bluuebunny/crossref_metadata_2025_split huggingface dataset:
Male squirting: Analysis of one case using color Doppler ultrasonography
Authors: Hara Ryoei , Nagai Atsushi , Nakatsuka Tohta , Ohira Shin , Fujii Tomohiro , Miyaji Yoshiyuki 
Published: October 2018

IntroductionThere is no scientific evidence for the mechanism of male squirting, although the term is common in mass media. Here, we describe the first recording of male squirting using color Doppler ultrasonography.Case presentationWe recruited a 25‐year‐old male volunteer who was able to have male squirting. A transrectal ultrasound probe was inserted into the rectum and male squirting was observed following normal ejaculation. With penis stimulation for a further 20 s after ejaculation, translucent misty fluids with a creatine level similar to that of urine came from the extraurethral orifice for about 60 s. Color Doppler ultrasonography recorded strong contraction of the prostate and pelvic striated muscles just before male squirting, and then the stream went from the urinary bladder through the prostatic urethra.ConclusionIn male squirting, urine in the bladder gushes out from the external urethral orifice due to strong contraction of the prostate and pelvic striated muscles.
MiR‐143‐3p suppresses cell proliferation, migration, and invasion by targeting Melanoma‐Associated Antigen A9 in laryngeal squamous cell carcinoma
Authors: Han Liang , Tang Mingming , Xu Xinjiang , Jiang Bin , Wei Yingze , Qian Hongyan , Lu Xueguan 
Published: October 2018

AbstractPreviously we found that melanoma‐associated antigen‐A9 (MAGE‐A9) was a significantly upregulated biomarker in laryngeal squamous cell carcinoma (LSCC). A high expression of MAGE‐A9 indicates an unfavorable survival outcome, and the MAGE‐A9 expression level is an independent prognostic factor of LSCC. To explore the mechanism of MAGE‐A9 upregulation, several predicted regulatory microRNAs were screened and validated in LSCC cells. In the current study, we found that miR‐143‐3p (MAGE‐A9 related miRNAs) expression levels correlated negatively with the MAGE‐A9 protein expression in LSCC tissues. Dual‐luciferase reporter assays and Western blot analysis revealed MAGE‐A9 to be a direct target of miR‐143‐3p. Furthermore, a series of in vitro gain‐ and loss‐of‐function assays revealed that miR‐143‐3p inhibited LSCC cell proliferation, migration, and invasion. Also, miR‐143‐3p suppressed LSCC tumorigenesis in vivo. These effects were clinically relevant, as a lower expression of miR‐143‐3p occurred in severer clinical stages and represented poor overall survival in patients with LSCC. Taken together, these results suggest that downregulation of miR‐143‐3p contributes to tumor progression through upregulation of MAGE‐A9. The expression level of these two key molecules maintained LSCC progression, thus, highlighting the potential of miR‐143‐3p as a therapeutic target for human LSCC.
Computational insights into pH‐dependence of structure and dynamics of pyrazinamidase: A comparison of wild type and mutants
Authors: Esmaeeli Reza , Mehrnejad Faramarz , Mir‐Derikvand Mohammad , Gopalpoor Niloofar 
Published: October 2018

AbstractThe mycobacterial enzyme pyrazinamidase (PZase) is the target of key tuberculosis drug, pyrazinamide. Mutations in PZase cause drug resistance. Herein, three point mutations, W68G, L85P, and V155G, were investigated through over 8 µs of molecular dynamics simulations coupled with essential dynamics and binding pocket analysis at neutral (pH = 7) and acidic (pH = 4) ambient conditions. The 51‐71 flap region exhibited drastic displacement leading to enlargement of binding cavity, especially at the lower pH. Accessibility of solvent to the active site of the mutant enzymes was also reduced. The protonation of key surface residues at low pH results in more contribution of these residues to structural stability and integrity of the enzyme and reduced interactions with solvent molecules, which acts as a cage, keeping the enzyme together. The observed results suggest a pattern of structural alterations due to point mutations in PZase, which is consistent with other experimental and theoretical investigations and, can be harnessed for drug design purposes.
Angiotensin‐converting enzyme insertion/deletion (rs106180) and angiotensin type 1 receptor A1166C (rs106165) genotypes and psoriasis: Correlation with cellular immunity, lipid profile, and oxidative stress markers
Authors: Tanhapour Maryam , Falahi Badieh , Vaisi‐Raygani Asad , Bahrehmand Fariborz , Kiani Amir , Rahimi Zohreh , Vaisi‐Raygani Ali‐Akbar , Shakiba Ebrahim , Pourmotabbed Tayebeh 
Published: October 2018

