bluuebunny/crossref_metadata_2025_split huggingface dataset:
MAPKs and NF‐κB‐mediated acrylamide‐induced neuropathy in rat striatum and human neuroblastoma cells SY5Y
Authors: Yan Dandan , Pan Xiaoqi , Yao Jianling , Wang Dun , Wu Xu , Chen Xiaoyi , Shi Nian , Yan Hong 
Published: October 2018

AbstractAcrylamide (ACR) is a potent neurotoxin that can be produced during high‐temperature food processing, but the underlying toxicological mechanism remains unclear. In this study, the detrimental effects of ACR on the striatal dopaminergic neurons and the roles of mitogen‐activated protein kinases (MAPKs) and nuclear factor κB (NF‐κB) in ACR‐induced neuronal apoptosis were investigated. Acute ACR exposure caused dopaminergic neurons loss and apoptosis as revealed by decreased tyrosine hydroxylase (TH)‐positive cells and TH protein level and increased terminal deoxynucleotidyl transferase dUTP nick‐end labeling (TUNEL)‐positive cells in the striatum. ACR‐decreased glutathione content, increased levels of malondialdehyde, proinflammatory cytokines tumor necrosis factor α, and interleukin 6. In addition, nuclear NF‐κB and MAPKs signaling pathway with c‐Jun N‐terminal kinase (JNK) and p38 were activated by ACR. Specific inhibitors were used to explore the roles of MAPKs and NF‐κB pathways in ACR‐induced apoptosis in SH‐SY5Y cells. Pretreatment with JNK‐specific inhibitors SP600125 markedly upregulated the reduced B‐cell lymphoma 2 (Bcl‐2) content and downregulated the increased Bcl‐2‐associated X protein (Bax) level and thereby eventually reduced the proportions of early and late apoptotic cells induced by ACR, while p38 suppression by SB202190 only reversed the decrease in Bcl‐2 expression. Inhibition of NF‐κB by BAY 11‐7082 markedly upregulated Bax level and decreased Bcl‐2 expression, and eventually increasing the proportions of neuronal apoptosis compared with that in ACR alone. These results suggested that JNK contributed to ACR‐induced apoptosis, while NF‐κB acted as a protective regulator in response to ACR‐induced neuropathy. This study helps to offer a deeper insight into the mechanism of ACR‐induced neuropathy.
MiR‐542‐3p controls hepatic stellate cell activation and fibrosis via targeting BMP‐7
Authors: Ji Feihong , Wang Kuifeng , Zhang Yu , Mao Xin‐Li , Huang Qin , Wang Jun , Ye Liping , Li Youming 
Published: October 2018

AbstractThere has been an increasing number of studies about microRNAs as key regulators in the development of hepatic fibrosis. Here, we demonstrate that miR‐542‐3p can promote hepatic fibrosis by downregulating the expression of bone morphogenetic protein 7 (BMP‐7), which is known to antagonize transforming growth factor β1 (TGFβ1)‐mediated fibrogenesis effect. The expression of miR‐542‐3p is increased in activated hepatic stellate cells (HSCs). Downregulation of MiR‐542‐3p by antisense inhibitors can inhibit HSCs activation markers, including α‐smooth muscle actin (α‐SMA) and collagen as well as TGFβ signaling pathways. MiR‐542‐3p was significantly upregulated in carbon tetrachloride (CCl4)‐induced hepatic fibrosis in mice, and downregulation of miR‐542‐3p by lentivirus could prevent the development of hepatic fibrosis. In addition, miR‐542‐3p can directly bind to the 3′‐untranslated region of BMP‐7 mRNA, indicating that its profibrotic effect appears to be caused by its inhibition of BMP‐7. Our results suggest that downregulation of miR‐542‐3p prevents liver fibrosis both in vitro and in vivo, highlighting its potential as a novel biomarker or therapeutic target for hepatic fibrosis.
New insight into BIRC3: A novel prognostic indicator and a potential therapeutic target for liver cancer
Authors: Fu Pei‐Yao , Hu Bo , Ma Xiao‐Lu , Yang Zhang‐Fu , Yu Min‐Cheng , Sun Hai‐Xiang , Huang Ao , Zhang Xin , Wang Jian , Hu Zhi‐Qiang , Zhou Chen‐Hao , Tang Wei‐Guo , Ning Ren , Xu Yang , Zhou Jian 
Published: October 2018

