bluuebunny/crossref_metadata_2025_split huggingface dataset:
Downregulation of microRNA‐214 improves therapeutic potential of allogeneic bone marrow–derived mesenchymal stem cell by targeting PIM‐1 in rats with acute liver failure
Authors: Yang Juan , Li Rui , Zhao Dan , Zheng Sheng 
Published: April 2019

AbstractAcute liver failure (ALF) is a disease resulted from diverse etiology, which generally leads to a rapid degenerated hepatic function. However, transplantation bone marrow–derived mesenchymal stem cells (BMSCs) transplantation has been suggested to relieve ALF. Interestingly, microRNA‐214 (miR‐214) could potentially regulate differentiation and migration of BMSCs. The present study aims to inquire whether miR‐214 affects therapeutic potential of BMSCs transplantation by targeting PIM‐1 in ALF. 120 male Wistar rats were induced as ALF model rats and transplanted with BMSCs post‐alteration of miR‐214 or PIM‐1 expression. Further experiments were performed to detect biochemical index (alanine aminotransferase [ALT], aspartate transaminase [AST], total bilirubin [TBiL]), and expression of miR‐214, PIM‐1, hepatocyte growth factor (HGF), caspase 3, tumor necrosis factor‐α (TNF‐α), and interleukin‐10 (IL‐10) in rat serum. Apart from the above detection, apoptosis of hepatocytes and Ki67 protein expression in hepatic tissues of rats were additionally assessed. After BMSCs transplantation with miR‐214 inhibition, a decreased expression of ALT, AST, and TBiL yet an increased expression of HGF was shown, coupled with a decline in the expression of caspase 3, TNF‐α, and IL‐10. Meanwhile, alleviated hepatic injury and decreased apoptotic index of hepatic cells were observed and the positive rate of Ki67 protein expression was significantly increased. Moreover, miR‐214 and caspase 3, TNF‐α, and IL‐10 decreased notably, while PIM‐1 was upregulated in response to miR‐214 inhibition. Strikingly, the inhibition of PIM‐1 reversed effects triggered by miR‐214 inhibition. These findings indicated that downregulation of miR‐214 improves therapeutic potential of BMSCs transplantation by upregulating PIM‐1 for ALF.
Efficacy of ten interventions for endometriosis: A network meta‐analysis
Authors: Chen Yan , Wang Hua , Wang Saili , Shi Xinying , Wang Qin , Ren Qingling 
Published: April 2019

AbstractObjectiveClinical trials comparing the efficacy of different interventions for endometriosis are limited and controversial. The aim of the present study is to perform a network meta‐analysis on the efficacy of various interventions for endometriosis.MethodsWe searched PubMed and Ovid EMBASE through 1 June, 2018, for trials reporting the pain score and 1‐year pregnancy rate of patients including at least one pair of direct control group. The mean difference of pain score, odds ratio of 1‐year pregnancy rate, and their associated 95% credible intervals (CrI) were used to describe efficacy. The surface under the cumulative ranking curve (SUCRA) was calculated to illustrate the rank probability of various treatments for different outcomes, on the basis of network meta‐analysis.ResultsOur meta‐analysis enrolled six studies for the evaluation of reducing pain and 10 studies for the 1‐year pregnancy rate. All involved trials were sufficiently powered with a low risk of bias. Expectant management (EM), progesterone (PR), and gonadotropin‐releasing hormone (GnRH)‐agonist (GN) were significantly effective to reduce pain when compared with the placebo; EM ranked the highest on the SUCRA curve. For the 1‐year pregnancy rate, no significant difference between the interventions was evident. Ablation ranked the highest with a SUCRA value of 0.6328. The rank of EM was acceptable with a SUCRA value of 0.4452. Our experimental results need to be verified by more high‐quality randomized controlled trial articles.ConclusionLimited available evidence showed that EM, PR, and GN were significantly effective to reduce pain when compared with the placebo. Due to a lack of convincing evidence favoring surgery or medication, we recommend considering EM.
Relationship between microbial diversity and nitrogenase activity of Stipagrostis pennata rhizosheath
Authors: Tian Yongzhi , Ma Xiaolin , Li Yuanting , Cheng Cong , Ge Fengwei , An Dengdi 
Published: April 2019

