bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chromosomal fragile sites FRA3B and FRA16D show correlated expression and association with failure of apoptosis in lymphocytes from patients with thyroid cancer
Authors: Sbrana Isabella , Veroni Franca , Nieri Maria , Puliti Aldamaria , Barale Roberto 
Published: January 2006

AbstractIt has been suggested that common fragile sites (cFSs) are related to cancer development. This appears to be the case for FRA3B and FRA16D, localized in two tumor‐suppressor genes (FHIT and WWOX, respectively) that are altered by deletions or loss of heterozygosity (LOH) in many cancers. The features responsible for fragility have not yet been identified. Furthermore, it is still unclear whether instability at these regions causes chance deletions and loss of function of the associated genes, or whether the gene function itself is related to the appearance of fragility. In this study, we analyzed cFS expression in lymphocytes from 20 healthy or thyroid cancer–affected subjects exposed to radiation after the Chernobyl accident. The same cells were examined for apoptosis, a principal function of both the FHIT and WWOX genes. Exceptionally elevated chromosome fragility was observed, particularly in cancer patients, affecting FRA3B, FRA16D, and a cluster of less highly expressed cFSs; levels of chromosome fragility were found to be correlated among these cFSs. Interestingly, most expressed cFSs were sites of LOH reported for thyroid tumors; moreover, cells with the highest fragility also had a reduced ability to undergo apoptosis. These findings reveal previously unknown genetic interactions affecting fragile loci, suggestive of a shared function inside mitotic cells. Attenuation of checkpoint control and apoptosis resistance seem to be the cell phenotypes associated with unusual chromosome fragility. We propose that breakage at specific cFS could derive from early epigenetic events at loci involved in radiation carcinogenesis. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat. © 2006 Wiley‐Liss, Inc.
Identification of NUP98 abnormalities in acute leukemia: JARID1A (12p13) as a new partner gene
Authors: van Zutven Laura J. C. M. , Önen Emine , Velthuizen Sandra C. J. M. , van Drunen Ellen , von Bergh Anne R. M. , van den Heuvel‐Eibrink Marry M. , Veronese Angelo , Mecucci Cristina , Negrini Massimo , de Greef Georgine E. , Beverloo H. Berna 
Published: January 2006

AbstractChromosome rearrangements are found in many acute leukemias. As a result, genes at the breakpoints can be disrupted, forming fusion genes. One of the genes involved in several chromosome aberrations in hematological malignancies is NUP98 (11p15). As NUP98 is close to the 11p telomere, small translocations might easily be missed. Using a NUP98‐specific split‐signal fluorescence in situ hybridization (FISH) probe combination, we analyzed 84 patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia, or myelodysplastic syndrome with either normal karyotypes or 11p abnormalities to investigate whether there are unidentified 11p15 rearrangements. Neither NUP98 translocations nor deletions were identified in cases with normal karyotypes, indicating these aberrations may be very rare in this group. However, NUP98 deletions were observed in four cases with unbalanced 11p aberrations, indicating that the breakpoint is centromeric of NUP98. Rearrangements of NUP98 were identified in two patients, both showing 11p abnormalities in the diagnostic karyotype: a t(4;11)(q1?3;p15) with expression of the NUP98–RAP1GDS1 fusion product detected in a 60‐year‐old woman with AML‐M0, and an add(11)(p15) with a der(21)t(11;21)(p15;p13) observed cytogenetically in a 1‐year‐old boy with AML‐M7. JARID1A was identified as the fusion partner of NUP98 using 3′ RACE, RT‐PCR, and FISH. JARID1A, at 12p13, codes for retinoblastoma binding protein 2, a protein implicated in transcriptional regulation. This is the first report of JARID1A as a partner gene in leukemia. © 2006 Wiley‐Liss, Inc.
Spatiotemporal gene control by the Cre‐ERT2 system in melanocytes
Authors: Yajima Ichiro , Belloir Elodie , Bourgeois Yveline , Kumasaka Mayuko , Delmas Véronique , Larue Lionel 
Published: January 2006

