bluuebunny/crossref_metadata_2025_split huggingface dataset:
Upregulation of SNHG14 suppresses cell proliferation and metastasis of colorectal cancer by targeting miR‐92b‐3p
Authors: Zhang Wei , Duan Wenfei , Mo Zhifeng , Wang Jianen , Yang Wenbin , Wu Wenrong , Li Xian , Lin Shuihua , Tan Yuanfei , Wei Wei 
Published: November 2019

AbstractAmple evidence have demonstrated that long noncoding RNAs small nucleolus RNA host gene 14 (SNHG14) serves as a master regulator in various cancers. However, the exact mechanism of SNHG14 in colorectal cancer (CRC) remains unknown. In the present study, we concentrate on the potential function of SNHG14 in the pathogenesis of CRC. From the quantitative reverse transcription‐polymerase chain reaction results, SNHG14 was found to be downregulated in CRC tissues compared with the normal mucous samples, and its low expression was significantly correlated with poor clinical outcomes. Overexpression of SNHG14 inhibited cell growth, induced cell apoptosis, suppressed migration and invasion by inhibiting epithelial‐mesenchymal transition process. Furthermore, mechanistic studies revealed that miR‐92b‐3p could rescue the CRC progress induced by SNHG14. Consequently, SNHG14 exhibited low expression in CRC tissues and involved in CRC progression and metastasis by competing for miR‐92b‐3p, and SNHG14 could be used as a valuable biomarker and therapeutic target for CRC.
Impact of modulation of telomerase and cancer stem‐cell marker OCT4 axis in cervical cancer pathogenesis with underlying HPV16 infection
Authors: Tiwari Diptika , Ray Das Chandana , Sultana Rizwana , Kakoti Shantipriya , Aasif Khan Mohammad , Dongre Anita , Husain Syed Akhtar , Bose Purabi Deka , Bose Sujoy 
Published: November 2019

AbstractLacunae exist in the molecular event(s) specificity associated with cervical cancer (CaCx) pathogenesis. The present study aimed to evaluate the significance of telomerase‐cervical cancer stem cells (CSCs) modulation in CaCx pathogenesis with underlying HPV16 infection. The study included HPV16 positive cases only (N = 65) of the total enrolled cases from Northeast India. The analysis of viral load and the differential messenger RNA expression of E6, E7, hTERT, hTR, and cancer stem‐cell markers was studied by real‐time polymerase chain reaction. Further the protein and colocalization study for E6, hTERT, and oct4 was performed by immunofluorescence. The real‐time polymerase chain reaction based analysis showed an upregulation of HPV16 viral oncoprotein E6 and E7, and telomerase component hTERT and hTR expression and their correlation in CaCx susceptibility and severity. The hTERT expression correlated with viral load; while the E6 and telomerase protein expression colocalized in the nucleus. The CSCs marker octamer‐binding transcription factor 4 (OCT4) was significantly upregulated in CaCx cases, was associated with CaCx susceptibility and severity, and colocalized with E6 expression in the nucleus as revealed from the immunofluorescence studies. To conclude, the telomerase‐OCT4 axis modulation holds key in HPV16 CaCx pathogenesis mediated by HPV16 E6 viral oncoprotein expression, and underlines its potential for therapeutic targeting.
Retracted: AIB1 induces epithelial‐mesenchymal transition in gastric cancer via the PI3K/AKT signaling
Authors: Diao Lei , Li Yang , Mei Qiao , Han Wei , Hu Jing 
Published: November 2019

