bluuebunny/crossref_metadata_2025_split huggingface dataset:
Broad tumor spectrum in a mouse model of multiple endocrine neoplasia type 1
Authors: Loffler Kelly A. , Biondi Christine A. , Gartside Michael , Waring Paul , Stark Mitchell , Serewko‐Auret Magdalena M. , Muller H. Konrad , Hayward Nicholas K. , Kay Graham F. 
Published: October 2006

AbstractMultiple endocrine neoplasia type 1 (MEN1) is an inherited cancer predisposition syndrome typified by development of tumors in parathyroid, pituitary and endocrine pancreas, as well as less common sites including both endocrine and nonendocrine organs. Deletion or mutation of the tumor suppressor gene MEN1 on chromosome 11 has been identified in many cases of MEN1 as well as in sporadic tumors. The molecular biology of menin, the protein encoded by MEN1, remains poorly understood. Here we describe a mouse model of MEN1 in which tumors were seen in pancreatic islets, pituitary, thyroid and parathyroid, adrenal glands, testes and ovaries. The observed tumor spectrum therefore includes types commonly seen in MEN1 patients and additional types. Pancreatic pathology was most common, evident in over 80% of animals, while other tumor types developed with lower frequency and generally later onset. Tumors of multiple endocrine organs were observed frequently, but progression to carcinoma and metastasis were not evident. Tumors in all sites showed loss of heterozygosity at the Men1 locus, though the frequency in testicular tumors was only 36%, indicating that a different molecular mechanism of tumorigenesis occurs in those Leydig tumors that do not show loss of the normal Men1 allele. Menin expression was below the level of detection in ovary, thyroid and testis, but loss of nuclear menin immunoreactivity was observed uniformly in all pancreatic islet adenomas and in some hyperplastic islet cells, suggesting that complete loss of Men1 is a critical point in islet tumor progression in this model. © 2006 Wiley‐Liss, Inc.
Effects of copper on gill structure and transport function in the rainbow trout, oncorhynchus mykiss
Authors: Sola François , Isaia Jacques , Masoni Armand 
Published: October 2006

AbstractEffects of copper were studied in freshwater adapted rainbow trout using the perfused head preparation. In its monovalent chemical form, copper at millimolar concentrations had no significant effects on Na+ and water transport. By contrast, the divalent form produced an increase in gill perfusion pressure, a significant reduction in Na+ influx and water fluxes and reversed Na+ net flux. Observations by light microscopy showed important cell damage (oedema, mucus production, cellular desquamation). By electron microscopy there was smoothing of apical membranes, swelling of the tubular system and destruction of mitochondria. The Na, K‐ATPase activity was totally suppressed and residual ATPase activity largely inhibited by 1 mM Cu2+. There was inhibition of the Na, K‐ATPase activity with an IC50 of ± 10 μM of total copper (free and bound cupric fractions). As active sodium transport is located on the secondary lamellae, our results show that its entry mechanism is inhibited at that level by cupric ions only. Results are discussed in relation to hydromineral balance of the trout.
Oxidative modifications produced in HL‐60 cells on exposure to benzene metabolites
Authors: Rao Nimmagudda R. , Snyder Robert 
Published: October 2006

AbstractWe have studied the effects of the benzene metabolites hydroquinone, p‐benzoquinone or 1,2,4‐benzenetriol on cytotoxicity, active oxygen formation, hydrogen peroxide (i.e. hydroperoxide) production and nitric oxide formation in HL‐60 cells. We also examined the effects of these compounds on antioxidant enzymes and intracellular antioxidants in these cells. The cytotoxicity of benzene metabolites to HL‐60 cells was found to be of the order of p‐benzoquinone>hydroquinone>benzenetriol. No appreciable changes in the basal levels of either superoxide anion production or nitric oxide formation were observed following exposures to the benzene metabolites, but significant increases in superoxide were seen on stimulation with TPA for each metabolite, whereas hydroquinone and p‐benzoquinone, but not 1,2,4‐benzenetriol, increased nitric oxide production under these conditions. Following exposure to the benzene metabolites, HL‐60 cells showed significant rises in hydrogen peroxide formation compared to controls. The study of antioxidant enzymes and intracellular antioxidants suggested that the benzene metabolites inhibit or reduce the levels of different antioxidant mechanisms and, thereby, cause the accumulation of free radicals in these cells predisposing them for oxidative damage.
Distinctive gene expression of prostatic stromal cells cultured from diseased versus normal tissues
Authors: Zhao Hongjuan , Ramos Cristiane F. , Brooks James D. , Peehl Donna M. 
Published: October 2006

