bluuebunny/crossref_metadata_2025_split huggingface dataset:
Simulated microgravity decreases DNA repair capacity and induces DNA damage in human lymphocytes
Authors: Kumari Ragini , Singh Kamaleshwar P. , DuMond James W. 
Published: May 2009

AbstractThe effect of simulated microgravity on DNA damage and apoptosis is still controversial. The objective of this study was to test whether simulated microgravity conditions affect the expression of genes for DNA repair and apoptosis. To achieve this objective, human lymphocyte cells were grown in a NASA‐developed rotating wall vessel (RWV) bioreactor that simulates microgravity. The same cell line was grown in parallel under normal gravitational conditions in culture flasks. The effect of microgravity on the expression of genes was measured by quantitative real‐time PCR while DNA damage was examined by comet assay. The result of this study revealed that exposure to simulated microgravity condition decreases the expression of DNA repair genes. Mismatch repair (MMR) class of DNA repair pathway were more susceptible to microgravity condition‐induced gene expression changes than base excision repair (BER) and nucleotide excision repair (NER) class of DNA repair genes. Downregulation of genes involved in cell proliferation (CyclinD1 and PCNA) and apoptosis (Bax) was also observed. Microgravity‐induced changes in the expression of some of these genes were further verified at the protein level by Western blot analysis. The findings of this study suggest that microgravity may induce alterations in the expression of these DNA repair genes resulting in accumulation of DNA damage. Reduced expression of cell‐cycle genes suggests that microgravity may cause a reduction in cell growth. Downregulation of pro‐apoptotic genes further suggests that extended exposure to microgravity may result in a reduction in the cells' ability to undergo apoptosis. Any resistance to apoptosis seen in cells with damaged DNA may eventually lead to malignant transformation of those cells. J. Cell. Biochem. 107: 723–731, 2009. © 2009 Wiley‐Liss, Inc.
Caspases and p53 modulate FOXO3A/Id1 signaling during mouse neural stem cell differentiation
Authors: Aranha Márcia M. , Solá Susana , Low Walter C. , Steer Clifford J. , Rodrigues Cecília M.P. 
Published: May 2009

AbstractNeural stem cells (NSCs) differentiate into neurons and glia, and a large percentage undergoes apoptosis. The engagement and activity of apoptotic pathways may favor either cell death or differentiation. In addition, Akt represses differentiation by up‐regulating the inhibitor of differentiation 1 (Id1), through phosphorylation of its repressor FOXO3A. The aim of this study was to investigate the potential cross‐talk between apoptosis and proliferation during mouse NSC differentiation. We determined the time of neurogenesis and gliogenesis using neuronal β‐III tubulin and astroglial GFAP to confirm that both processes occurred at ∼3 and 8 days, respectively. p‐Akt, p‐FOXO3A, and Id1 were significantly reduced throughout differentiation. Caspase‐3 processing, p53 phosphorylation, and p53 transcriptional activation increased at 3 days of differentiation, with no evidence of apoptosis. Importantly, in cells exposed to the pancaspase inhibitor z‐VAD.fmk, p‐FOXO3A and Id1 were no longer down‐regulated, p53 phosphorylation and transcriptional activation were reduced, while neurogenesis and gliogenesis were significantly delayed. The effect of siRNA‐mediated silencing of p53 on FOXO3A/Id1 was similar to that of z‐VAD.fmk only at 3 days of differentiation. Interestingly, caspase inhibition further increased the effect of p53 knockdown during neurogenesis. In conclusion, apoptosis‐associated factors such as caspases and p53 temporally modulate FOXO3A/Id1 signaling and differentiation of mouse NSCs. J. Cell. Biochem. 107: 748–758, 2009. © 2009 Wiley‐Liss, Inc.
Regulation and function of proline oxidase under nutrient stress
Authors: Pandhare Jui , Donald Steven P. , Cooper Sandra K. , Phang James M. 
Published: May 2009