AbstractAmplified in breast cancer 1 (AIB1) is overexpression in various cancers and promotes tumor cell proliferation, survival, and invasiveness. However, the role of AIB1 in the regulation of gastric cancer (GC) cell epithelial‐mesenchymal transition (EMT) is still largely unclear. In the present study, immunohistochemistry showed that AIB1 was upregulated in our cohort of patients with GC and correlated with poor survival. Knockdown of AIB1 reduced the invasive ability of GC cells, downregulated the expression of epithelial cell marker E‐cadherin, and upregulated mesenchymal cell marker vimentin. AIB1 overexpression elicited the opposite effect. PI‐103, the inhibitor of the PI3K/AKT signaling, partially reversed AIB1 overexpression mediated a decrease in E‐cadherin and an increase in vimentin. The present data demonstrated that AIB1 augmented the EMT via activation of PI3K/AKT signaling. In conclusion, our results suggested a novel role of AIB1 in GC invasion and EMT and raised the possibility of using this molecule as an indicator for GC treatment.
Mediator subunit MED1 modulates intranuclear dynamics of the thyroid hormone receptor
Authors: Femia Matthew R. , Evans Rochelle M. , Zhang Jibo , Sun Xiaopeng , Lebegue Caroline J. , Roggero Vincent R. , Allison Lizabeth A. 
Published: November 2019

AbstractThe thyroid hormone receptors (TRs) mediate thyroid hormone (T3)‐dependent gene expression. The nuclear import and export signals that direct TR shuttling are well characterized, but little is known about factors modulating nuclear retention. We used fluorescence‐based nucleocytoplasmic scoring and fluorescence recovery after photobleaching in transfected cells to investigate whether Mediator subunits MED1 and MED13 play a role in nuclear retention of TR. When MED1 was overexpressed, there was a striking shift towards a greater nuclear localization of TRβ1 and the oncoprotein v‐ErbA, subtypes with cytosolic populations at steady‐state, and TRβ1 intranuclear mobility was reduced. For TRα1, there was no observable change in its predominantly nuclear distribution pattern or mobility. Consistent with a role for MED1 in nuclear retention, the cytosolic TRα1 and TRβ1 population were significantly greater in MED1−/− cells, compared with MED1+/+ cells. Exposure to T3 and epidermal growth factor, which induces MED1 phosphorylation, also altered TR intranuclear dynamics. Overexpression of miR‐208a, which downregulates MED13, led to a more cytosolic distribution of nuclear‐localized TRα1; however, overexpression of MED13 had no effect on TRβ1 localization. The known binding site of MED1 overlaps with a transactivation domain and nuclear export signal in helix 12 of TR's ligand‐binding domain (LBD). Coimmunoprecipitation assays demonstrated that TR's LBD interacts directly with exportins 5 and 7, suggesting that binding of exportins and MED1 to TR may be mutually exclusive. Collectively, our data provide evidence that MED1 promotes nuclear retention of TR, and highlight the dual functionality of helix 12 in TR transactivation and nuclear export.
Next‐generation sequencing reveals unique combination of mutations in cis of CSF3R in atypical chronic myeloid leukemia
Authors: Yun Jae Won , Yoon Jung , Jung Chul Won , Lee Ki‐O , Kim Jong Won , Kim Sun‐Hee , Kim Hee‐Jin 
Published: November 2019

AbstractBackgroundAtypical chronic myeloid leukemia (aCML) is a hematologic disorder characterized by leukocytosis with increased dysplastic neutrophils and their precursors. In CSF3R gene, the activation mutation including T618I is frequently reported in aCML but is rarely accompanied by truncation mutations. Herein, we report a unique aCML patient with two CSF3R mutations (T618I and Y779*) in the same DNA strand.MethodsHigh‐coverage next‐generation sequencing for 40 genes related with myeloid leukemia was performed. Sanger sequencing was performed to confirm CSF3R mutations. To confirm whether two CSF3R mutations are in cis or not, TA cloning was used. Clinical information and bone marrow pathology were reviewed by two hematopathologists.ResultsIn the patient diagnosed with aCML in bone marrow study, two CSF3R mutations, (T618I and Y779*) a SETBP1 mutation (G870S) and an U2AF1 mutation (Q157P), were identified by high‐coverage next‐generation sequencing. The two CSF3R mutations were confirmed to be located in the same DNA strand by TA cloning, indicating that the two mutations are harbored in one malignant clone. The SETBP1 mutation is known to be related with poor prognosis in aCML. Likewise, the patient was refractory to hydroxyurea and showed disease progression. Additionally, we discussed the potential therapeutic targets by reviewing the molecular profile of the patient.ConclusionWe believe that the accurate diagnosis and maximum therapeutic chance could be achieved by profiling the mutations and their characteristics.
The role of relationship proximity to witnessed community violence and youth outcomes
Authors: Elsaesser Caitlin , Kennedy Traci M. , Tredinnick Lorin 
Published: November 2019