AbstractBackgroundPrognosis of hepatocellular carcinoma (HCC) remains poor due to high recurrence rate and ineffective treatment options, highlighting the need to better understand the mechanism of recurrence and metastasis in HCC.MethodsWe first collected messenger RNA (mRNA) expression data from 442 cases of HCC patients from The Cancer Genome Atlas (TCGA) database as well as 251 HCC patients from Zhongshan Hospital during 2009 and 2010 to analyze the expression pattern from tissue microarray (TMA) of baculoviral IAP repeat containing 3 (BIRC3). Then, we used BIRC3 gain‐of‐function (overexpression) and loss‐of‐function (knockdown) studies to examine the effect of BIRC3 on HCC cell proliferation and invasion. In addition, we also investigated the undying mechanism by which BIRC3 contributes to HCC tumor progression. Functionally, we also used a BIRC3‐specific inhibitor AT‐406 in HCC xenograft model to explore the potential therapeutic benefit of targeting BIRC3 in liver cancer.ResultsBIRC3 serves as a novel prognostic indicator for HCC patients undergoing curative resection. BIRC3 promotes HCC epithelial‐mesenchymal transition (EMT), cell migration, and metastasis via upregulating MAP3K7, therefore, inducing ERK1/2 phosphorylation. The specific BIRC3 inhibitor AT‐406 can inhibit HCC cell proliferation and reduce pulmonary metastases.ConclusionBIRC3 induces tumor proliferation and metastasis in vitro and in vivo. BIRC3 may serve as a novel therapeutic target for liver cancer.
Retracted: Propranolol suppresses HUVEC viability, migration, VEGF expression, and promotes apoptosis by downregulation of miR‐4295
Authors: Zhao Feng , Yang Xiaoliang , Xu Guangqi , Bi Jianhai , Lv Renrong , Huo Ran 
Published: October 2018

AbstractInfantile hemangioma (IH) is a common benign tumor. Human umbilical vein endothelial cells (HUVECs) have the potential of stem cells, which has been widely used in vascular endothelial cell experiments. Oral propranolol was first reported to treat hemangioma in 2008. However, the role of propranolol in IH remains unclear. Therefore, in this study, we investigated the effects of propranolol on HUVECs in vitro, to explore the underlying mechanism of propranolol in IH. HUVECs were treated with 0.15, 1.5, and 15 μM of propranolol, and transfected with microRNA‐4295 (miR‐4295) mimic. Cell viability, migration, and apoptosis were examined using Cell Counting Kit‐8, transwell assay, and flow cytometry analysis, respectively. In addition, the expressions and concentrations of miR‐4295, vascular endothelial growth factor (VEGF), VEGF‐A, FLT1, FLT2, and FOXF1 were assessed using real‐time polymerase chain reaction, Western blot assay, and enzyme‐linked immunosorbent assay. We found that 15 μM of propranolol decreased HUVEC viability the most. Then, cell migration and the concentrations of VEGF and VEGF‐A were reduced, and apoptosis was increased when treated with propranolol. Meanwhile, the expressions of VEGF, VEGF‐A, FLT1, FLT2, and FOXF1 were downregulated by propranolol exposure. Further study showed that miR‐4295 expression was upregulated in IH tissues, and propranolol treatment downregulated miR‐4295 expression in HUVECs. MiR‐4295 overexpression alleviated the reductions of viability, migration, and factors expression, as well as the increase of apoptosis. Propranolol suppressed HUVEC viability, migration, the expression of VEGF, VEGF‐A, FLT1/2, FOXF1, and promoted apoptosis via downregulation of miR‐4295. This study lays a foundation for further study of the effect of propranolol on IH.
Facile and greener hydrothermal honey‐based synthesis of Fe3O4/Au core/shell nanoparticles for drug delivery applications
Authors: Rasouli Elisa , Basirun Wan Jeffrey , Johan Mohd Rafie , Rezayi Majid , Darroudi Majid , Shameli Kamyar , Shanavaz Zohreh , Akbarzadeh Omid , Izadiyan Zahra 
Published: October 2018