AbstractUnder conditions of nutrient stress, cells switch to a survival mode catabolizing cellular and tissue constituents for energy. Proline metabolism is especially important in nutrient stress because proline is readily available from the breakdown of extracellular matrix (ECM), and the degradation of proline through the proline cycle initiated by proline oxidase (POX), a mitochondrial inner membrane enzyme, can generate ATP. This degradative pathway generates glutamate and α‐ketoglutarate, products that can play an anaplerotic role for the TCA cycle. In addition the proline cycle is in a metabolic interlock with the pentose phosphate pathway providing another bioenergetic mechanism. Herein we have investigated the role of proline metabolism in conditions of nutrient stress in the RKO colorectal cancer cell line. The induction of stress either by glucose withdrawal or by treatment with rapamycin, stimulated degradation of proline and increased POX catalytic activity. Under these conditions POX was responsible, at least in part, for maintenance of ATP levels. Activation of AMP‐activated protein kinase (AMPK), the cellular energy sensor, by 5‐aminoimidazole‐4‐carboxamide ribonucleoside (AICAR), also markedly upregulated POX and increased POX‐dependent ATP levels, further supporting its role during stress. Glucose deprivation increased intracellular proline levels, and expression of POX activated the pentose phosphate pathway. Together, these results suggest that the induction of proline cycle under conditions of nutrient stress may be a mechanism by which cells switch to a catabolic mode for maintaining cellular energy levels. J. Cell. Biochem. 107: 759–768, 2009. © 2009 Wiley‐Liss, Inc.
FGF‐8b induces growth and rich vascularization in an orthotopic PC‐3 model of prostate cancer
Authors: Valta Maija P. , Tuomela Johanna , Vuorikoski Heikki , Loponen Niina , Väänänen Riina‐Minna , Pettersson Kim , Väänänen H. Kalervo , Härkönen Pirkko L. 
Published: May 2009

AbstractFibroblast growth factor 8 (FGF‐8) is expressed at an increased level in a high proportion of prostate cancers and it is associated with a poor prognosis of the disease. Our aim was to study the effects of FGF‐8b on proliferation of PC‐3 prostate cancer cells and growth of PC‐3 tumors, and to identify FGF‐8b‐associated molecular targets. Expression of ectopic FGF‐8b in PC‐3 cells caused a 1.5‐fold increase in cell proliferation in vitro and a four‐ to fivefold increase in the size of subcutaneous and orthotopic prostate tumors in nude mice. Tumors expressing FGF‐8b showed a characteristic morphology with a very rich network of capillaries. This was associated with increased spread of the cancer cells to the lungs as measured by RT‐qPCR of FGF‐8b mRNA. Microarray analyses revealed significantly altered, up‐ and downregulated, genes in PC‐3 cell cultures (169 genes) and in orthotopic PC‐3 tumors (61 genes). IPA network analysis of the upregulated genes showed the strongest association with development, cell proliferation (CRIP1, SHC1), angiogenesis (CCL2, DDAH2), bone metastasis (SPP1), cell‐to‐cell signaling and energy production, and the downregulated genes associated with differentiation (DKK‐1, VDR) and cell death (CYCS). The changes in gene expression were confirmed by RT‐qPCR. In conclusion, our results demonstrate that FGF‐8b increases the growth and angiogenesis of orthotopic prostate tumors. The associated gene expression signature suggests potential mediators for FGF‐8b actions on prostate cancer progression and metastasis. J. Cell. Biochem. 107: 769–784, 2009. © 2009 Wiley‐Liss, Inc.
A proteomic approach to the identification of molecular targets in subsequent apoptosis of HEL cells after diosgenin‐induced megakaryocytic differentiation
Authors: Cailleteau Clementine , Liagre Bertrand , Beneytout Jean‐L. 
Published: May 2009