AbstractNitrogen is the key factor for plant survival and growth, especially in the desert. Stipagrostis pennata, a sand born drought‐resistant plant, could colonize pioneerly in Gurbantunggut Desert during revegetation. One strategy for their environment adaptation was the rhizosheath formatted by root‐hair, mucilaginous exudates, microbial components, and soil particles, for which not only provides a favorable living microenvironment but also supplies essential nutrients. To understand the relationship between microorganisms living in rhizosheaths and the nitrogen nutrition supply, the microbial diversity and nitrogenase activity was estimated during the growth of S. pennata. Five samples of the rhizosheath, which based on the development periods of the plant, regreen, flowering, filling, seed maturating, and withering period, were collected. The nitrogenase activity was estimated by acetylene reduction and the microbial diversity was analyzed by 16S rRNA high‐throughput sequencing. The results showed that the nitrogenase activity was increased slowly during regreen to flowering, while reached a peak rapidly at filling sample and then decreased gradually. A total of 274 operational taxonomic units (OTUs) were identified and significant differences in community structure and composition at each growth period. Among them, the main phyla included Actinobacteria and Proteus, which were the most abundant phyla in all periods. In addition, the microbial diversity in the grain filling period was higher than other periods in view of the analysis of alpha diversity and beta diversity. Furthermore, principal component analysis (PCA) analysis showed that the microbial communities in the filling period was low in similarity with other periods. Most importantly, the OTUs associated with nitrogen fixation is the most during the filling period, involving Phagecidae and Fucoraceae. Overall, the study not only revealed the differences in nitrogenase activity among different developmental periods in S. pennata, but also explored the potential bridges between it and community structure and diversity of bacteria.
Bioprospection of anti‐inflammatory phytochemicals suggests rutaecarpine and quinine as promising 15‐lipoxygenase inhibitors
Authors: Gurung Arun Bahadur , Pamay Pezaiwi , Tripathy Debabrata , Biswas Koel , Chatterjee Anupam , Joshi S.R. , Bhattacharjee Atanu 
Published: April 2019

Abstract15‐Lipoxygenase (15‐LOX) belongs to the family of nonheme iron containing enzymes that catalyzes the peroxidation of polyunsaturated fatty acids (PUFAs) to generate eicosanoids that play an important role in signaling pathways. The role of 15‐LOX has been demonstrated in atherosclerosis as well as other inflammatory diseases. In the present study, drug‐like compounds were first screened from a set of anti‐inflammatory phytochemicals based on Lipinski's rule of five (ROF) and in silico toxicity filters. Two lead compounds‐quinine (QUIN) and rutaecarpine (RUT) were shortlisted by analyzing molecular interactions and binding energies of the filtered compounds with the target using molecular docking. Molecular dynamics simulation studies indicate stable trajectories of apo_15‐LOX and docked complexes (15‐LOX_QUIN and 15‐LOX_RUT). In vitro 15‐LOX inhibition studies shows that both QUIN and RUT have lower inhibitory concentration (IC50) value than the control (quercetin). Both QUIN and RUT exhibit moderate antioxidant activities. The cell viability study of these compounds suggests no significant toxicity in HEK‐293 cell lines. Further, QUIN and RUT both did not show any inhibition against selected Gram‐positive and Gram‐negative bacterial species. Thus, based on our present findings, rutaecarpine and quinine may be suggested as promising 15‐LOX inhibitor for the prevention of the atherosclerosis development.
Evaluation of cord blood immunoglobulin E and its association with maternal factors in a group of Iranian newborns
Authors: Fereidouni Mohammad , Nami Fateme Arefe , Serki Elham , Arefi Majid 
Published: April 2019

