bluuebunny/crossref_metadata_2025_split huggingface dataset:
Insulin induces the low density lipoprotein receptor‐related protein 1 (LRP1) degradation by the proteasomal system in J774 macrophage‐derived cells
Authors: Ceschin Danilo G. , Sánchez María C. , Chiabrando Gustavo A. 
Published: December 2008

AbstractLow‐density lipoprotein receptor‐related protein 1 (LRP1) is an endocytic receptor, which binds and internalizes diverse ligands such as activated α2‐macroglobulin (α2M*). LRP1 promotes intracellular signaling, which downstream mediates cellular proliferation and migration of different types of cells, including macrophages. Unlike the LDL receptor, LRP1 expression is not sensitive to cellular cholesterol levels but appears to be responsive to insulin. It has been previously demonstrated that insulin increases the cell surface presentation of LRP1 in adipocytes and hepatocytes, which is mediated by the intracellular PI3K/Akt signaling activation. The LRP1 protein distribution is similar to other insulin‐regulated cell surface proteins, including transferring receptor (Tfr). However, in macrophages, the insulin effect on the LRP1 distribution and expression is not well characterized. Considering that macrophages play a central role in the pathogenesis of atherosclerosis, herein we evaluate the effect of insulin on the cellular expression of LRP1 in J774 macrophages‐derived cells using Western blot and immunofluorescence microscopy. Our data demonstrate that insulin induces a significant decrease in the LRP1 protein content, without changing the specific mRNA level of this receptor. Moreover, insulin specifically affected the protein expression of LRP1 but not Tfr. The insulin‐induced protein degradation of LRP1 in J774 cells was mediated by the activation of the PI3K/Akt pathway and proteasomal system by an enhanced ubiquitin–receptor conjugation. The decreased content of LRP1 induced by insulin affected the cellular internalization of α2M*. Thus, we propose that the protein degradation of LRP‐1 induced by insulin in macrophages could have important effects on the pathogenesis of atherosclerosis. J. Cell. Biochem. 106: 372–380, 2009. © 2008 Wiley‐Liss, Inc.
Autophosphorylation of carboxy‐terminal residues inhibits the activity of protein kinase CK1α
Authors: Budini Mauricio , Jacob Germaine , Jedlicki Ana , Pérez Carolina , Allende Catherine C. , Allende Jorge E. 
Published: December 2008

AbstractCK1 constitutes a protein kinase subfamily that is involved in many important physiological processes. However, there is limited knowledge about mechanisms that regulate their activity. Isoforms CK1δ and CK1ε were previously shown to autophosphorylate carboxy‐terminal sites, a process which effectively inhibits their catalytic activity. Mass spectrometry of CK1α and splice variant CK1αL has identified the autophosphorylation of the last four carboxyl‐end serines and threonines and also for CK1αS, the same four residues plus threonine‐327 and serine‐332 of the S insert. Autophosphorylation occurs while the recombinant proteins are expressed in Escherichia coli. Mutation of four carboxy‐terminal phosphorylation sites of CK1α to alanine demonstrates that these residues are the principal but not unique sites of autophosphorylation. Treatment of autophosphorylated CK1α and CK1αS with λ phosphatase causes an activation of 80–100% and 300%, respectively. Similar treatment fails to stimulate the CK1α mutants lacking autophosphorylation sites. Incubation of dephosphorylated enzymes with ATP to allow renewed autophosphorylation causes significant inhibition of CK1α and CK1αS. The substrate for these studies was a synthetic canonical peptide for CK1 (RRKDLHDDEEDEAMS*ITA). The stimulation of activity seen upon dephosphorylation of CK1α and CK1αS was also observed using the known CK1 protein substrates DARPP‐32, β‐catenin, and CK2β, which have different CK1 recognition sequences. Autophosphorylation effects on CK1α activity are not due to changes in Kmapp for ATP or for peptide substrate but rather to the catalytic efficiency per pmol of enzyme. This work demonstrates that CK1α and its splice variants can be regulated by their autophosphorylation status. J. Cell. Biochem. 106: 399–408, 2009. © 2008 Wiley‐Liss, Inc.
Protein kinase‐A affects sorting and conformation of the sodium‐dependent glucose co‐transporter SGLT1
Authors: Subramanian Supriya , Glitz Petra , Kipp Helmut , Kinne Rolf K.H. , Castaneda Francisco 
Published: December 2008

