bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improving hypertension control through a collaboration between an academic medical center and a chain community pharmacy
Authors: Vordenberg Sarah E. , Lindell Valerie , Sheerer Krystal , Settles Amy , Fan Audrey L. , Serlin David C. , Parker‐Featherstone Ebony , Bernstein Steven J. , Choe Hae M. 
Published: July 2019

AbstractIntroductionApproximately one‐third of adults in the United States have hypertension (HTN), leading to increased morbidity and mortality.ObjectivesThis quality improvement intervention was designed to improve HTN control among community‐dwelling adults through collaboration between patient‐centered medical homes (PCMH) within an academic medical center and chain community pharmacies.MethodsFour PCMH sites in Ann Arbor, Michigan that were in close proximity to two Meijer pharmacies participated in this study between September 2016 and March 2017, which compared HTN outcomes for patients seen at two community pharmacies where the pharmacists received training on HTN management for patients who received usual care at their PCMH. The primary outcome was percent of patients who met their blood pressure (BP) goal of either <140/90 mmHg or < 150/90 mmHg compared with matched controls who received usual care at the PCMH. Secondary outcomes included number of medication recommendations made, percent of recommendations accepted by the primary care provider (PCP), and patient satisfaction.ResultsPatients who received care at the community pharmacy (n = 155) had a higher rate of BP control at 3 months than matched controls (61.8% vs 47.7%, P = 0.013). A total of 29 medication recommendations were made by community pharmacists and 26 were accepted by the PCP. Nearly 95% of patients rated the care they received as excellent or very good and over 95% stated that they would recommend the pharmacist at the Meijer pharmacy to their family and friends.ConclusionPatients who received HTN management services as part of a collaboration between an academic medical center and chain community pharmacy were significantly more likely to have controlled BP at 3 months compared with matched controls who received standard care. This model shows promise as being a strategy to expand access to care for patients while being mutually beneficial for community pharmacies and health systems.
Laser‐induced plasmon‐mediated treatment of retinoblastoma in viscous vitreous phantom
Authors: Darviot Cécile , Hardy Pierre , Meunier Michel 
Published: July 2019

AbstractRetinoblastoma (RB) is a rare form of cancer of the retina most prevalent in young children. We successfully show that laser‐induced cell disruption, mediated by gold plasmonic nanoparticle (NP), is a potential and efficient therapy to kill the cancerous cells. The proof of concept is demonstrated in vitro on cultured Y79 RB cancer cells with a nanosecond laser at 527 nm, for both attached cells at the bottom of a Petri dish and for floating, clustered cells in a viscous vitreous phantom comprised of hyaluronan. We report a cellular death of 82% after irradiation in classic culture medium and a cellular death of 98% in vitreous phantom, for similar number of NPs in each sample. It is found that the NPs efficiently penetrate the floating Y79 clusters cells in the vitreous phantom, leading to a cellular death of over 85% even within the centre of the aggregates. The proposed treatment technique is based on a similar nanosecond laser used to eliminate floaters in the vitreous, but with much lower (100‐1000 times) fluences of 20 J cm−2.
lncRNA ZFPM2‐AS1 promotes proliferation via miR‐18b‐5p/VMA21 axis in lung adenocarcinoma
Authors: Xue Min , Tao Weimin , Yu Suyun , Yan Zhijun , Peng Qing , Jiang Fan , Gao Xiwen 
Published: July 2019

AbstractLung cancer has been proved to be one of the most common kinds of cancers around the globe. Meanwhile, as the predominant type of lung cancer, lung adenocarcinoma (LUAD) has received increasing attention in cancer research. Long noncoding RNAs (lncRNAs) are known to be associated with oncogenesis and progression of various cancers. However, many lncRNAs have not been thoroughly detected in LUAD. In this study, through bioinformatics analysis we found that zinc finger protein multitype 2 antisense RNA 1 (ZFPM2‐AS1) was associated with poor prognosis of LUAD patients. Also, ZFPM2‐AS1 was detected to be overexpressed in LUAD tissues and cells. Furthermore, ZFPM2‐AS1 could promote the proliferation of LUAD cells. Next, miR‐18b‐5p was found to bind with and negatively regulated by ZFPM2‐AS1. VMA21, target gene of miR‐18b‐5p, could bind with and be negatively regulated by miR‐18b‐5p. More importantly, both ZFPM2‐AS1 and VMA21 were found to be attached to the RNA‐induced silencing complex constructed from miR‐18b‐5p and Ago2. Also, ZFPM2‐AS1 could regulate the expression of VMA21. Therefore, ZFPM2‐AS1 were confirmed to regulate VMA21 by competitively binding with miR‐18b‐5p. Finally, rescue assays confirmed that ZFPM2‐AS1 could regulate LUAD cell proliferation via miR‐18b‐5p/VMA21 axis.
Insight into the molecular mechanism of LINC00152/miR‐215/CDK13 axis in hepatocellular carcinoma progression
Authors: Wang Jianchu , Zhang Ying , Lu Libai , Lu Yuan , Tang Qianli , Pu Jian 
Published: July 2019

AbstractHepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world. Nevertheless, its underlying molecular mechanisms are largely unknown. LINC00152 are recently investigated in several cancer types. In our current investigation, we observed LINC00152 was obviously upregulated in HCC cells. LINC00152 was significantly downregulated by infecting LV‐shLINC00152 in HepG2 and SNU449 cells. Loss of LINC00152 remarkably repressed HCC cell proliferation, cell colony formation, induced cell apoptosis, and restrained cell migration/invasion. Growing evidence has reported long noncoding RNAs can sponge microRNAs to modulate cancer process. Here, we indicated miR‐215 was greatly decreased in HCC and LINC00152 regulated HCC development via sponging miR‐215. For another, the binding association between LINC00152 and miR‐215 was proved by a series of functional assays. CDK13 was predicted as the target of miR‐215. Upregulation of miR‐215 greatly depressed CDK13 in HCC cells. Subsequently, the in vivo results demonstrated that silence of LINC00152 restrained HCC development via modulating miR‐215 to up‐regulate CDK13. Therefore, it was revealed that LINC00152 contributed to the progression of HCC by the modulation of miR‐215 and CDK13.
miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene
Authors: Li Cui , Zhang Yinmin , Zhao Wei , Cui Shoubin , Song Yuchun 
Published: July 2019

AbstractThe study of either miR‐153‐3p or MCL1 gene in ovarian carcinoma (OVC) has been reported; however, the interaction between miR‐153‐3p and MCL1 gene in OVC as well as the influence of their interaction on OVC progression has not been reported yet. Herein we intended to study the effects of miR‐153‐3p/MCL1 axis in OVC. Web‐based bioinformatics algorithms including DIANA TarBase 8.0, PicTar, and TargetScan Human 7.2 were used to predict the microRNAs (miRNAs) that could target MCL1 mRNA. Patient characteristics data collection and tissue sample immunohistochemical staining were used to determine the expression level of miR‐153‐3p and MCL1. We determined to unravel the effects of the pairing‐up of miR‐153‐3p and MCL1 mRNA in OVC cell lines (OVCAR3 cell line and A2780) and xenografts (immunodeficient(immunodeficient Rag−/− mice) using several methods including real‐time quantitative reverse transcription polymerase chain reaction, westernWestern blot, colony formation assay, wound healing assay, Transwell invasion assay, flow cytometry assay, and xenograft assay. These experiments were performed to study OVC cellular activities such as cell growth and death and so forth in vitro and in vivo. Plenty of miRNAs that can target MCL1 mRNA have been identified, and we have narrowed them down to miR‐153‐3p. MCL1 gene was found overexpressed in OVC tissues and OVC cell lines at RNA and protein levels, whereas miR‐153‐3p was found under‐expressed in OVC tissues and cells. miR‐153‐3p was found to target MCL1 mRNA and interfered OVC progression. The repression of MCL1 gene expression caused by either miR‐153‐3p or small interfering RNA technique led to significantly reduced OVC cell growth and invasion in vitro. Lastly, the engraftment of transfected human OVC cells into Rag−/− mice confirmed the in vitro results. MCL1 gene acts as a cancer facilitator in OVC. In this study, we revealed the role of miR‐153‐3p on OVC progression by targeting MCL1 gene. Our work could comprehend the current understanding of OVC progression and contribute to the underlying aggression mechanism of this cancer.
Depletion of NBR1 in urothelial carcinoma cells enhances rapamycin‐induced apoptosis through impaired autophagy and mitochondrial dysfunction
Authors: Kim Myeong Joo , Hwang Gwang Yong , Cho Min Ji , Chi Byung Hoon , Park Serk In , Chang In Ho , Whang Young Mi 
Published: July 2019

