bluuebunny/crossref_metadata_2025_split huggingface dataset:
The determination of the potential anticancer effects of Coriandrum sativum in PC‐3 and LNCaP prostate cancer cell lines
Authors: Elmas Levent , Secme Mücahit , Mammadov Ramazan , Fahrioglu Umut , Dodurga Yavuz 
Published: November 2018

AbstractCoriander (Coriandrum sativum L.) is such an herb from the Apiaceae family, used both for its medicinal and nutritional properties for many centuries. In this study, the effects of C. sativum extract on gene expression, viability, colony formation, migration, and invasion of PC‐3 and LNCaP prostate cancer cell lines have been investigated. The half maximal inhibitory concentration (IC50) dose in PC‐3 and LNCaP cells was detected to be 2 and 5 mg/mL at the 24th hour, respectively. C. sativum extracts have been observed to cause a significant decrease in the expression of Akt and Bcl‐2 in the PC‐3 cells and just Akt in LNCaP cells while increasing in the expression of p53, caspase‐9, caspase‐10, PTEN, DR5, TRADD, PUMA, and NOXA. DR4 expression was increased in LNCaP cell line but not PC‐3, and APAF and BID had increased expression in PC‐3 but not the LNCaP cells. Our observations have shown that C. sativum extract decreased colony formation while inhibiting cell invasion and migration. Cell migration was hindered in PC‐3 but not the LNCaP cells. In conclusion, this data present a valuable addition to the very limited data available out there on the potential use of C. sativum in prostate cancer treatment.
The effect of VDR gene polymorphisms and vitamin D level on blood pressure, risk of preeclampsia, gestational age, and body mass index
Authors: Rezavand Negin , Tabarok Saba , Rahimi Ziba , Vaisi‐Raygani Asad , Mohammadi Ehsan , Rahimi Zohreh 
Published: November 2018

AbstractWe investigated the influence of vitamin D receptor (VDR) polymorphisms and vitamin D level on the blood pressure and the risk of preeclampsia. In a case‐control study, 200 pregnant women, including 100 individuals with preeclampsia along with 100 healthy pregnant women, were studied for VDR FokI, TaqI, and BmsI polymorphisms and serum 25 (OH)‐D level using polymerase chain reaction‐restriction fragment length polymorphism method and commercial kit, respectively. The mean level of 25 (OH)‐D in preeclamptic patients was significantly lower (16.6 ± 4.2 ng/mL, P < 0.001) compared with controls (19.6 ± 3.8 ng/mL). Among all women, a significantly higher systolic blood pressure and before‐pregnancy body mass index and also lower gestational age were observed in the presence of 25 (OH)‐D level < 20 ng/mL compared with the 20 to 30 ng/mL. A significantly higher frequency of VDR FokI C allele in preeclamptic patients (83%) than controls (74%) was associated with a 1.72‐fold increased risk of preeclampsia. In all the studied individuals, the systolic and diastolic blood pressures were significantly higher in the presence of the FokI CC genotype compared with the TC and TT+TC genotypes. Neither VDR Taq1 nor VDR BmsI was associated with the risk of preeclampsia. The haplotype FokI C, TaqI C and BmsI A (CCA) compared with haplotype CTG increased the risk of preeclampsia by 1.4‐fold (P = 0.33). Our study suggests an association between VDR FokI polymorphism and an insufficient serum level of 25 (OH)‐D with the risk of preeclampsia and also the influence of insufficient 25 (OH)‐D level and VDR FokI polymorphism on maternal factors, including blood pressure.
Decellularized Wharton's jelly extracellular matrix as a promising scaffold for promoting hepatic differentiation of human induced pluripotent stem cells
Authors: Kehtari Mousa , Beiki Bahareh , Zeynali Bahman , Hosseini Fatemeh Sadat , Soleimanifar Fatemeh , Kaabi Mohammad , Soleimani Masoud , Enderami Seyed Ehsan , Kabiri Mahboubeh , Mahboudi Hossein 
Published: November 2018