AbstractIn Chinese hamster ovary cells expressing rabbit sodium‐dependent glucose transporter (rbSGLT1) protein kinase A (PKA) activators (forskolin and 8‐Br‐cAMP) stimulated α‐methyl D‐glucopyranoside uptake. Kinetic analysis revealed an increase in both Vmax and affinity of the transport. Immunohistochemistry and biotinylation experiments showed that this stimulation was accompanied by an increased amount of SGLT1 localized into the plasma membrane, which explains the higher Vmax of the transport. Cytochalasin D only partly attenuated the effect of forskolin as did deletion of the PKA phosphorylation site of SGLT1 in transient transfection studies. Experiments using an anti‐phosphopeptide antibody revealed that forskolin also increased the extent of phosphorylation of SGLT1 in the membrane fraction. These results suggested that regulation of SGLT1 mediated glucose transport involves an additional direct effect on SGLT1 by phosphorylation. To evaluate this assumption further, phosphorylation studies of recombinant human SGLT1 (hSGLT1) in vitro were performed. In the presence of the catalytic subunit PKA and [32P] ATP 1.05 mol of phosphate were incorporated/mol of hSGLT1. Additionally, phosphorylated hSGLT1 demonstrated a reduction in tryptophan fluorescence intensity and a higher quenching by the hydrophilic Trp quencher acrylamide, particularly in the presence of D‐glucose. These results indicate that PKA‐mediated phosphorylation of SGLT1 changes the conformation of the empty carrier and the glucose carrier complex, probably causing the increase in transport affinity. Thus, PKA‐mediated phosphorylation of the transporter represents a further mechanism in the regulation of SGLT1‐mediated glucose transport in epithelial cells, in addition to a change in surface membrane expression. J. Cell. Biochem. 106: 444–452, 2009. © 2008 Wiley‐Liss, Inc.
T‐box 3 negatively regulates osteoblast differentiation by inhibiting expression of osterix and runx2
Authors: Govoni K.E. , Linares G.R. , Chen S‐T. , Pourteymoor S. , Mohan S. 
Published: December 2008

AbstractT‐box (Tbx)3, a known transcriptional repressor, is a member of a family of transcription factors, which contain a highly homologous DNA binding domain known as the Tbx domain. Based on the knowledge that mutation of the Tbx3 gene results in limb malformation, Tbx3 regulates osteoblast proliferation and its expression increases during osteoblast differentiation, we predicted that Tbx3 is an important regulator of osteoblast cell functions. In this study, we evaluated the consequence of transgenic overexpression of Tbx3 on osteoblast differentiation. Retroviral overexpression increased Tbx3 expression >100‐fold at the mRNA and protein level. Overexpression of Tbx3 blocked mineralized nodule formation (28 ± 8 vs. 7 ± 1%) in MC3T3‐E1 cells. In support of these data, alkaline phosphatase (ALP) activity was reduced 33–70% (P < 0.05) in both MC3T3‐E1 cells and primary calvaria osteoblasts overexpressing Tbx3. In contrast, Tbx3 overexpression did not alter ALP activity in bone marrow stromal cells. Tbx3 overexpression blocked the increase in expression of key osteoblast marker genes, ALP, bone sialoprotein, and osteocalcin that occurs during normal osteoblast differentiation, but had little or no effect on expression of proliferation genes p53 and Myc. In addition, Tbx3 overexpression abolished increased osterix and runx2 expression observed during normal osteoblast differentiation, but the change in Msx1 and Msx2 expression over time was similar between control and Tbx3 overexpressing cells. Interestingly, osterix and runx2, but not Msx1 and Msx2, contain Tbx binding site in the regulatory region. Based on these data and our previous findings, we conclude that Tbx3 promotes proliferation and suppresses differentiation of osteoblasts and may be involved in regulating expression of key transcription factors involved in osteoblast differentiation. J. Cell. Biochem. 106: 482–490, 2009. © 2008 Wiley‐Liss, Inc.
Prediction of human cytochrome P450 2B6‐substrate interactions using hierarchical support vector regression approach
Authors: Leong Max K. , Chen Yen‐Ming , Chen Tzu‐Hsien 
Published: December 2008

