human normal cervical epithelial cell, the expression of lncRNA NOC2L‐4.1 was significantly increased and the expression of miR‐630 was decreased in cell lines of cervical cancer. Moreover, luciferase reporter assay showed that miR‐630 was a target of lncRNA NOC2L‐4.1. The in vitro study found that downregulation of lncRNA NOC2L‐4.1 suppressed cervical cancer cell migration (transwell assays) and proliferation (cell counting kit‐8 and cloning formation assays). miR‐630 specific inhibitor treatment reversed the inhibitory effect of lncRNA NOC2L‐4.1 on cell proliferation and migration. Further studies also found that yes‐associated protein 1 (YAP1) was the target of miR‐630. Overexpression YAP1 suppressed miR‐630 overexpression induced cell proliferation and inhibition of migration. Tumors induced by implantation of lncRNA NOC2L‐4.1‐knockdown Hela cells in nude mice showed that lncRNA NOC2L‐4.1 silencing decreased the growth of tumors in both volume and weight by regulation of miR‐630/YAP1. Taken together, our study reveals the important role of lncRNA NOC2L‐4.1/miR‐630/YAP1 regulatory network in cervical cancer, which provides new insights concerning the pathogenesis of cervical cancer.
MicroRNA signature predicts survival in papillary thyroid carcinoma
Authors: Chengfeng Xiong , Gengming Cai , Junjia Zhang , Yunxia Lv 
Published: May 2019

AbstractPapillary thyroid cancer (PTC) accounts for the majority of malignant thyroid tumors. Recently, several microRNA (miRNA) expression profiling studies have used bioinformatics to suggest miRNA signatures as potential prognostic biomarkers in various malignancies. However, a prognostic miRNA biomarker has not yet been established for PTC. The aim of the present study was to identify miRNAs with prognostic value for the overall survival (OS) of patients with PTC by analyzing high‐throughput miRNA data and their associated clinical characteristics downloaded from The Cancer Genome Atlas database. From our dataset, 150 differentially expressed miRNAs were identified between tumor and nontumor samples; of these miRNAs, 118 were upregulated and 32 were downregulated. Among the 150 differentially expressed miRNAs, a four miRNA signature was identified that reliably predicts OS in patients with PTC. This miRNA signature was able to classify patients into a high‐risk group and a low‐risk group with a significant difference in OS (P < .01). The prognostic value of the signature was validated in a testing set (
P < .01). The four miRNA signature was an independent prognostic predictor according to the multivariate analysis and demonstrated good performance in predicting 5‐year disease survival with an area under the receiver operating characteristic curve area under the curve (AUC) score of 0.886. Thus, this signature may serve as a novel biomarker for predicting the survival of patients with PTC.
Involvement of microRNAs in physiological and pathological processes in asthma
Authors: Mousavi Seyed Reza , Ahmadi Ali , Jamalkandi Sadegh Azimzadeh , Salimian Jafar 
Published: May 2019

AbstractAsthma is the most common respiratory disease accompanied by lung inflammatory disorders. The main symptoms are airway obstruction, chronic inflammation due to mast cell and eosinophil activity, and the disturbance of immune responses mostly mediated by the Th2 response. Genetic background and environmental factors also contribute to the pathogenesis of asthma. Today, microRNAs (miRNAs) are known as remarkable regulators of gene expression. As a small group of noncoding single‐strand RNAs, mature miRNAs (~21 nucleotides) modulate the gene expression by targeting complement RNAs at both transcriptional and posttranscriptional levels. The role of miRNAs in the pathogenesis of many diseases such as allergies, asthma, and autoimmunity has been vastly studied. This review provides a thorough research update on the role of miRNAs in the pathogenesis of asthma and their probable role as diagnostic and/or therapeutic biomarkers.