AbstractTo obtain a comprehensive view of the transcriptional programs in prostatic stromal cells of different histological/pathological origin, we profiled 18 adult human stromal cell cultures from normal transition zone (TZ), normal peripheral zone (PZ), benign prostatic hyperplasia (BPH), and prostate cancer (CA) using cDNA microarrays. A hierarchical clustering analysis of 714 named unique genes whose expression varied at least threefold from the overall mean abundance in at least three samples in all 18 samples demonstrated that cells of different origin displayed distinct gene expression profiles. Many of the differentially expressed genes are involved in biological processes known to be important in the development of prostatic diseases including cell proliferation and apoptosis, cell adhesion, and immune response. Significance Analysis of Microarrays (SAM) analysis identified genes that showed differential expression with statistical significance including 24 genes between cells from TZ versus BPH, 34 between BPH versus CA, and 101 between PZ versus CA. S100A4 and SULF1, the most up‐ and downregulated genes in BPH versus TZ, respectively, showed expression at the protein level consistent with microarray analysis. In addition, sulfatase assay showed that BPH cells have lower SULF1 activity compared to TZ cells. Quantitative real‐time polymerase chain reaction (qRT‐PCR) analysis confirmed differential expression of ENPP2/autotoxin and six other genes between PZ versus CA, as well as differential expression of six genes between BPH versus CA. Our results support the hypothesis that prostatic stromal cells of different origin have unique transcriptional programs and point towards genes involved in actions of stromal cells in BPH and CA. J. Cell. Physiol. 210: 111–121, 2007. © 2006 Wiley‐Liss, Inc.
Bone anabolic effects of parathyroid hormone are blunted by deletion of the Wnt antagonist secreted frizzled‐related protein‐1
Authors: Bodine Peter V.N. , Seestaller‐Wehr Laura , Kharode Yogendra P. , Bex Frederick J. , Komm Barry S. 
Published: October 2006

AbstractSecreted frizzled‐related protein (sFRP)‐1 is a Wnt antagonist that when deleted in mice leads to increased trabecular bone formation in adult animals after 13 weeks of age. Treatment of mice with parathyroid hormone (PTH) also increases trabecular bone formation, and some of the anabolic actions of this hormone may result from altered expression of Wnt pathway components. To test this hypothesis, we treated +/+ and −/− female sFRP‐1 mice with PTH 1–34 for 30 days and measured distal femur trabecular bone parameters by peripheral quantitative computed tomography (pQCT) and high‐resolution micro‐computed tomography. During the course of the 32‐week study, volumetric bone mineral density (vBMD) declined 41% in vehicle‐treated +/+ mice, but increased 24% in vehicle‐treated −/− animals. At 8 weeks of age when vBMD was not altered by deletion of sFRP‐1, treatment of +/+ and −/− mice with PTH increased vBMD by 147 and 163%, respectively. In contrast, at 24 weeks of age when vBMD was 75% higher in −/− mice than in +/+ controls, treatment with PTH increased vBMD 164% in +/+ animals, but only 58% in −/− mice. Furthermore, at 36 weeks of age when vBMD was 117% higher in −/− mice than in +/+ controls, treatment with PTH increased vBMD 74% in +/+ animals, while no increase was observed in −/− mice. At each of these time points, PTH treatment increased vBMD to a similar level in +/+ and −/− mice, and this level declined with age. In addition, at 36 weeks of age, the vBMD level reached by PTH treatment of +/+ mice was the same as that achieved solely by deletion of sFRP‐1. These results indicate that loss of sFRP‐1 and PTH treatment increase vBMD to a similar extent. Moreover, as the effects of sFRP‐1 deletion on vBMD increase, the ability of PTH to enhance vBMD declines suggesting that there are overlapping mechanisms of action. J. Cell. Physiol. 210: 352–357, 2007. © 2006 Wiley‐Liss, Inc.
AMP‐activated protein kinase mediates preconditioning in cardiomyocytes by regulating activity and trafficking of sarcolemmal ATP‐sensitive K+ channels
Authors: Sukhodub Andrey , Jovanović Sofija , Du Qingyou , Budas Grant , Clelland Allyson K. , Shen Mei , Sakamoto Kei , Tian Rong , Jovanović Aleksandar 
Published: October 2006