AbstractIn the present research, we report a greener, faster, and low‐cost synthesis of gold‐coated iron oxide nanoparticles (Fe3O4/Au‐NPs) by different ratios (1:1, 2:1, and 3:1 molar ratio) of iron oxide and gold with natural honey (0.5% w/v) under hydrothermal conditions for 20 minutes. Honey was used as the reducing and stabilizing agent, respectively. The nanoparticles were characterized by X‐ray diffraction (XRD), UV‐visible spectroscopy, field emission scanning electron microscope (FESEM), energy‐dispersive X‐ray spectroscopy (EDXS), transmission electron microscopy (TEM), selected area electron diffraction (SAED), vibrating sample magnetometer (VSM), and fourier transformed infrared spectroscopy (FT‐IR). The XRD analysis indicated the presence of Fe3O4/Au‐NPs, while the TEM images showed the formation of Fe3O4/Au‐NPs with diameter range between 3.49 nm and 4.11 nm. The VSM study demonstrated that the magnetic properties were decreased in the Fe3O4/Au‐NPs compared with the Fe3O4‐NPs. The cytotoxicity threshold of Fe3O4/Au‐NPs in the WEHI164 cells was determined by using the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay. It was demonstrated no significant toxicity in higher concentration up to 140.0 ppm which can become the main candidates for biological and biomedical applications, such as drug delivery.
Association of MCP‐1 promoter polymorphism with susceptibility to nasopharyngeal carcinoma
Authors: Niu Yuguang , Zhou Guangming , Wang Yahui , Qin Jianing , Ping Jie , Zhang Qing , Han Bo‐Wei , Liu Yu‐Xiang , Yang Chenning , Zhai Yun , Zhang Hongxing , He Fuchu , Mai Hai‐Qiang , Bei Jin‐Xin , Li Yuanfeng , Zhou Gangqiao 
Published: October 2018

AbstractNasopharyngeal carcinoma (NPC) is prevalent among populations from southern China and is influenced by both genetic and environmental risk factors. The monocyte chemoattractant protein‐1 (MCP‐1), a member of cysteine‐cysteine chemokine family, plays critical roles in cancers. A polymorphism within the MCP‐1 promoter, rs1024611, has been shown to be significantly associated with the risk of several cancers. Our purpose was to assess the role of rs1024611 in NPC susceptibility. By polymerase chain reaction‐restriction fragment length polymorphism method, we genotyped rs1024611 in 593 patients with NPC (cases) and 480 cancer‐free subjects (controls) among Guangxi population from southern China. We observed that the G allele of rs1024611 was significantly associated with the increased risk of NPC in an additive model and dominant model, respectively (P = 0.018 and 0.010, odds ratio = 1.25 and 1.41, respectively). No appreciable variation of the effects was found across the subgroups stratified by age, sex, nationality, smoking and drinking status, and smoking level. In addition, significantly higher messenger RNA (mRNA) expression level of MCP‐1 was observed in NPC tissues than that in normal nasopharyngeal tissues, and the G allele of rs1024611 was significantly associated with elevated mRNA expression level of MCP‐1 in Epstein‐Barr virus‐transformed lymphocytes. In conclusion, our findings suggested that rs1024611 at the MCP‐1 promoter may be a risk factor for NPC. Further studies with larger sample size are necessary to confirm these findings.
SATB1 3′‐UTR and lncRNA‐UCA1 competitively bind to miR‐495‐3p and together regulate the proliferation and invasion of gastric cancer
Authors: Sun Li , Liu Lina , Yang Junshu , Li Hai , Zhang Can 
Published: October 2018

