bluuebunny/crossref_metadata_2025_split huggingface dataset:
Runx2‐mediatedbcl‐2gene expression contributes to nitric oxide protection against hydrogen peroxide‐induced osteoblast apoptosis
Authors: Ho Wei‐Pin , Chan Wing‐Pong , Hsieh Ming‐Shium , Chen Ruei‐Ming 
Published: September 2009

AbstractNitric oxide (NO) can regulate osteoblast activities. This study was aimed to evaluate the protective effects of pretreatment with sodium nitroprusside (SNP) as a source of NO on hydrogen peroxide‐induced osteoblast insults and its possible mechanisms. Exposure of human osteosarcoma MG63 cells to hydrogen peroxide significantly increased cellular oxidative stress, but decreased ALP activity and cell viability, inducing cell apoptosis. Pretreatment with 0.3 mM SNP significantly lowered hydrogen peroxide‐induced cell insults. Treatment of human MG63 cells with hydrogen peroxide inhibited Bcl‐2 mRNA and protein production, but pretreatment with 0.3 mM SNP significantly ameliorated such inhibition. Sequentially, hydrogen peroxide decreased the mitochondrial membrane potential, but increased the levels of cytochromecand caspase‐3 activity. Pretreatment with 0.3 mM SNP significantly lowered such alterations. Exposure to hydrogen peroxide decreased Runx2 mRNA and protein syntheses. However, pretreatment with 0.3 mM SNP significantly lowered the suppressive effects. Runx2 knockdown using RNA interference inhibited Bcl‐2 mRNA production in human MG63 cells. Protection of pretreatment with 0.3 mM SNP against hydrogen peroxide‐induced alterations in ALP activity, caspase‐3 activity, apoptotic cells, and cell viability were also alleviated after administration of Runx2 small interference RNA. Thus, this study shows that pretreatment with 0.3 mM SNP can protect human MG63 cells from hydrogen peroxide‐induced apoptotic insults possibly via Runx2‐involved regulation ofbcl‐2gene expression. J. Cell. Biochem. 108: 1084–1093, 2009. © 2009 Wiley‐Liss, Inc.
Physiological and coordinate downregulation of the NPC1 and NPC2 genes are associated with the sequestration of LDL‐derived cholesterol within endocytic compartments
Authors: Jelinek David , Patrick Sarah Mount , Kitt Khameeka N. , Chan Teddy , Francis Gordon A. , Garver William S. 
Published: September 2009

AbstractThe Niemann‐Pick C1 and C2 (NPC1 and NPC2) proteins have a central role in regulating the transport of lipoprotein‐derived cholesterol from endocytic compartments to the endoplasmic reticulum for esterification by acyl‐CoA:cholesterol acyltransferase (ACAT) and feedback inhibition of the sterol regulatory element‐binding protein (SREBP) pathway. Since the NPC1 gene/protein has recently been shown to be downregulated by feedback inhibition of the SREBP pathway, the present study was performed to determine whether physiological downregulation of the NPC1 gene/protein alters the transport and metabolism of low‐density lipoprotein (LDL)‐derived cholesterol in human fibroblasts. To perform this study, three different culture conditions were used that included fibroblasts grown in lipoprotein‐deficient serum (LPDS), LPDS supplemented with LDL, and LPDS supplemented with LDL, followed by equilibration in the absence of LDL to allow the transport of LDL‐derived cholesterol from endocytic compartments and equilibration of cellular sterol pools. The results from this study indicated that in addition to the NPC1 gene/protein, the NPC2 gene/protein was also downregulated by LDL‐derived cholesterol‐dependent feedback inhibition and that downregulation of both the NPC1 and NPC2 genes/proteins was associated with the sequestration of LDL‐derived cholesterol within endocytic compartments, including late endosomes/lysosomes after equilibration. Therefore, it is proposed that physiological and coordinate downregulation of the NPC1 and NPC2 genes/proteins promotes the sequestration of LDL‐derived cholesterol within endocytic compartments and serves a role in maintaining intracellular cholesterol homeostasis. J. Cell. Biochem. 108: 1102–1116, 2009. © 2009 Wiley‐Liss, Inc.
Generation of a human immunodeficiency virus type 1 chronically infected monkey B cell line expressing low levels of endogenous TRIM5α
Authors: Ridolfi Barbara , Catone Stefania , Sgarbanti Marco , Sernicola Leonardo , Battistini Angela , Parolin Cristina , Titti Fausto , Borsetti Alessandra 
Published: September 2009