AbstractLiver tissue engineering as a therapeutic option for restoring of damaged liver function has a special focus on using native decellularized liver matrix, but there are limitations such as the shortage of liver donor. Therefore, an appropriate alternative scaffold is needed to circumvent the donor shortage. This study was designed to evaluate hepatic differentiation of human induced pluripotent stem cells (hiPSCs) in decellularized Wharton's jelly (WJ) matrix as an alternative for native liver matrix. WJ matrices were treated with a series of detergents for decellularization. Then hiPSCs were seeded into decellularized WJ scaffold (DWJS) for hepatic differentiation by a defined induction protocol. The DNA quantitative assay and histological evaluation showed that cellular and nuclear materials were efficiently removed and the composition of extracellular matrix was maintained. In DWJS, hiPSCs‐derived hepatocyte‐like cells (hiPSCs‐Heps) efficiently entered into the differentiation phase (G1) and gradually took a polygonal shape, a typical shape of hepatocytes. The expression of hepatic‐associated genes (albumin, TAT, Cytokeratin19, and Cyp7A1), albumin and urea secretion in hiPSCs‐Heps cultured into DWJS was significantly higher than those cultured in the culture plates (2D). Altogether, our results suggest that DWJS could provide a proper microenvironment that efficiently promotes hepatic differentiation of hiPSCs.
Cyadox regulates the transcription of different genes by activation of the PI3K signaling pathway in porcine primary hepatocytes
Authors: Guo Ju , Cui Luqing , Lu Qirong , Zhang Yinfeng , Liu Qianying , Wang Xu , Wang Yulian , Liu Zhenli , Yuan Zonghui , Dai Menghong 
Published: November 2018

AbstractCyadox, a new derivative of quinoxalines, has been ascertained as an antibiotic with significant growth promoting, low poison, quick absorption, swift elimination, brief residual period, and noncumulative effect. Seven differential expressed genes, including Insulin‐like Growth Factor‐1 (
IGF‐1),
Epidermal Growth Factor (
EGF),
Poly ADP‐ribose polymerase (
PARP),
the Defender Against Apoptotic Death 1 (
DAD1),
Complement Component 3 (
C3),
Transketolase (
TK) and a
New gene, were induced by cyadox in swine liver tissues by messenger RNA differential display reverse transcription polymerase chain reaction (DDRT‐PCR) in our laboratory. However, the signal mechanism that cyadox altered these genes expression is not completely elucidated. The signaling pathways involved in the expressions of seven genes induced by cyadox were determined in porcine primary hepatocytes by RT‐qPCR and the application of various signal pathway inhibitors. 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay revealed that cyadox could stimulate proliferation of porcine primary hepatocytes in a time‐dependent manner. In porcine primary cultured hepatocytes, phosphoinositide 3‐kinase (PI3K) and transforming growth factor‐β (TGF‐β) signal pathways were the main signal pathways involved in the expressions of seven genes induced by cyadox. Taken together, these results demonstrate for the first time that seven cyadox‐related genes expressions in porcine primary hepatocytes treated with cyadox are mediated mainly through the PI3K signaling pathway, potentially leading to enhanced cell growth and cell immunity.
EGF might be the early response gene of cyadox, and a primary regulator of the other gene expressions such as
IGF‐1 and
DAD1, playing an important role in cell proliferation promoted by cyadox.
Ameliorative effects of autophagy inducer, simvastatin on alcohol‐induced liver disease in a rat model
Authors: Atef Marwa Mohamed , Hafez Yasser Mostafa , Alshenawy Hanan Alsaeed , Emam Marwa Nagy 
Published: November 2018