AbstractHigh expression of special AT‐rich‐binding protein 1 (SATB1) correlates with the advanced TNM stage and short overall and recurrence‐free survival of gastric cancer (GC). A bioinformatic analysis revealed that SATB1 3′‐untranslated region (3′‐UTR) and long noncoding RNA UCA1 (lncRNA‐UCA1) might competitively bind to microRNA‐495‐3p (miR‐495‐3p). Interestingly, lncRNA‐UCA1 is also an important contributor to GC. The current study aimed to demonstrate the potential interaction among SATB1/miR‐495‐3p/lncRNA‐UCA1 network and their effects on GC proliferation and invasion. The expression in GC and paracancerous normal tissues were assessed using real‐time polymerase chain reaction and Western blot analysis. Luciferase reporter, RNA pull‐down, and transfection assays were performed to determine the interaction among SATB1/miR‐495‐3p/lncRNA‐UCA1 network in GC cells. GC proliferation and invasion were evaluated using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide, transwell invasion, and colony formation assays. Results showed higher expression of SATB1 and lncRNA‐UCA1 but lower miR‐495‐3p expression in GC than in the normal tissues. In luciferase reporter assay, miR‐495‐3p bound to three seed sequences in SATB1 3′‐UTR but only one in lncRNA‐UCA1. SATB1 knockdown increased the combination of miR‐495‐3p with lncRNA‐UCA1 but decreased lncRNA‐UCA1 expression. Decreased lncRNA‐UCA1 was also observed with the mimics increased miR‐495‐3p. These data suggested that SATB1 3′‐UTR functions as a competing endogenous RNA of miR‐495‐3p and positively regulates lncRNA‐UCA1. LncRNA‐UCA1 knockdown only decreased SATB1 expression in MKN‐45 cells but not in BGC‐823 cells, which suggested that the regulatory effect of lncRNA‐UCA1 on SATB1 by sponging miR‐495‐3p is cell‐dependent. This study further identified that SATB1/miR‐495‐3p/lncRNA‐UCA1 network is implicated in GC proliferation and invasion. The current study firstly revealed that SATB1 interacts with miR‐495‐3p/lncRNA‐UCA1 network, whereby enhancing GC proliferation and invasion.
Paeoniflorin attenuated bupivacaine‐induced neurotoxicity in SH‐SY5Y cells via suppression of the p38 MAPK pathway
Authors: Chen Long , Li Qiushi , Wang Hao , Chen Quan , Wu Yuanyuan , Shang You 
Published: October 2018

AbstractBupivacain, a common local anesthetic, can cause neurotoxicity and permanent neurological disorders. Paeoniflorin has been widely reported as a potential neuroprotective agent in neural injury models. However, the roles and molecular basis of paeoniflorin in bupivacaine‐induced neurotoxicity are still undefined. In the current study, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay was performed to detect cell viability. Apoptotic rate was measured through double‐staining of Annexin V‐FITC and propidium iodide on a flow cytometer. Western blot assay was carried out to examine the protein levels of p38 mitogen‐activated protein kinase (p38 MAPK), phosphorylated‐p38 MAPK (p‐p38 MAPK), Bcl‐2, and Bax. caspase‐3 activity was determined using a caspase‐3 activity assay kit. We found that paeoniflorin dose‐dependently attenuated bupivacaine‐induced viability inhibition and apoptosis in SH‐SY5Y cells. Moreover, paeoniflorin inhibited bupivacaine‐induced activation of p38 MAPK pathway in SH‐SY5Y cells. Paeoniflorin alone showed no significant effect on cell viability, apoptosis and p38 MAPK signaling in SH‐SY5Y cells. Inhibition of p38 MAPK signaling by SB203580 or small interfering RNA targeting p38 (si‐p38) abated bupivacaine‐induced viability inhibition and apoptosis in SH‐SY5Y cells. In conclusion, paeoniflorin alleviated bupivacaine‐induced neurotoxicity in SH‐SY5Y cells via suppression of the p38 MAPK pathway, highlighting the potential values of paeoniflorin in relieving bupivacaine‐induced neurotoxicity.
Ameliorative effect of carnosine and N‐acetylcysteine against sodium nitrite induced nephrotoxicity in rats
Authors: Ansari Fariheen Aisha , Khan Aijaz Ahmed , Mahmood Riaz 
Published: October 2018