AbstractBrief periods of ischemia and reperfusion that precede sustained ischemia lead to a reduction in myocardial infarct size. This phenomenon, known as ischemic preconditioning, is mediated by signaling pathway(s) that is complex and yet to be fully defined. AMP‐activated kinase (AMPK) is activated in cells under conditions associated with ATP depletion and increased AMP/ATP ratio. In the present study, we have taken advantage of a cardiac phenotype overexpressing a dominant negative form of the α2 subunit of AMPK to analyze the role, if any, that AMPK plays in preconditioning the heart. We have found that myocardial preconditioning activates AMPK in wild type, but not transgenic mice. Cardiac cells from transgenic mice could not be preconditioned, as opposed to cells from the wild type. The cytoprotective effect of AMPK was not related to the effect that preconditioning has on mitochondrial membrane potential as revealed by JC‐1, a mitochondrial membrane potential‐sensitive dye, and laser confocal microscopy. In contrast, experiments with di‐8‐ANEPPS, a sarcolemmal‐potential sensitive dye, has demonstrated that intact AMPK activity is required for preconditioning‐induced shortening of the action membrane potential. The preconditioning‐induced activation of sarcolemmal KATP channels was observed in wild type, but not in transgenic mice. HMR 1098, a selective inhibitor of sarcolemmal KATP channels opening, inhibited preconditioning‐induced shortening of action membrane potential as well as cardioprotection afforded by AMPK. Immunoprecipitation followed by Western blotting has shown that AMPK is essential for preconditioning‐induced recruitment of sarcolemmal KATP channels. Based on the obtained results, we conclude that AMPK mediates preconditioning in cardiac cells by regulating the activity and recruitment of sarcolemmal KATP channels without being a part of signaling pathway that regulates mitochondrial membrane potential. J. Cell. Physiol. 210: 224–236, 2007. © 2006 Wiley‐Liss, Inc.
Constitutive internalization of murine MHC class I molecules
Authors: Mahmutefendić Hana , Blagojević Gordana , Kučić Natalia , Lučin Pero 
Published: October 2006