AbstractAlcoholic liver disease (ALD) encompasses a variety of liver injuries with various underlying mechanisms but still no effective treatment. So we aimed to monitor the influence of simvastatin on alcohol‐induced liver injury and elucidate the underlying mechanisms of its cytoprotective effect. Thirty male albino rats were randomly divided into five equal groups. Group 1 (control): received a standard diet; group 2: received simvastatin (10 mg kg−1 day
−1) once a day orally for 8 weeks; group 3: received 20% ethanol (7.9 g kg
−1 day
−1) daily orally for 8 weeks; group 4: received 20% ethanol along with same simvastatin dose daily for 8 weeks; group 5: received 20% ethanol orally for 8 weeks then received the same simvastatin dose for the next 8 weeks. Serum alanine aminotransferase, aspartate aminotransferase, total cholesterol, triglycerides, high‐density lipoprotein cholesterol, and low‐density lipoprotein cholesterol were measured. Liver tissue malondialdehyde, reduced glutathione levels, and superoxide dismutase activity were estimated. B‐cell lymphoma 2 and C/EBP homologous protein levels were evaluated by enzyme linked immunosorbent assay (ELISA). Light chain 3‐II and peroxisome proliferation‐activated receptor gamma messenger RNA expression was assessed by real‐time polymerase chain reaction. Immunohistochemical staining was performed using anti‐rat tumor necrosis factor‐alpha antibody. Our results revealed that simvastatin treatment was able to ameliorate alcohol‐induced liver damage; the improved biochemical data were confirmed by histopathological evaluation. Simvastatin being an autophagy inducer was able to prevent and reverse alcohol‐induced liver changes via induction of autophagy, attenuation of oxidative stress, inflammation, and endoplasmic reticulum stress‐induced apoptosis. Therefore, our findings suggest that treatment with simvastatin may be a useful approach in the management strategy of ALD.
Adenosine protects pancreatic beta cells against apoptosis induced by endoplasmic reticulum stress
Authors: Shahrestanaki Mohammad Keyvanloo , Arasi Fatemeh Panahi , Aghaei Mahmoud 
Published: November 2018

AbstractChronic exposure to high glucose induces endoplasmic reticulum (ER) stress in pancreatic beta cells (PBCs). The previous evidence showed that adenosine modulate PBCs viability and insulin secretion. The aim of this study was to evaluate possible involvement of adenosine in protection of MIN6 β‐cells from Tunicamycin (Tu)‐induced ER stress.MIN6 cells were cotreated with Tu and different concentrations of adenosine. Cell viability, proliferation, and apoptosis were evaluated using 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide (MTT), 5‐bromo‐2′‐deoxyuridine (Brdu), and colony formation assays. Caspase‐12 activity was assayed using the fluorometric method. Thioflavin T (ThT) staining was used for the evaluation of protein aggregation. Insulin secretion was evaluated using specific an ELISA kit. Ca2+ mobilization assayed using Fura2/AM probe. BIP, CHOP, XBP‐1, and XBP‐1s expression in both messenger RNA (mRNA) and protein levels were evaluated using the reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot analysis, respectively. Bcl‐2, p‐eIF2α/eIF2α, and GADD34 levels also determined with Western blot analysis.Adenosine protected MIN6 cells against Tu‐induced ER stress in a dose‐dependent manner and increased their proliferation. Decreased caspase‐12 activity and upregulated Bcl‐2 protein may explain antiapoptotic effects of adenosine. ThT staining indicated an attenuated aggregation of misfolded proteins. Adenosine effectively increased insulin secretion in Tu‐treated cells. BIP, CHOP, XBP1, and sXBP1 expression were decreased significantly in cotreated cells, indicating alleviation of ER stress. However, adenosine potentiated the expression of GADD34 and decreased p‐eIF2α/eIF2α ratio. Adenosine increased cytosolic Ca
2+ levels, which may promote adenosine triphosphate (ATP) synthesis in mitochondria, helping ER to preserve protein hemostasis.Taken together, adenosine upregulated Bcl‐2 and GADD34 to protect PBCs against Tu‐induced apoptosis and increase Insulin secretion.
Rab6A GTPase contributes to phenotypic modulation in pulmonary artery smooth muscle cells under hypoxia
Authors: Wang Fang , Xu Xingxiang , Tang Weian , Min Lingfeng , Yang Junjun 
Published: November 2018