AbstractAimsThis study examines whether the relational proximity to the victim or perpetrator of witnessed community violence is associated with youth symptoms.MethodsData come from the Longitudinal Studies of Child Abuse and Neglect, a national high‐risk sample. The sample included 12‐year‐old youth (N = 720) who had witnessed violence in their lifetimes. Ordinary least squares (OLS) regressions tested whether relationship proximity differentiated youth functioning (social competency, withdrawal, anxiety/depression, delinquency, and aggression), and whether gender moderated these effects.ResultsWitnessing violence toward a parent was associated with greater withdrawal, delinquency, and aggression symptoms. Witnessing violence perpetrated by a stranger was associated with lower social competency, higher anxiety/depression, and higher delinquency. Two perpetrator associations differed by gender.ConclusionFindings suggest important differences in outcomes based on relational proximity to victims and perpetrators. The particularly widespread associations between witnessing violence against a parent and youth functioning underscore the importance of targeting interventions toward youth with parent victims.
Mesenchymal stem cells as carrier of the therapeutic agent in the gene therapy of blood disorders
Authors: Shomali Navid , Gharibi Tohid , Vahedi Ghasem , Mohammed Rebar N. , Mohammadi Hamed , Salimifard Sevda , Marofi Faroogh 
Published: November 2019

AbstractNonhematopoietic stem cells as a delivery platform of therapeutic useful genes have attracted widespread attention in recent years, owing to gained a long lifespan, easy separation, high proliferation, and high transfection capacity. Mesenchymal stem/stromal cells (MSCs) are the choice of the cells for gene and cell therapy due to high self‐renewal capacity, high migration rate to the site of the tumor, and with immune suppressive and anti‐inflammatory properties. Hence, it has a high potential of safety genetic modification of MSCs for antitumor gene expression and has paved the way for the clinical application of these cells to target the therapy of cancers and other diseases. The aim of gene therapy is targeted treatment of cancers and diseases through recovery, change, or enhancement cell performance to the sustained secretion of useful therapeutic proteins and induction expression of the functional gene in intended tissue. Recent developments in the vectors designing leading to the increase and durability of expression and improvement of the safety of the vectors that overcome a lot of problems, such as durability of expression and the host immune response. Nowadays, gene therapy approach is used by MSCs as a delivery vehicle in the preclinical and the clinical trials for the secretion of erythropoietin, recombinant antibodies, coagulation factors, cytokines, as well as angiogenic inhibitors in many blood disorders like anemia, hemophilia, and malignancies. In this study, we critically discuss the status of gene therapy by MSCs as a delivery vehicle for the treatment of blood disorders. Finally, the results of clinical trial studies are assessed, highlighting promising advantages of this emerging technology in the clinical setting.
Astrocyte elevated gene 1 (AEG‐1) promotes anoikis resistance and metastasis by inducing autophagy in hepatocellular carcinoma
Authors: Zhu Hai‐Dan , Liu Lian , Deng Huan , Li Zheng‐Bo , Sheng Jia‐Qi , He Xing‐Xing , Tian De‐An , Li Pei‐Yuan 
Published: November 2019