AbstractAllergic disorders are among the most common diseases around the world especially in children. Many factors contribute to the pathogenesis of atopic disorders, but early events during the pregnancy are very important. The aim of this study was to evaluate the level of cord blood immunoglobulin E (CB‐IgE) and its association with maternal in a group of Iranian newborns. In a cross‐sectional study, 163 pregnant women randomly selected and information about pregnancy and atopy were taken by questionnaire. Blood samples of mothers and matched cord blood were collected and total serum IgE levels were measured by enzyme‐linked immunosorbent assay (ELISA) method. To rolling out the possibility of contamination with maternal blood, total IgA was checked for all the cord blood samples. Sixteen percent of mothers had the history of atopic diseases and the mean IgE level was significantly higher in an atopic than nonatopic mothers (241 vs 102, P < 0.001). About 73.9% of cord blood samples, had high IgE level (>0.9 IU/mL). The level of cord blood IgE (CB‐IgE) was not significantly different in male and female newborns (2.14 vs 2.15 IU/mL). There was no significant correlation between maternal factors such as age, pregnancy variables, allergens exposure, smoking, and maternal IgE with cord blood IgE. The results of this study showed that CB‐IgE is high in a remarkable number of samples; independent of maternal or fetal factors. Further studies need to evaluate the reasons for the high level of IgE in cord blood in our area.
The inflammatory cytokine TNF‐α regulates the biological behavior of rat nucleus pulposus mesenchymal stem cells through the NF‐κB signaling pathway in vitro
Authors: Cheng Shi , Li Xiaochuan , Jia Zhiwei , Lin Linghan , Ying Jinwei , Wen Tianyong , Zhao Yachao , Guo Ziming , Zhao Xiyan , Li Dandan , Ji Wei , Wang Deli , Ruan Dike 
Published: April 2019

AbstractNucleus pulposus (NP) mesenchymal stem cells (NPMSCs) are a potential cell source for intervertebral disc (IVD) regeneration; however, little is known about their response to tumor necrosis factor‐α (TNF‐α), a critical inflammation factor contributing to accelerating IVD degeneration. Accordingly, the aim of this study was to investigate the regulatory effects of TNF‐α at high and low concentrations on the biological behaviors of healthy rat NPMSCs, including proliferation, migration, and NP differentiation. In this study, NPMSCs were treated with different concentration of TNF‐α (0‐200 ng/mL). Then we used annexin V/propidium iodide flow cytometry analysis to detect the apoptosis rate of NPMSCs. Cell Counting Kit‐8, Edu assay, and cell cycle test were used to examine the proliferation of NPMSCs. Migration ability of NPMSCs was detected by wound healing assay and transwell migration assay. Pellets method was used to induce NP differentiation of NPMSCs, and immunohistochemical staining, real‐time polymerase chain reaction, and Western blot analysis were used to examine the NPC phenotypic genes and proteins. The cells were further treated with the nuclear factor‐κB (NF‐κB) pathway inhibitor Bay 11‐7082 to determine the role of the NF‐κB pathway in the mechanism underlying the differentiation process. Results showed that treatment with a high concentration of TNF‐α (50‐200 ng/mL) could induce apoptosis of NPMSCs, whereas a relatively low TNF‐α concentration (0.1‐10 ng/mL) promoted the proliferation and migration of NPMSCs, but inhibited their differentiation toward NP cells. Moreover, we identified that the NF‐κB signaling pathway is activated during the TNF‐α‐inhibited differentiation of NPMSCs, and the NF‐κB signal inhibitor Bay 11‐7082 could partially eliminate the adverse effect of TNF‐α on the differentiation of NPMSCs. Therefore, our findings provide important insight into the dynamic biological behavior reactivity of NPMSCs to TNF‐α during IVD degeneration process, thus may help us understanding the underlying mechanism of IVD degeneration.
The N‐terminal His‐tag affects the triglyceride lipase activity of hormone‐sensitive lipase in testis
Authors: Wang Feng , Ren Xiao‐Fang , Chen Zheng , Li Xiao‐Long , Zhu Hai‐Jing , Li Sen , Ou Xiang‐Hong , Zhang Cheng , Zhang Fei‐Xiong , Zhu Bao‐Chang 
Published: April 2019

