bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transfection efficiency and cytotoxicity of polyethyleneimine‐coated magnetic iron oxide nanoparticles in rooster sperm cells
Authors: Katebi Samira , Esmaeili Abolghasem , Ghaedi Kamran , Salimi Parvin 
Published: October 2018

AbstractSince the morphology of the rooster spermatozoa is different to other animal spermatozoa, the aim of the current study was to investigate the transfection efficiency and cytotoxicity of polyethyleneimine (PEI) coated magnetic iron oxide nanoparticles (MION) on these cells. Liposome/nucleic acid (NA) complexes and PEI‐coated MION linked to the labeled oligonucleotides were used. Viability and percentage of exogenous nucleic acid uptake of spermatozoa were measured by flow cytometry analyses. The results showed a significant increase in exogenous nucleic acid uptake by rooster spermatozoa (P < 0.001) when treated with MION‐NA complexes in comparison to liposome/NA. There were no significant differences between efficiency of lipid‐based transfection agent and MION (P > 0.05) during short incubation period. MION with or without magnetic field, did not show significant cytotoxicity while the lipid‐based transfection agent significantly decreased (P < 0.05) the viability of rooster spermatozoa. Results of this study showed that magnetofection and lipofection were both effective methods which increased exogenous nucleic acid uptake by rooster spermatozoa. However, the magnetofection method was more successful in maintaining the cell's survival than lipofection method.
Evaluation of the two polymorphisms rs1801133 in MTHFR and rs10811661 in CDKN2A/B in breast cancer
Authors: Hesari Amirreza , Maleksabet Amir , Tirkani Abolfazl Nosrati , Ghazizadeh Hamideh , Iranifar Elmira , Mohagheg Fatoalah , Anoshrvani Ali Arash , Ghasemi Faezeh 
Published: October 2018

AbstractThe 5,10‐Methylenetetrahydrofolate reductase (MTHFR) was the rate‐limiting enzyme in the methyl cycle, which was encoded by the MTHFR gene. MTHFR played a key role in homocysteine plasma level and was associated with the risk of breast cancer. The cyclin‐dependent kinase (CDK) inhibitor (CDKN2A/B) was the tumor suppressor in the cell cycle regulation. The single‐nucleotide polymorphism was thought to be associated with the predisposition of breast cancer and in subsequent immune response in different populations. The current study was conducted on a peripheral blood sample of 100 Iranian women with breast carcinoma and 142 cancer‐free healthy female volunteers. The TaqMan real‐time polymerase chain reaction technique was applied for genotyping of participants. The correlation of both variants and demographic data were investigated with the risk of breast cancer. Our data showed that the MTHFR allele T and TT genotype had the higher prevalence in patients (P < 0.0001) than the control group. The frequency of risk C allele into the CDKN2A/B rs10811661 was 72%. The correlations of menarche and underlying hormonal disorder with the risk of breast cancer were investigated; also our results showed that the menopause status was statistically significant between patients and controls (P = 0.036). Our investigations demonstrated that the MTHFR rs180113 and CDKN2A/B rs10811661 had a significant correlation with the elevated risk of breast cancer and they might be potentially valuable to apply as a prognostic factor for individual health care.
Strategies for targeting energy metabolism in Kirsten rat sarcoma viral oncogene homolog ‐mutant colorectal cancer
Authors: Wang Gang , Wang Jun‐Jie , Yin Pei‐Hao , Xu Ke , Wang Yu‐Zhu , Shi Feng , Gao Jing , Fu Xing‐Li 
Published: October 2018

AbstractAlterations in cellular energy metabolism play critical roles in colorectal cancer (CRC). These alterations, which correlate to KRAS mutations, have been identified as energy metabolism signatures. This review summarizes the relationship between colorectal tumors associated with mutated KRAS and energy metabolism, especially for the deregulated energy metabolism that affects tumor cell proliferation, invasion, and migration. Furthermore, this review will concentrate on the role of metabolic genes, factors and signaling pathways, which are coupled with the primary energy source connected with the KRAS mutation that induces metabolic alterations. Strategies for targeting energy metabolism in mutated KRAS CRC are also introduced. In conclusion, deregulated energy metabolism has a close relationship with KRAS mutations in colorectal tumors. Therefore, selective inhibitors, agents against metabolic targets or KRAS signaling, may be clinically useful for colorectal tumor treatment through a patient‐personalized approach.
Zellweger spectrum disorder patient–derived fibroblasts with the PEX1‐Gly843Asp allele recover peroxisome functions in response to flavonoids
Authors: MacLean Gillian E. , Argyriou Catherine , Di Pietro Erminia , Sun Xuting , Birjandian Sara , Saberian Panteha , Hacia Joseph G. , Braverman Nancy E. 
Published: October 2018