AbstractRapamycin is well‐recognized in the clinical therapeutic intervention for patients with cancer by specifically targeting mammalian target of rapamycin (mTOR) kinase. Rapamycin regulates general autophagy to clear damaged cells. Previously, we identified increased expression of messenger RNA levels of NBR1 (the neighbor of BRCA1 gene; autophagy cargo receptor) in human urothelial cancer (URCa) cells, which were not exhibited in response to rapamycin treatment for cell growth inhibition. Autophagy plays an important role in cellular physiology and offers protection against chemotherapeutic agents as an adaptive response required for maintaining cellular energy. Here, we hypothesized that loss of NBR1 sensitizes human URCa cells to growth inhibition induced by rapamycin treatment, leading to interruption of protective autophagic activation. Also, the potential role of mitochondria in regulating autophagy was tested to clarify the mechanism by which rapamycin induces apoptosis in NBR1‐knockdown URCa cells. NBR1‐knockdown URCa cells exhibited enhanced sensitivity to rapamycin associated with the suppression of autophagosomal elongation and mitochondrial defects. Loss of NBR1 expression altered the cellular responses to rapamycin treatment, resulting in impaired ATP homeostasis and an increase in reactive oxygen species (ROS). Although rapamycin treatment‐induced autophagy by adenosine monophosphate‐activated protein kinase (AMPK) phosphorylation in NBR1‐knockdown cells, it did not process the conjugated form of LC3B‐II after activation by unc‐51 like autophagy‐activating kinase 1 (ULK1). NBR1‐knockdown URCa cells exhibited rather profound mitochondrial dysfunctions in response to rapamycin treatment as evidenced by Δψm collapse, ATP depletion, ROS accumulation, and apoptosis activation. Therefore, our findings provide a rationale for rapamycin treatment of NBR1‐knockdown human urothelial cancer through the regulation of autophagy and mitochondrial dysfunction by regulating the AMPK/mTOR signaling pathway, indicating that NBR1 can be a potential therapeutic target of human urothelial cancer.
Screening and identification of hub genes in pancreatic cancer by integrated bioinformatics analysis
Authors: Chen Qing , Yu Dongmei , Zhao Yingying , Qiu Jiajun , Xie Yufeng , Tao Min 
Published: July 2019

AbstractPancreatic cancer (Pa) is a malignant tumor of the digestive tract with high degree of malignancy, this study aimed to obtain the hub genes in the tumorigenesis of Pa. Microarray datasets GSE15471, GSE16515, and GSE62452 were downloaded from Gene Expression Omnibus (GEO) database, GEO2R was conducted to screen the differentially expressed genes (DEGs), and functional enrichment analyses were carried out by Database for Annotation, Visualization and Integrated Discovery (DAVID). The protein‐protein interaction (PPI) network was constructed with the Search Tool for the Retrieval of Interacting Genes (STRING), and the hub genes were identified by Cytoscape. Totally 205 DEGs were identified, consisting of 51 downregulated genes and 154 upregulated genes enriched in Gene Ontology terms including extracellular matrix (ECM) organization, collagen binding, cell adhesion, and pathways associated with ECM‐receptor interaction, focal adhesion, and protein digestion. Two modules in the PPI were chosen and biological process analyses showed that the module genes were mainly enriched in ECM and cell adhesion. Twenty‐four hub genes were confirmed, the survival analyses from the cBioPortal online platform revealed that topoisomerase (DNA) II α (TOP2A), periostin (POSTN), plasminogen activator, urokinase (PLAU), and versican (VCAN) may be involved in the carcinogenesis and progression of Pa, and the receiver‐operating characteristic curves indicated their diagnostic value for Pa. Among them, TOP2A, POSTN, and PLAU have been previously reported as biomarkers for Pa, and far too little attention has been paid to VCAN. Analysis from R2 online platform showed that Pa patients with high VCAN expression were more sensitive to gemcitabine than those with low level, suggesting that VCAN may be an indicator to guide the use of the chemotherapeutic drug. In vitro experiments also showed that the sensitivity of the VCAN siRNA group to gemcitabine was lower than that of the control group. In conclusion, this study discerned hub genes and pathways related to the development of Pa, and VCAN was identified as a novel biomarker for the diagnose and therapy of Pa.
Genome‐wide identification of lncRNAs as novel prognosis biomarkers of glioma
Authors: Song Lianhao , Zhang Shengkun , Duan Chenwei , Ma Shuai , Hussain Sajjad , Wei Lanlan , Chu Ming 
Published: July 2019

