bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pain, Quality of Life, and Safety Outcomes of Kyphoplasty for Vertebral Compression Fractures: Report of a Task Force of the American Society for Bone and Mineral Research
Authors: Rodriguez Alexander J , Fink Howard A , Mirigian Lynn , Guañabens Nuria , Eastell Richard , Akesson Kristina , Bauer Douglas C , Ebeling Peter R 
Published: May 2017

ABSTRACT

The relative efficacy and harms of balloon kyphoplasty (BK) for treating vertebral compression fractures (VCF) are uncertain. We searched multiple electronic databases to March 2016 for randomized and quasi-randomized controlled trials comparing BK with control treatment (nonsurgical management [NSM], percutaneous vertebroplasty [PV], KIVA VCF treatment system [Benvenue Medical, Inc., Santa Clara, CA, USA], vertebral body stenting, or other) in adults with VCF. Outcomes included back pain, back disability, quality of life, new VCF, and adverse events (AEs). One reviewer extracted data, a second checked accuracy, and two rated risk of bias (ROB). Mean differences and 95% confidence intervals (CIs) were calculated using inverse-variance models. Risk ratios of new VCF and AE were calculated using Mantel-Haenszel models. Ten unique trials enrolled 1837 participants (age range, 61 to 76 years; 74% female), all rated as having high or uncertain ROB. Versus NSM, BK was associated with greater reductions in pain, back-related disability, and better quality of life (k = 1 trial) that appeared to lessen over time, but were less than minimally clinically important differences. Risk of new VCF at 3 and 12 months was not significantly different (k = 2 trials). Risk of any AE was increased at 1 month (RR = 1.73; 95% CI, 1.36 to 2.21). There were no significant differences between BK and PV in back pain, back disability, quality of life, risk of new VCF, or any AE (k = 1 to 3 trials). Limitations included lack of a BK versus sham comparison, availability of only one RCT of BK versus NSM, and lack of study blinding. Individuals with painful VCF experienced symptomatic improvement compared with baseline with all interventions. The clinical importance of the greater improvements with BK versus NSM is unclear, may be due to placebo effect, and may not counterbalance short-term AE risks. Outcomes appeared similar between BK and other surgical interventions. Well-conducted randomized trials comparing BK with sham would help resolve remaining uncertainty about the relative benefits and harms of BK. © 2017 American Society for Bone and Mineral Research.
Nucleophosmin Regulates Intracellular Oxidative Stress Homeostasis via Antioxidant PRDX6
Authors: Liu Guo‐Yan , Shi Jing‐Xian , Shi Song‐Lin , Liu Fan , Rui Gang , Li Xiao , Gao Li‐Bin , Deng Xiao‐Ling , Li Qi‐Fu 
Published: May 2017

ABSTRACTReactive oxygen species (ROS) play both deleterious and beneficial roles in cancer cells. Nucleophosmin (NPM) is heavily implicated in cancers of diverse origins, being its gene over‐expression in solid tumors or frequent mutations in hematological malignancies. However, the role and regulatory mechanism of NPM in oxidative stress are unclear. Here, we found that NPM regulated the expression of peroxiredoxin 6 (PRDX6), a member of thiol‐specific antioxidant protein family, consequently affected the level and distribution of ROS. Our data indicated that NPM knockdown caused the increase of ROS and its relocation from cytoplasm to nucleoplasm. In contrast, overexpression or cytoplasmic localization of NPM upregulated PRDX6, and decreased ROS. In addition, NPM knockdown decreased peroxiredoxin family proteins, including PRDX1, PRDX4, and PRDX6. Co‐immunoprecipitation further confirmed the interaction between PRDX6 and NPM. Moreover, NSC348884, an inhibitor specifically targeting NPM oligomerization, decreased PRDX6 and significantly upregulated ROS. These observations demonstrated that the expression and localization of NPM affected the homeostatic balance of oxidative stress in tumor cells via PRDX6 protein. The regulation axis of NPM/PRDX/ROS may provide a novel therapeutic target for cancer treatment. J. Cell. Biochem. 118: 4697–4707, 2017. © 2017 Wiley Periodicals, Inc.
The Therapeutic Potential of PI3K/Akt/mTOR Inhibitors in Breast Cancer: Rational and Progress
Authors: Bahrami Afsane , Khazaei Majid , Shahidsales Soodabeh , Hassanian Seyed Mahdi , Hasanzadeh Malihe , Maftouh Mina , Ferns Gordon A. , Avan Amir 
Published: May 2017