AbstractZellweger spectrum disorder (ZSD) results from biallelic mutations in PEX genes required for peroxisome biogenesis. PEX1‐G843D is a common hypomorphic allele in the patient population that is associated with milder disease. In prior work using a PEX1‐G843D/null patient fibroblast line expressing a green fluorescent protein (GFP) reporter with a peroxisome‐targeting signal (GFP‐PTS1), we demonstrated that treatments with the chemical chaperone betaine and flavonoid acacetin diacetate recovered peroxisome functions. To identify more effective compounds for preclinical investigation, we evaluated 54 flavonoids using this cell‐based phenotype assay. Diosmetin showed the most promising combination of potency and efficacy (EC50 2.5 µM). All active 5′,7′‐dihydroxyflavones showed greater average efficacy than their corresponding flavonols, whereas the corresponding flavanones, isoflavones, and chalcones tested were inactive. Additional treatment with the proteostasis regulator bortezomib increased the percentage of import‐rescued cells over treatment with flavonoids alone. Cotreatments of diosmetin and betaine showed the most robust additive effects, as confirmed by three independent functional assays in primary PEX1‐G843D patient cells, but neither agent was active alone or in combination in patient cells homozygous for the PEX1 c.2097_2098insT null allele. Moreover, diosmetin treatment increased PEX1, PEX6, and PEX5 protein levels in PEX1‐G843D patient cells, but none of these proteins increased in PEX1 null cells. We propose that diosmetin acts as a pharmacological chaperone that improves the stability, conformation, and functions of PEX1/PEX6 exportomer complexes required for peroxisome assembly. We suggest that diosmetin, in clinical use for chronic venous disease, and related flavonoids warrant further preclinical investigation for the treatment of PEX1‐G843D–associated ZSD.
Protective effect of ginsenoside Rg3 on lung injury in diabetic rats
Authors: Wang Heyuan , Wu Wei , Wang Guixia , Xu Wenzhou , Zhang Fuqiang , Wu Bing , Tian Yaping 
Published: October 2018

AbstractGinsenoside has been used to treat diabetes, while ginsenoside Rg3 is the main active ingredient component of ginseng and is used to study its effects on lung tissue damage in diabetic rats. In this paper, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay and flow cytometry were applied to detect the proliferation and apoptosis of BEAS‐2B cells treated with different concentrations of Rg3. The inflammatory response and pathological change in the lung tissue of diabetic rats treated with Rg3 were evaluated by enzyme‐linked immunosorbent assay, quantative real‐time polymerase chain reaction, and hematoxylin and eosin staining immunohistochemistry. Meanwhile, PI3K and MAPK signaling pathway proteins in lung tissue were determined by Western blot analysis. The results showed that ginsenoside Rg3 had no significant influence on the proliferation and apoptosis of BEAS‐2B cells. Ginsenoside Rg3 can inhibit inflammatory response and promote the activation of PI3K and MAPK signaling pathways to prevent damages of lung tissues induced by hyperglycemia. The protective effect provided by ginsenoside Rg3 indicates that ginsenoside Rg3 is a potential drug for the treatment of diabetes.
Integrative analysis of mRNA and microRNA expression profiles in laryngeal squamous cell carcinoma
Authors: Ekmekci Cumhur Gokhan , Coskunpinar Ender , Avci Hakan , Farooqi Ammad Ahmad , Orhan Kadir Serkan , Akbas Fahri 
Published: October 2018