AbstractThe organ‐specific and temporal control of gene activation/inactivation is a key issue in the understanding of protein function during normal and pathological development and during oncogenesis. We generated transgenic mice bearing a tamoxifen‐dependent Cre recombinase (Tyr::Cre‐ERT2) gene expressed under the control of a 6.1 kb murine tyrosinase promoter in order to facilitate targeted spatiotemporally controlled somatic recombination in melanoblasts/melanocytes. Cre‐ERT2 production was detected in tissues containing melanocytes. After tamoxifen induction at various times during embryogenesis and adulthood in a Cre‐responsive reporter mouse strain, genetic recombination was detected in the melanoblasts and melanocytes of the skin. Thus, the Tyr::Cre‐ERT2 transgenic mice provides a valuable tool for following this cell lineage and for investigating gene function in melanocyte development and transformation. genesis 44:34–43, 2006. © 2006 Wiley‐Liss, Inc.
On the reversible O2 binding of the Fe–porphyrin complex
Authors: Nakashima Hiroyuki , Hasegawa Jun‐Ya , Nakatsuji Hiroshi 
Published: January 2006

AbstractElectronic mechanism of the reversible O2 binding by heme was studied by using Density Functional Theory calculations. The ground state of oxyheme was calculated to be open singlet state [Fe(S =1/2) + O2(S = 1/2)]. The potential energy surface for singlet state is associative, while that for triplet state is dissociative. Because the ground state of the O2+ deoxyheme system is triplet in the dissociation limit [Fe(S = 2) + O2(S = 1)], the O2 binding process requires relativistic spin‐orbit interaction to accomplish the intersystem crossing from triplet to singlet states. Owing to the singlet‐triplet crossing, the activation energies for both O2 binding and dissociation become moderate, and hence reversible. We also found that the deviation of the Fe atom from the porphyrin plane is also important reaction coordinate for O2 binding. The potential surface is associative/dissociative when the Fe atom locates in‐plane/out‐of‐plane. © 2006 Wiley Periodicals, Inc. J Comput Chem 4: 426–433, 2006
HMGB1 expression and release by bone cells
Authors: Charoonpatrapong Kanokwan , Shah Rita , Robling Alexander G. , Alvarez Marta , Clapp D. Wade , Chen Shi , Kopp Ryan P. , Pavalko Fredrick M. , Yu Jun , Bidwell Joseph P. 
Published: January 2006

AbstractImmune and bone cells are functionally coupled by pro‐inflammatory cytokine intercellular signaling networks common to both tissues and their crosstalk may contribute to the etiologies of some immune‐associated bone pathologies. For example, the receptor activator of NF‐κB ligand (RANKL)/osteoprotegerin (OPG)/receptor activator of NF‐κB (RANK) signaling axis plays a critical role in dendritic cell (DC) function as well as bone remodeling. The expression of RANKL by immune cells may contribute to bone loss in periodontitis, arthritis, and multiple myeloma. A recent discovery reveals that DCs release the chromatin protein high mobility group box 1 (HMGB1) as a potent immunomodulatory cytokine mediating the interaction between DCs and T‐cells, via HMGB1 binding to the membrane receptor for advanced glycation end products (RAGE). To determine whether osteoblasts or osteoclasts express and/or release HMGB1 into the bone microenvironment, we analyzed tissue, cells, and culture media for the presence of this molecule. Our immunohistochemical and immunocytochemical analyses demonstrate HMGB1 expression in primary osteoblasts and osteoclasts and that both cells express RAGE. HMGB1 is recoverable in the media of primary osteoblast cultures and cultures of isolated osteoclast precursors and osteoclasts. Parathyroid hormone (PTH), a regulator of bone remodeling, attenuates HMGB1 release in cultures of primary osteoblasts and MC3T3‐E1 osteoblast‐like cells but augments this release in the rat osteosarcoma cell line UMR 106‐01, both responses primarily via activation of adenylyl cyclase. PTH‐induced HMGB1 discharge by UMR cells exhibits similar release kinetics as reported for activated macrophages. These data confirm the presence of the HMGB1/RAGE signaling axis in bone. J. Cell. Physiol. 207: 480–490, 2006. © 2006 Wiley‐Liss, Inc.
S100B stimulates myoblast proliferation and inhibits myoblast differentiation by independently stimulating ERK1/2 and inhibiting p38 MAPK
Authors: Riuzzi Francesca , Sorci Guglielmo , Donato Rosario 
Published: January 2006