ABSTRACTBreast cancer (BC) is the most commonly diagnosed cancer in women. The PI3K/AKT/mTOR pathway is among the most frequently dysregulated pathways in patients with BC. The activation of this pathway is associated with increased cell growth and clinical outcome, and its overexpression is associated with a poor prognosis. It has been proposed that it may be of importance as a potential therapeutic target in the treatment of BC. The aim of current review is to provide an overview of the potential utility of PI3K/Akt/mTOR inhibitors in patients with BC, with particular emphasis on recent preclinical and clinical studies. J. Cell. Biochem. 119: 213–222, 2018. © 2017 Wiley Periodicals, Inc.
Gingerenone A Attenuates Monocyte‐Endothelial Adhesion via Suppression of I Kappa B Kinase Phosphorylation
Authors: Kim Hee Joo , Son Joe Eun , Kim Jae Hwan , Lee Charles C. , Yang Hee , Yaghmoor Soonham Sami , Ahmed Youssri , Yousef Jehad Mustafa , Abualnaja Khalid Omer , Al‐Malki Abdulrahman Labeed , Kumosani Taha Abdullah , Kim Jong Hun , Yoon Park Jung Han , Lee Chang Yong , Kim Jong‐Eun , Lee Ki Won 
Published: May 2017

ABSTRACTDuring the early stages of atherosclerosis, monocytes bind and migrate into the endothelial layer, promoting inflammation within the aorta. In order to prevent the development of atherosclerosis, it is critical to inhibit such inflammation. The therapeutic effects of ginger have been investigated in several models of cardiovascular disease. However, although a number of previous studies have focused on specific compounds, the mechanisms of action responsible remain unclear. Here, we investigated five major compounds present in ginger, and observed that gingerenone A exhibited the strongest inhibitory effects against tumor necrosis factor (TNF)‐α and lipopolysaccharide (LPS) induced monocyte‐endothelial adhesion. Furthermore, gingerenone A significantly suppressed the expression of TNF‐α and LPS‐induced vascular cell adhesion molecule‐1 (VCAM‐1) and chemokine (C‐C motif) ligand 2 (CCL2), key mediators of the interaction between monocytes, and endothelial cells. Transactivation of nuclear factor‐κB (NF‐κB), which is a key transcription factor of VCAM‐1 and CCL2, was induced by TNF‐α and LPS, and inhibited by treatment of gingerenone A. Gingerenone A also inhibited the phosphorylation of NF‐κB inhibitor (IκB) α and IκB Kinase. Taken together, these results demonstrate that gingerenone A attenuates TNF‐α and LPS‐induced monocyte adhesion and the expression of adhesion factors in endothelial cells via the suppression of NF‐κB signaling. J. Cell. Biochem. 119: 260–268, 2018. © 2017 Wiley Periodicals, Inc.
Pleiotropic Effects of Chronic Phorbol Ester Treatment to Improve Glucose Transport in Insulin‐Resistant Cardiomyocytes
Authors: Viglino Christelle , Khoramdin Bahareh , Praplan Guillaume , Montessuit Christophe 
Published: May 2017

ABSTRACTStimulation of glucose transport is an important determinant of myocardial susceptibility to ischemia and reperfusion. Stimulation of glucose transport is markedly impaired in cardiomyocytes exposed to free fatty acids (FFA). Deactivation of the Focal Adhesion Kinase (FAK) by FFA contributes to glucose transport impairment, and could be corrected by chronic treatment with the phorbol ester TPA. However, TPA must have effects in addition to FAK reactivation to restore stimulated glucose transport. Chronic treatment with TPA improved basal and stimulated glucose transport in FFA‐exposed, but not in control cardiomyocytes. Chronic FFA exposure induced the activation of PKCδ and PKCϵ. TPA markedly downregulated the expression of PKCα, PKCδ, and PKCϵ, suggesting that PKCδ or PKCϵ activation could contribute to inhibition of glucose transport by FFA. Rottlerin, a specific PKCδ inhibitor, improved glucose transport in FFA‐exposed cardiomyocytes; and PKCδ was reduced in the particulate fraction of FFA + TPA‐exposed cardiomyocytes. TPA also activated Protein Kinase D 1(PKD1) in FFA‐exposed cardiomyocytes, as assessed by autophosphorylation of PKD1 on Y916. Pharmaceutical inhibition of PKD1 only partially prevented the improvement of glucose transport by TPA. Chronic TPA treatment also increased basal and stimulated glycolysis and favored accumulation of lipid droplets in FFA‐exposed cardiomyocytes. In conclusion, basal and stimulated glucose transport in cardiomyocytes is reduced by chronic FFA exposure, but restored by concomitant treatment with a phorbol ester. The mechanism of action of phorbol esters may involve downregulation of PKCδ, activation of PKD1 and a general switch from fatty acid to glucose metabolism. J. Cell. Biochem. 9999: 4716–4727, 2017. © 2017 Wiley Periodicals, Inc.
Retracted: Potential Role of Long Non‐Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on Proliferation and Migration by Targeting miR‐323
Authors: Zhang Hong , Wang Xiuli , Chen Xinxin 
Published: May 2017