AbstractLarynx cancer is a therapeutically challenging disease. Rapidly evolving experimentally validated data have significantly improved our understanding of the complex role of numerous RNA, DNA, and proteins that play a role in the development and progression of cancer. Based on the insights from approximately two decades of research, it seems clear that microRNAs (miRNAs) have revolutionized our concepts related to the main role of noncoding RNAs in different cancers’ progression, development, and metastasis. Mechanistically, miRNAs have been reported to regulate different RNAs and finally protein‐coding genes. The expression profiling of miRNAs and messenger RNA (mRNAs) was conducted for a deeper analysis of the miRNAs and mRNAs which play an essential role in larynx cancer. Downregulation or upregulation over twofolds in the miRNAs was considered to be significant, and that of sixfolds or below was considered to be significant for the mRNAs. In accordance with this approach, the expression levels of 43 miRNAs were increased in this study, whereas the expression levels of 129 were decreased. Accordingly, all the genomic expression studies provided evidence of upregulation of 97 genes, whereas 128 genes were found to be downregulated. Among these miRNAs, hsa‐miR‐20a‐3p and hsa‐miR‐1972 were noted to be important in the etiology of larynx cancer.
Current progress in CRISPR‐based diagnostic platforms
Authors: Khambhati Khushal , Bhattacharjee Gargi , Singh Vijai 
Published: October 2018

AbstractThe CRISPR‐Cas system is a key technology for genome editing and regulation in a wide range of organisms and cell types. Recently, CRISPR‐Cas–based diagnostic platform has shown idealistic properties for pathogen detection. Integrating the CRISPR‐Cas platform along with lateral flow system allows rapid, sensitive, specific, cheap, and reliable diagnostic. It has the potential to be in frontline for not only pathogen detection during the epidemic outbreak, but also cancer, and genetic diseases.
Oncostatic treatment effect of triple negative breast cancer cell line with copper (I)‐nicotinate complex
Authors: Abdel‐Mohsen Mohamed A. , Toson Elshahat A. , Helal Marihan A. 
Published: October 2018

AbstractThe treatment of triple‐negative breast cancer (TNBC) remains a major challenge. The present study aimed to throw more light on the role of copper (I)‐nicotinate complex (CNC) as an antitumor as well as a proapoptotic agent. In this study, the HCC‐1806 cell line was used as a model for TNBC. Cell cycle, apoptosis assay, and programmed cell death protein‐1 were investigated by flowcytometry. Besides, the comet assay was performed using a fluorescence microscope. The enzyme‐linked immunosorbent assay technique was used for the detection of phospho‐Chk1 at ser 317 and caspase‐3. Moreover, the gene expression of survivin was identified by real‐time polymerase chain reaction. Finally, superoxide dismutase (SOD) was calorimetrically assayed. The viability of HCC‐1806 cells treated with CNC was decreased in a dose‐dependent manner. The tendency for apoptotic machinery was observed through the increase in the sub G0 peak, the percentage of early and late apoptotic phases, and the elevation in caspase‐3 levels associated with a downregulation of the survivin gene expression. The antioxidant property of the complex, reflected by elevated SOD activity, may contribute to mediate the cell death pathways. Low concentrations of CNC were found to favor the apoptotis‐mediated mechanism. However, one cannot neglect the abundance of cell necrosis–mediated death of cells via CNC, especially at higher concentrations.
Exosomes derived from miR‐146a‐modified adipose‐derived stem cells attenuate acute myocardial infarction−induced myocardial damage via downregulation of early growth response factor 1
Authors: Pan Junjie , Alimujiang Maimaitijiang , Chen Qiying , Shi Haiming , Luo Xinping 
Published: October 2018

AbstractMultiple studies demonstrated that early growth response factor 1 (EGR1) induces myocardial damage after acute myocardial infarction (AMI). Recent evidence indicates that microRNAs (miRNA) play an important role in exosome‐mediated cardioprotection after AMI. Bioinformatics analysis has shown that miR‐146a can regulate the expression of EGR1, so the aim of this study was to determine if miR‐146a plays a role in exosome‐mediated cardioprotection by regulation of EGR1 after AMI. Exosomes were isolated from wild‐ or miR‐146a‐modified adipose‐derived stem cells (ADSCs), and the therapeutic effect of exosomes was assessed in an AMI model in rats and hypoxic‐induced H9c2 model cells. The results showed that miR‐146a containing exosomes had more effect than the exosome treatment group on the suppression of AMI‐induced apoptosis, inflammatory response, and fibrosis in an AMI rat model. Both in vivo and in vitro experiments found that miR‐146a interacted with the 3′‐untranslated region of EGR1 and suppressed posttranscriptional EGR1 expression, which was confirmed by the luciferase reporter assay. We also found that suppressed EGR1 expression reversed AMI or hypoxia‐induced TLR4/NFκB signal activation, which played an important role in the promotion of myocardial cell apoptosis, inflammatory response, and fibrosis. Taken together, these findings suggested that exosomes derived from miR‐146a‐modified ADSCs attenuated AMI‐induced myocardial damage via downregulation of EGR1.
Effects of alpha lipoic acid and its derivative “andrographolid‐lipoic acid‐1” on ulcerative colitis: A systematic review with meta‐analysis of animal studies
Authors: Moeinian Mahsa , Abdolghaffari Amir Hossein , Nikfar Shekoufeh , Momtaz Saeideh , Abdollahi Mohammad 
Published: October 2018