AbstractThe Ca2+‐modulated protein of the EF‐hand type, S100B, was shown to inhibit rat L6 myoblast differentiation and myotube formation by interacting with a high affinity with an unidentified receptor (Sorci et al., 2003). We show here that S100B independently inhibits the MKK6‐p38 MAPK pathway and stimulates the Ras‐MEK‐ERK1/2 pathway. The inhibitory effect of S100B on p38 MAPK translates into a defective induction of the muscle‐specific transcription factor myogenin and the antiproliferative factor p21WAF1, while S100B's stimulatory effect on ERK1/2 results in stimulation of myoblast proliferation via cyclin D1 induction and Rb phosphorylation and protection against apoptosis via activation of NF‐κB transcriptional activity. Also, the S100B's effects that are mediated by the Ras‐MEK‐ERK1/2 pathway that is, stimulation of proliferation and protection against apoptosis, depend on reactive oxygen species production, being inhibited by antioxidants, while the S100B inhibitory effect on the MKK6‐p38 MAPK pathway is not. We propose that S100B might participate in the regulation of myoblast differentiation by stimulating myoblast proliferation, protecting myoblasts against apoptosis, and modulating myotube formation. J. Cell. Physiol. 207: 461–470, 2006. © 2006 Wiley‐Liss, Inc.
Intraocular injection of an aptamer that binds PDGF‐B: A potential treatment for proliferative retinopathies
Authors: Akiyama Hideo , Kachi Shu , E Silva Raquel Lima , Umeda Naoyasu , Hackett Sean F. , McCauley Dilara , McCauley Thomas , Zoltoski Anna , Epstein David M. , Campochiaro Peter A. 
Published: January 2006

AbstractPlatelet‐derived growth factor‐B (PDGF‐B) has been implicated in the pathogenesis of proliferative retinopathies and other scarring disorders in the eye. In this study, we sought to test the therapeutic potential of an aptamer that selectively binds PDGF‐B, ARC126, and its PEGylated derivative, ARC127. Both ARC126 and ARC127 blocked PDGF‐B‐induced proliferation of cultured fibroblasts with an IC50 of 4 nM. Pharmacokinetic studies in rabbits showed similar peak vitreous concentrations of approximately 110 µM after intravitreous injection of 1 mg of either ARC126 or ARC127, but the terminal half‐life was longer for ARC127 (98 versus 43 h). Efficacy was tested in rho/PDGF‐B transgenic mice that express PDGF‐B in photoreceptors and develop severe proliferative retinopathy resulting in retinal detachment. Compared to eyes injected with 20 µg of scrambled aptamer in which five of six developed detachments (three total and two partial), eyes injected with ARC126 (no detachment in five of six and one partial detachment), or ARC127 (no detachment in six of six) had significantly fewer retinal detachments. They also showed a significant reduction in epiretinal membrane formation. These data demonstrate that a single intravitreous injection of an aptamer that specifically binds PDGF‐B is able to significantly reduce epiretinal membrane formation and retinal detachment in rho/PDGF‐B mice. These striking effects in an aggressive model of proliferative retinopathy suggest that ARC126 and ARC127 should be considered for treatment of diseases in which PDGF‐B has been implicated, including ischemic retinopathies such as proliferative diabetic retinopathy, proliferative vitreoretinopathy (PVR), and choroidal neovascularization. J. Cell. Physiol. 207: 407–412, 2006. © 2006 Wiley‐Liss, Inc.
Protein kinase C theta co‐operates with calcineurin in the activation of slow muscle genes in cultured myogenic cells
Authors: D'Andrea M. , Pisaniello A. , Serra C. , Senni M.I. , Castaldi L. , Molinaro M. , Bouché M. 
Published: January 2006

AbstractAdult skeletal muscle fibers can be divided into fast and slow twitch subtypes on the basis of specific contractile and metabolic properties, and on distinctive patterns of muscle gene expression. The calcium, calmodulin‐dependent protein phosphatase, calcineurin, stimulates slow fiber‐specific genes (myoglobin (Mb), troponin I slow) in cultured skeletal muscle cells, as well as in transgenic mice, through the co‐operation of peroxisome‐proliferation‐activator receptor γ co‐activator 1α (PGC1α) myocyte enhancer factor 2 (MEF2), and nuclear factor of activated T cells (NFAT) transcription factors. Specific protein kinase C isoforms have been shown to functionally co‐operate with calcineurin in different cellular models. We investigated whether specific protein kinase C isoforms are involved in calcineurin‐induced slow skeletal muscle gene expression. By pharmacological inhibition or exogenous expression of mutant forms, we show that protein kinase C theta (the protein kinase C isoform predominantly expressed in skeletal muscle) is required and co‐operates with calcineurin in the activation of the Mb promoter, as well as in the induction of slow isoforms of myosin and troponin I expression, in cultured muscle cells. This co‐operation acts primarily regulating MEF2 activity, as shown by using reporter gene expression driven by the Mb promoter mutated in the specific binding sites. MEF2 activity on the Mb promoter is known to be dependent on both PGC1α and inactivation of histone deacetylases (HDACs) activity. We show in this study that protein kinase C theta is required for, even though it does not co‐operate in, PGC1α‐dependent Mb activation. Importantly, protein kinase C theta regulates the HDAC5 nucleus/cytoplasm location. We conclude that protein kinase C theta ensures maximal activation of MEF2, by regulating both MEF2 transcriptional complex formation and HDACs nuclear export. J. Cell. Physiol. 207: 379–388, 2006. © 2006 Wiley‐Liss, Inc.
The MEK/MAPK pathway is involved in the resistance of breast cancer cells to the EGFR tyrosine kinase inhibitor gefitinib
Authors: Normanno Nicola , Luca Antonella De , Maiello Monica R. , Campiglio Manuela , Napolitano Maria , Mancino Mario , Carotenuto Adele , Viglietto Giuseppe , Menard Sylvie 
Published: January 2006