AbstractThe human cytochrome P450 2B6 can metabolize a number of clinical drugs. Inhibition of CYP2B6 by coadministered multiple drugs may lead to drug–drug interactions and undesired drug toxicity. The aim of this investigation is to develop anin silicomodel to predict the interactions between P450 2B6 and novel inhibitors using a novel hierarchical support vector regression (HSVR) approach, which simultaneously takes into account the coverage of applicability domain (AD) and the level of predictivity. Thirty‐seven molecules were deliberately selected and rigorously scrutinized from the literature data, of which 26 and 11 molecules were treated as the training set and the test set to generate the models and to validate the generated models, respectively. The generated HSVR model gave rise to anr2value of 0.97 for observed versus predicted pKmvalues for the training set, aq2value of 0.93 by the 10‐fold cross‐validation, and anr2value of 0.82 for the test set. Additionally, the predicted results show that the HSVR model outperformed the individual local models, the global model, and the consensus model. Thus, this HSVR model provides an accurate tool for the prediction of human cytochrome P450 2B6‐substrate interactions and can be utilized as a primary filter to eliminate the potential selective inhibitor of CYP2B6. © 2008 Wiley Periodicals, Inc. J Comput Chem, 2009
Investigation of chemical bond characteristics, thermal expansion coefficients and bulk moduli of α‐R2MoO6 and R2Mo2O7 (R = rare earths) by using a dielectric chemical bond method
Authors: Li Huaiyong , Zhang Siyuan , Zhou Shihong , Cao Xueqiang 
Published: December 2008

AbstractTheoretical researches are performed on the α‐R2MoO6 (R = Y, Gd, Tb Dy, Ho, Er, Tm and Yb) and pyrochlore‐type R2Mo2O7 (R = Y, Nd, Sm, Gd, Tb and Dy) rare earth molybdates by using chemical bond theory of dielectric description. The chemical bonding characteristics and their relationship with thermal expansion property and compressibility are explored. The calculated values of linear thermal expansion coefficient (LTEC) and bulk modulus agree well with the available experimental values. The calculations reveal that the LTECs and the bulk moduli do have linear relationship with the ionic radii of the lanthanides: the LTEC decreases from 6.80 to 6.62 10−6/K and the bulk modulus increases from 141 to 154 GPa when R goes in the order Gd, Tb Dy, Ho, Er, Tm, and Yb in the α‐R2MoO6 series; while in the R2Mo2O7 series, the LTEC ranges from 6.80 to 6.61 10−6/K and the bulk modulus ranges from 147 to 163 GPa when R varies in the order Nd, Sm, Gd, Tb and Dy. © 2008 Wiley Periodicals, Inc. J Comput Chem, 2009
Genome based cell population heterogeneity promotes tumorigenicity: The evolutionary mechanism of cancer
Authors: Ye Christine J. , Stevens Joshua B. , Liu Guo , Bremer Steven W. , Jaiswal Aruna S. , Ye Karen J. , Lin Ming‐Fong , Lawrenson Lesley , Lancaster Wayne D. , Kurkinen Markku , Liao Joshua D. , Gairola C. Gary , Shekhar Malathy P.V. , Narayan Satya , Miller Fred R. , Heng Henry H.Q. 
Published: December 2008

