bluuebunny/crossref_metadata_2025_split huggingface dataset:
Masseter corticomotor excitability is decreased after intramuscular administration of nerve growth factor
Authors: Costa Yuri M. , Exposto Fernando G. , Kothari Mohit , Castrillon Eduardo E. , Conti Paulo César R. , Bonjardim Leonardo R. , Svensson Peter 
Published: June 2019

AbstractBackgroundQuantification of motor‐evoked potentials (MEPs) can contribute to better elucidate the central modulation of motor pathways in response to nociceptive inputs. The primary aim of this study was to assess the modulatory effects of nerve growth factor (NGF) injection on masseter corticomotor excitability.MethodsThe healthy participants of this randomized, double blind placebo‐controlled experiment were assigned to have injected into the right masseter muscle either NGF (n = 25) or isotonic saline (IS, n = 17). The following variables were assessed at baseline and 48 hr after the injection: right masseter MEP amplitude and corticomotor mapping and clinical assessment of jaw pain intensity and function. Repeated Measures ANOVA was applied to the data.ResultsNGF caused jaw pain and increased jaw functional disability after the injection (p < 0.050). Also, the participants in the NGF group decreased the MEP amplitude (p < 0.001) but the IS group did not present any significant modulation after the injection (p > 0.050). Likewise, the participants in the NGF group reduced corticomotor map area and volume (p < 0.001), but the IS group did not show any significant corticomotor mapping changes after the injection (p > 0.050). Finally, there was a significant correlation between the magnitude of decreased corticomotor excitability and jaw pain intensity on chewing 48 hr after the NGF injection (r = −0.51, p = 0.009).ConclusionNGF‐induced masseter muscle soreness can significantly reduce jaw muscle corticomotor excitability, which in turn is associated with lower jaw pain intensity and substantiates the occurrence of central changes that most likely aim to protect the musculoskeletal orofacial structures.SignificanceIntramuscular administration of nerve growth factor into masseter muscle causes inhibitory corticomotor plasticity, which likely occurs to prevent further damage and seems associated with lower pain intensity on function.
Associations between pain thresholds for heat, cold and pressure, and Pain Sensitivity Questionnaire scores in healthy women and in women with persistent pelvic pain
Authors: Grundström Hanna , Larsson Britt , Arendt‐Nielsen Lars , Gerdle Björn , Kjølhede Preben 
Published: June 2019

AbstractBackgroundThe Pain Sensitivity Questionnaire (PSQ) is a self‐rating instrument developed as a time‐ and cost‐saving alternative to quantitative sensory testing (QST). The aims of the study were to assess (a) the associations between PSQ scores and QST in women with persistent pelvic pain and in pain‐free controls and (b) to what extent demographic variables and psychological distress influenced PSQ scores.MethodsFifty‐five healthy women and 37 women with persistent pelvic pain participated. All filled in the PSQ and Hospital Anxiety and Depression Scale and had QST (heat, cold and pressure pain thresholds) performed on six locations on the body. Information on age, body mass index, smoking habits and pain duration were collected. Principal component analysis and orthogonal partial least square regressions were used.ResultsThe patients scored significantly higher on PSQ than the controls. Significant multivariate correlations between pain thresholds and PSQ scores were found only in the patient group. In the patient group, the heat and cold pain thresholds correlated more strongly with PSQ scores than the pressure pain threshold.ConclusionsThe PSQ score was significantly higher in pelvic pain patients, and correlations between QSTs and the PSQ were only found for patients.SignificanceThe PSQ reflects pain sensitivity in women with PPP and can be used as a non‐invasive and painless way to assess this condition in clinical practice.
Recent Ecosystem Disturbance in the Northern California Current
Authors: Morgan Cheryl A , Beckman Brian R , Weitkamp Laurie A , Fresh Kurt L 
Published: June 2019

Abstract
An extended marine heat wave occurred across the North Pacific during 2014–2016, including the formation of the warm “Blob” followed by a strong El Niño in 2016. Coincident with this marine heat wave, we documented unprecedented biological changes in plankton and nekton in the Northern California Current (NCC) within pelagic surveys conducted over 20 years (1998–2017). The recent warm period was dominated by warmwater gelatinous invertebrates and fishes, some of which were previously either extremely rare or absent. Mixing of organisms originating from more southern or western regions with those previously present in the NCC may have resulted in novel and unpredictable trophic interactions that produced some of the observed changes in relative abundance. Continued long-term monitoring is needed to determine whether this is a temporary ecosystem disturbance or a fundamental change in the very productive NCC upwelling region.
Verifying the impact of corporate governance on hospital performance on HIV and malaria control: A structural equation modelling approach
Authors: Afriyie Stephen Owusu , Kong Yusheng , Ampimah Benjamin Chris , Akuamoah Collins Danso , Vanderpuije Leslie Nii Otu , Xinlei Zhao 
Published: June 2019