AbstractPsoriasis is a chronic inflammatory skin condition and angiotensin‐converting enzyme (ACE) is a key circulating enzyme converting angiotensin (Ang) I to the vasoactive peptide Ang II. The exact role of ACE insertion (I)/deletion (D) polymorphism (rs106180) in psoriasis is not clear. We aimed to examine whether the ACE I/D and Ang II type 1 receptor (AT1R) A1166C‐polymorphisms (rs106165), lipid profile, and stress oxidative are associated with susceptibility to psoriasis. One hundred patients with psoriasis and 100 sex‐ and age‐matched unrelated healthy controls were recruited for this case‐control study. ACE I/D and AT1R A1166C polymorphisms were identified by the polymerase chain reaction (PCR) and PCR‐restriction fragment length polymorphism, respectively, malondialdehyde (MDA) was detected by the high‐performance liquid chromatography, serum arylesterase (ARE) activity of paraoxonase and catalase activities were detected by the spectrophotometry, superoxide dismutase (SOD) activity and vascular adhesion protein (VAP)‐1 were measured by ELISA. The presence of C allele of AT1R A1166C and I allele of ACE considerably increased the risk of psoriasis by 6.42‐fold (P < 0.001). The distribution of II‐genotype of ACE was significantly higher in psoriasis patients than in control group and increased the risk of disease by 3.11‐times (P = 0.023). The higher levels of MDA in patients and the higher activity of SOD, ARE, and CAT was observed in healthy controls with I/D+I/I‐genotype of ACE I/D. This study for the first time demonstrated that the ACE I/D and AT1R A 1166C genes polymorphisms robustly increases the risk of developing psoriasis in population from west of Iran. In addition, these individuals had significantly higher VAP‐1 and MDA concentration and lower enzymatic and nonenzymatic antioxidant‐status, suggesting that psoriatic patients carrying C allele of AT1R1166 polymorphism may be more susceptible to cardiovascular disease and myocardial infarction compared with A allele.
TrkC‐miR2 regulates TGFβ signaling pathway through targeting of SMAD3 transcript
Authors: Dokanehiifard Sadat , Soltani Bahram M. 
Published: October 2018

AbstractTrkC,neurotrophin receptor, functions inside and outside of the nervous system and has a crucial effect on the regulation of cardiovascular formation. Recently, we introducedTrkC‐miR2as a novel microRNA located inTrkCgene, which is a regulator of the Wnt signaling pathway. Here, we presented a lot of evidence showing thatTrkC‐miR2also regulates the transforming growth factor‐beta (TGFβ) signaling pathway. Bioinformatics studies predictedSMAD3as one of the bona fideTrkC‐miR2target genes. Quantitative reverse transcription PCR (RT‐qPCR), Western blot analysis, and dual luciferase assay analysis confirmed thatSMAD3is targeted byTrkC‐miR2. On the other hand, overexpression ofTrkC‐miR2in cardiosphere‐derived cells (CDCs) rendered downregulation ofTGFβR1,TGFβR2, andSMAD7detected by RT‐qPCR. Consistently, an inverse correlation of expression betweenTrkC‐miR2andSMAD3genes was detected during the course of CDC differentiation, and also during the course of human embryonic stem cells differentiation to cardiomyocytes. Overall, we conclude thatTrkC‐miR2downregulates the expression ofSMAD3and potentially regulates the TGFβ signaling pathway. Knowing its approved effect on Wnt signaling,TrkC‐miR2here is introduced as a common regulator of both the Wnt and TGFβ signaling pathways. Therefore, it may be a potential key element in controlling both of these signaling pathways in cell processes like colorectal cancer and cardiogenesis.
Upregulation of lincRNA‐p21 in thoracic aortic aneurysms is involved in the regulation of proliferation and apoptosis of vascular smooth muscle cells by activating TGF‐β1 signaling pathway
Authors: Hu Wenxian , Wang Zhaowei , Li Qiang , Wang Jinjun , Li Lin , Jiang Guixi 
Published: October 2018