AbstractThe total number of cell surface glycoprotein molecules at the plasma membrane results from a balance between their constitutive internalization and their egress to the cell surface from intracellular pools and/or biosynthetic pathway. Constitutive internalization is net result of constitutive endocytosis and endocytic recycling. In this study we have compared spontaneous internalization of murine major histocompatibility complex (MHC) class I molecules (Kd, Dd, full Ld, and empty Ld) after depletion of their egress to the cell surface (Cycloheximide [CHX], brefeldin A [BFA]) and internalization after external binding of monoclonal antibody (mAb). MHC class I alleles differ regarding their cell surface stability, kinetics, and in the way of internalization and degradation. Kd and Dd molecules are more stable at the cell surface than Ld molecules and, thus, constitutively internalized more slowly. Although the binding of mAbs to cell surface MHC class I molecules results in faster internalization than depletion of their egress, it is still slow and, thereby, can serve as a model for tracking of MHC class I endocytosis. Internalization of fully conformed MHC class I molecules (Kd, Dd, and Ld) was neither inhibited by chlorpromazine (CP) (inhibitor of clathrin endocytosis), nor with filipin (inhibitor of lipid raft dependent endocytosis), indicating that fully conformed MHC class I molecules are internalized via the bulk pathway. In contrast, internalization of empty Ld molecules was inhibited by filipin, indicating that non‐conformed MHC class I molecules require intact cholesterol‐rich membrane microdomains for their constitutive internalization. Thus, conformed and non‐conformed MHC class I molecules use different endocytic pathways for constitutive internalization. J. Cell. Physiol. 210: 445–455, 2007. © 2006 Wiley‐Liss, Inc.
Effects of TGF‐β and glucocorticoids on map kinase phosphorylation, IL‐6/IL‐11 secretion and cell proliferation in primary cultures of human lung fibroblasts
Authors: Pelaia Girolamo , Gallelli Luca , D'Agostino Bruno , Vatrella Alessandro , Cuda Giovanni , Fratto Donatella , Renda Teresa , Galderisi Umberto , Piegari Elena , Crimi Nunzio , Rossi Francesco , Caputi Mario , Costanzo Francesco S. , Vancheri Carlo , Maselli Rosario , Marsico Serafino A. 
Published: October 2006

AbstractTransforming growth factor‐β1 (TGF‐β1) is crucially involved in the fibrotic events characterizing interstitial lung diseases (ILDs), as well as in the airway remodeling process typical of asthma. Within such a context, the aim of our study was to investigate, in primary cultures of normal and fibrotic human lung fibroblasts (HLFs), the effects of TGF‐β1 on mitogen‐activated protein kinase (MAPK) phosphorylation, cell proliferation, and production of interleukins 6 (IL‐6) and 11 (IL‐11), in the presence or absence of a pretreatment with budesonide (BUD). MAPK phosphorylation was detected by Western blotting, cell viability and proliferation were evaluated using Trypan blue staining and [3H]‐thymidine incorporation assay, respectively, and the release of IL‐6 and IL‐11 into cell culture supernatants was assessed by ELISA. TGF‐β1 (10 ng/ml) significantly stimulated MAPK phosphorylation (P < 0.01), and also enhanced cell proliferation as well as the secretion of both IL‐6 and IL‐11, which reached the highest increases at the 72nd h of cell exposure to this growth factor. All such effects were prevented by BUD (10−8 M) and, with the exception of IL‐6 release, also by a mixture of MAPK inhibitors. Therefore, our findings suggest that the fibrotic action exerted by TGF‐β1 in the lung is mediated at least in part by MAPK activation and by an increased synthesis of the profibrogenic cytokines IL‐6 and IL‐11; all these effects appear to be prevented by corticosteroids via inhibition of MAPK phosphorylation. J. Cell. Physiol. 210: 489–497, 2007. © 2006 Wiley‐Liss, Inc.
Alterations of hHrd1 expression are related to hyperphosphorylated tau in the hippocampus in Alzheimer's disease
Authors: Hou Hai‐Long , Shen Yu‐Xian , Zhu Hong‐Yan , Sun Hao , Yan Xue‐Bo , Fang Hui , Zhou Jiang‐Ning 
Published: October 2006