AbstractWe aimed to review and meta‐analyze the inflammatory and oxidative factors following alpha lipoic acid (ALA) and its derivative “andrographolid‐lipoic acid‐1” (AL‐1) in ulcerative colitis (UC). ALA plays an important role in scavenging intracellular radicals and inflammatory elements. AL‐1 is found in herbal medicines with potent anti‐inflammatory properties. Data were collected from the Google Scholar, PubMed, Scopus, Evidence‐based medicine/clinical trials, and Cochrane library database until 2017, which finally resulted in 22 animal studies (70 rats and 162 mice). The beneficial effects of ALA or AL‐1 on the most important parameters of UC were reviewed; also, studies were considered separately in mice and rats. Administration of ALA and AL‐1 significantly reduced the tumor necrosis factor‐α level compared with the controls, while data were not noteworthy in the meta‐analysis (mean differences = −18.57 [95% CI = −42.65 to 5.51],
P = 0.13). In spite of insignificant decrease in meta‐analysis outcomes (differences = 6.92 [95% CI = −39.33 to 53.16],
P = 0.77), a significant reduction in myeloperoxidase activity was shown following ALA or AL‐1 treatment compared with the controls. Despite significant differences in each study, we had to exclude some studies to homogenize data for meta‐analyzing as they showed insignificant results. Interleukin 6, cyclooxygenase‐2, glutathione, malondialdehyde, superoxide dismutase, histopathological score, macroscopic and microscopic scores, disease activity index, body weight change, and colon length were also reviewed. Most studies have emphasized on significant positive effects of ALA and AL‐1. Comprehensive clinical trials are obligatory to determine the precious position of ALA or AL‐1 in the management of UC.
Administration of losartan improves aortic arterial stiffness and reduces the occurrence of acute coronary syndrome in aged patients with essential hypertension
Authors: Zhang Zhi‐Mian , Wang Bing‐Xiang , Ou Wen‐Sheng , Lv Yan‐Hong , Li Ming‐Min , Miao Zhang , Wang Shuang‐Xi , Fei Jian‐Chun , Guo Tao 
Published: October 2018

AbstractBackgrounds and AimsIncreased arterial stiffness may increase cardiovascular morbidity and mortality. Angiotensin II type 1 receptor blocker losartan is potentially useful in controlling the central blood pressure and arterial stiffness in mild to moderate essential hypertension, while the effects of losartan in aged patients with essential hypertension are not entirely investigated.MethodsThe carotid‐femoral arterial pulse wave velocity (PWV) was measured in aged patients with essential hypertension.ResultsIn a cross‐sectional study, PWV value was significantly higher in these old patients with essential hypertension, compared with patients without essential hypertension. Logistic regression analysis indicated that age, hypertension duration, and losartan treatment are risk factors of arterial stiffness. In a perspective study, long‐term administration of losartan (50 mg/d) remarkably reduced PWV in aged patients with essential hypertension. In a longitudinal study, PWV is an independent predictor of the occurrence of acute coronary syndrome (ACS) in elderly patients with essential hypertension by using multivariate analysis. Further, the ACS occurrence was reduced by long‐term administration of losartan in aged patients with essential hypertension, compared with the old hypertensive patients without taking losartan.ConclusionLosartan treatment is a negative risk factor of arterial stiffness and reduces the risk of ACS in aged patients with essential hypertension.
CTRP3 inhibits high glucose–induced human glomerular mesangial cell dysfunction
Authors: Hu Tian‐ying , Li La‐mei , Pan Yan‐zi 
Published: October 2018