AbstractSeveral innate cellular antiviral factors exist in mammalian cells that prevent the replication of retroviruses. Among them, the tripartite motif protein (TRIM)5α has been shown to block human immunodeficiency virus type 1 (HIV‐1) infection in several types of Old World monkey cells. Here we report a novel HIV‐1 chronically infected monkey B cell line, F6/HIV‐1, characterized by very low levels of TRIM5α expression that allows HIV‐1 to overcome the restriction. Virus produced by F6/HIV‐1 cells fails to infect monkey cells but retains the ability to infect human peripheral blood mononuclear cells (PBMCs) and T cell lines, although with a reduced infectivity compared to the input virus. Ultrastructural analyses revealed the presence of budding virions at the F6/HIV‐1 cells plasma membrane characterized by a typical conical core shell. To our knowledge F6/HIV‐1 is the first monkey cell line chronically infected by HIV‐1 and able to release infectious particles thus representing a useful tool to gain further insights into the molecular mechanisms of HIV‐1 pathogenesis. J. Cell. Physiol. 221: 760–765, 2009. © 2009 Wiley‐Liss, Inc.
Expression of RIZ1 protein (Retinoblastoma‐interacting zinc‐finger protein 1) in prostate cancer epithelial cells changes with cancer grade progression and is modulated in vitro by DHT and E2
Authors: Rossi Valentina , Staibano Stefania , Abbondanza Ciro , Pasquali Daniela , De Rosa Caterina , Mascolo Massimo , Bellastella Giuseppe , Visconti Daniela , De Bellis Annamaria , Moncharmont Bruno , De Rosa Gaetano , Puca Giovanni Alfredo , Bellastella Antonio , Sinisi Antonio Agostino 
Published: September 2009

AbstractThe nuclear protein methyl‐transferase Retinoblastoma‐interacting zinc‐finger protein 1 (RIZ1) is considered to be a downstream effector of estrogen action in target tissues. Silencing of RIZ1 expression is common in many tumors. We analyzed RIZ1 expression in normal and malignant prostate tissue and evaluated whether estradiol (E2) or dihydrotestosterone (DHT) treatment modulated RIZ1 in cultured prostate epithelial cells (PEC). Moreover, we studied the possible involvement of RIZ1 in estrogen action on the EPN prostate cell line, constitutively expressing both estrogen receptor (ER)‐α and β. RIZ1 protein, found in the nucleus of normal PECs by immunohistochemistry, was progressively lost in cancer tissues as the Gleason score increased and was only detected in the cytoplasmic compartment. RIZ1 transcript levels, as assayed by semi‐quantitative RT‐PCR in primary PEC cultures, were significantly reduced in cancer cells (P < 0.05). In EPN DHT treatment significantly increased RIZ1 transcript and protein levels (P < 0.05); E2 induced a reduction of S phase without significant changes of RIZ1 expression. In E2‐treated EPN cell extracts RIZ co‐immunoprecipitated with ERβ and ERα. Our data demonstrate that RIZ1 is expressed in normal PECs and down‐regulated in cancer cells, with a switch of its sub‐cellular localization from the nucleus to the cytoplasm upon cancer grade progression. RIZ1 expression levels in the PECs were modulated by DHT or E2 treatment in vitro. Furthermore, the E2 effects on ER‐expressing prostate cells involve RIZ1, which confirms a possible role for ER‐mediated pathways in a non‐classic E2‐target tissue. J. Cell. Physiol. 221: 771–777, 2009. © 2009 Wiley‐Liss, Inc.
ROCK pathway participates in the processes that 15‐hydroxyeicosatetraenoic acid (15‐HETE) mediated the pulmonary vascular remodeling induced by hypoxia in rat
Authors: Ma Jun , Liang Shujun , Wang Zhigang , Zhang Lei , Jiang Jing , Zheng Jinhua , Yu Lei , Zheng Xiaodong , Wang Ruifang , Zhu Daling 
Published: September 2009