AbstractAstrocyte elevated gene 1 (AEG‐1) is overexpressed in hepatocellular carcinoma (HCC) and is strongly associated with tumor metastasis. Anoikis resistance and autophagy may play an important role in the survival of circulating tumor cells. However, the relationship among AEG‐1, anoikis resistance, autophagy, and metastasis in HCC is still not clear. The results of this study indicate that AEG‐1 expression is increased in HCC cell lines grown in suspension culture. AEG‐1 could enhance anoikis resistance to promote the survival of detached HCC cells. Moreover, the anoikis resistance appears to be partly dependent on autophagy. Regulating AEG‐1 expression changed the autophagy levels to modulate anoikis resistance, likely acting via the protein kinase RNA‐like ER kinase (PERK)‐eIF2α‐ATF4‐CHOP signaling axis. Finally, inhibiting autophagy by RNA interference prevented the AEG‐1‐promoted metastasis of HCC xenografts to the liver and lungs of nude mice. Taken together, AEG‐1 is a key contributor to anoikis resistance and metastasis by inducing autophagy in vitro and in vivo, and it may be a potential target for therapeutic intervention in HCC.
Diagnostic and prognostic significance of serum miRNA‐146‐a expression in Egyptian children with sepsis in a pediatric intensive care unit
Authors: Karam Rehab A. , Zidan Haidy E. , Karam Nehad A. , Abdel Rahman Doaa M. , El‐Seifi Omnia S. 
Published: November 2019

AbstractBackgroundPrevious studies have suggested a strong genetic effect on sepsis pathogenesis. The present study aimed to investigate the role of miRNA‐146‐a expression in pediatric sepsis.MethodsThe study included 55 pediatric sepsis patients and 60 control children of the same age and sex. Serum miRNA‐146‐a expression was measured using a quantitative real‐time polymerase chain reaction. C‐reactive protein, interleukin‐6, tumor necrosis factor‐α and procalcitonin levels were measured by an enzyme‐linked immunosorbent assay. The outcome of the pediatric sepsis group was determined at 28 days of follow up.ResultsThe results obtained revealed that serum miRNA‐146‐a levels were significantly decreased in sepsis group compared to the control group. Serum level of miRNA‐146a correlated with sepsis severity, with the pediatric septic shock group having the lowest level, followed by the severe sepsis and sepsis groups. The miRNA‐146‐a level could indicate sepsis (area under curve = 0.803). Serum miRNA‐146‐a expression was negatively associated with C‐reactive protein, pro‐calcitonin, interleukin‐6 and tumor necrosis factor‐α. Patients with miRNA‐146‐a at a level lower than 0.4 had an increased mortality rate.ConclusionsmiRNA‐146‐a is of significant diagnostic and prognostic value in pediatric sepsis and could be used for planning therapeutic strategies.
MiR‐6838‐5p suppresses cell metastasis and the EMT process in triple‐negative breast cancer by targeting WNT3A to inhibit the Wnt pathway
Authors: Liu Guozhu , Wang Ping , Zhang Hao 
Published: November 2019