SummaryBackgroundThe research aims to study the impact of corporate governance on hospital performance regarding HIV and malaria control, using the Ghana health industry as a case. The nation is making frantic effort to control HIV and malaria, since they continue to be among the deadliest diseases that attract holistic attention; hence, there is the need to put structures in place to curb the spread.MethodsA total of 1005 precoded questionnaires were administered to 125 hospitals, for responses from staff, managers, board, and chief executive officers (CEOs). The collated data were analysed using structural equation modelling approach.ResultsOur research revealed that corporate governance has a positive effect on hospital performance, regarding the control of the two deadly diseases (HIV and malaria). The interventions in Ghana health delivery have brought a level of improvement in malaria control, since the disease mortality has significantly declined from 19% in 2010 to 4% in 2016. Through the implementation of systems and policies, the national HIV prevalence has admirably reduced from 2.9% in 2000 to 1.6% in 2017.ConclusionsHospitals are therefore encouraged to continue to implement effective corporate governance mechanisms to facilitate efficient, well‐organised, and prudent practices that can deliver more institutional performance in HIV and malaria control.
Class I and II aminoacyl‐tRNA synthetase tRNA groove discrimination created the first synthetase–tRNA cognate pairs and was therefore essential to the origin of genetic coding
Authors: Carter Charles W. , Wills Peter R. 
Published: June 2019

AbstractThe genetic code likely arose when a bidirectional gene replicating as a quasi‐species began to produce ancestral aminoacyl‐tRNA synthetases (aaRS) capable of distinguishing between two distinct sets of amino acids. The synthetase class division therefore necessarily implies a mechanism by which the two ancestral synthetases could also discriminate between two different kinds of tRNA substrates. We used regression methods to uncover the possible patterns of base sequences capable of such discrimination and find that they appear to be related to thermodynamic differences in the relative stabilities of a hairpin necessary for recognition of tRNA substrates by Class I aaRS. The thermodynamic differences appear to be exploited by secondary structural differences between models for the ancestral aaRS called synthetase Urzymes and reinforced by packing of aromatic amino acid side chains against the nonpolar face of the ribose of A76 if and only if the tRNA CCA sequence forms a hairpin. The patterns of bases 1, 2, and 73 and stabilization of the hairpin by structural complementarity with Class I, but not Class II, aaRS Urzymes appear to be necessary and sufficient to have enabled the generation of the first two aaRS–tRNA cognate pairs, and the launch of a rudimentary binary genetic coding related recognizably to contemporary cognate pairs. As a consequence, it seems likely that nonrandom aminoacylation of tRNAs preceded the advent of the tRNA anticodon stem‐loop. Consistent with this suggestion, coding rules in the acceptor‐stem bases also reveal a palimpsest of the codon–anticodon interaction, as previously proposed. © 2019 IUBMB Life, 2019 © 2019 IUBMB Life, 71(8):1088–1098, 2019
Determination of the metabolic index using the fluorescence lifetime of free and bound nicotinamide adenine dinucleotide using the phasor approach
Authors: Ranjit Suman , Malacrida Leonel , Stakic Milka , Gratton Enrico 
Published: June 2019

AbstractThe fluorescence lifetime of nicotinamide adenine dinucleotide (NADH) is commonly used in conjunction with the phasor approach as a molecular biomarker to provide information on cellular metabolism of autofluorescence imaging of cells and tissue. However, in the phasor approach, the bound and free lifetime defining the phasor metabolic trajectory is a subject of debate. The fluorescence lifetime of NADH increases when bound to an enzyme, in contrast to the short multiexponential lifetime displayed by NADH in solution. The extent of fluorescence lifetime increase depends on the enzyme to which NADH is bound. With proper preparation of lactate dehydrogenase (LDH) using oxalic acid (OA) as an allosteric factor, bound NADH to LDH has a lifetime of 3.4 ns and is positioned on the universal semicircle of the phasor plot, inferring a monoexponential lifetime for this species. Surprisingly, measurements in the cellular environments with different metabolic states show a linear trajectory between free NADH at about 0.37 ns and bound NADH at 3.4 ns. These observations support that in a cellular environment, a 3.4 ns value could be used for bound NADH lifetime. The phasor analysis of many cell types shows a linear combination of fractional contributions of free and bound species NADH.
ARPC4 promotes bladder cancer cell invasion and is associated with lymph node metastasis
Authors: Xu Ning , Qu Gen‐Yi , Wu Yu‐Peng , Lin Yun‐Zhi , Chen Dong‐Ning , Li Xiao‐Dong , Chen Shao‐Hao , Huang Jin‐Bei , Zheng Qing‐Shui , Xue Xue‐Yi , Wei Yong 
Published: June 2019