AbstractCancer progression represents an evolutionary process where overall genome level changes reflect system instability and serve as a driving force for evolving new systems. To illustrate this principle it must be demonstrated that karyotypic heterogeneity (population diversity) directly contributes to tumorigenicity. Five well characterized in vitro tumor progression models representing various types of cancers were selected for such an analysis. The tumorigenicity of each model has been linked to different molecular pathways, and there is no common molecular mechanism shared among them. According to our hypothesis that genome level heterogeneity is a key to cancer evolution, we expect to reveal that the common link of tumorigenicity between these diverse models is elevated genome diversity. Spectral karyotyping (SKY) was used to compare the degree of karyotypic heterogeneity displayed in various sublines of these five models. The cell population diversity was determined by scoring type and frequencies of clonal and non‐clonal chromosome aberrations (CCAs and NCCAs). The tumorigenicity of these models has been separately analyzed. As expected, the highest level of NCCAs was detected coupled with the strongest tumorigenicity among all models analyzed. The karyotypic heterogeneity of both benign hyperplastic lesions and premalignant dysplastic tissues were further analyzed to support this conclusion. This common link between elevated NCCAs and increased tumorigenicity suggests an evolutionary causative relationship between system instability, population diversity, and cancer evolution. This study reconciles the difference between evolutionary and molecular mechanisms of cancer and suggests that NCCAs can serve as a biomarker to monitor the probability of cancer progression. J. Cell. Physiol. 219: 288–300, 2009. © 2008 Wiley‐Liss, Inc.
The relative potency and safety of endothelial progenitor cells and unselected mononuclear cells for recovery from myocardial infarction and ischemia
Authors: Sekiguchi Haruki , II Masaaki , Losordo Douglas W. 
Published: December 2008

AbstractEndothelial progenitor cells (EPCs) are a subset of the total mononuclear cell population (tMNCs) that possess an enhanced potential for differentiation within the endothelial‐cell lineage. Typically, EPCs are selected from tMNCs via the expression of both hematopoietic stem‐cell markers and endothelial‐cell markers, such as CD34, or by culturing tMNCs in media selective for endothelial cells. Both EPCs and tMNCs participate in vascular growth and regeneration, and their potential use for treatment of myocardial injury or disease has been evaluated in early‐phase clinical studies. Direct comparisons between EPCs and tMNCs are rare, but the available evidence appears to favor EPCs, particularly CD34+ cells, and the potency of EPCs may be increased as much as 30‐fold through genetic modification. However, these observations must be interpreted with caution because clinical investigations of EPC therapy are ongoing. We anticipate that with continued development, EPC therapy will become a safe and effective treatment option for patients with acute myocardial infarction or chronic ischemic disease. J. Cell. Physiol. 219: 235–242, 2009. © 2008 Wiley‐Liss, Inc.
A model forL‐methionine production describing oxygen–productivity relationship
Authors: Ranjan Amalendu P. , Nayak Rajib , Gomes James 
Published: December 2008

AbstractBACKGROUND:The state‐time profile of cell mass, substrate and methionine concentrations of a methionine synthesis process shows strongly nonlinear features. A mathematical representation of this process was developed that conformed to systems analysis required for monitoring and controlling methionine production. The specific growth rate was defined by an exponential term to describe the lag phase in growth, extended before the onset of methionine production and substrate inhibition observed for this process. A switching function was used to describe the relation between methionine synthesis and dissolved oxygen concentration. In addition, the product formation kinetics of this model described the reutilization of methionine feedback regulation whenever the residual substrate concentration dropped below a critical value.RESULTS:The parameters for the model were determined from experimental data using a nonlinear regression technique. A complete nonlinear systems analysis of the model proved that using this model, the system was controllable and observable. The model prediction of methionine production in controlled and uncontrolled environments was satisfactory. Six statistical measures were employed to validate model prediction and its adequacy was shown through simulations.CONCLUSIONS:The proposed model for methionine production possesses the correct system architecture for application in process control. It predicts satisfactorily the relationship between methionine synthesis and dissolved oxygen, and time profiles of state variables. Copyright © 2008 Society of Chemical Industry
Technical and economic comparison of conventional and electrochemical coagulation processes
Authors: Cañizares Pablo , Martínez Fabiola , Jiménez Carlos , Sáez Cristina , Rodrigo Manuel A. 
Published: December 2008