AbstractBackgroundTriple‐negative breast cancer (TNBC) has become a common tumor that harms women's physical and mental health, as characterized by a relatively rapid recurrence and a high incidence of brain metastasis. Research increasingly suggests that microRNAs play key roles in the progress of TNBC. However, the function of miR‐6838‐5p in TNBC has not yet been reported, and requires additional exploration.MethodsIn the present study, we uncovered miR‐6838‐5p expression in TNBC cells via a quantitative reverse transcriptase‐polymerase chain reaction. Functionally, the impacts of up‐regulated or down‐regulated miR‐6838‐5p on TNBC invasiveness, Wnt pathway activation and epithelial–mesenchymal transition (EMT) were investigated via transwell and western blot assays. Mechanical analyses were utilized to unmask the miR‐6838‐5p mechanism in TNBC, including luciferase reporter, western blot and RIP assays. Rescue assays manifested the miR‐6838‐5p/WNT3A network in TNBC invasiveness through the Wnt pathway.ResultsUnder‐expressed miR‐6838‐5p was found in TNBC cells. Up‐regulation of miR‐6838‐5p suppressed TNBC cell invasion, migration and blockade of the Wnt pathway. However, down‐regulation of miR‐6838‐5p led to opposite results. Furthermore, we found, via luciferase reporter, western blot and RIP assays, that miR‐6838‐5p could bind with WNT3A and negatively regulate WNT3A expression. Through rescue experiments, we demonstrated that the overexpression of WNT3A partially rescued the miR‐6838‐5p overexpression‐mediated inhibitory effect, and knockdown of WNT3A partially rescued the miR‐6838‐5p suppression‐mediated promotive effect on the progression of TNBC.ConclusionsIn summary, the results of the present study indicate that miR‐6838‐5p suppresses cell proliferation, metastasis and the EMT process in TNBC by targeting WNT3A to inhibit the Wnt pathway, which may provide a new insight into the therapeutic strategies of TNBC.
Immunological recovery failure in cART-treated HIV-positive patients is associated with reduced thymic output and RTE CD4+ T cell death by pyroptosis
Authors: Carvalho-Silva Wlisses Henrique Veloso , Andrade-Santos José Leandro , Souto Fabrício Oliveira , Coelho Antonio Victor Campos , Crovella Sergio , Guimarães Rafael Lima 
Published: November 2019

Abstract
Despite more than three decades of studies and advances in combination antiretroviral therapy (cART) against human immunodeficiency virus (HIV), the mechanisms that precisely determine immune reconstitution failure have not been completely elucidated yet. Thus, this study aimed to investigate the thymic function, immune activation, and cell death by pyroptosis and apoptosis in virologically suppressed HIV-positive patients receiving cART. Immunophenotyping analyses were performed in 57 cART-treated HIV-infected patients with undetectable plasma viral load, who were classified as immunological nonresponders (INR = 29) and immunologic responders (IR = 28). Sociodemographic and clinical data were also assessed from medical records. Twelve healthy volunteers were also included in this study. The INR showed lower pretreatment CD4+ T cell count that remained low even after 1 yr of treatment, lower CD4/CD8 ratio, lower percentage of recent thymic emigrant (RTE) CD4+ T cell (CD45RA+CD31+) and naïve CD4+ T cell (CD45RA+CD62L+), higher levels of effector memory CD4+ T cells (CD45RA-CD62L-), and higher pyroptosis levels of RTE CD4+ T cells (CD31+FLICA-Caspase1+) when compared with IR. Our findings indicate that reduced thymic function and RTE CD4+ T cell death by pyroptosis are the major mechanisms of immunological recovery failure in HIV-infected patients receiving cART.
Optimization of a minimal sample preparation protocol for imaging mass spectrometry of unsectioned juvenile invertebrates
Authors: Zink Katherine E. , Tarnowski Denise A. , Mandel Mark J. , Sanchez Laura M. 
Published: November 2019

AbstractTissue sections have long been the subject matter for the application of imaging mass spectrometry, but recently the technique has been adapted for many other purposes including bacterial colonies and 3D cell culture. Here, we present a simple preparation method for unsectioned invertebrate tissue without the need for fixing, embedding, or slicing. The protocol was used to successfully prepare a Hawaiian bobtail squid hatchling for analysis, and the resulting data detected ions that correspond to compounds present in the host only during its symbiotic colonization by Vibrio fischeri.
Two‐dimensional FIR filters model order reduction and frequency transformation: Maximum error invariance
Authors: Bouhamla Lakhdar , Adamou‐Mitiche Amel Baha Houda , Mitiche Lahcène 
Published: November 2019