AbstractThe sterility of hormone‐sensitive lipase (HSL) knockout mice clearly shows the link between lipid metabolism and spermatogenesis. However, which substrate or product of this multifunctional lipase affects spermatogenesis is unclear. We found that an HSL protein with a His‐tag at the N‐terminus preserved the normal hydrolase activity of cholesteryl ester (CE) but the triglyceride lipase (TG) activity significantly decreased in vitro. Therefore, mice with this functionally incomplete HSL (His‐HSL) were produced on a background of HSL deficiency (HSL−/−h). As a result, HSL−/−h testis has an 8.65‐fold higher CE activity than wild‐type testis but a twofold higher TG activity than wild‐type testis. To compare His‐HSL and wild‐type HSL in vitro and in vivo, we confirmed that the His‐tag significantly suppressed HSL TG activity. From our results, we believe that TG activity was affected by the His‐tag insertion, but CE activity was not influenced. Furthermore, the His‐tag protected HSL from binding to the inhibitor BAY. From our study, TG activity and BAY binding sites were affected by N‐terminal His‐tag insertion.
Epigenetic modulation of BRCA‐1 and MGMT genes, and histones H4 and H3 are associated with breast tumors
Authors: Paydar Parisa , Asadikaram Gholamreza , Nejad Hamid Zeynali , Akbari Hamed , Abolhassani Moslem , Moazed Vahid , Nematollahi Mohammad Hadi , Ebrahimi Ghasem , Fallah Hossein 
Published: April 2019

AbstractAberrant patterns in promoter methylation of tumor‐suppressor genes and posttranslational modifications of histone proteins are considered as major features of malignancy. In this study, we aimed to investigate promoter methylation of three tumor‐suppressor genes (BRCA‐1, MGMT, and P16) and three histone marks (H3K9ac, H3K18ac, and H4K20me3) in patients with breast tumors. This case‐control study included 27 patients with malignant breast tumors (MBT) and 31 patients with benign breast tumors (BBT). The methylation‐specific PCR was used for determining promoter methylation of BRCA‐1, MGMT, and P16 genes. Western blot analysis was performed to detect histone lysine acetylation (H3K9ac and H3K18ac) and lysine methylation (H4K20me3). BRCA‐1 promoter methylation was detected in 44.4% of the MBT whereas this alteration was found in 9.7% of BBT (P = 0.005). The Kaplan‐Meier analysis indicated that hypermethylation in BRCA‐1 promoter was significantly associated with poor overall survival of patients with breast cancer (P = 0.039). MGMT promoter methylation was identified in 18.5% of MBT and 0.0% of the BBT (P = 0.01). The frequency of P16 promoter methylation was 25.8% in BBT and 11.1% in MBT (P = 0.12). As compared with BBT, MBT samples displayed the aberrant patterns of histones marks with hypomethylation of H4K20 and hypoacetylation of H3K18 (P = 0.03 and P = 0.04, respectively). There was a negative significant correlation between H3K9ac levels and tumor size in MBT group (r = −0.672; P = 0.008). The present findings suggest that promoter hypermethylation of MGMT and BRCA‐1 genes along with alterations in H3K18ac and H4K20me3 levels may have prognostic values in patients with breast cancer. Moreover, the detection of these epigenetic modifications in breast tumors could be helpful in finding new methods for breast cancer therapy.
Long noncoding RNAs expression in gastric cancer
Authors: Esfandi Farbod , Taheri Mohammad , Kholghi Oskooei Vahid , Ghafouri‐Fard Soudeh 
Published: April 2019