AbstractThe widespread use of sodium nitrite (NaNO2) for various industrial purposes has increased human exposure to alarmingly high levels of nitrate/nitrite. Because NaNO
2 is a strong oxidizing agent, induction of oxidative stress is one of the mechanisms by which it can exert toxicity in humans and animals. We have investigated the possible protection offered by carnosine (CAR) and N‐acetylcysteine (NAC) against NaNO
2‐induced nephrotoxicity in rats. Animals orally received CAR at 100 mg/kg body weight/d for seven days or NAC at 100 mg/kg body weight/d for five days followed by a single oral dose of NaNO
2 at 60 mg/kg body weight. The rats were killed after 24 hours, and the kidneys were removed and processed for various analyses. NaNO
2 induced oxidative stress in kidneys, as shown by the decreased activities of antioxidant defense, brush border membrane, and metabolic enzymes. DNA‐protein crosslinking and DNA fragmentation were also observed. CAR/NAC pretreatment significantly protected the kidney against these biochemical alterations. Histological studies supported these findings, showing kidney damage in NaNO
2‐treated animals and reduced tissue impairment in the combination groups. The protection offered by CAR and NAC against NaNO
2‐induced damage, and their nontoxic nature, makes them potential therapeutic agents against nitrite‐induced nephrotoxicity.
Association between CASP3 polymorphisms and overall cancer risk: A meta‐analysis of case‐control studies
Authors: Hashemi Mohammad , Moazeni‐Roodi Abdolkarim , Ghavami Saeid 
Published: October 2018

AbstractSeveral studies inspected the relationship between caspase‐3 (CASP3) polymorphisms and the risk of several human cancers, but the findings remain controversial. We conducted a meta‐analysis aiming to inspect the association between CASP3 rs1049216 T>C, rs12108497 C>T, rs4647603 G>A, rs4647602 C>A, rs6948 T>G, rs2705897 A>C, and rs113420705 G>A polymorphisms and cancer risk. Eligible studies were recognized by searching the Web of Science, PubMed, Scopus, and Google Scholar databases. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to quantitatively evaluate the association between each polymorphism of CASP3 and cancer risk. The rs4647603 variant significantly increased the risk of cancer in an overdominant (OR, 1.44; 95% CI, 1.03‐2.01; P = 0.03; AG vs AA+GG) inheritance model. Regarding the rs4647602 variant, the findings revealed that this variant was associated with protection against cancer in homozygous codominant (OR, 0.67; 95% CI, 0.56‐0.80;
P < 0.00001; AA vs CC), dominant (OR, 0.84; 95% CI, 0.73‐0.96;
P = 0.009; AC+AA vs CC), recessive (OR, 0.70; 95% CI, 0.61‐0.79;
P < 0.00001; AA vs AC+CC), and allele (OR, 0.81; 95% CI, 0.75‐0.88;
P = 0.00001; A vs C) models. The findings suggested that the rs2705897 variant significantly decreased the risk of cancer in heterozygous codominant (OR, 0.80; 95% CI, 0.67‐0.94;
P = 0.009; AC vs AA), dominant (OR, 0.81; 95% CI, 0.69‐0.95;
P = 0.009; AC+CC vs AA), overdominant (OR, 0.80; 95% CI, 0.68‐0.95;
P = 0.01; AC vs CC+AA), and allele (OR, 0.85; 95% CI, 0.74‐0.97;
P = 0.02; C vs A) models. The results did not support an association between CASP3 rs1049216 and rs6948 polymorphisms and cancer risk. In summary, the findings of this meta‐analysis support an association between CASP3 polymorphisms and cancer risk. Larger and well‐designed studies are desired to evaluate these associations in detail.
Provider perspectives on a novel moral injury treatment for veterans: Initial assessment of acceptability and feasibility of the Impact of Killing treatment materials
Authors: Burkman Kristine , Purcell Natalie , Maguen Shira 
Published: October 2018