AbstractThe degradation of aberrantly phosphorylated tau in neurons plays an important role in the pathogenesis of Alzheimer's disease (AD). hHrd1 is a newly identified ubiquitin ligase involved in the endoplasmic reticulum (ER)‐associated protein degradation. The expression and function of hHrd1 in AD brain remains elusive. In the present study, the expression of hHrd1 in AD hippocampus and the morphological relations between hHrd1 expression and pretangle formation were studied by using immunohistochemical single‐ and double‐labeling methods. The results showed that hHrd1 was expressed in neurons and reactive astrocytes, especially in the CA2–CA4 hippocampal subfields. The ratio of hHrd1‐positive neurons/astrocytes to total neurons/astrocytes was increased in the CA1 subfield in AD hippocampus compared with the age‐matched controls (P < 0.05). Most Alz‐50 labeled pretangles were colocalized with hHrd1, and the expression levels showed an inversed change, implied that hHrd1 might be associated with the degradation of hyperphosphorylated tau. © 2006 Wiley‐Liss, Inc.
Contribution of valine 7′ of TMD2 to gating of neuronal α3 receptor subtypes
Authors: Nieves‐Cintrón Madeline , Caballero‐Rivera Daniel , Navedo Manuel F. , Lasalde‐Dominicci José A. 
Published: October 2006

AbstractThe second transmembrane domain (TMD2) of the Cys‐loop family of ligand‐gated ion channels forms the channel pore. The functional role of the amino acid residues contributing to the channel pore in neuronal nicotinic α3 receptors is not well understood. We characterized the contribution of TMD2 position V7′ to channel gating in neuronal nicotinic α3 receptors. Site‐directed mutagenesis was used to substitute position α3 (V7′) with four different amino acids (A, F, S, or Y) and coexpressed each mutant subunit with wild‐type (WT) β2 or β4 subunits inXenopusoocytes. Whole‐cell voltage clamp experiments show that substitution for an alanine, serine, or phenylalanine decreased by 2.3–6.2‐fold the ACh‐EC50for α3β2 and α3β4 receptor subtypes. Interestingly, mutation V7′Y did not produce a significant change in ACh‐EC50when coexpressed with the β2 subunit but showed a significant approximately two‐fold increase with β4. Similar responses were obtained with nicotine as the agonist. The antagonist sensitivity of the mutant channels was assessed by using dihydro‐β‐erythroidine (DHβE) and methyllycaconitine (MLA). The apparent potency of DHβE as an antagonist increased by ∼3.7‐ and 11‐fold for the α3β2 V7′S and V7′F mutants, respectively, whereas no evident changes in antagonist potency were observed for the V7′A and V7′Y mutants. The V7′S and V7′F mutations increase MLA antagonist potency for the α3β4 receptor by ∼6.2‐ and ∼9.3‐fold, respectively. The V7′A mutation selectively increases the MLA antagonist potency for the α3β4 receptor by ∼18.7‐fold. These results indicate that position V7′ contributes to channel gating kinetics and pharmacology of the neuronal nicotinic α3 receptors. © 2006 Wiley‐Liss, Inc.
A method for measuring bending stresses based on electromagnetic actuation and Raman spectroscopy
Authors: Ren Yongfeng , Xu Wenqiang , Xue Chenyang , Zhang Wendong , Zheng Lina 
Published: October 2006

AbstractBending stress and fracture strength of micromachined structures are the parameters determining the function and life span of microelectromechanical systems (MEMS) and are also indispensable data for MEMS design. This paper reports the results of a study in which a bending stress measurement method based on electromagnetic actuation and Raman spectroscopy has been examined. In this study, an eight‐cantilever mass structure is chosen as the experimental object. The results have indicated that it can accurately measure the bending stresses and fracture strength. Copyright © 2006 John Wiley & Sons, Ltd.
Isolation of eriocitrin (eriodictyol 7‐O‐rutinoside) as an arachidonate lipoxygenase inhibitor from Lumie fruit (Citrus lumia) and its distribution in Citrus species
Authors: Nogata Yoichi , Ohta Hideaki , Ishii Toshinao , Sekiya Keizo 
Published: October 2006