AbstractDiosgenin is a plant steroid which is able to induce megakaryocytic differentiation of human erythroleukemia (HEL) cells followed by apoptosis at a later stage. Apoptosis markers and phospho‐kinases involved during the subsequent apoptosis of megakaryocytes after diosgenin‐induced differentiation in these cells were detected using a proteomic approach. In mature megakaryocytes undergoing apoptosis, we observed increased expression of intrinsic apoptosis markers such as Bax/Bcl‐2 ratio and cleaved caspase‐9 as well as extrinsic apoptosis markers including cell death receptors and cleaved caspase‐8. Furthermore, we demonstrated the link between both apoptotic pathways by Bid cleavage and confirmed the executive phase of apoptosis by caspase‐3 cleavage. For the first time, we examined kinase activation and showed that kinases including Src, Tor, Akt, CREB, RSK and Chk2 may be implicated in signalling of subsequent apoptosis of mature megakaryocytes after diosgenin‐induced differentiation of HEL cells. J. Cell. Biochem. 107: 785–796, 2009. © 2009 Wiley‐Liss, Inc.
Caspase‐3‐mediated cyclic stretch‐induced myoblast apoptosis via a Fas/FasL‐independent signaling pathway during myogenesis
Authors: Liu Jiaqiang , Liu Jing , Mao Jing , Yuan Xiao , Lin Zhu , Li Yongming 
Published: May 2009

AbstractSkeletal muscle cells are exposed to mechanical stretch during embryogenesis. Increased stretch may contribute to cell death, and the molecular regulation by stretch remains incompletely understood. The aim of this study was to investigate the effects of cyclic stretch on cell death and apoptosis in myoblast using a Flexercell Strain Unit. Apoptosis was studied by annexin V binding and PI staining, DNA size analysis, electron microphotograph, and caspase assays. Fas/FasL expression was determined by Western blot. When myoblasts were cultured on a flexible membrane and subjected to cyclic strain stress, apoptosis was observed in a time‐dependent manner. We also determined that stretch induced cleavage of caspase‐3 and increased caspase‐3 activity. Caspase‐3 inhibition reduced stretch‐induced apoptosis. Protein levels of Fas and FasL remained unchanged. Our findings implicated that stretch‐induced cell death is an apoptotic event, and that the activation of caspase cascades is required in stretch‐induced cell apoptosis. Furthermore, we had provided evidence that caspase‐3 mediated cyclic stretch‐induced myoblast apoptosis. Mechanical forces induced activation of caspase‐3 via signaling pathways independent of Fas/FasL system. J. Cell. Biochem. 107: 834–844, 2009. © 2009 Wiley‐Liss, Inc.
Increased bone resorption and osteopenia in Dlx5 heterozygous mice
Authors: Samee Nadeem , Geoffroy Valérie , Marty Caroline , Schiltz Corinne , Vieux‐Rochas Maxence , Clément‐Lacroix Philippe , Belleville Cécile , Levi Giovanni , de Vernejoul Marie‐Christine 
Published: May 2009

AbstractDistal‐less (Dlx) homeobox transcription factors play a central role in the control of osteogenesis. In particular, Dlx5 regulates osteoblasts/osteoclasts coupling during perinatal bone formation. We analyze here the effect of Dlx5 allelic reduction in the control of bone remodeling. We first show that Dlx5 expression persists during postnatal bone development. We then compare the skeletal phenotype of 10‐ and 20‐week‐old Dlx5+/− mice to that of wild‐type (WT) littermates. Dlx5+/− male mice exhibit lower bone mineral density (BMD) at both ages while only 20‐week‐old females are affected. µCT analyses reveal a reduction in cortical thickness of femoral midshafts in Dlx5+/− mice. Histomorphometry on distal femora shows no changes in trabecular structure and confirms a reduction in Dlx5+/− cortical thickness. The cortical decrease of 10‐week‐old mice does not derive from a reduction in periosteal bone apposition, but results from increased bone resorption with a significantly higher number of endosteal osteoclasts per bone surface and a larger marrow diameter. Urinary level of deoxypyridinoline is also higher in heterozygous mice confirming an increase in bone resorption activity. Our findings might be relevant for understanding complex, multifactorial diseases such as osteoporosis in which quantitative deregulation of gene expression leads to disruption of bone homeostasis. J. Cell. Biochem. 107: 865–872, 2009. © 2009 Wiley‐Liss, Inc.
Thyroid state and tolerance of mammalian myocardium to hypoxia
Authors: Brooks Wesley W. , Cicogna Antonio C. , Conrad Chester H. , Robinson Kathleen G. , Sen Subha , Bing Oscar H.L. 
Published: May 2009