AbstractBackgroundGlioma is the primary cancer of the central nervous system, and defining the prognosis of glioma is of great significance in the clinical. The long noncoding RNAs (lncRNAs) emerge as important regulators of pathological processes. This study aimed to identify lncRNAs which could function as potential prognosis biomarkers of glioma.Material and MethodsGlioma RNA‐seq data from TCGA and CGGA were analyzed to identify neoplasm grade associated lncRNAs by DEseq. 2R and weighted gene co‐expression network analysis. Consensus module genes were analyzed in Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway to predict lncRNAs biological functions. Then neutrophil immune estimations were analyzed by Tumor Immune Estimation Resource. Transcrption factors of these lncRNAs were predicted by PROMO. Overall survival and receiver operating characteristic (ROC) analyses were applied to test the accuracy of predicted lncRNAs as the markers of prognosis.ResultsWe identified four lncRNAs most correlated with both higher neoplasm grade and worse prognosis, including AC064875.2, HOTAIRM1, LINC00908, and RP11‐84A19.3. Neutrophil‐mediated immunity and cell adhesion junction were considered as the main biological functions of these lncRNAs. In addition, the correlation of these four lncRNAs with glioma prognosis was validated.ConclusionNeutrophil immune infiltration is implicated in higher neoplasm grade and worse prognosis of glioma. AC064875.2, HOTAIRM1, LINC00908, and RP11‐84A19.3 may serve as potential prognosis biomarkers of glioma.
Retracted: DLX5 gene regulates the Notch signaling pathway to promote glomerulosclerosis and interstitial fibrosis in uremic rats
Authors: Wang Xin‐Fang , Zhang Bei‐Hao , Lu Xiao‐Qing , Wang Rui‐Qiang 
Published: July 2019

AbstractUremia largely results from the accumulation of organic waste products normally cleared by the kidneys, which commonly accompanies kidney failure and chronic kidney disease. However, genetic investigations in a uremia remain largely unclear. This study aimed to determine the expression patterns of distal‐less homeobox 5 (DLX5) in uremia rat model and further to study its effects on glomerulosclerosis and interstitial fibrosis. Uremic expression chip was applied to screen differentially expressed genes in uremia. Next, we used small interfering RNA‐mediated RNA interference to specifically silence DLX5 in experimental uremic rats to understand the regulatory mechanism of DLX5. To understand effect of Notch1 signaling pathway in uremia, we also treated experimental uremic rats with γ‐secretase inhibitor (GSI), an inhibitor of Notch1 signaling pathway. The expression of fibronectin (FN), laminin (LN), transforming growth factor‐β1 (TGF‐β1), Hes1, Hes5, and Jagged2 was determined. The semiquantitative assessment was applied to verify the effects of DLX5 on glomerulosclerosis. In the uremic expression chip, we found that DLX5 was upregulated in uremia samples, and considered to regulate the Notch signaling pathway. We found that small interfering RNA‐mediated DLX5 inhibition or Notch1 signaling pathway inhibitory treatment relieved and delayed the kidney injury and glomerulosclerosis in uremia. Meanwhile, inhibition of DLX5 or Nothch1 signaling pathway reduced expression of FN, LN, Nothch1, TGF‐β1, Hes1, Hes5, and Jagged2. Intriguingly, we discovered that Notch1 signaling pathway was inhibited after silencing DLX5. In conclusion, these findings highlight that DLX5 regulates Notch signaling, which may, in turn, promote complications of uremia such as kidney fibrosis, providing a novel therapeutic target for treating uremia.
Cover Image, Volume 94, Issue 8
Authors: Ait El Fakir Abdellah , Anfar Zakaria , Benafqir Mohamed , Jada Amane , El Alem Noureddine 
Published: July 2019