ABSTRACTMedulloblastoma (MB) is a common primary tumor of the central nervous system diagnosed in pediatric patients. Survivors of MB are frequently accompanied by severe side effects, thus it is urgent to explore novel therapeutic target. First of all, the level of antisense non‐coding RNA in the INK4 locus (ANRIL) in normal cerebellum and DAOY cells were evaluated. Then, the effect of ANRIL on DAOY cell proliferation, migration, and apoptosis were tested. Then, qRT‐PCR was performed to explore whether ANRIL acted as a sponge of miR‐323. The effects of miR‐323 inhibition on ANRIL silence‐induced alterations of cell proliferation, migration, and apoptosis were estimated. Predicted by TargetScan, the possible target gene of miR‐323 was screened, followed by validation with luciferase assay. The abnormally expressed BRI3 on cell proliferation, migration, apoptosis, and signaling pathways were all evaluated. ANRIL was up‐regulated in MB and its silence significantly lowered cell viability and migration but promoted cell apoptosis. ANRIL acted as a sponge of miR‐323 and its silence functioned through up‐regulating miR‐323. BRI3 and CDK6 were target genes of miR‐323 and the effect of BRI3 on DAOY cells was the same as ANRIL. Moreover, ANRIL suppression could reduce phosphorylated levels of p38 MAPK, ERK and AKT, and inhibit Wnt signaling pathway through positively regulating BRI3. ANRIL inhibition repressed cell proliferation and migration but promoted cell apoptosis through miR‐323‐mediated regulation of BRI3, which could activate p38 MAPK, ERK, and AKT as well as Wnt signaling pathway. J. Cell. Biochem. 118: 4735–4744, 2017. © 2017 Wiley Periodicals, Inc.
β3‐Adrenergic Regulation of EPC Features Through Manipulation of the Bone Marrow MSC Niche
Authors: Vafaei Rana , Nassiri Seyed Mahdi , Siavashi Vahid 
Published: May 2017

ABSTRACTMesenchymal stem cells (MSCs) reside in a specific niche in the bone marrow, however, biological features of this niche are still not fully understood. Given the interactions of MSCs with endothelial cells in different tissues, bone marrow MSC niche may influence the biological features of endothelial progenitor cells (EPCs). To understand the role of the sympathetic nervous system in regulation of the MSC niche, we examined whether the manipulation of the MSC niche via β3‐adrenergic signals will affect EPC features. A selective β3 agonist (BRL37344) or a β3 antagonist (SR59230A) was administered in mice for 2 weeks to determine the potential effects of these regimens on the population of CD133+ stem cells in the bone marrow. Then, bone marrow‐derived MSCs and EPCs were harvested and expanded from the mice to examine the effect of changes in the MSC niche on EPC features. Improved MSC colony forming potency with increased bone marrow stromal cell‐derived factor 1 (SDF‐1) (also known as C‐X‐C motif chemokine 12 [CXCL12]) expression was shown as a result of intensification of the bone marrow adrenergic signals through BRL37344 injection. On the other hand, the blockage of these signals limited the expression level of SDF‐1 and resulted in bone marrow enrichment of CD133+ cells. Manipulation of the MSC niche and decreased SDF‐1 expression via SR59230A injection also prompted EPCs to form more colonies with augmented proliferation and differentiation capacity. Overall, our results indicate that the β3‐adrenergic signals regulate the MSC niche, thereby resulting in modulation of EPC biological features. J. Cell. Biochem. 118: 4753–4761, 2017. © 2017 Wiley Periodicals, Inc.
Rapid diagnosis of sepsis with TaqMan‐Based multiplex real‐time PCR
Authors: Liu Chang‐Feng , Shi Xin‐Ping , Chen Yun , Jin Ye , Zhang Bing 
Published: May 2017