AbstractAn inhibitory compound acting against rat platelet 12‐lipoxygenase was isolated from the peel of Lumie fruit (Citrus lumia) by activity‐guided separation. It was identified as eriocitrin (eriodictyol 7‐O‐rutinoside) by spectroscopic analyses. Eriocitrin inhibited 5‐lipoxygenase (IC5029.1 µmol L−1) from rat peritoneal polymorphonuclear leukocytes in addition to 12‐lipoxygenase (IC5022.3 µmol L−1). Its aglycone, eriodictyol (5,7,3′, 4′‐tetrahydroxyflavanone), was a much more potent inhibitor of both 12‐lipoxygenase (IC500.07 µmol L−1) and 5‐lipoxygenase (IC500.20 µmol L−1). It also inhibited the production of leukotriene B4 in intact peritoneal polymorphonuclear leukocytes stimulated with calcium ionophore A23187 (IC5012.7 µmol L−1). The distribution of eriocitrin in 39 citrus fruits was investigated by high‐performance liquid chromatography analysis. Lumie, eureka lemon (Citrus limon), Sambokan (Citrus sulcata), Sudachi (Citrus sudachi) and Koji (Citrus leiocarpa) fruits were found to contain high levels of eriocitrin in both peel and juice vesicles. Copyright © 2006 Society of Chemical Industry
Evaluation of antioxidant capacity of some fruit and vegetable foods: efficiency of extraction of a sequence of solvents
Authors: Pellegrini Nicoletta , Colombi Barbara , Salvatore Sara , Brenna Oreste V , Galaverna Gianni , Del Rio Daniele , Bianchi Marta , Bennett Richard N , Brighenti Furio 
Published: October 2006

AbstractAll methods for assessing the total antioxidant capacity (TAC) of food samples are strongly affected by the solvents used during extraction. In recent years a sequential solvent extraction procedure utilising water and acetone has been widely used for TAC measurements of foods. To better understand the efficiency of this procedure in terms of the amount of extracted antioxidants and the subsequent measurement of TAC, two vegetables (onion and spinach) and two fruits (orange and tomato) were sequentially extracted with water, acetone and chloroform. Each extract fraction was analysed separately for its content of known antioxidant compounds by specific procedures and for its TAC by the Trolox equivalent antioxidant capacity assay. The results showed that the compounds in the water and acetone extracts were the main contributors to TAC. The chloroform extracts did not contribute to TAC, with the exception of the spinach extract, owing to the presence of low levels of carotenoids. In conclusion, the analysed extraction procedure was more effective for foods rich in water‐soluble antioxidants than for those rich in lipid‐soluble antioxidants. Copyright © 2006 Society of Chemical Industry
Effectiveness of chitosan‐based coating in improving shelf‐life of eggs
Authors: Caner Cengiz , Cansiz Ozge 
Published: October 2006

AbstractDespite eggs having a natural packaging—shell—they are perishable and can lose their quality during storage. Chitosan‐based coatings were applied to shell eggs to examine potential effects on egg quality properties (weight loss, Haugh unit, yolk index) during 4 weeks of storage. Mineral amounts in yolks were also evaluated after 4 weeks of storage. Three chitosan‐based coatings produced with organic acids (acetic‐(C‐AA), lactic‐(C‐LA), and propionic (C‐PA)) were evaluated on shelf‐life enhancements of fresh egg quality. All chitosan‐coated eggs showed greater interior quality than the non‐coated eggs. The coatings significantly maintained weight loss compared to the control specimen (4.96%). Lower weight loss (3.45% for C‐PA, 3.53% for C‐LA) was observed in the coated eggs. Eggshell chitosan coat containing lactic and propionic acids maintained higher Haugh unit and yolk index than eggs coated with acetic acid. Uncoated (UC) eggs changed from grade ‘A’ to ‘B’ after 1 week of storage. Chitosan‐based coating containing lactic and propionic acids maintained eggs in grade ‘A’ for 4 weeks. Haugh unit showed that C‐LA and C‐PA effectively maintained eggs at grade ‘A’ quality for at least 3 weeks more than control and 1 week more than C‐AA. Results also indicated that the chitosan coating maintained mineral amounts at nutritional values (especially calcium, iron and magnesium concentration) in yolks after 4 weeks storage. Copyright © 2006 Society of Chemical Industry