Abstract15‐Hydroxyeicosatetraenoic acid (15‐HETE), a product of arachidonic acid (AA) catalyzed by 15‐lipoxygenase (15‐LO), plays an essential role in hypoxic pulmonary arterial hypertension. We have previously shown that 15‐HETE inhibits apoptosis in pulmonary artery smooth muscle cells (PASMCs). To test the hypothesis that such an effect is attributable to the hypoxia‐induced pulmonary vascular remodeling (PVR), we performed these studies. We found subtle thickening of proximal media/adventitia of the pulmonary arteries (PA) in rats that had been exposed to hypoxia. This was associated with an up‐regulation of the anti‐apoptotic Bcl‐2 expression and down‐regulation of pro‐apoptotic caspase‐3 and Bax expression in PA homogenates. Nordihydroguaiaretic acid (NDGA), which inhibits the generation of endogenous 15‐HETE, reversed all the alterations following hypoxia. In situ hybridization histochemistry and immunocytochemistry showed that the 15‐LO‐1 mRNA and protein were localized in pulmonary artery endothelial cells (PAECs), while the 15‐LO‐2 mRNA and protein were localized in both PAECs and PASMCs. Furthermore, the Rho‐kinase (ROCK) pathway was activated by both endogenous and exogenous 15‐HETE, alleviating the serum deprivation (SD)‐induced PASMC apoptosis. Thus, these findings indicate that 15‐HETE protects PASMC from apoptosis, contributing to pulmonary vascular medial thickening, and the effect is, at least in part, mediated via the ROCK pathway. J. Cell. Physiol. 222:82–94, 2010. © 2009 Wiley‐Liss, Inc.
The utility of thoracic ultrasound before local anesthetic video‐assisted thoracoscopy in patients with suspected pleural malignancy
Authors: Medford Andrew R. L. 
Published: September 2009

AbstractVideo‐assisted thoracoscopy under local anesthesia (VAT‐LA) is a key investigation in the diagnosis and management of suspected malignant pleural effusion. Two problems encountered at VAT‐LA are accessing the pleural space and fibrinous intrapleural septa. Thoracic sonography (TUS) is known to facilitate thoracocentesis after dry tap but has not been studied in detail before VAT‐LA. We report a case of lateral decubitus pre‐VAT TUS that helped locate the optimal access to the pleural space and demonstrated fibrinous intrapleural septation, thereby affecting the decision to avoid thoracoscopic pleurodesis. © 2009 Wiley Periodicals, Inc. J Clin Ultrasound, 2009
Survival, differentiation, and reversal of heroin neurobehavioral teratogenicity in mice by transplanted neural stem cells derived from embryonic stem cells
Authors: Kazma Meital , Izrael Michal , Revel Michel , Chebath Judith , Yanai Joseph 
Published: September 2009

