bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evolution and development of Hertwig's epithelial root sheath
Authors: Luan Xianghong , Ito Yoshihiro , Diekwisch Thomas G.H. 
Published: January 2006

AbstractPeriodontal regeneration and tissue engineering has re‐awakened interest in the role of Hertwig's Epithelial Root Sheath (HERS), an epithelial tissue layer first discovered in amphibians more than a century ago. Using developmental, evolutionary, and cell biological approaches, we have, therefore, performed a careful analysis of the role of HERS in root formation and compared our data with clinical findings. Our developmental studies revealed HERS as a transient structure assembled in the early period of root formation and elongation and, subsequently, fenestrated and reduced to epithelial rests of Malassez (ERM). Our comparative evolutionary studies indicated that HERS fenestration was closely associated with the presence of a periodontal ligament and a gomphosis‐type attachment apparatus in crocodilians and mammals. Based on these studies, we are proposing that HERS plays an important role in the regulation and maintenance of periodontal ligament space and function. Additional support for this hypothesis was rendered by our meta‐analysis of recent clinical reports related to HERS function. Developmental Dynamics 235:1167–1180, 2006. © 2006 Wiley‐Liss, Inc.
Dynamic expression patterns of zebrafish 1G5 (1G5z), a calmodulin kinase‐like gene in the developing nervous system
Authors: Won Minho , Ro Hyunju , Park Hae‐Chul , Kim Kyoon E. , Huh Tae‐Lin , Kim Cheol‐Hee , Rhee Myungchull 
Published: January 2006

AbstractEvolutionarily well‐conserved Ca2+/calmodulin‐dependent protein kinase (CaMK) proteins are known for their role as Ca2+ signaling mediators. 1G5 encodes a CaMK like protein, which belongs to a calmodulin (CaM) kinase gene family. Here, we report the isolation of zebrafish homologue of mammalian 1G5, which we named 1G5z. 1G5z is composed of three major domains: (1) an N‐terminal serine/threonine kinase domain, (2) a central calmodulin‐binding domain, and (3) a C‐terminal alanine‐rich domain, the 1G5z‐specific domain. 1G5z shares 83∼84% homology with other vertebrate 1G5 proteins. Spatiotemporal expression studies found that 1G5z is expressed by means of zygotic transcription and appears in various neuronal tissues from the 20‐somite stage. 1G5z transcripts are more regionalized in the brain and spinal cord at 24 hr postfertilization (hpf). At 35 hpf, 1G5z transcripts are exclusively present in the anterior trunk spinal cord as well as in the hindbrain, tegmentum, hypothalamus, and telencephalon. This expression pattern lasts until 48 hpf but ceases in the trunk. At 72 hpf, 1G5z is abundantly transcribed particularly in the specific region of the tectum and eye. We further observed that the number of 1G5z‐positive cells is dramatically increased in the mindbomb mutant embryos but abolished in the trigeminal ganglion and caudal trunk sensory neuron of the neurogenin1 morphant at 24 hpf. In addition, bromodeoxyuridine staining further confirmed that the 1G5z‐positive cells were postmitotic sensory and interneurons. Developmental Dynamics 235:835–842, 2006. © 2006 Wiley‐Liss, Inc.
Vascular anatomy of the developing medaka, Oryzias latipes: A complementary fish model for cardiovascular research on vertebrates
Authors: Fujita Misato , Isogai Sumio , Kudo Akira 
Published: January 2006