AbstractPrevious studies have demonstrated that hypoxia can induce phenotypic modulation of pulmonary smooth muscle cells; however, the mechanisms remain unclear. The present study aimed to investigate the effect of the GTPase Rab6A‐mediated phenotypic modulation and other activities of rat pulmonary artery smooth muscle cells (RPASMCs). We revealed that Rab6A was induced by hypoxia (1% O2) and was involved in a hypoxia‐induced phenotypic switch and endoplasmic reticulum stress (ERS) in RPASMCs. After 48 hours of hypoxia, the expression of the phenotype marker protein smooth muscle actin was downregulated and vimentin (VIM) expression was upregulated. Rab6A was upregulated after 48 hours of hypoxia, and the level of glucose‐regulated protein, 78 kDa (GRP78) after 12 hours of hypoxic stimulation was also increased. After transfection with a Rab6A short interfering RNA under hypoxic conditions, the expression levels of GRP78 and VIM in RPASMCs were downregulated. Overall, hypoxia‐induced RPASMCs to undergo ERS followed by phenotypic transformation. Rab6A is involved in this hypoxia‐induced phenotypic modulation and ERS in RPASMCs.
Is neighborhood poverty harmful to every child? Neighborhood poverty, family poverty, and behavioral problems among young children
Authors: Kim Yeonwoo , Lee Sharon , Jung Hyejin , Jaime Jose , Cubbin Catherine 
Published: November 2018

AbstractThis longitudinal study investigates the association between neighborhood poverty and behavioral problems among young children. This study also examines whether social environments mediate the relationship between neighborhood poverty and behavioral problems. We used data from the third and fourth waves of the Fragile Families and Child Wellbeing study to assess behavioral problems separately for children who experienced no family poverty, moved out of family poverty, moved into family poverty, and experienced long‐term family poverty. Regression models assessed the effect of neighborhood poverty on behavioral problem outcomes among children aged 5 years, after controlling for sociodemographic characteristics and earlier behavioral problems. Results showed an association between neighborhood poverty and lower social cohesion and safety, which lead to greater externalizing problems among children with long‐term family poverty living in high‐poverty neighborhoods compared with those in low‐poverty neighborhoods. Policies and community resources need to be allocated to improve neighborhood social environments, particularly for poor children in high‐poverty neighborhoods.
Effects of microRNA‐217 on proliferation, apoptosis, and autophagy of hepatocytes in rat models of CCL4‐induced liver injury by targeting NAT2
Authors: Yang Cheng‐Liang , Zheng Xiao‐Li , Ye Ke , Sun Ya‐Nan , Lu Yu‐Fei , Ge Hong , Liu Hui 
Published: November 2018

AbstractLiver injury is an important cause of serious liver disease. This study aims to explore the effects of miR‐217 targeting NAT2 on hepatocyte proliferation, apoptosis, and autophagy following carbon tetrachloride (CCL4)‐induced liver injury. Rat models of CCL4‐induced liver injury were established. Healthy Wistar rats were randomized into the normal, blank, negative control (NC), microRNA‐217 (miR‐217) mimic, miR‐217 inhibitor, small interfering RNA (siRNA)‐N‐acetyltransferase 2 (NAT2), and miR‐217 inhibitor + siRNA‐NAT2 groups. NAT2 activity was evaluated with reversed‐phase high‐performance liquid chromatographic method. Immunohistochemistry was used to detect NAT2 protein positive rate. Reverse transcription quantitative polymerase chain reaction and western blot analysis were used to examine expressions of miR‐217, NAT2, Bcl‐2, Bax, p35, LC3‐II, Becline‐1, and the ratio of caspase‐3/cleaved caspase‐3. Autophagy, proliferation, and cell cycle distribution were determined by electron microscope, CCK‐8, and flow cytometry. NAT2 protein positive rate and miR‐217, NAT2, Bcl‐2, and p35 expressions were higher and Bax, LC3‐II, and Becline‐1 expressions and the ratio of caspase‐3/cleaved caspase‐3 lower in the normal group than the other six groups. Compared with the blank and NC groups, in the miR‐217 mimic and siRNA‐NAT2 groups, Bax, LC3‐II, and Becline‐1 expressions and the ratio of caspase‐3/cleaved caspase‐3, and hepatocyte apoptosis and autophagy increased, while NAT2, Bcl‐2, and p35 expressions and hepatocyte proliferation decreased; opposite results were observed in the miR‐217 inhibitor group. Collectively, miR‐217 targeting NAT2 inhibits proliferation and promotes apoptosis and autophagy of hepatocytes in CCL4‐induced liver injury.
Integrative proteomics and immunochemistry analysis of the factors in the necrosis and repair in acetaminophen‐induced acute liver injury in mice
Authors: Feng Qin , Zhao Ningwei , Xia Wenkai , Liang ChengJie , Dai Guoxin , Yang Jian , Sun Jingxia , Liu Lanying , Luo Lan , Yang Jie 
Published: November 2018