AbstractThe significance of actin‐related protein 2/3 complex subunit 4 (ARPC4) expression in bladder cancer, and its potential role in the invasion and migration of bladder cancer cells, has yet to be determined. This study was to identify the correlation between ARPC4 and lymph node metastasis, and to determine the role of ARPC4 in the invasive migration of T24 bladder cancer cells. One hundred and ninety‐eight bladder cancer tissues and 40 normal bladder and lymph node tissues were examined. Tissue microarrays were constructed and subjected to immunohistochemical stating for ARPC4. Multiple logistic analysis was used to determine risk factors associated with bladder cancer metastasis. ARPC4 expression in T24 bladder cancer cells was suppressed using small interfering RNA and changes in protein levels were determined by Western blot analysis. The proliferation of bladder cancer cells after knocking down of ARPC4 was determined by cell counting kit‐8. The effects of ARPC4 knockdown on T24 cell invasion and migration was determined using transwell and wound healing assays. Immunofluorescence analysis was performed to examine changes in pseudopodia formation and actin cytoskeleton structure. The expression of ARPC4 was elevated in bladder cancer tissues than normal tissues (84.3% vs 27.5%, P < 0.001). The multivariate logistic analysis demonstrated that the level of ARPC4, as a risk factor, was correlated with lymphatic metastasis (P < 0.05). ARPC4 knockdown attenuated proliferation, migration, invasion, and pseudopodia formation in T24 cells. ARPC4 expression, as a risk factor, is associated with lymphatic metastasis and is upregulated in bladder cancer tissues in comparison with normal tissues. Inhibition of ARPC4 expression significantly attenuates the proliferation, migration, and invasion of bladder cancer cell, possibly due to defects in pseudopodia formation.
Propofol induces impairment of mitochondrial biogenesis through inhibiting the expression of peroxisome proliferator–activated receptor‐γ coactivator‐1α
Authors: Qin Jing , Li Yizhen , Wang Kai 
Published: June 2019

AbstractPropofol is a commonly used general anesthetic in patient care. Recent studies have shown that propofol has neurological side effects especially in young children, which raises a concern regarding the safety of its use. We explored the effects of the molecular mechanism of propofol on neuronal mitochondrial function in SH‐SY5Y cells. Our results demonstrate that clinically relevant doses of propofol reduce the expression of peroxisome proliferator–activated receptor‐γ coactivator‐1α (PGC‐1α) in a dose‐ and time‐dependent manner. At a concentration of 2%, propofol suppresses the mitochondrial regulator nuclear respiratory factor 1 and mitochondrial transcription factor A and impairs neuronal mitochondrial biogenesis. These impairments involve reduction of mitochondrial mass and reduction of the ratio of mitochondrial to nuclear DNA as well as reduction of cytochrome C oxidase activity. Propofol treatment reduces intracellular adenosine triphosphate (ATP) production, the mitochondrial respiratory rate, and increases mitochondrial reactive oxygen species production, implying that it disturbs neuronal mitochondrial function. Overexpression of PGC‐1α rescued propofol‐induced reduced mitochondrial mass, ATP production, and respiratory rate, indicating that PGC‐1α is the mediator of the effect of propofol on mitochondrial function. Finally, we demonstrate that propofol suppresses PGC‐1α by inhibiting cAMP‐response element binding protein (CREB) activation and promoting PKA RI expression, and the addition of cyclic adenosine monophosphate rescues propofol‐mediated reduced PGC‐1α. In conclusion, PGC‐1α is the central mediator of propofol‐induced impairment of mitochondrial biogenesis and neuronal mitochondrial dysfunction. Our study demonstrates the molecular mechanism behind propofol‐induced neurotoxicity and provides valuable information regarding its side effects in clinical practice.
Overexpression of LINC00261 inhibits non–small cell lung cancer cells progression by interacting with miR‐522‐3p and suppressing Wnt signaling
Authors: Shi Jingli , Ma Huimin , Wang Huaixi , Zhu Weiyan , Jiang Shuting , Dou Rui , Yan Beizhan 
Published: June 2019