AbstractObjectiveLong intergenic noncoding RNA‐p21 (lincRNA‐p21) has been proved in the pathogenesis of aortic aneurysms, while its functionality in thoracic aortic aneurysms (TAA) and the mechanism of function remains unclear. Therefore our study aimed to investigate the role of lincRNA‐p21 in TAA.MethodsAortic media specimens and blood samples were collected from both patients with TAA and healthy controls. Expression of lincRNA‐p21 in those tissues was detected by reverse‐transcription quantitative polymerase chain reaction (qRT‐PCR). Diagnostic values of lincRNA‐p21 in aortic media and blood for TAA were evaluated by receiver operating characteristic curve analysis. LincRNA‐p21 overexpression human vascular smooth muscle cells (VSMCs) were prepared and the effects of lincRNA‐p21 overexpression on cell proliferation and apoptosis were explored by cell counting kit‐8 assay and 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide assay, respectively. Expression of lincRNA‐p21 and transforming growth factor β1 (TGF‐β1) in VSMCs with different treatment was detected by qRT‐PCR and Western blot analysis, respectively.ResultsExpression of lincRNA‐p21 in aortic media tissues and blood was significantly upregulated in TAA patients than in healthy controls. Expression of lincRNA‐p21 in aortic media and blood can be used to effectively distinguish TAA patients form healthy controls. LincRNA‐p21 overexpression inhibited proliferation and promoted apoptosis of VSMCs, while TGF‐β1 inhibitor reduced those effects. LincRNA‐p21 overexpression upregulated TGF‐β1 expression, while TGF‐β1 activator showed no significant effects on lincRNA‐p21 expression in VSMC.ConclusionLincRNA‐p21 participates in TAA by regulating the proliferation and apoptosis of VSMCs through the activation of TGF‐β1 signaling pathway.
Comparing the efficacy of pain managements after total hip arthroplasty: A network meta‐analysis
Authors: Liu Pengcheng , Wu Yingbo , Liang Zhiquan , Deng Yingjie , Meng Qingcai 
Published: October 2018

AbstractThe aim of our current study is to compare efficiency of various interventions implemented for pain management after total hip arthroplasty (THA). PubMed and EMBASE were searched for randomized clinical trials (RCTs) reporting the pain scales for evaluate the efficacy of pain control after THA including at least one pair of direct control groups. Pain scale values and the associated 95% credible interval (CrI) were used to describe efficacy. Surface under the cumulative ranking curve (SUCRA) of each means of pain control was calculated to compare the relative ranking of different interventions. Thirty‐five eligible literatures were involved in data analysis. The interventions for postoperative pain management we examined were psoas compartment block (PCB), posterior nerve block (PNB), fascia iliaca block (FIB), periarticular injection (PAI), femoral nerve block (FNB), lumbar plexus block (LPB), spinal anesthesia (SA), epidural analgesia (EPI), intrathecal morphine (IA), intravenous patient‐controlled analgesia (IV‐PCA), patient‐controlled analgesia (PCA), onsteroidal anti‐inflammatory drug (NSAID), local infiltration analgaesia (LIA), and reverse LIA (rLIA). In 0 to 6 hours analysis, patients under SA were found to have significantly lower pain score and SA was ranked the best. In 6 to 12 hours analysis, SA was found to be significantly more effective than other interventions and its SUCRA was the highest. No intervention showed a significant effect on reducing pain score for 12 to 24 hours and 24 to 48 hours after THA. SA is the best intervention to reduce THA postoperative pain in the first 24 hours. LPB is a better choice to reduce pain 12 to 48 hours after THA.
Identification of differentially expressed long noncoding RNAs in human knee osteoarthritis
Authors: Xiao Ke , Yang Yuemei , Bian Yanyan , Feng Bin , Li Zeng , Wu Zhihong , Qiu Guixing , Weng Xisheng 
Published: October 2018

AbstractLong noncoding RNAs (lncRNAs) are considered a novel class of regulatory factors in many diseases, but their biological function and the signaling pathway involved in osteoarthritic (OA) remain unknown. To identify the lncRNAs specifically expressed in OA cartilage, the expression of lncRNAs in OA cartilage was measured using an illumina sequencing platform. Furthermore, differentially expressed transcripts of uncertain coding potential (TUCPs) and messenger RNAs (mRNAs) were identified. The colocated target genes and the possible role of lncRNAs as a competing endogenous RNA (ceRNA) were predicted. Based on 19 samples from osteoarthritis patients of knees, 580 significantly dysregulated lncRNAs as well as differently expressed TUCPs and mRNAs were identified. Four differently expressed lncRNAs (SNHG5, ZFAS1, GAS5, and DANCR) involved in OA cartilage were analyzed by protein‐protein interactions network and ceRNA regulatory network. Part of our results were consistent with previous studies, and 96 novel differently expressed lncRNAs were identified in OA. These results could expand our knowledge of the OA mechanism.
Embryonic poly(A)‐binding protein is differently expressed and interacts with the messenger RNAs in the mouse oocytes and early embryos
Authors: Uysal Fatma , Ozturk Saffet 
Published: October 2018