AbstractAcetaminophen (APAP) overdose‐induced acute liver injury (AILI) is a significant clinical problem worldwide, the hepatotoxicity mechanisms are well elucidated, but the factors involved in the necrosis and repair still remain to be investigated. APAP was injected intraperitoneally in male Institute of Cancer Research (ICR) mice. Quantitative proteome analysis of liver tissues was performed by 2‐nitrobenzenesulfenyl tagging, two‐dimensional‐nano high‐performance liquid chromatography separation, and matrix‐assisted laser desorption/ionization–time of flight mass spectrometry analysis. Diffrenetial proteins were verified by the immunochemistry method. 36 and 44 differentially expressed proteins were identified, respectively, at 24 hr after APAP (200 or 300 mg·kg
−1) administration. The decrease in the mitochondrial protective proteins Prdx6, Prdx3, and Aldh2 accounted for the accumulation of excessive reactive oxygen species (ROS) and aldehydes, impairing mitochondria structure and function. The Gzmf combined with Bax and Apaf‐1 jointly contributed to the necrosis. The blockage of Stat3 activation led to the overexpression of unphosphorylated Stat3 and the overproduction of Bax. The overexpression of unphosphorylated Stat3 represented necrosis; the alternation from Stat3 to p‐Stat3 in necrotic regions represented hepatocytes from death to renewal. The high expressions of P4hα1, Ncam, α‐SMA, and Cygb were involved in the liver repair, they were not only the markers of activated HSC but also represented an intermediate stage of hepatocytes from damage or necrosis to renewal. Our data provided a comprehensive report on the profile and dynamic changes of the liver proteins in AILI; the involvement of Gzmf and the role of Stat3 in necrosis were revealed; and the role of hepatocyte in liver self‐repair was well clarified.
Ectopic nerve growth factor prevents proliferation in glioma cells by senescence induction
Authors: Meco Daniela , Di Francesco Angela Maria , Melotti Linda , Ruggiero Antonio , Riccardi Riccardo 
Published: November 2018