AbstractThyroid hormone is known to affect myocardial glycogen stores and thereby possibly limit anaerobic performance of mammalian cardiac muscle. Thyroid hormone administration (3,5,3′‐triiodo‐L‐thyroxine, 300 µg/kg/day, sc) for 10 days decreased left ventricle (LV) glycogen concentration relative to euthyroid animals (2.78±0.46 vs. 4.28±0.29 mg/g of LV (mean±SEM)) while increasing the percent of V1 myosin isozyme, contractile activity and cardiac mass. In contrast, thyroidectomy increased myocardial glycogen stores (8.50±0.56 mg/g of LV) and shifted the myosin isozyme toward V3, prolonged contractile activity and decreased LV mass. Thyroxine administration for 3, 7 and 10 days to thyroidectomized animals progressively decreased contractile duration and increased LV mass. Thyroxine administration for 3 or 7 days to thyroidectomized rats did not reduce glycogen stores (7.75±1.02 and 9.62±1.16 mg/g of LV, respectively), whereas myocardial glycogen declined to 3.30±0.58 mg/g of LV after 10 days of treatment. During hypoxia, cardiac muscle from thyroidectomized rats maintained greater active force and developed less contracture relative to euthyroid and, to a greater extent, than hyperthyroid rats. Removal of glucose from the bath decreased anaerobic performance and impaired recovery; however, myocardium from thyroidectomized rats remained more tolerant to hypoxia than the euthyroid group. Overall, the intrinsic LV glycogen content was positively correlated to anaerobic performance. These data demonstrate that the thyroid state profoundly affects myocardial growth, contractility and anaerobic performance of rat myocardium. Although energy demand may affect function during hypoxia, anaerobic substrate reserve (cardiac glycogen concentration) appears to be the primary factor determining tolerance to hypoxic stress. J. Exp. Zool. 311A:399–407, 2009. © 2009 Wiley‐Liss, Inc.
Retention time of attenuated response to diacetyl after pre‐exposure to diacetyl in Caenorhabditis elegans
Authors: Matsuura Tetsuya , Suzuki Seiko , Musashino Ayaka , Kanno Ryo , Ichinose Mitsuyuki 
Published: May 2009

AbstractThe retention time of attenuated chemotactic response to continuous presentation of odorant diacetyl was investigated in the nematode Caenorhabditis elegans. The level of chemotactic response of nematodes pre‐exposed to diacetyl for 90 min was significantly smaller than that of nonexposed control nematodes. In this study, wild‐type (N2) nematodes were maintained at 15, 20 and 25°C after pre‐exposure to diacetyl. At 20°C, there was a decrease in response to diacetyl continuing for up to 6 hr after pre‐exposure to the chemical, but not up to 12 hr. Interestingly, the decrease in response to diacetyl did not continue up to 2 hr in nematodes bred at 15°C, although it continued beyond 12 hr in nematodes bred at 25°C. These results indicate that the retention time of attenuated chemotactic response to diacetyl is dependent on the environmental breeding temperature of nematodes. The breeding temperature correlated with aging speed of nematodes, suggesting that a short life span (higher aging speed) prolongs the retention time of attenuated chemotactic response to diacetyl after pre‐exposure to diacetyl. In the long‐lived daf‐2, age‐1, clk‐1 and isp‐1 mutants, the effect of diacetyl did not continue up to 2 hr. The short‐lived daf‐16, daf‐18, mev‐1 and gas‐1 mutants showed a longer duration of decrease in response to diacetyl, that is, the retention time of attenuated chemotactic response to diacetyl continued beyond 12 hr. There is a possibility that the duration of decrease in response to diacetyl after pre‐exposure to diacetyl was inversely related to the length of nematodes' life span. J. Exp. Zool. 311A:483–495, 2009. © 2009 Wiley‐Liss, Inc.
Evolutionary conservation of mammalian HTRA3 and its developmental regulation in the rat ovary
Authors: Bowden Marissa , Drummond Ann E. , Salamonsen Lois A. , Findlay Jock K. , Nie Guiying 
Published: May 2009