BackgroundThe survival rate of septic patients mainly depends on a rapid and reliable diagnosis. A rapid, broad range, specific and sensitive quantitative diagnostic test is the urgent need. Thus, we developed a TaqMan‐Based Multiplex real‐time PCR assays to identify bloodstream pathogens within a few hours.MethodsPrimers and TaqMan probes were designed to be complementary to conserved regions in the 16S rDNA gene of different kinds of bacteria. To evaluate accurately, sensitively, and specifically, the known bacteria samples (Standard strains, whole blood samples) are determined by TaqMan‐Based Multiplex real‐time PCR. In addition, 30 blood samples taken from patients with clinical symptoms of sepsis were tested by TaqMan‐Based Multiplex real‐time PCR and blood culture.ResultsThe mean frequency of positive for Multiplex real‐time PCR was 96% at a concentration of 100 CFU/mL, and it was 100% at a concentration greater than 1000 CFU/mL. All the known blood samples and Standard strains were detected positively by TaqMan‐Based Multiplex PCR, no PCR products were detected when DNAs from other bacterium were used in the multiplex assay. Among the 30 patients with clinical symptoms of sepsis, 18 patients were confirmed positive by Multiplex real‐time PCR and seven patients were confirmed positive by blood culture.ConclusionTaqMan‐Based Multiplex real‐time PCR assay with highly sensitivity, specificity and broad detection range, is a rapid and accurate method in the detection of bacterial pathogens of sepsis and should have a promising usage in the diagnosis of sepsis.
The Utility of a Population Approach in Drug–Drug Interaction Assessments: A Simulation Evaluation
Authors: Wang Diane D. , Yu Yanke , Kassir Nastya , Zhu Min , Hanley William D. , Earp Justin C. , Chow Andrew T. , Gupta Manish , Hu Chuanpu 
Published: May 2017

AbstractThis study aims at evaluating the utility of the population pharmacokinetics approach in therapeutic protein drug‐drug‐interaction (DDI) assessment. Simulations were conducted for 2 representative victim drugs, methotrexate and trastuzumab, using a parallel‐group design with and without the interaction drug. The effect of a perpetrator on the exposure of the victim drug is described as the ratio of clearance/apparent clearance of the victim drug given with or without the perpetrator. The power of DDI assessment was calculated as the percentage of runs with 90% confidence interval of the estimated DDI effect within 80% to 125% for the scenarios of no DDI, benchmarked with the noncompartmental approach with intensive sampling. The impact of the number of subjects, the number of sampling points per subject, sampling time error, and model misspecification on the power of DDI determination were evaluated. Results showed that with equal numbers of subjects in each arm, the population pharmacokinetics approach with sparse sampling may need about the same or a higher number of subjects compared to a noncompartmental approach in order to achieve similar power. Increasing the number of subjects, even if only in the study drug alone arm, can increase the power. Sampling or dosing time error had notable impacts on the power for methotrexate but not for trastuzumab. Model misspecification had no notable impacts on the power for trastuzumab. Overall, the population pharmacokinetics approach with sparse sampling built in phase 2/3 studies allows appropriate DDI assessment with adequate study design and analysis and can be considered as an alternative to dedicated DDI studies.
Effect of Pentoxifylline in Ameliorating Myocardial Injury in Patients With Myocardial Infarction Undergoing Thrombolytic Therapy: A Pilot Randomized Clinical Trial
Authors: Namdar Hossein , Zohori Rasoul , Aslanabadi Naser , Entezari‐Maleki Taher 
Published: May 2017

AbstractCell death following acute myocardial infarction (MI) is the hallmark pathology of cardiovascular disease, leading to considerable mortality and morbidity. Platelet and neutrophil activation and inflammatory cytokines, prominently TNF‐α, play an important role in the development of cell death. Because pentoxifylline inhibits platelet and neutrophil activation and reduces TNF‐α, this study was performed to assess the potential benefit of pentoxifylline in the reduction of myocardial injury following acute MI. In this randomized clinical trial, 98 patients with acute MI were randomly divided into 2 groups. The intervention group received an oral dose of 1200 mg of pentoxifylline immediately before thrombolytic therapy (TLT). All patients received the same standard protocol for treatment of MI. Cardiac enzymes were checked over 48 hours. ST resolution was measured over 90 minutes. Then all patients were followed up for a 1‐month period to assess major adverse cardiac effects (MACEs). There were no significant differences in peak levels of CPK (P = .18) and CK‐MB (P = .33) between the 2 groups, whereas peak level of troponin I was significantly lower in the pentoxifylline group (16.8 ± 10.4 vs 21.3 ± 11.6; P = .048). No significant change between the groups was observed in biomarkers levels, ST segment resolution, cardiac ejection fraction, and MACEs. The results showed that pentoxifylline significantly reduced the peak value of troponin I in patients with acute MI receiving TLT. No significant change was observed in the other studied parameters. Further outcome‐based studies are needed to show the clinical relevance of differences between the groups in troponin peak.
Milk pancreatitis with hypertriglyceridemia and diabetic ketoacidosis
Authors: Shinotsuka Manami , Tokuda Yasuharu 
Published: May 2017