AbstractCell therapies in animal models of neurobehavioral defects are normally derived from neural stem cells (NSC) of the developing cortex. However, the clinical feasibility of NSC therapies would be greatly improved by deriving transplanted cells and from a tissue culture source that is self‐renewing, containing cells that potentially differentiate into the desired neuronal phenotypes. These cultures can be engineered to contain the appropriate factors to support their therapeutic action and likely evoke lesser immune reactions. In the current study, we employed our model of mice neurobehaviorally impaired via prenatal exposure to heroin, to test the therapeutic efficacy of NSC derived from murine embryonic stem cells culture (ESC). The culture contained elongated bipolar cells, 90% of which are positive for nestin, the intermediate filament protein found in neural precursors. After removal of growth factors, the NSC differentiated into neurons (34.0% ± 3.8% NF‐160 positive), including cholinergic cells (ChAT positive), oligodendrocytes (29.9% ± 4.2% O4), and astrocytes (36.1% ± 4.7% GFAP positive). Rreverse transcriptase polymerase chain reaction (RT‐PCR) analysis confirmed the immunocytochemical findings. Mice made deficient in Morris maze behavior by prenatal heroin exposure (10 mg/kg heroin S.C. on gestational days 9–18) were transplanted into the hippocampusregion on postnatal day 35 with the ES culture‐derived NSC (ES‐NSC) labeled with dialkylcarbocyanine (Dil) cell tracker. Dil+ and NF160+ cells were detected in the hippocampal region (50% ± 8% survival). The transplantation completely restored maze performance to normal; e.g., on day 3, transplantation improved the behavior from the deficient level of 11.9‐sec latency to the control of 5.6‐sec latency (44.5% improvement). © 2009 Wiley‐Liss, Inc.
Immediate anti‐tumor necrosis factor‐α (etanercept) therapy enhances axonal regeneration after sciatic nerve crush
Authors: Kato Kinshi , Liu Huaqing , Kikuchi Shin‐ichi , Myers Robert R. , Shubayev Veronica I. 
Published: September 2009

AbstractPeripheral nerve regeneration begins immediately after injury. Understanding the mechanisms by which early modulators of axonal degeneration regulate neurite outgrowth may affect the development of new strategies to promote nerve repair. Tumor necrosis factor‐α (TNF‐α) plays a crucial role in the initiation of degenerative cascades after peripheral nerve injury. Here we demonstrate using real‐time Taqman quantitative RT‐PCR that, during the time course (days 1–60) of sciatic nerve crush, TNF‐α mRNA expression is induced at 1 day and returned to baseline at 5 days after injury in nerve and the corresponding dorsal root ganglia (DRG). Immediate therapy with the TNF‐α antagonist etanercept (fusion protein of TNFRII and human IgG), administered systemically (i.p.) and locally (epineurially) after nerve crush injury, enhanced the rate of axonal regeneration, as determined by nerve pinch test and increased number of characteristic clusters of regenerating nerve fibers distal to nerve crush segments. These fibers were immunoreactive for growth associated protein‐43 (GAP‐43) and etanercept, detected by anti‐human IgG immunofluorescence. Increased GAP‐43 expression was found in the injured nerve and in the corresponding DRG and ventral spinal cord after systemic etanercept compared with vehicle treatments. This study established that immediate therapy with TNF‐α antagonist supports axonal regeneration after peripheral nerve injury. © 2009 Wiley‐Liss, Inc.
“Juvenile stress” alters maturation‐related changes in expression of the neural cell adhesion molecule L1 in the limbic system: Relevance for stress‐related psychopathologies
Authors: Tsoory M.M. , Guterman A. , Richter‐Levin G. 
Published: September 2009

AbstractL1 is critically involved in neural development and maturation, activity‐dependent synaptic plasticity, and learning processes. Among adult rats, chronic stress protocols that affect L1 functioning also induce impaired cognitive and neural functioning and heightened anxiety reminiscent of stress‐induced mood and anxiety disorders. Epidemiological studies indicate that childhood trauma is related predominantly to higher rates of both mood and anxiety disorders in adulthood and is associated with altered limbic system functioning. Exposing rats to stress during the juvenile period (“juvenile stress”) has comparable effects and was suggested as a model of induced predisposition for these disorders. This study examined the effects of juvenile stress on rats aversive learning and on L1 expression soon after exposure and in adulthood, both following additional exposure to acute stress and in its absence. Adult juvenile‐stressed rats exhibited enhanced cued fear conditioning, reduced novel‐setting exploration, and impaired avoidance learning. Furthermore, juvenile stress increased L1 expression in the BLA, CA1, DG, and EC both soon after the stressful experience and during adulthood. It appears that juvenile stress affects the normative maturational decrease in L1 expression. The results support previous indications that juvenile stress alters the maturation of the limbic system and further support a role for L1 regulation in the mechanisms that underlie the predisposition to exhibit mood and/or anxiety disorders in adulthood. Furthermore, the findings support the “network hypothesis,” which postulates that information‐processing problems within relevant neural networks might underlie stress‐induced mood and anxiety disorders. © 2009 Wiley‐Liss, Inc.
Uptake of ferrous iron by cultured rat astrocytes
Authors: Tulpule Ketki , Robinson Stephen R. , Bishop Glenda M. , Dringen Ralf 
Published: September 2009