AbstractLong noncoding RNA LINC00261 has been experimentally validated to function as a tumor suppressor in several cancers, but its pathological role and functional mechanism in non–small cell lung cancer (NSCLC) are largely unclear. In this study, LINC00261 was delineated in NSCLC to be significantly downregulated in cancer tissues compared with corresponding adjacent normal tissues. Low expression of LINC00261 predicted worse survival for patients with NSCLC. Overexpression of LINC00261 in NSCLC cell lines inhibited cell proliferation and invasion, meanwhile promoted apoptosis. Subcellular fractionation assay showed that LINC00261 existed mainly in the cytoplasm of NSCLC A549 cells and luciferase assay validated its direct interaction with miR‐522‐3p. Overexpression of miR‐522‐3p significantly ameliorated suppressive effects of LINC00261 on proliferation and invasion of NSCLC cells. Besides, miR‐522‐3p was found to be able to directly combine with the 3′‐untranslated region of SFRP2, which was generally regarded as a suppressor of Wnt signaling. Further quantitative reverse transcription polymerase chain reaction and Western blot experiments showed that LINC00261 upregulation potentiated the expression of SFRP2 and inhibited Wnt signaling pathway, which could both be reversely modulated by miR‐522‐3p. Taken together, our study demonstrated that LINC00261 suppressed NSCLC cells progression via sponging miR‐522‐3p and inhibiting Wnt signaling. These results supported us to better understand the pathogenic mechanism of NSCLC and revealed a potential molecular target for this fatal disease.
Retracted: miR‐124a enhances therapeutic effects of bone marrow stromal cells transplant on diabetic nephropathy‐related epithelial‐to‐mesenchymal transition and fibrosis
Authors: Cai Xiaojun , Wang Lei , Wang Xuling , Hou Fengyan 
Published: June 2019

AbstractBackgroundEpithelial‐to‐mesenchymal transition (EMT) has been gradually considered as one of the major pathways that causes the production of interstitial myofibroblasts in diseased kidneys.Materials and MethodsThe study was done to investigate the effect of a bone marrow stromal cell (BMSCs) transplant on rat podocytes and diabetic nephropathy (DN) rats in high‐glucose concentration, and to explore the effect of miR‐124a on BMSC therapy. High glucose–injured podocytes and streptozotocin‐induced DN rats have been respectively used as injury models in in vitro and in vivo studies. Podocyte viability was measured using the Cell Counting Kit‐8 assay. Renal pathological examination was observed by HE staining and Masson staining. The messenger RNA and protein levels were determined via real‐time polymerase chain reaction and Western blotting, respectively.ResultsBy mediating the activation of caveolin‐1 (cav‐1) and β‐catenin and affecting the expression levels of EMT biomarkers including p‐cadherin, synaptopodin, fibroblast‐specific protein‐1, α‐smooth muscle actin and snail, our in vitro study confirmed that miR‐124a played a significant role in the treatment of high glucose–induced podocyte injury by BMSCs. The therapeutic effects of the BMSC transplant on DN rats were also proved to be further enhanced by miR‐124a overexpression in BMSCs, and such a phenomenon was accompanied by the improvement of renal fibrosis and mitigation of DN‐related kidney impairment. Regulation of fibronectin, collagen1, and EMT‐related proteins was closely implicated with the mechanism, and the activation of cav‐1 and β‐catenin was also possibly involved.ConclusionThe study demonstrated the pivotal effect of miR‐124a on BMSC therapy for DN rats via mitigating EMT and fibrosis. Our results provide a novel insight into how therapeutic effects of BMSCs can be improved at the posttranscriptional level.
Downregulation of HDAC3 by ginsenoside Rg3 inhibits epithelial–mesenchymal transition of cutaneous squamous cell carcinoma through c‐Jun acetylation
Authors: Zhang Li , Shan Xiu , Chen Qun , Xu Dayu , Fan Xinling , Yu Ming , Yan Qiu , Liu Jiwei 
Published: June 2019