AbstractThe zebrafish has become a very useful vertebrate model for cardiovascular research, but detailed morphogenetic studies have revealed that it differs from mammals in certain aspects of the primary circulatory system, in particular, the early vitelline circulation. We searched for another teleost species that might serve as a complementary model for the formation of these early primary vessels. Here (and online at http://www.shigen.nig.ac.jp/medaka/atlas/), we present a detailed characterization of the vascular anatomy of the developing medaka embryo from the stage 24 (1 day 20 hr) through stage 30 (3 days 10 hr). Three‐dimensional images using confocal microangiography show that the medaka, Oryzias latipes, follows the common embryonic circulatory pattern consisting of ventral aorta, aortic arches, dorsal aorta, transverse vessels, vitelline capillary plexus, and marginal veins. The medaka, thus, may serve as a valuable model system for genetic analysis of the primary vasculature of vertebrates. Developmental Dynamics 235:734–746, 2006. © 2006 Wiley‐Liss, Inc.
Treatment integrity in a home‐based pre‐reading intervention programme
Authors: van Otterloo Sandra G. , van der Leij Aryan , Veldkamp Esther 
Published: January 2006

AbstractTreatment integrity is an underexposed issue in the phonological awareness intervention research. The current study assessed the integrity of treatment of the families (N=32) participating in the experimental condition of a home‐based pre‐reading intervention study. The participating kindergartners were all genetically at risk for developing dyslexia. Two aspects of treatment integrity, the number of lessons completed (quantity) and the quality of the administration of the programme (observed in a videotaped session), were investigated. The level of treatment integrity turned out to be 66% when completion of all lessons was taken as quantitative criterion, and about 74% when quality of the parent–child interaction was assessed. The two measures could predict the pre‐reading skills at the end of kindergarten. Together they accounted for 43% of the variance in this dependent variable. Together with pre‐reading scores at the pre‐test the total predicted variance was 87%. The number of lessons completed still contributed 12% to the prediction after controlling for pre‐test scores. The results indicated that treatment integrity indeed appears to be an important aspect of treatment outcome and should therefore be included in intervention studies. Copyright © 2006 John Wiley & Sons, Ltd.
Redox Chemistry in the Reaction of Oxovanadium(V) with Thiolate‐Containing Ligands: the Isolation and Characterization of Non‐Oxo Vanadium(IV) Complexes Containing Disulfide and Thioether Groups
Authors: Hsu Hua‐Fen , Su Chia‐Ling , Gopal Neeruganti O. , Wu Chi‐Chin , Chu Wei‐Cheng , Tsai Yi‐Fang , Chang Ya‐Ho , Liu Yi‐Hung , Kuo Ting‐Shen , Ke Shyue‐Chu 
Published: January 2006

AbstractThe reactions of VVO(O‐iPr)3 with [PS3′]H3 and [PS3]H3 {[PS3′]H3 = P(C6H3‐5‐Me‐2‐SH)3, [PS3]H3 = P(C6H4‐2‐SH)3} led to the formation of [VIV(L)] [L = P2S4′ (1a), P2S4 (1b)], where L was formed by the oxidative coupling of two PS3′ or PS3 ligands by a disulfide bond. When the reaction of VVO(O‐iPr)3 with [PS3′]H3 was conducted in the presence of methoxide followed by the addition of a cation, [VIV(PS3′)(PS2SMe′)]X [X = N(C2H5)4 (2a), N(C2H5)3(CH2Ph) (2b)] was isolated, where PS2SMe′ is a bis(benzenethiolato)phenylmethylthioetherphosphane ligand generated from the methylation of one thiolate group in PS3′. The structures of complexes 1a,b and 2a,b, determined by X‐ray crystallography, contain six‐ and seven‐coordinate non‐oxo vanadium(IV) centers, respectively, with an octahedral geometry for 1a,b and a pentagonal‐bipyramidal geometry for 2a,b. The electronic, magnetic, and electrochemical properties of these complexes were determined by UV/Vis and EPR spectroscopy, SQUID measurements, and cyclic voltammetry. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Direct Preparation of [Ru(η2‐O2CO)(η6‐arene)(L)] Carbonate Complexes (L = Phosphane, Carbene) and Their Use as Precursors of [RuH2(p‐cymene)(PCy3)] and [Ru(η6‐arene)(L)(MeCN)2][BF4]2: X‐ray Crystal Structure Determination of [Ru(η2‐O2CO)(p‐cymene)(PCy3)]·1/2CH2Cl2 and [Ru(η2‐O2CO)(η6‐C6Me6)(PMe3)]·H2O
Authors: Demerseman Bernard , Mbaye Mbaye Diagne , Sémeril David , Toupet Loïc , Bruneau Christian , Dixneuf Pierre H. 
Published: January 2006