AbstractAstrocytes are considered to play an important role in iron homeostasis of the brain, yet the mechanisms involved in the uptake of iron into astrocytes remain elusive. To investigate the uptake of iron into astrocytes, we have applied ferric ammonium citrate (FAC) to rat astrocyte‐rich primary cultures. These cultures express the mRNAs of two membrane‐bound ferric reductases, Dcytb and SDR2, and reduce extracellular ferric iron (100 μM) with a rate of 3.2 ± 0.4 nmol/(hr × mg). This reduction rate is substantially lower than the rate of cellular iron accumulation from 100 μM FAC [24.7 ± 8.9 nmol/(hr × mg)], which suggests that iron accumulation from FAC does at best partially depend on extracellular ferric reduction. Nonetheless, when the iron in FAC was almost completely reduced by an excess of exogenous ascorbate, astrocytes accumulated iron in a time‐ and concentration‐dependent manner with specific iron accumulation rates that increased linearly for concentrations of up to 100 μM ferrous iron. This accumulation was attenuated by lowering the incubation temperature, by the presence of ferrous iron chelators, or by lowering the pH from 7.4 to 6.8. These data indicate that, in addition to the DMT1‐mediated uptake of ferrous iron, astrocytes can accumulate ferric and ferrous iron by mechanisms that are independent of DMT1 or transferrin. © 2009 Wiley‐Liss, Inc.
Characterization of green‐tissue protein extract from alfalfa (Medicago sativa) exploiting a 3‐D technique
Authors: Aguilar Oscar , Glatz Charles E. , Rito‐Palomares Marco 
Published: September 2009

AbstractThere is a growing interest of pharmaceutical companies for plant‐based production systems. To facilitate the general acceptance of plants as bioreactors, the establishment of efficient downstream operations is critical. It has been proposed that a better understanding of the properties of the contaminant proteins can benefit downstream processing design and operation. The coupled application of 2‐DE with aqueous two‐phase partitioning has been suggested as a practical 3‐D method to characterize potential contaminant proteins from plant extracts. The application of this novel 3‐D approach to a complex protein extract from alfalfa (Medicago sativa) containing a model recombinant protein (human granulocyte colony stimulating factor (hG‐CSF)) resulted in the quantification of 55 protein spots. The 3‐D properties (Mr, pI, and Kp) obtained for 17 proteins comprising 69% of the alfalfa proteins, allowed the proposal of a prefractionation step as well as the identification of the target molecule (rG‐CSF) from bulk of alfalfa proteins. The information obtained from this experimental approach was useful for the identification of the potential contaminant proteins that will occur in alfalfa when this plant is used as a host for recombinant proteins. Additionally, this method will assist in the design of adequate purification strategies for recombinant proteins expressed in alfalfa green tissue.
MEKC determination of vanadium from mineral ore and crude petroleum oil samples using precapillary chelation with bis(salicylaldehyde)tetramethyl‐ethylenediimine
Authors: Mirza Muhammad Aslam , Kandhro Abdul Jabbar , Khuhawar Muhammad Yar , Arain Rafee 
Published: September 2009