AbstractC1q/tumour necrosis factor–related protein‐3 (CTRP3) is a member of CTRP family, and its blood level is reduced in human and rodent models of obesity and diabetes. However, the role of CTRP3 in diabetic nephropathy remains unclear. This study was designed to examine the effects of CTRP3 on cell proliferation and extracellular matrix (ECM) accumulation in human glomerular mesangial cells (MCs) in response to high glucose (HG), and explore the potential molecular mechanisms. Our results demonstrated that the expression of CTRP3 was significantly decreased by HG stimulation in MCs. In addition, CTRP3 overexpression inhibited MCs proliferation, reactive oxygen species level, and ECM production in HG‐stimulated MCs. Mechanistically, CTRP3 overexpression inhibited the activation of the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) pathway in HG‐stimulated MCs. Taken together, these findings indicated that CTRP3 attenuated HG‐induced MC proliferation and ECM production through the inactivation of the JAK2/STAT3 signaling pathway. Thus, CTRP3 may be a potential therapeutic target for the treatment of diabetic nephropathy.
Priming with oxytocin and relaxin improves cardiac differentiation of adipose tissue–derived stem cells
Authors: Taha Masoumeh Fakhr , Javeri Arash , Karimipour Mojtaba , Yamaghani Mojtaba Saghafi 
Published: October 2018

AbstractPrevious studies have identified the heart as a source and a target tissue for oxytocin and relaxin hormones. These hormones play important roles in the regulation of cardiovascular function and repair of ischemic heart injury. In the current study, we examined the impact of oxytocin and relaxin on the development of cardiomyocytes from mesenchymal stem cells. For this purpose, mouse adipose tissue–derived stem cells (ADSCs) were treated with different concentrations of oxytocin or relaxin for 4 days. Three weeks after initiation of cardiac induction, differentiated ADSCs expressed cardiac‐specific genes, Gata4,
Mef2c, Nkx2.5,
Tbx5, α‐ and
β‐Mhc,
Mlc2v,
Mlc2a and
Anp, and cardiac proteins including connexin 43, desmin and α‐actinin. 10
−7 M oxytocin and 50 ng/mL relaxin induced the maximum upregulation in the expression of cardiac markers. A combination of oxytocin and relaxin induced cardiomyocyte differentiation more potently than the individual factors. In our experiment, oxytocin‐relaxin combination increased the population of cardiac troponin I‐expressing cells to 6.84% as compared with 2.36% for the untreated ADSCs, 3.7% for oxytocin treatment and 3.41% for relaxin treatment groups. In summary, the results of this study indicated that oxytocin and relaxin hormones individually and in combination can improve cardiac differentiation of ADSCs, and treatment of the ADSCs and possibly other mesenchymal stem cells with these hormones may enhance their cardiogenic differentiation and survival after transplantation into the ischemic heart tissue.
The experimental research of pregnancy immune tolerance induced by FTY720 via blocking S1P signal transduction pathway
Authors: Xiong Miao , Xu Lang , Li Li , Liu Yang , Zhou Fangfang , Wang Jun , Zhu Jieping 
Published: October 2018

AbstractObjectiveTo investigate the effects of pregnancy immune tolerance induced by FTY720 via blocking S1P signal transduction pathway.MethodsImmunohistochemistry was used to detect the expression of S1P in the decidua of pregnant rats. We have constructed S1P gene small interfering RNA (siRNA) lentiviral vector and overexpression
S1P gene lentiviral vector and they are transferred into dendritic cell (DC), then observing the effect of adoptive transferring of FTY720 on the embryo loss rate of spontaneous abortion mouse model after transferring this two kinds of lentiviral vectors.Results(1) FTY720 had no significant effect on the embryo loss rate of the normal pregnant rats; (2) Adoptive transferring of FTY720 can significantly reduce the embryo loss rate of the spontaneous abortion mouse model. The expression of S1P in the decidua of spontaneous abortion mouse model was lower than that of normal pregnant rat (P < 0.05). (3) After transferring of S1P‐siRNA lentiviral vector transfected DC, FTY720 could mild reduce the embryo loss rate of abortion mouse model (embryo loss rate was 11.5%) (
P < 0.05). However, the effect is far less than that of before adoptive transferring of S1P‐siRNA lentivirus transfected DC. After the transferring of the overexpression of
S1P gene lentiviral vector transfected DC, FTY720 can significantly reduce the rate of embryo loss in the spontaneous abortion mouse model (embryo loss rate decreased to 1.95%) (
P < 0.01). The effect was more obvious than that of no transfecting
S1P gene lentiviral vector transfected DC.ConclusionFTY720 is secured in inducing immune tolerance during pregnancy by blocking the S1P signaling pathway.