Abstract[RuCl2(η6‐arene)(PR3)] complexes react with K2CO3 in the presence of water to afford the carbonatoruthenium(II) derivatives [Ru(η2‐O2CO)(η6‐arene)(PR3)] (2; arene = p‐cymene, R = Cy, Ph, or Me; arene = hexamethylbenzene, R = Me) involving a planar Ru(η2‐O2CO) moiety as shown by X‐ray crystal structure determination of 2a (p‐cymene, PCy3) and 2d (hexamethylbenzene, PMe3). The complex [Ru(η2‐O2CO)(p‐cymene)(PCy3)] is cleanly converted in hot methanol into the dihydride [RuH2(p‐cymene)(PCy3)]. The related complexes [Ru(η2‐O2CO)(η6‐arene)(IMes)] [arene = p‐cymene or hexamethylbenzene, IMes = 1,3‐bis(2,4,6‐trimethylphenyl)imidazol‐2‐ylidene] are straightforwardly prepared by treating [RuCl2(η6‐arene)]2 precursors with 1,3‐bis(2,4,6‐trimethylphenyl)imidazolium chloride and K2CO3 in THF at reflux. The removal of the carbonato ligand from complexes 2 with HBF4 in the presence of acetonitrile leads to the dicationic derivatives [Ru(η6‐arene)(L)(MeCN)2][BF4]2 (L = PR3 or IMes). (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
A Theoretical Study of the Stereoselectivities of the Diels–Alder Addition of Cyclopentadiene to Ethyl‐(S)‐lactyl Acrylate Catalyzed by Aluminium Chloride
Authors: Bakalova Snezhana M. , Santos A. Gil 
Published: January 2006

AbstractWe have studied the AlCl3‐catalyzed cycloaddition of ethyl‐(S)‐lactyl acrylate (ELA) and cyclopentadiene (CPD) by MP2 and DFT (B3LYP) methods using the 6‐31G(d,p) basis set, with or without solvent effects. Four types of dienophile–Lewis acid (LA) complexes were considered — two types of ELA·AlCl3, ELA·2AlCl3 and ELA·AlCl2+. The stereochemical predictions of these models were compared with available experimental data. The participation of lactate‐bound ELA·AlCl3 complexes is insignificant because of their relatively high TS energies. The diastereofacial selectivities exhibited by the chelated ELA·AlCl2+ complex do not agree with experimental data, suggesting that this type of complex is not very probable, even with ligands having an appropriate carbonyl orientation. Our results show the dominating role of ELA·2AlCl3 in the catalyzed reaction, in agreement with experimental data. The observed diastereofacial stereoselectivities are due to a delicate equilibrium of electrostatic and steric interactions in the different transition states between the two LA groups and between these two groups and the cyclopentadiene moiety. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Molecular cytogenetic characterization of doxorubicin‐resistant neuroblastoma cell lines: Evidence that acquired multidrug resistance results from a unique large amplification of the 7q21 region
Authors: Flahaut Marjorie , Mühlethaler‐Mottet Annick , Martinet Danielle , Fattet Sarah , Bourloud Katia Balmas , Auderset Katya , Meier Roland , Schmutz Nathalie Besuchet , Delattre Olivier , Joseph Jean‐Marc , Gross Nicole 
Published: January 2006