AbstractAn analytical procedure has been developed for the separation of Cu(II), Ni(II), Co(II), Fe(II), Pd(II), Th(IV), V(IV), and determination of Fe(II), Co(II), Ni(II), and V(IV) by MEKC after chelation with bis(salicylaldehyde)tetramethylethylenediimine (H2SA2Ten). Uncoated fused silica capillary was used with an applied voltage of 30 kV with photo‐diode array detection at 228 nm. SDS was added as micellar medium at pH 8.2 with sodium tetraborate buffer (0.1 M). Linear calibrations were established within 0.015–1000 μg/mL of each element with LOD within 5–67 ng/mL. The method was applied for the determination of vanadium from crude oil and ore samples in the range 0.34–2.40 and 114.2–720.7 μg/g with RSD 1.7–3.8 and 0.98–2.30% (n = 3), respectively. Fe, Ni, and Co present in crude oil and ore samples were also determined with RSD 1.3–2.8, 1.1–4.1, and 1.2–3.5% (n = 3), respectively. The results were compared with that of supplier's specifications and atomic absorption spectrometry (AAS). Method was evaluated by standard addition technique.
Comparison of solidification of floating drop and homogenous liquid–liquid microextractions for the extraction of two plasticizers from the water kept in PET‐bottles
Authors: Yamini Yadollah , Ghambarian Mahnaz , Khalili‐Zanjani Mohammad Reza , Faraji Mohammad , Shariati Shahab 
Published: September 2009

AbstractTwo approaches based on solidification of floating drop microextraction (SFDME) and homogenous liquid–liquid microextraction (HLLE) were compared for the extraction and preconcentration of di‐(2‐ethylhexyl) phthalate (DEHP) and di‐(2‐ethylhexyl) adipate (DEHA) from the mineral water samples. In SFDME, a floated drop of the mixture of acetophenone/1‐undecanol (1:8) was exposed on the surface of the aqueous solution and extraction was permitted to occur. In HLLE, a homogenous ternary solvent system was used by water/methanol/chloroform and the phase separation phenomenon occurred by salt addition. Under the optimal conditions, the LODs for the two target plasticizers (DEHA and DEHP), obtained by SFDME–GC‐FID and HLLE–GC‐FID, were ranged from 0.03 to 0.01 μg/L and 0.02 to 0.01 μg/L, respectively. HLLE provided higher preconcentration factors (472.5‐ and 551.2‐fold) within the shorter extraction time as well as better RSDs (4.5–6.9%). While, in SFDME, high preconcentration factors in the range of 162–198 and good RSDs in the range of 5.2–9.6% were obtained. Both methods were applied for the analysis of two plasticizers in different water samples and two target plasticizers were found in the bottled mineral water after the expiring time and the boiling water was exposed to a polyethylene vial.
Inherent peak compression of charged analytes in electrochromatography
Authors: Nischang Ivo , Tallarek Ulrich 
Published: September 2009

AbstractThis work resolves peak compression of charged analytes in CEC with strong cation‐exchange stationary phase particles. By combining electrochromatographic peak shape analysis with the results of numerical simulations and confocal laser scanning microscopy in the packed capillaries, we identify electrical field‐induced concentration polarization as the key physical phenomenon responsible for the inherent existence of local electrical field gradients on the scale of an individual support particle. Consequently, positive and negative field gradients exist between and inside the particles along the whole packing. Their intensity depends on the particles cation‐selectivity (governed by the particles volume charge density and the mobile phase ionic strength) and the applied field strength. The interplay of these local field gradients with the analytes retention (intraparticle adsorption) determines whether fronting, tailing, or spiked analyte peaks are observed, and it provides a mechanism by which strongly retained analytes can be eluted over long distances with little zone dispersion. Our analysis explains the “anomalous” peak compression effects with strong cation‐exchange particles, which have been reported more than a decade ago (Smith, N. W., Evans, M. B., Chromatographia 1995, 41, 197–203) and since then remained largely unresolved.