AbstractObjectiveWe assessed whether treatment providers specializing in evidence‐based treatment for posttraumatic stress disorder found the Impact of Killing (IOK), a novel treatment for moral injury among combat veterans, acceptable, and feasible.MethodsTen providers from a large veterans administration (VA) medical center were provided with materials from IOK. We audio‐recorded a semistructured interview with each provider where we elicited open‐ended feedback as well as asked five structured questions about the relative advantage, compatibility, complexity/simplicity, trialability, and observability of IOK.ResultsAll providers found IOK feasible, acceptable, and something they could incorporate into their existing practice. Providers reported that the spiritual and moral concerns addressed in IOK were novel, and that self‐forgiveness and making amends were critical components promoting healing from moral injury not emphasized in other treatments.ConclusionsAmong trauma providers, IOK was found acceptable and feasible, offering a novel approach to addressing moral injury among combat veterans.
Family environment moderates the relation of sluggish cognitive tempo to attention‐deficit/hyperactivity disorder inattention and depression
Authors: Fredrick Joseph W. , Luebbe Aaron M. , Mancini Kathryn J. , Burns G. Leonard , Epstein Jeffery N. , Garner Annie A. , Jarrett Matthew A. , Becker Stephen P. 
Published: October 2018

AbstractObjectivesThe current study investigated whether a maladaptive family environment would moderate the strength of the relations of sluggish cognitive tempo (SCT) to attention‐deficit/hyperactivity disorder inattention (ADHD‐IN) and to depressive symptoms in a large sample of college students.MethodsParticipants (n = 3,172), between the ages of 18–29 (M ± SDage = 19.24 ± 1.52; 69.8% women; 80.4% White) and enrolled in five universities in the United States completed self‐report measures of symptomatology, interparental conflict, and family expressiveness of emotions.ResultsA negative emotional climate strengthened relations of SCT with ADHD‐IN and depressive symptoms. Moreover, the lack of a positive emotional climate strengthened the co‐occurrence of SCT with depressive symptoms, though not with ADHD‐IN.ConclusionsThe current study is the first to demonstrate that the family environment moderates the association between SCT and co‐occurring symptomatology in young adults.
American Psychological Association practice guidelines for psychopharmacology: Ethical practice considerations for psychologists involving psychotropic use with children and adolescents
Authors: Goldberg Susan G. , Wagner Kathryn 
Published: October 2018

AbstractObjectivesThis study discusses the implications of the American Psychological Association’s 2011 Practice Guidelines for Pharmacology as they apply to psychologists working with juvenile clients. Special considerations apply due to concerns about the developmental side effects that occur when psychotropic medications are prescribed to children and adolescents.Methods or DesignThis study provides recommendations for implementing each of the Practice Guidelines. Constructive criticism of the Practice Guidelines is also discussed with the aim of improving service delivery.ResultsThis study provides specific recommendations for psychologists regarding obtaining adequate knowledge about psychopharmacology to inform clients or consult with physicians. Suggestions are made for continuing education requirements for psychologists who work with juveniles.ConclusionsRecommendations are made for psychologists working with juveniles to increase their knowledge of psychotropic medications for a more ethical and informed voice regarding the prescribing of such medications.
I heard it through the grapevine: Where and what parents learn about youth mental health treatments
Authors: O’Connor Erin E. , Langer David A. 
Published: October 2018

AbstractObjectiveThis study investigates where parents learn about, and what parents know about child mental health services. Parents who are better informed about mental health services may be more likely to utilize services for their children.MethodsIn a national online survey, 196 parents of children between the ages of 4 and 17 years reported on their information‐seeking behaviors and their familiarity and experience with psychosocial approaches.ResultsParents reported utilizing multiple information sources with mental health providers, pediatricians, and social networks being the most prominent. Parents’ trust in different sources varied, with parents generally trusting healthcare professionals the most. Parents exposed to mental health services were more aware of specific therapeutic approaches.ConclusionsData on how parents receive and understand mental health‐related information contributes to ongoing dissemination and implementation efforts.