AbstractNeuroblastoma is a heterogeneous neural crest–derived embryonic childhood neoplasm that is the second most common solid tumor found in children. Despite recent advances in combined therapy, the overall survival of patients with high‐stage disease has not improved in the last decades. Treatment failure is in part attributed to multidrug resistance. To address the mechanisms involved in the development of multidrug resistance, we have generated two doxorubicin‐resistant neuroblastoma cell lines (IGRN‐91R and LAN‐1R). These cells were shown to overexpress theMDR1gene coding for the P‐glycoprotein and were resistant to other MDR1‐ and non‐MDR1‐substrate drugs. Indeed, the MDR1 inhibitor verapamil only partially restored sensitivity to drugs, confirming that P‐glycoprotein‐mediated drug efflux was not responsible for 100% resistance. High‐resolution and array‐based comparative genomic hybridization analyses revealed the presence of an amplicon in the 7q21 region as the unique genomic alteration common to both doxorubicin‐resistant cell lines. In addition to theMDR1locus, this large amplified region is likely to harbor additional genes potentially involved in the development of drug resistance. This study represents the first molecular cytogenetic and genomic approach to identifying genomic regions involved in the multidrug‐resistant phenotype of neuroblastoma. These results could lead to the identification of relevant target genes for the development of new therapeutic modalities. © 2006 Wiley‐Liss, Inc.
High antineoplastic activity of new heterocyclic compounds in cancer cells with resistance against classical DNA topoisomerase II‐targeting drugs
Authors: Lage Hermann , Aki‐Sener Esin , Yalcin Ismail 
Published: January 2006

AbstractTwenty previously synthesized fused heterocyclic DNA‐topoisomerase II (Topo II)‐inhibiting compounds were investigated for their potential efficacy in various human cancer cell lines that were derived from different tumor entities. Moreover, different multidrug‐resistant variants of these cancer cell lines with decreased Topo II expression were investigated. In parental, drug‐sensitive cells merely the compounds BD3 and G35 showed efficacies, in terms of μM, which were similar to that of the classical Topo II inhibitor etoposide. On the other hand, most of the tested heterocyclic compounds were found more effective in drug‐resistant cells than in the parental, drug‐sensitive ones, and some of the compounds showed high antineoplastic efficacy in several drug‐resistant cell models. Compounds BD13, BD14 and BD16 exhibited high antineoplastic activities against the drug‐resistant sublines EPG85‐257RNOV and EPG85‐257RDB derived from gastric carcinoma, EPP85‐181RNOV and EPP85‐181RDB derived from pancreatic carcinoma, MCF‐7/Adr derived from breast cancer, D79/86RNOV derived from fibrosarcoma, and MeWoETO1 derived from melanoma. Furthermore, compound D23 was found highly efficient in the multidrug‐resistant variants HT‐29RNOV and HT‐29RDB derived from colon carcinoma, and compound D24 exhibited the highest antineoplastic activity among the tested compounds in the drug‐resistant subline MDA‐MB‐231ROV derived from breast cancer. In conclusion, compounds BD 13, BD 14, BD 16, D 23 and D 24 may be useful for the treatment of different multidrug‐resistant cancer cells with cross resistance against “classical” Topo II‐targeting drugs. © 2006 Wiley‐Liss, Inc.
Nuclear targeting of a midregion PTHrP fragment is necessary for stimulating growth in breast cancer cells
Authors: Kumari Rajendra , Robertson John F. , Watson Sue A. 
Published: January 2006