AbstractThe high‐temperature requirement factor A (HtrA) family of serine proteases is evolutionarily conserved from bacteria to mammals. We have previously identified Htra3 in the mouse and human (HTRA3) and reported its expression in the ovary. In this study, we analyzed the rat Htra3 gene and determined its developmental regulation in the rat ovary. We localized the rat Htra3 gene on chromosome 14q21 and identified two alternatively spliced mRNA variants. The two protein sequences deduced from these mRNAs enabled the prediction of the domain organization of the two protein isoforms. Our comparative analysis has established that the key gene features of Htra3 including its genomic structure, intron–exon junction and alternative splicing are well conserved among the mouse, rat and human. The similarities are even higher at the levels of primary protein sequence and protein domain architecture, suggesting that the functions of Htra3 are highly conserved during evolution from rodents to primates. We demonstrate that Htra3 expression in the rat ovary is developmentally regulated; expression was initiated on day 12 after birth and up‐regulated during ovarian maturation with the highest levels found in the mature cycling ovary. In the mature ovary, Htra3 was expressed in granulosa cells, in a follicle‐stage specific manner, with the level of expression being dependent on the positioning of the granulosa cells relative to the oocyte in late stage follicles. The luteinizing granulosa cells of the corpus luteum expressed the highest levels of Htra3. Collectively, these results suggest an important role for Htra3 in ovarian development, granulosa cell differentiation and luteinization. J. Exp. Zool. (Mol. Dev. Evol.) 312B:701–713, 2009. © 2009 Wiley‐Liss, Inc.
Innovative e‐commerce model for food tourism products
Authors: Huang Ting‐Chung , Lee Timothy Jeonglyeol , Lee Kuan‐Huei 
Published: May 2009

AbstractThe applications and opportunities for e‐commerce are increasing. The unique features of the Internet have changed the styles and competition of enterprises. The key factor for the survival of enterprises in this competitive environment is whether they know how to make use of these features to maximise advantages and to make profits. Different enterprises' e‐commerce business models were investigated in the food souvenir industry in Hualien, Taiwan. This study combines the characteristics of network marketing and develops a business model for e‐commerce. This innovative business model in e‐commerce suggests a new paradigm for traditional industries. Copyright © 2009 John Wiley & Sons, Ltd.
Laser cooling of solids [Laser Photon. Rev. 3, No. 1–2, 67–84 (2009)]
Authors: Sheik‐Bahae M. , Epstein R.I. 
Published: May 2009

AbstractFig. 7b and Figs. 14a and b in the paper published in Laser Photon. Rev. 3, 67–84 have not been referenced completely. Please find the correct figure captions here.
Near‐wall hydrodynamic effects related to flow‐induced localized corrosion
Authors: Yabuki A. 
Published: May 2009

AbstractThe relationship between near‐wall hydrodynamic conditions and flow‐induced localized corrosion of copper alloys was investigated. Flow‐induced localized corrosion tests for copper alloys were conducted in corrosive solutions using a jet‐in‐slit testing apparatus, in which various hydrodynamic conditions were reproduced. To evaluate local damage, the profiles of the specimens were measured using a surface roughness meter. In addition, the near‐wall hydrodynamic conditions on the material surface in the apparatus were measured by pressure gauges to determine the distribution of near‐wall velocities and velocity fluctuations. In the equation used to predict corrosion damage, three types of hydrodynamic conditions were applied as parameters related to the mass transfer coefficient in the film of corrosion products. The damage profiles calculated from the equation could be fitted to that obtained from the corrosion test.
Effect of the long‐term service of the gas pipeline on the properties of the ferrite–pearlite steel
Authors: Nykyforchyn H. , Lunarska E. , Tsyrulnyk O. , Nikiforov K. , Gabetta G. 
Published: May 2009