AbstractThis paper presents a numerical study of the maximum error in model order reduction (MOR) for finite impulse response (FIR) 2‐D digital filter under frequency transformation, which is based on the Roesser state‐space formulation. This study discuss the maximum error obtained from the 2‐D balanced truncation method after and before using the frequency transformation. Several numerical examples are realized to show the invariant of the maximum error in all frequency transformation cases (single variable, two‐variable, and hybrid variable transformations).
Effect of nitrogen deficiency on the physiology and biochemical composition of microalga Scenedesmus rotundus‐MG910488
Authors: Dixit Rishibha , Singh Surendra , Singh Ajeet 
Published: November 2019

AbstractThe present investigation ascertains the impact of gradient concentrations of sodium nitrate on the physiology and biochemical composition of isolated microalga Scenedesmus rotundus‐MG910488. The concentrations of nitrate were selected as 0, 3.5, 7.0, 10.5, 14.0, and 17.6 mM/L in BG11 medium. The lower concentrations of nitrogen were found to be significantly decreasing the cell count and photosynthetic activity in the microalga as well as changing cell morphology. The amount of biomass, its productivity and lipid yield were significantly affected. The highest biomass of 689.15 ± 14.27 mg/L was achieved in the concentration of 17.6 mM/L with the biomass productivity of 38.28 ± 0.78 mg/L. The highest lipid accumulation of 41.46 ± 1.94% dry‐cell weight was obtained at a concentration of 3.5 mM/L, whereas the lowest lipid accumulation of 29.22 ± 1.65% at the concentration of 17.6 mM/L sodium nitrate. The fatty acid composition determines the quality of the fuel, so the characterization of fatty acid methyl esters (FAMEs) was performed by GC, and the assessment of methyl esters of fatty acid confirmed the existence of palmitic acid, oleic acid, and linoleic acid, which are essential components suitable for biodiesel production. FTIR confirms the presence of FAME components by estimating the bending and stretching of functional groups.
Endoscopic Sealing With a Polyglycolic Acid Sheet for Restoration of Vocal Fold Mucosa in Dogs
Authors: Mihashi Ryota , Chitose Shun‐ichi , Sato Fumihiko , Tanaka Hisaichiro , Sato Kiminori , Ono Takeharu , Fukahori Mioko , Sueyoshi Shintaro , Kurita Takashi , Sato Kiminobu , Umeno Hirohito 
Published: November 2019

Objectives/HypothesisVoice outcomes of cordectomy for early glottic cancer are often poor due to vocal fold scarring and tissue defects. Improvements in this aspect could make cordectomy a more acceptable treatment option than radiotherapy. We hypothesized that a polyglycolic acid (PGA) sheet could be used to cover vocal fold defects. The present study aimed to prevent vocal fold scarring after cordectomy using the PGA sheet.Study DesignAnimal experiment.MethodsNine male beagles were divided into three groups including a control group (n = 3). Following cordectomy, the vocal fold defect was covered with the PGA sheet plus fibrin glue (PGA group; n = 3) or with the PGA sheet plus fibrin glue containing basic fibroblast growth factor (bFGF; the PGA‐bFGF group, n = 3). Vocal folds were chronologically observed, and larynges were removed 6 months after surgery. Mucosal amplitude was measured using a high‐speed camera, and histological analysis was performed.ResultsThe re‐epithelialization process was delayed in the PGA and PGA‐bFGF groups compared with the control group. The mucosal amplitude was significantly more normalized and the thickness ratio significantly higher in the PGA and PGA‐bFGF groups compared with the control group. The PGA‐bFGF group had the highest elastic fiber density, followed by the PGA group and then the control group, with a significant difference between the PGA‐bFGF and control groups.ConclusionsThe PGA sheet plus fibrin glue could serve as an effective regenerative scaffold for reconstructing vocal fold morphology and function after cordectomy, with the potential benefit of establishing an endoscopic sealing method for vocal fold defects.Level of EvidenceNALaryngoscope, 130:E436–E443, 2020