AbstractLong noncoding RNAs (lncRNAs) have been involved in the pathogenesis of several human cancers including gastric cancer. In the current study, we selected five lncRNAs namely NEAT1, TUG1, PANDA, UCA1, and GHET1 to assess their expressions in gastric cancer samples compared with adjacent noncancerous tissues (ANCTs) from the same patients. Some previous reports have shown contribution of these lncRNAs in gastric cancer. However, we aimed to explore their associations with patients’ clinicopathological data and their potential as diagnostic biomarkers. Significant associations were found between site of primary tumor and relative expression of all lncRNAs in cancer samples compared with ANCTs. Besides, GHET1 relative expression was associated with lymph node status. The diagnostic power of GHET1 was higher from other lncRNAs. Combination of GHET1, TUG1, UCA1, and PANDA increased the diagnostic power and significance (AUC = 0.8; P < 0.0001). The current study supports participation of lncRNAs in the pathogenesis of gastric cancer and highlights their potential as diagnostic biomarkers.
PCR detection for syphilis diagnosis: Status and prospects
Authors: Zhou Chenglong , Zhang Xiaohong , Zhang Wei , Duan Junxia , Zhao Feijun 
Published: April 2019

Syphilis, a re‐emerging public health problem worldwide caused by Treponema pallidum subsp pallidum (T. pallidum), usually induces systemic and chronic inflammation in hosts who do not receive timely therapy after exposing to high‐risk factors such as leprous sexual contact. Before the treatment, rapid and accurate detection of syphilis is essential. However, the existing detection methods, which focus on the treponemal or non‐treponemal antibody test, both have inherent limitations. For instance, both of them cannot distinguish the stage and severity of syphilis. Non‐treponemal test such as RPR, which is generally deemed to be used for assessing treatment response, is influenced by biological false positives. Therefore, it is imperative to seek out a new and effective diagnostic test. With recent advancements in molecular biology and whole‐genome sequencing, the molecular diagnosis has increased in popularity, especially the use of polymerase chain reaction (PCR). Here, we firstly present a mini‐review on the research of PCR detection methods used for syphilis diagnosis over the past decade, and we then compare these methodologies to assess their potential and the challenges faced. This information can provide a fresh perspective to help researchers address the current challenges.
Human umbilical artery endothelial cells from Large‐for‐Gestational‐Age newborn have increased antioxidant efficiency and gene expression
Authors: Carrasco‐Wong Ivo , Hernández Cherie , Jara‐Gutiérrez Carlos , Porras Omar , Casanello Paola 
Published: April 2019

AbstractObesity is a public health problem worldwide, and especially in women in reproductive age where more than one in three have obesity. Maternal obesity is associated with an increased maternal, placental, and newborn oxidative stress, which has been proposed as a central factor in vascular dysfunction in large‐for‐gestational‐age (LGA) newborn. However, cellular and molecular mechanisms behind this effect have not been elucidated. Untreated human umbilical artery endothelial cells (HUAEC) from LGA (LGA‐HUAEC) presented higher O2− levels, superoxide dismutase activity and heme oxygenase 1 messenger RNA (mRNA) levels, paralleled by reduced GSH:GSSG ratio and NRF2 mRNA levels. In response to an oxidative challenge (hydrogen peroxide), only HUAEC from LGA exhibited an enhanced Glutathione Peroxidase 1 (GPX1) expression, as well as a more efficient antioxidant machinery measured by the biosensor probe, HyPer. An open state of chromatin in the TSS region of GPX1 in LGA‐HUAEC was evidenced by the DNase‐HS assay. Altogether, our data indicate that LGA‐HUAEC have an altered cellular and molecular antioxidant system. We propose that a chronic pro‐oxidant intrauterine milieu, as evidenced in pregestational obesity, could induce a more efficient antioxidant system in fetal vascular cells, which could be maintained by epigenetic mechanism during postnatal life.
The interplay between glioblastoma and microglia cells leads to endothelial cell monolayer dysfunction via the interleukin‐6‐induced JAK2/STAT3 pathway
Authors: Couto Marina , Coelho‐Santos Vanessa , Santos Liliana , Fontes‐Ribeiro Carlos , Silva Ana Paula , Gomes Célia M. F. 
Published: April 2019

AbstractGlioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor, with an average life expectancy of 12–15 months. GBM is highly infiltrated by microglial cells (MG) promoting tumor growth and invasiveness. Moreover, microglia activation and subsequent neuroinflammation seem to be involved in blood–brain barrier (BBB) dysfunction commonly observed in several central nervous system diseases, including brain tumors. Nevertheless, how the crosstalk between microglia and tumor cells interferes with BBB function is far from being clarified. Herein, we evaluated the effects of reciprocal interactions between MG and GBM cells in the barrier properties of brain endothelial cells (ECs), using an in vitro approach.The exposure of ECs to the inflammatory microenvironment mediated by MG‐GBM crosstalk induced a decrease in the transendothelial electric resistance and an increase in permeability across the ECs (macromolecular flux of 4 kDa‐fluorescein isothiocyanate and 70 kDa‐Rhodamine B isothiocyanate–Dextran). These effects were accompanied by a downregulation of the intercellular junction proteins, β‐catenin and zonula occludens. Moreover, the dynamic interaction between microglia and tumor cells triggered the release of interleukin‐6 (IL‐6) by microglia and subsequent activation of the downstream Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway. Interestingly, the depletion of IL‐6 or the blockade of the JAK/STAT3 signaling with AG490 were able to prevent the EC hyperpermeability. Overall, we demonstrated that IL‐6 released during MG‐GBM crosstalk leads to barrier dysfunction through the activation of the JAK/STAT3 pathway in ECs and downregulation of intercellular junction proteins. These results provide new insights into the mechanisms underlying the disruption of BBB permeability in GBM.
Osteogenic transdifferentiation of vascular smooth muscle cells isolated from spontaneously hypertensive rats and potential menaquinone‐4 inhibiting effect
Authors: Mandatori Domitilla , Pipino Caterina , Di Tomo Pamela , Schiavone Valeria , Ranieri Antonia , Pantalone Sara , Di Silvestre Sara , Di Pietrantonio Nadia , Ucci Mariangela , Palmerini Carola , Failli Paola , Di Pietro Natalia , Pandolfi Assunta 
Published: April 2019

AbstractVascular calcification (VC) is an active and cell‐mediated process that shares many common features with osteogenesis. Knowledge demonstrates that in the presence of risk factors, such as hypertension, vascular smooth muscle cells (vSMCs) lose their contractile phenotype and transdifferentiate into osteoblastic‐like cells, contributing to VC development. Recently, menaquinones (MKs), also known as Vitamin K2 family, has been revealed to play an important role in cardiovascular health by decreasing VC. However, the MKs' effects and mechanisms potentially involved in vSMCs osteoblastic transdifferentiation are still unknown. The aim of this study was to investigate the possible role of menaquinone‐4 (MK‐4), an isoform of MKs family, in the modulation of the vSMCs phenotype. To achieve this, vascular cells from spontaneously hypertensive rats (SHR) were used as an in vitro model of cell vascular dysfunction. vSMCs from Wistar Kyoto normotensive rats were used as control condition. The results showed that MK‐4 preserves the contractile phenotype both in control and SHR‐vSMCs through a γ‐glutamyl carboxylase‐dependent pathway, highlighting its capability to inhibit one of the mechanisms underlying VC process.Therefore, MK‐4 may have an important role in the prevention of vascular dysfunction and atherosclerosis, encouraging further in‐depth studies to confirm its use as a natural food supplement.