AbstractWe investigated the role of the MEK/MAPK pathway in the sensitivity/resistance of breast carcinoma cells to the EGFR tyrosine kinase inhibitor gefitinib (IRESSA). We assessed the effects of gefitinib on the growth of three breast cancer cell lines that showed high (SK‐Br‐3; IC50 4 µM), intermediate (MDA‐MB‐361; IC50 5.3 µM), and low (MDA‐MB‐468; IC50 6.8 µM) sensitivity to the drug. Although treatment with gefitinib inhibited EGFR activation in the three cell lines in a similar fashion, significant reduction of both p42/p44‐MAPK and AKT phosphorylation was observed in SK‐Br‐3 and MDA‐MB‐361, but not in MDA‐MB‐468 cells. The growth of MDA‐MB‐468 cells was significantly inhibited by treatment with either the PI3K‐inhibitor LY294002 or the MEK‐inhibitor PD98059. In agreement with these findings, treatment of MDA‐MB‐468 cells with a combination of PD98059 and gefitinib produced a synergistic anti‐tumor effect, whereas this combination was only additive in SK‐Br‐3 and MDA‐MB‐361 cells. The combination of gefitinib and PD98059 also produced a significant increase in the levels of apoptosis in MDA‐MB‐468 cells as compared with treatment with a single agent. This phenomenon was associated with a profound decrease in MAPK activation, reduction of BAD (ser112) phosphorylation and a paradoxical increase in the levels of AKT activation. Finally, overexpression of a constitutively activated form of p42‐MAPK in MCF‐10A non‐transformed human mammary epithelial cells resulted in a two‐ to three‐fold increase in the IC50 to gefitinib. Taken together, these data strongly support the role of the MEK/MAPK pathway in the resistance to gefitinib, and provide the rationale for novel therapeutic approaches based on combinations of signal transduction inhibitors. J. Cell. Physiol. 207: 420–427, 2006. © 2006 Wiley‐Liss, Inc.
From the “Modern Synthesis” to cybernetics: Ivan Ivanovich Schmalhausen (1884–1963) and his research program for a synthesis of evolutionary and developmental biology
Authors: Levit Georgy S. , Hossfeld Uwe , Olsson Lennart 
Published: January 2006

AbstractIvan I. Schmalhausen was one of the central figures in the Russian development of the “Modern Synthesis” in evolutionary biology. He is widely cited internationally even today. Schmalhausen developed the main principles of his theory facing the danger of death in the totalitarian Soviet Union. His great services to evolutionary and theoretical biology are indisputable. However, the received view of Schmalhausen's contributions to evolutionary biology makes an unbiased reading of his texts difficult. Here we show that taking all of his works into consideration (including those only available in Russian) paints a much more dynamic and exciting picture of what he tried to achieve. Schmalhausen pioneered the integration of a developmental perspective into evolutionary thinking. A main tool for achieving this was his approach to living objects as complex multi‐level self‐regulating systems. Schmalhausen put enormous effort into bringing this idea into fruition during the final stages of his career by combining evolutionary theory with cybernetics. His results and ideas remain thought‐provoking, and his texts are of more than just historical interest. J. Exp. Zool. (Mol. Dev. Evol.) 306B, 2006. © 2006 Wiley‐Liss, Inc.
Application of flow nephelometry to the analysis of the influence of carbohydrates on protein–tannin interactions
Authors: Carvalho Elisabete , Póvoas Maria João , Mateus Nuno , de Freitas Victor 
Published: January 2006