AbstractThe metastatic rate of human cutaneous squamous cell carcinoma (CSCC) has increased in recent years. Despite the current advances in therapies, effective treatments remain lacking. Ginsenoside 20(R)‐Rg3 is an effective antitumor monomer extracted from ginseng, but the role of Rg3 in CSCC remains unknown. It has been reported that aberrantly elevated histone deacetylase 3 (HDAC3) is involved in tumor malignancy in multiple malignant tumors. However, the effects of HDAC3 on the regulation of c‐Jun acetylation in tumor epithelial–mesenchymal transition (EMT) and migration have not been clearly illuminated. In our research, the immunohistochemistry staining results of skin tissue microarrays showed that HDAC3 staining was increased in CSCC compared with the normal dermal tissue. Then, we found that Rg3 treatment (25 and 50 μg/ml) inhibited CSCC cell (A431 and SCC12 cells) EMT through increasing E‐cadherin and decreasing N‐cadherin, vimentin, and Snail expression. Wound‐healing and transwell assays showed that Rg3 could inhibit migration. Meanwhile, Rg3 significantly downregulated the expression of HDAC3 in CSCC cells as detected by real‐time quantitative PCR, western blot, and immunofluorescence. Importantly, c‐Jun acetylation was increased by the downregulation of HDAC3 with HDAC3 shRNA, and the downregulation was associated with CSCC cell EMT inhibition. Collectively, our results showed that downregulation of HDAC3 by Rg3 or shHDAC3 treatment resulted in c‐Jun acetylation, which in turn inhibited CSCC cell EMT. These results indicate that HDAC3 could potentially serve as a therapeutic target therapeutic target for CSCC. Rg3 is an attractive and efficient agent that has oncotherapeutic effects and requires further investigation.
Retracted: LncRNA‐ROR alleviates hypoxia‐triggered damages by downregulating miR‐145 in rat cardiomyocytes H9c2 cells
Authors: Wang Pengxi , Yuan Yanran 
Published: June 2019

AbstractChronic hypoxic heart disease (CHD) is a common clinical type of congenital heart disease. Long noncoding RNA regulator of reprogramming (lncRNA‐ROR) exerts an important regulating effect in cardiovascular diseases. In our study, we explored the effect of lncRNA‐ROR and the possible mechanisms against hypoxia‐caused apoptosis in H9c2 cells. H9c2 cells were exposed to hypoxia (1% O2) to construct the in vitro model of CHD. The level of lncRNA‐ROR and microRNA (miRNA/miR)‐145 was detected. To upregulate the level of lncRNA‐ROR and miR‐145, transfection was carried out. Western blot assay was performed to quantified protein expression. The interaction of lncRNA‐ROR with miR‐145 was verified by RIP and Dual‐luciferase reporter assays. The expression of p53 and Bax was largely elevated and Bcl‐2 was suppressed by hypoxia induction. We found that lncRNA‐ROR was elevated by hypoxia. LncRNA‐ROR overexpression was able to relieve the damages of H9c2 cells induced by hypoxia through rescuing viability, suppressing apoptosis, and blocking Cytochrome c release. miR‐145 was suppressed by overexpressed lncRNA‐ROR and the combination of miR‐145 mimic was able to abolish the protective effect of lncRNA‐ROR. Moreover, we found that lncRNA‐ROR activated Ras/Raf/MEK/ERK and PI3K/AKT transduction cascades by suppressing miR‐145. Besides, lncRNA‐ROR directly targeted miR‐145 and negatively modulated the level of miR‐145. Our present study revealed that lncRNA‐ROR protected H9c2 cells against hypoxia‐caused damages by regulation of miR‐145 through activating Ras/Raf/MEK/ERK and PI3K/AKT.
miR‐4429 sensitized cervical cancer cells to irradiation by targeting RAD51
Authors: Sun Hongbo , Fan Guimei , Deng Chunxia , Wu Lin 
Published: June 2019

AbstractCervical cancer (CC) is a prevalent malignancy in women, with the feature of metastasis and easy recurrence is responsible for a large proportion of global cancer deaths. Radiotherapy is one of the common treatment tools for CC patients with unresectable tumors. However, radio‐resistance in patients could be a major reason for recurrence. Therefore, it is of significance to tunnel the molecular mechanism of radio‐resistance in CC. MicroRNAs (miRNAs) are increasingly reported in the regulation of cancer progression and cellular response to radiotherapy and chemotherapy. miR‐4429 is a newly discovered miRNA acting as a tumor‐suppressor gene in multiple cancers, but its function in CC has never been explored yet. The current study tried to explore the role of miR‐4429 in cell radio‐sensitivity in CC. First, we validated the downregulation of miR‐4429 in CC cells. Importantly, the association of miR‐4429 with radio‐resistance was validated by identifying the downregulation of miR‐4429 in radio‐resistant CC cells. Gain‐ and loss‐of‐function assays validated that miR‐4429 sensitized CC cells to irradiation. Through bioinformatics tools, RAD51 recombinase (RAD51) was identified to be a target for miR‐4429. RAD51 is known to be a crucial regulator for DNA damage repair and has been reported to influence cell radio‐resistance in cancers, including in CC. Luciferase reporter assay confirmed the interaction between miR‐4429 and RAD51. Finally, rescue assays indicated that miR‐4429 promoted CC cell radio‐sensitivity through RAD51. Consequently, our study showed that miR‐4429 sensitized CC cells to irradiation by targeting RAD51, providing a potential therapeutic target for CC patients.