AbstractThe thorough mechanical, corrosion‐mechanical, hydrogen permeation studies of X52 steel in as‐received condition and after 30 years of service in gas pipeline have shown the degradation of the bulk metal properties due to the exploitation. The structure degradation of exploited steels decreased the resistance to crack propagation, to stress corrosion cracking (SCC), HE and HIBC. The exploited steel exhibited specific anomalies of mechanical behaviour: (1) decrease in resistance to brittle fracture with simultaneous decrease in hardness; and (2) the opposite change of the plasticity parameters: decrease in the RA accompanied by the increase in elongation. Deformation ageing and formation of micro defects, assisted by entering and accumulated hydrogen evolved in corrosion processes which takes place in brine deposited inside the pipes, have been proposed to be responsible for the metal degradation and specific modification of the properties during the long‐term service of pipes. The extent of the steel degradation not being able to be detected by the standardized mechanical properties and routine microstructure observation can be efficiently determined by the specially modified methods and conditions. The information may be used in assessment of the conditions and of the life‐time of operated and newly constructed gas pipelines.
Corrosion characteristics of Al‐Si‐Mg/SiCp composites with varying Si/Mg molar ratio in neutral chloride solutions
Authors: Escalera‐Lozano R. , Pech‐Canul M. A. , Pech‐Canul M. I. , Quintana P. 
Published: May 2009

AbstractThe corrosion resistance of Al‐Mg‐Si/SiCp composites produced by the pressureless infiltration method [using SiCp preforms with 50% porosity containing rice hull ash (RHA) and four custom‐made alloys with varying Si/Mg molar ratio] was evaluated in neutral 0.1 M NaCl solutions. The deleterious phase Al4C3 was successfully suppressed in composites with Si/Mg molar ratios of 0.89 and 1.05, but not in those with lower Si/Mg molar ratios (0.12 and 0.49). Results of cyclic polarizations in deareated 0.1 M NaCl solutions showed that with increasing Si/Mg molar ratio, passive current density increased but pitting susceptibility decreased both for reinforced and unreinforced alloys. Immersion tests in aerated 0.1 M NaCl showed that for composites with Si/Mg molar ratios of 0.12 and 0.49 chemical degradation by hydrolysis of Al4C3 was followed by intense anodic dissolution at the matrix–reinforcement interface, while composites corresponding to Si/Mg molar ratios of 0.89 and 1.05 did not exhibit intense localized attack. Possible reasons for the improvement in resistance to localized corrosion are discussed.
The cyclic oxidation behavior of the single crystal TMS‐82+ superalloy in humidified air
Authors: Wu Y. , Narita T. 
Published: May 2009

AbstractThe cyclic oxidation behavior of a single crystal Ni‐based superalloy TMS‐82+ was studied at 800 and 900 °C for 200 h in water vapor (air plus 15% H2O). Regardless of the exposure temperature, time‐dependence of the growth rate of the scale for the superalloy was fitted by a subparabolic relationship. The oxidation rate was enhanced with increase in exposure temperature, which was evidenced by a higher mass gain and thicker scale. The oxides on the specimen at 800 °C consisted of (Ni,Co)O, CrTaO4, AlTaO4, Cr2O3, and θ‐Al2O3, whereas for the specimen exposed at 900 °C, spinels of NiCr2O4 and (Ni,Co)Al2O4 as well as α‐Al2O3 were observed. An innermost dense α‐Al2O3 layer was responsible for a stable growth rate of the scale after the initial rapid oxidation.