AbstractThe embryonic poly(A)‐binding protein (EPAB) functions in the translational regulation of the maternal messenger RNAs (mRNAs) required during oocyte maturation, fertilization, and early embryo development. Since there is no antibody specific to mammalian EPAB protein, all studies related to the Epab gene could be performed at the mRNA levels except for the investigations in the
Xenopus. In this study, we have produced an EPAB‐specific antibody. When we examined its expressional distribution in the mouse gonadal and somatic tissues, the EPAB protein was found to be expressed only in the mouse ovary and testis tissues, but it is undetectable level in the somatic tissues including stomach, liver, heart, small intestine, and kidney. Additionally, the spatial and temporal expression patterns of the EPAB and poly(A)‐binding protein cytoplasmic 1 (PABPC1) proteins were analyzed in the mouse germinal vesicle (GV) and metaphase II (MII) oocytes, one‐cell, and two‐cell embryos. While EPAB expression gradually decreased from GV oocytes to two‐cell embryos, the PABPC1 protein level progressively increased from GV oocytes to one‐cell embryos and remarkably declined in the two‐cell embryos (
P < 0.05). We have also described herein that the EPAB protein interacted with
Epab,
Pabpc1,
Ccnb1,
Gdf9, and
Bmp15 mRNAs dependent upon the developmental stages of the mouse oocytes and early embryos. As a result, we have first produced an EPAB‐specific antibody and characterized its expression patterns and interacting mRNAs in the mouse oocytes and early embryos. The findings suggest that EPAB in cooperation with PABPC1 implicate in the translational control of maternal mRNAs during oogenesis and early embryo development.
Photodynamic treatment with anionic nanoclays containing curcumin on human triple‐negative breast cancer cells: Cellular and biochemical studies
Authors: Khorsandi Khatereh , Hosseinzadeh Reza , Shahidi Fedora Khatibi 
Published: October 2018

AbstractPhotodynamic treatment is a minimally invasive and clinically approved procedure for eliminating selected malignant cells with activation of a photosensitizer agent at a specific light. Little is known, however, about the phototoxic properties of curcumin, as a natural phenolic compound, against different types of cancers. It is generally accepted that cellular damage occurs during photo treatment. There is a limitation in using of curcumin as a drug due to its low solubility, but nanoparticles such as anionic nanoclays or layered double hydroxide (LDH) could overcome it. The aim of this study was to investigate cellular responses to curcumin‐LDH nanoparticles after photodynamic treatment of MDA‐MB‐231 human breast cancer cells. For this purpose, the MDA‐MB‐231 human breast cancer cell line treated with curcumin‐LDH nanoparticle and then irradiated (photodynamic treatment). After irradiation, lactate dehydrogenase assay, clonogenic cell survival, cell death mechanisms such as autophagy and apoptosis were determined. Cell cycle distribution after photodynamic therapy (PDT) and also intracellular reactive oxygen species (ROS) generation were measured. The result showed that curcumin‐LDH–PDT has a cytotoxic and antiprolifrative effect on MDA‐MB‐231 human breast cancer cells. Curcumin‐LDH–PDT induced autophagy, apoptosis, and G0/G1 cell cycle arrest in human breast cancer cell line. Intracellular ROS increased in MDA‐MB‐231 cancer cell line after treatment with curcumin‐LDH along with irradiation. The results suggest that curcumin‐LDH nanoparticle could be considered as a novel approach in the photodynamic treatment of breast cancer.
miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1
Authors: Zhao Xuefeng , Xu Yan , Sun Xiaoya , Ma Yuan , Zhang Yan , Wang Yadong , Guan Hongya , Jia Zhen , Li Yuebai , Wang Yisheng 
Published: October 2018