AbstractExcessive milk intake may lead to diabetic ketoacidosis and acute pancreatitis. A 55‐year‐old milk salesperson with diabetes and dyslipidemia presented with a 5‐day history of fatigue and thirst. The patient had drunk a large amount of milk for 2 months prior to the admission. Laboratory data showed metabolic acidosis, hyperglycemia, ketonuria, hypertriglyceridemia, and elevated serum amylase. Abdominal CT with contrast material revealed the swelling of the pancreas. The patient received medical treatment for diabetic ketoacidosis and acute pancreatitis and was discharged uneventfully on day 18. Dietary advice for diabetics should include the avoidance of excessive amount of milk.
Natural history of intraductal papillary mucinous neoplasm and non‐neoplastic cyst: long‐term imaging follow‐up study
Authors: Hisada Yuya , Nagata Naoyoshi , Imbe Koh , Takasaki Yusuke , Sekine Katsunori , Tajima Tsuyoshi , Yanase Mikio , Fujimoto Kazuma , Akiyama Junichi , Uemura Naomi 
Published: May 2017

AbstractBackgroundTo identify differences in incidence and mortality of pancreatic cancer (PC) between intraductal papillary mucinous neoplasm (IPMN) and non‐neoplastic cyst.MethodsPatients with pancreatic cyst (n = 526; 263 with IPMN and 263 with non‐neoplastic cyst matched for age, sex, and diagnosis year) were periodically followed‐up with imaging. Hazard ratio (HR), standardized incidence ratio (SIR), and standardized mortality ratio (SMR) for PC and PC‐related mortality were estimated.ResultsDuring a mean follow‐up of 57.5 months with 3,376 computed tomography scans and 1,079 magnetic resonance imaging scans, 5‐year cumulative PC incidence was 4.0% for IPMN and 0% for non‐neoplastic cyst, respectively (HR 5.2; P = 0.031). During a mean follow‐up of 73.1 months, 5‐year cumulative PC‐related mortality was 2.6% for IPMN and 0% for non‐neoplastic cyst, respectively (HR 4.5; P = 0.05). Compared with the general population in Japan, patients with IPMN, but not those with non‐neoplastic cyst, had significantly increased risks of PC incidence (SIR 22.03) and related mortality (SMR 15.9).ConclusionsDuring long‐term imaging follow‐up, patients with IPMN developed PC over time, whereas none of the patients with non‐neoplastic cyst developed it within 5 years. Compared with the general population, patients with IPMN, but not those with non‐neoplastic cyst, were at risk of PC and related mortality.
ZL006 promotes migration and differentiation of transplanted neural stem cells in male rats after stroke
Authors: Wang Dong‐Liang , Qian Xiao‐Dan , Lin Yu‐Hui , Tian Bin‐Bin , Liang Hai‐Ying , Chang Lei , Wu Hai‐Yin , Zhu Dong‐Ya , Luo Chun‐Xia 
Published: May 2017

AbstractNew strategies must be developed to resolve the problems of stroke treatment. In recent years, stem cell–based therapy after stroke has come into the public and academic lens. Previously we have shown that uncoupling neuronal nitric oxide synthase (nNOS) from the postsynaptic density protein‐95 (PSD‐95) by ZL006, a small molecular compound, can ameliorate ischemic damage and promote neuronal differentiation of endogenous neural stem cells (NSCs) in focal cerebral ischemic male rats. In this study, we transplanted exogenous NSCs into the ipsilateral hemisphere of male rats in combination with ZL006 treatment after ischemic stroke. We show that ZL006 treatment facilitates the migration of transplanted NSCs into the ischemia‐injured area and promotes neuronal differentiation of these cells, which is not due to a direct effect of ZL006 on exogenous NSCs but is associated with increased phosphorylation of cAMP response element–binding protein (CREB) in neurons and favorable microenvironment. Moreover, improved functional outcome in the ZL006‐treated group was also found. Taken together, our data indicate that ZL006, uncoupling nNOS–PSD‐95 in neurons, positively regulates the fate of transplanted NSCs and benefits the functional outcome after stroke in male rats.