AbstractObjectiveThe neurotrophin nerve growth factor (NGF) affects survival, regulation and differentiation of both central and peripheral nervous system neurons. NGF exerts its effects primarily through tropomyosin receptor kinase A (TrkA), inducing a cascade of tyrosine kinase‐initiated responses. In spite of its importance, the general behavior of NGF looks contradictory: its effects can be both stimulatory and inhibitory. The present study aims to explore the molecular mechanisms induced by NGF in glioma cancer cells.MethodsThe effects of NGF were investigated in high grade glioma and low grade pediatric glioma (PLGG) cell lines through comparative studies. In particular, we investigated TrkA‐mediated cellular pathways, molecular signaling, proliferation, cell cycle and cellular senescence.ResultsWe found that exposure of PLGG cells to NGF produced stable growth arrest with the features of a senescence phenotype but without the expression of anti‐poly(ADP‐ribose) polymerase cleavage, a marker of apoptosis. Moreover, NGF treatment promoted the phosphorylation of extracellular signal‐regulated kinase1/2 (ERK1/2), signal transducer and activator of transcription 3 (STAT3), and phosphatidylinositol‐3‐kinase (PI3K)/protein kinase B (AKT) signaling. In addition, K252a, a TrkA inhibitor, significantly reduced the phosphorylation of the aforementioned signaling pathways, suggesting that NGF‐activated ERK1/2 and AKT signaling take place downstream of TrkA‐neurotrophin interaction.ConclusionsThese findings provide the first evidence that NGF can induce senescence of PLGG cells in a receptor‐mediated fashion, thus supporting the hypothesis that in the clinical setting NGF might be beneficial to pediatric glioma patients.
Estrogen deprivation aggravates intracellular calcium dyshomeostasis in the heart of obese‐insulin resistant rats
Authors: Palee Siripong , Minta Wanitchaya , Mantor Duangkamol , Sutham Wissuta , Kerdphoo Sasiwan , Pratchayasakul Wasana , Chattipakorn Siriporn C. , Chattipakorn Nipon 
Published: November 2018

AbstractThe incidence of cardiovascular disease and metabolic syndrome increases after the onset of menopause, giving evidence for the vital role of estrogen. Intracellular calcium [Ca2+]i regulation plays an important role in the maintenance of left ventricular (LV) contractile function. Although either estrogen deprivation or obesity has been shown to strongly affect the metabolic status and LV function, the effects of estrogen deprivation on the cardiometabolic status and cardiac [Ca
2+]i regulation in the obese‐insulin resistant condition have never been investigated. Our hypothesis was that estrogen deprivation aggravates LV dysfunction through the increased impairment of [Ca
2+]i homeostasis in obese‐insulin resistant rats. Female rats were fed on either a high‐fat (HFD, 59.28% fat) or normal (ND, 19.77% fat) diet for 13 weeks. Then, rats were divided into sham (HFS and NDS) operated or ovariectomized (HFO and NDO) groups. Six weeks after surgery, metabolic status, LV function and incidence of [Ca
2+]i transients were determined. NDO, HFS, and HFO rats had evidence of obese‐insulin resistance indicated by increased body weight with hyperinsulinemia and euglycemia. Although NDO, HFS, and HFO rats had markedly reduced %LV fractional shortening, E/A ratio and decreased [Ca
2+]i transient amplitude and decay rate, HFO rats had the most severe impairments. These findings indicate that estrogen deprivation had a strong impact on abnormal LV function through [Ca
2+]i regulation. In addition, evidence was found that in obese‐insulin resistant rats, estrogen deprivation severely aggravates LV dysfunction via increased impairment of [Ca
2+]i homeostasis.
Long‐term evaluation of corneal sub‐basal nerve recovery after photorefractive keratectomy and influence of pars plana vitrectomy
Authors: Tosi Gian Marco , Martone Gianluca , Bacci Tommaso , Tarantello Antonio , Baiocchi Stefano , Marigliani Davide , Cevenini Gabriele , Menicacci Flavia , Virgili Gianni , Massaro‐Giordano Giacomina 
Published: November 2018

AbstractThe corneal sub‐basal nerve (SBN) plexus is destroyed during photorefractive keratectomy (PRK) and its recovery is still a matter of debate. In vivo confocal microscopy (IVCM) was used to evaluate SBN plexus in 23 patients at a distance of 10–25 years (mean 15.6 years) from myopic PRK. Because 8 out of the 23 PRK patients underwent pars plana vitrectomy (PPV) for rhegmatogenous retinal detachment, IVCM was also performed on those patients 6 months after PPV. Thirteen patients matched for age and myopia served as controls (non‐PRK). SBN plexus was markedly reduced after PRK compared with non‐PRK eyes and showed a slow, continuous but incomplete recovery up to the end of our follow‐up (range 10–25 years). PRK and non‐PRK eyes showed a marked reduction in SBN density 6 months after PPV, thus demonstrating a detrimental effect exerted by PPV on SBN plexus.