The cover image is based on the Research Article Polyaniline coated hematite sand supported on graphene oxide (HS@PANI‐GO) as a new magnetic material for advanced catalytic oxidation based on sulfate radicals: optimization using response surface methodology by Abdellah Ait El Fakir et al., DOI: 10.1002/jctb.6070.
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Fetal echocardiography gives a clue for the maternal diagnosis of tuberous sclerosis complex
Authors: Pasieczna Monika , Koleśnik Adam , Królicki Leszek , Duczkowski Marek , Bekiesińska‐Figatowska Monika , Szymkiewicz‐Dangel Joanna 
Published: July 2019

AbstractThe detection of multiple cardiac tumors during fetal echocardiography allowed us to make the diagnosis of tuberous sclerosis complex in the mother and establish the reason of her first epileptic seizures.
Cellular identities in an unusual presentation of cyclopia in a chick embryo
Authors: Palmquist‐Gomes Paul , Pérez‐Pomares José María , Guadix Juan Antonio 
Published: July 2019

AbstractCyclopia is a congenital anomaly characterized by the presence of a single or partially divided eye in a single orbit at the body midline. This condition is usually associated with other severe facial malformations, such as the absence of the nose and, on rare occasions, the presence of a proboscis located above the ocular structures. The developmental origin of cyclopia in vertebrates is the failure of the embryonic prosencephalon to divide properly during the formation of the two bilateral eyes. Although the developmental origin of the cyclopia‐associated proboscis is not clear, it has been suggested that this unique structure results from the disrupted morphogenesis of the olfactory placodes, the main organizers of the developing nose. In this study, we report a spontaneous congenital case of cyclopia with a proboscis‐like appendage in a chick embryo. By means of both conventional histology and immunohistochemical methods, we have analyzed this anomaly in detail to suggest an alternative identity for the anatomical embryonic features of cyclopic vertebrate embryos displaying a proboscis. Our findings are discussed in the context of previously reported cases of cyclopia, and provide additional insight into this complex congenital malformation.
Implementation of “Treat‐all” at adult HIV care and treatment sites in the Global IeDEA Consortium: results from the Site Assessment Survey
Authors: Brazier Ellen , Maruri Fernanda , Duda Stephany N , Tymejczyk Olga , Wester C William , Somi Geoffrey , Ross Jeremy , Freeman Aimee , Cornell Morna , Poda Armel , Musick Beverly S , Zhang Fujie , Althoff Keri N , Mugglin Catrina , Kimmel April D , Yotebieng Marcel , Nash Denis ,   the IeDEA Consortium
Published: July 2019

AbstractIntroductionSince 2015, the World Health Organization (WHO) has recommended that all people living with HIV (PLHIV) initiate antiretroviral treatment (ART), irrespective of CD4+ count or clinical stage. National adoption of universal treatment has accelerated since WHO's 2015 “Treat All” recommendation; however, little is known about the translation of this guidance into practice. This study aimed to assess the status of Treat All implementation across regions, countries, and levels of the health care delivery system.MethodsBetween June and December 2017, 201/221 (91%) adult HIV treatment sites that participate in the global IeDEA research consortium completed a survey on capacity and practices related to HIV care. Located in 41 countries across seven geographic regions, sites provided information on the status and timing of site‐level introduction of Treat All, as well as site‐level practices related to ART initiation.ResultsAlmost all sites (93%) reported that they had begun implementing Treat All, and there were no statistically significant differences in site‐level Treat All introduction by health facility type, urban/rural location, sector (public/private) or country income level. The median time between national policy adoption and site‐level introduction was one month. In countries where Treat All was not yet adopted in national guidelines, 69% of sites reported initiating all patients on ART, regardless of clinical criteria, and these sites had been implementing Treat All for a median period of seven months at the time of the survey. The majority of sites (77%) reported typically initiating patients on ART within 14 days of confirming diagnosis, with 60% to 62% of sites implementing Treat All in East, Southern and West Africa reporting same‐day ART initiation for most patients.ConclusionsBy mid‐ to late‐2017, the Treat All strategy was the standard of care at almost all IeDEA sites, including rural, primary‐level health facilities in low‐resource settings. While further assessments of site‐level capacity to provide high‐quality HIV care under Treat All and to support sustained viral suppression after ART initiation are needed, the widespread introduction of Treat All at the service delivery level is a critical step towards global targets for ending the HIV epidemic as a public health threat.