AbstractBACKGROUND: Electrocoagulation is an alternative to the conventional coagulation method, to treat different types of waters and wastewaters. Although there have been many reports on the technical suitability of electrocoagulation, no study has made a direct comparison of the economics of the two processes.RESULTS: Concerning the technical feasibility, no significant differences were found in the results achieved by the two technologies in the treatment of synthetic suspensions, emulsions and solutions of dyes, when the same values of pH and aluminium concentration were adopted in the reaction systems. Regarding the economic comparison, the electrocoagulation process presents lower operating costs for low and intermediate aluminium doses, but results depend on the particular coagulant reagent selected at high doses. The highest operational costs were obtained with conventional coagulation with aluminium sulphate (in the range 3–60 mg dm−3 aluminium). Comparing electrocoagulation and conventional coagulation with aluminium polychloride, the electrocoagulation process presents lower operational costs for low and intermediate doses. However, this situation changes for high aluminium doses.CONCLUSION: Coagulation and electrocoagulation techniques give very similar yields in the removal of different types of pollutants; therefore an economic comparison is of major importance in order to recommend the use of one of the technologies. Nevertheless, it has to be noted that operational costs are of the same order of magnitude for the two processes. Thus, the cost of the electrocoagulation process compares favourably with that of conventional coagulation for small coagulant demands, but the results at high doses depend on the particular coagulant reagent selected. Copyright © 2008 Society of Chemical Industry
Design‐based life cycle assessment of hazardous air pollutant control options at pulp and paper mills: a comparison of thermal oxidation to photocatalytic oxidation and biofiltration
Authors: Babbitt Callie W. , Stokke Jennifer M. , Mazyck David W. , Lindner Angela S. 
Published: December 2008

AbstractBACKGROUND: The forest products industry produces valuable industrial chemicals, wood products, and consumer goods, but is also responsible for the emission of significant quantities of hazardous air pollutants. Although many air pollution control options are available, little is known about the overall environmental impacts of implementing each option. Therefore, a life cycle assessment (LCA) was conducted to compare energy and raw material inputs, air emissions, and environmental impacts associated with construction and operation of two air pollution control systems: regenerative thermal oxidation (RTO) with wet scrubbing and photocatalytic oxidation (PCO) with biofiltration.RESULTS: LCA results indicated that environmental impacts to resource depletion, photochemical oxidant formation, and acidification were 20% higher for the use of a RTO‐scrubber than for the PCO‐biofilter. In addition, at least 25% of the RTO impacts were due to infrastructure requirements. However, the PCO‐biofilter system was responsible for more environmental impact in categories of global warming and human toxicity, because of the packing materials required and the electricity use for the PCO reactor.CONCLUSIONS: The PCO‐biofilter system could be a promising, environmentally‐friendly alternative to traditional RTO devices, provided that this system is modified to decrease resource and energy demands. Copyright © 2008 Society of Chemical Industry
Influence of calcitonin administration on ultimobranchial and parathyroid glands of pigeon, Columba livia
Authors: Yadav Seema , Srivastav Ajai Kumar 
Published: December 2008

AbstractPigeons were divided into two numerically equal groups (A and B) containing 30 specimens each. Birds from group A were intraperitoneally injected daily with 0.1 mL/100 g body wt of vehicle (0.1 M acetate buffer, pH 4.3 containing 0.1% gelatin). Specimens from group B were intraperitoneally injected daily with 1 μg/100 g body wt of salmon calcitonin. Six birds were sacrificed from each group 2 h after the last injection on 1st, 3rd, 5th, 10th, and 15th day of the experiment. After collection of blood samples, ultimobranchial and parathyroid glands were fixed for histological studies. In calcitonin‐treated C. livia, the plasma calcium levels exhibit a progressive decline from day 1 till day 5. On day 15, the levels become more or less similar to the control value. No change has been noticed on day 1 in the plasma phosphate levels of calcitonin‐treated C. livia. The levels decrease progressively from day 3 to day 5; thereafter, it exhibits an elevation so that on day 15, normal plasma phosphate levels is achieved. The ultimobranchial gland of C. livia exhibits no change up to day 5 following calcitonin treatment. The nuclear volume of ultimobranchial cells exhibits a decrease on day 10. This response progresses up to day 15. Few degenerating cells are also discerned following 15 days calcitonin treatment. The parathyroid gland of calcitonin‐treated C. livia exhibits no histological alteration up to day 3. The nuclear volume of parathyroidal cells exhibits a progressive increase from day 3 till the close of the experiment (day 15). Moreover, the gland exhibits more compactness on day 10 and day 15. Few degenerating cells are encountered after day 15 following calcitonin treatment. Microsc. Res. Tech. 2009. © 2008 Wiley‐Liss, Inc.