AbstractMicroRNA‐17‐5p (miR‐17‐5p) and epithelial‐mesenchymal transition (EMT) have been reported to participate in the development and progression of multiple cancers. However, the relationship between the miR‐17‐5p and EMT in osteosarcoma (OS) is still poorly understood. This study was to investigate the effects of the miR‐17‐5p and its potential mechanism in regulating proliferation, apoptosis, and EMT of human OS. Quantitative real‐time PCR was used to detect the miR‐17‐5p and SRC kinase signaling inhibitor 1 (SRCIN1) messenger RNA expression in OS specimens and cell lines. After transfection with miR‐17‐5p inhibitors, proliferation, apoptosis, migration, and invasion of OS cells were assessed by using the Cell Counting Kit‐8, the annexin V‐FITC apoptosis, wound‐healing, and transwell assays. The SRCIN1 was validated as a target of the miR‐17‐5p through bioinformatics algorithms and luciferase reporter assay. Moreover, the expression of EMT markers, E‐cadherin, N‐cadherin, and Snail was identified by the Western blot analysis. MiR‐17‐5p was significantly upregulated in OS tumor samples and cell lines. It inhibited proliferation and EMT, and promoted apoptosis in OS. The SRCIN1 was identified as a direct target of the miR‐17‐5p. Silenced miR‐17‐5p could change the expression of EMT markers, such as upregulating the expression of E‐cadherin, and downregulating the expression of N‐cadherin and Snail through targeting the antioncogenic SRCIN1. These findings suggest that the miR‐17‐5p promotes cell proliferation, and EMT in human OS by directly targeting the SRCIN1, and reveal a branch of the miR‐17‐5p/SRCIN1/EMT signaling pathway involved in the progression of OS.
A novel agent attenuates cardiotoxicity and improves antitumor activity of doxorubicin in breast cancer cells
Authors: Zhang Ying , Deng Hongkuan , Zhou Hefeng , Lu Yucong , Shan Luchen , Lee Simon Ming‐Yuen , Cui Guozhen 
Published: October 2018

AbstractDoxorubicin (Dox) is a well‐known chemotherapeutic agent used in the treatment of various cancers. However, Dox‐induced cardiotoxicity limits its further clinical use. We have previously reported a small molecular named biotin‐conjugated ADTM analog (BAA) that exhibits cytoprotective effects against oxidative stress–induced cell injury in cardiomyoblast H9c2 cells. Here, the protective effects of BAA, indexed by attenuation of the cardiotoxicity induced by Dox as well as synergistic antitumor activity that increases the chemotherapeutic efficacy of Dox were investigated. Our results demonstrated that BAA significantly ameliorated Dox‐induced toxicity in the H9c2 cells and zebrafish models. In addition, BAA attenuated Dox‐induced endoplasmic reticulum (ER) stress in H9c2 cells. An ER stress inhibitor, 4‐phenylbutyric acid, reversed the protective effect of BAA in H9c2 cells. In contrast, in human breast tumor MDA‐MB‐231 cells, BAA significantly enhanced Dox‐induced cytotoxicity through upregulating Dox‐induced ER stress response. Taken together, our findings indicate that Dox combined with BAA can significantly enhance its antitumor activity in breast cancer cells and reduce its cardiotoxicity, at least in part, by mediating ER stress activation.
Retracted: Role of RKIP in human hepatic stellate cell proliferation, invasion, and metastasis
Authors: Huang Quanfang , Wei Jinbin , Wei Ling , Zhang Xiaolin , Bai Facheng , Wen Shujuan , Wei Yuanyuan , Tan Shimei , Lu Zhongpeng , Lin Xing 
Published: October 2018

AbstractThe purpose of this study was to investigate the effect of Raf kinase inhibitor protein (RKIP) on the growth, apoptosis, invasion, and metastasis of human hepatic stellate cell line (LX‐2). A recombinant plasmid (pcDNA3.1‐RKIP) or RKIP‐targeting small interfering RNA (siRNA) vector (siRNA‐RKIP) was transfected into LX‐2 cells to interfere with the RKIP expression. The results demonstrated that increased RKIP expression significantly reduced cell viability, clonogenic growth, and invasion. Further, it promoted cell apoptosis and induced cell cycle arrest in the G1 phase. Overexpression of RKIP led to inactivation of LX‐2 cells, as evidenced by the decrease in the expression levels of collagen I and α‐smooth muscle actin (α‐SMA). In addition, increased RKIP expression significantly reduced the phosphorylation of Raf/extracellular signal‐regulated kinase (ERK)/mitogen‐activated protein kinase (MAPK), the transcriptional activity of nuclear factor‐κB (NF‐κB), and the levels of matrix metalloproteinases‐1 and ‐2. In conclusion, these findings clearly demonstrate that RKIP inhibits LX‐2 cell growth, metastasis, and activation, primarily by downregulating the ERK/MAPK and NF‐κB signaling pathways.