AbstractThe flow nephelometric technique was recently introduced to study the interaction between tannins and proteins. This technique was employed here to study the ability of the polysaccharides xanthan, dextran and gum arabic to disrupt the interactions between condensed tannin fractions from grape seed and bovine serum albumin (BSA). Xanthan was shown to have a higher ability to inhibit the aggregate formation of tannins and BSA than the other polysaccharides. Xanthan's ability to inhibit protein‐tannin complex formation was higher for condensed tannin fractions of smaller size and lower complexity. Copyright © 2006 Society of Chemical Industry
Tea, obesity, and diabetes
Authors: Kao Yung‐Hsi , Chang Hsin‐Huei , Lee Meng‐Jung , Chen Chia‐Lin 
Published: January 2006

AbstractTea has been found to possess widespread biological functions based on a variety of laboratory data. The effects of tea on obesity and diabetes have received increasing attention. This paper reviews the evidence for the connections among tea catechins, and obesity and diabetes. Tea catechins, especially (–)‐epigallocatechin gallate (EGCG), appear to have antiobesity and antidiabetic effects. While few epidemiological and clinical studies show the health benefits of EGCG on obesity and diabetes, the mechanisms of its actions are emerging based on the various laboratory data. These mechanisms may be related to certain pathways, such as through the modulations of energy balance, endocrine systems, food intake, lipid and carbohydrate metabolism, the redox status, and activities of different types of cells (i. e., fat, liver, muscle, and β‐pancreatic cells). Because the EGCG receptor, the so‐called 67‐kDa laminin receptor (LR), has been discovered with colocalization of other types of LR and cytoskeleton in both cancer cells and normal cells, this may explain that EGCG possesses numerous actions. The mechanistic results of this review may possibly be utilized in the treatment of obesity, diabetes, and other related diseases using tea‐ and EGCG‐based folk medicines.
Recent progress in high resolution lithography
Authors: Bratton Daniel , Yang Da , Dai Junyan , Ober Christopher K. 
Published: January 2006

AbstractThe nanotechnology revolution of the past decade owes much to the science of lithography, an umbrella term which encompasses everything from conventional photolithography to “unconventional” soft lithography and the self‐assembly of block polymers. In this review, some of the recent advances in lithography are summarized with special reference to the microelectronics industry. The next generation photolithography, two‐photon lithography, step‐and‐flash imprint lithography and nanofabrication using block copolymers are covered, in an attempt to describe more recent work in this vibrant and active field of research. Copyright © 2006 John Wiley & Sons, Ltd.
Photoinitiators with functional groups. IX. Hydrophilic bisacylphosphine oxides for acidic aqueous formulations
Authors: Ullrich G. , Ganster B. , Salz U. , Moszner N. , Liska R. 
Published: January 2006

AbstractBecause of the poor photoreactivity of camphorquinone–amine‐based photoinitiator systems in dental acidic aqueous primer formulations, we were interested to evaluate a commercially available bisacylphosphine oxide as photoinitiator. Because of the promising results on photoreactivity and storage stability, new oligo(ethylene glycol)‐substituted bisacylphosphine oxides were synthesized and investigated. Beside good solubility and significantly increased reactivity in aqueous acidic formulations, sufficient storage stability was found. Additionally, the influence of the type of substitution on the photopolymerization behavior in aqueous, hydrophilic, and hydrophobic resins is discussed. © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 1686–1700, 2006
Computational study of the synthesis of benzoin derivatives from benzil
Authors: Topal Kevser Göçmen , Unaleroglu Canan , Aviyente Viktorya 
Published: January 2006

AbstractBenzil (1,2‐diphenylethane‐1,2‐dione) undergoes cyanide catalyzed condensation with benzaldehyde to yield O‐benzoylated benzoin (2‐benzoyl‐1,2‐diphenylethanone). In this study, the experimentally suggested mechanism has been modeled with PM3 and verified with B3LYP. The effect of the substituent on the reaction yield has been rationalized by considering two benzil derivatives; 1,2‐bis(2‐chlorophenyl)ethane‐1,2‐dione and 1,2‐bis(2‐fluorophenyl)ethane‐1,2‐dione and three benzaldehyde derivatives; o‐fluorobenzaldehyde, o‐methylbenzaldehyde and 2‐pyridinecarboxaldehyde. The effect of the solvent has been modeled by using the isodensity‐surface polarizable continuum (IPCM) model. Reactivity descriptors have been used to justify the reactivity differences of the various substituents. © 2006 Wiley Periodicals, Inc. Int J Quantum Chem, 2006