AbstractParathyroid‐hormone related protein (PTHrP) is the primary factor in humoral hypercalcemia of malignancy and is highly secreted by breast cancers. The pro‐hormone undergoes post‐translational processing and cleavage to give rise to mature secretory peptides, one of which is midregion PTHrP (38‐94/95/101) containing a nuclear localisation sequence (NLS) in amino acids (87‐106). The current study investigates whether the NLS in midregion PTHrP is important in breast cancer growth. PTHrP‐(67‐101), a midregion PTHrP fragment containing NLS‐(87‐101) significantly increased growth of MCF‐7 and MDA‐MB231 cells (126.3 and 121.3% of control respectively in serum conditions), independent of PTHR1 whereas PTHrP‐(67‐86), which lacks the NLS did not. Fluorescent‐labelled PTHrP‐(67‐101) translocated to the nucleus, whereas PTHrP‐(67‐86) remained cytosolic and a scrambled(+NLS) peptide was not internalised. In comparison, no growth influence or uptake was seen in non‐tumour breast cells (Hs578Bst). Increases in intracellular calcium mobilisation were observed in breast cancer cells stimulated with both PTHrP‐(67‐101) and PTHrP‐(67‐86) (EC50 of 3.2 pM and 2.2 pM respectively for MCF‐7 cells), whereas inositide turnover was not detected. Both nuclear uptake and calcium signalling were attenuated in the presence of EGTA, but not with U73122 or N‐terminal PTHrP peptides. Our studies indicate that the NLS‐containing midregion PTHrP peptide is dependent on both internalisation and nuclear translocation to induce growth in breast cancer cells. These findings highlight the importance of midregion PTHrP and its receptor in breast cancer growth and may provide potential targets for future therapeutic intervention. © 2006 Wiley‐Liss, Inc.
Cytokine‐containing gelfoam implants at a postsurgical tumor excision site to stimulate local immune reactivity
Authors: Young M. Rita I. 
Published: January 2006

AbstractWe previously demonstrated increased numbers of CD34+ progenitor cells in the peripheral blood of tumor bearers. Also demonstrated was the feasibility of chemoattracting these cells by sponge implants containing VEGF. The present study used a murine Lewis lung carcinoma (LLC) model to test if CD34+ cells that are chemoattracted to a tumor excision site can be differentiated in situ into dendritic cells and whether this leads to increased local immune reactivity. After surgically excising established LLC tumors, mice received at the excision site gelatin sponge implants containing VEGF to chemoattract CD34+ cells, and/or GM‐CSF plus SCF to induce CD34+ cell differentiation into dendritic cells. In some studies, lysates of GFP‐transfected LLC cells (LLCGFP) were also included in the implants as a source of tumor antigen. After 2 weeks, implants and local lymph nodes were removed and analyzed. Implants containing VEGF, GM‐CSF/SCF or VEGF/GM‐CSF/SCF had a higher proportion of CD34+ cells compared to control implants. However, the number of dendritic cells was higher in implants containing GM‐CSF/SCF or VEGF/GM‐CSF/SCF than those containing either VEGF or diluent. Regional lymph node from mice containing GM‐CSF/SCF or VEGF/GM‐CSF/SCF implants showed increased dendritic cell levels. However, when lysates from LLCGFP were added to the implants, the highest proportion of dendritic cells associated with GFP was in lymph nodes of mice containing GM‐CSF/SCF implants. Lymph node cells from mice with GM‐CSF/SCF or VEGF/GM‐CSF/SCF had a higher level of proliferation and IFN‐γ secretion in response to in vitro LLC lysate challenge, with the greatest response being from lymph node cells of mice with GM‐CSF/SCF implants. These results suggest the feasibility of using GM‐CSF/SCF‐containing implants to increase dendritic cell levels, uptake of tumor antigens, trafficking to lymph nodes and stimulation of immune reactivity at tumor excision sites with residual tumor. © 2006 Wiley‐Liss, Inc.
Cigarette smoking, elevated fasting serum glucose, and risk of pancreatic cancer in Korean men
Authors: Yun Ji Eun , Jo Inho , Park Jungyong , Kim Miyong T. , Gun Ryu Hwang , Odongua Nemekhee , Kim Eunkyung , Jee Sun Ha 
Published: January 2006

AbstractPancreatic cancer is one of the most fatal human cancers and continues to be a major unsolved health problem. The goal of this study was to estimate the independent effects and interactions between cigarette smoking and diabetes on the risk of pancreatic cancer in Korean male population. Cigarette smoking and the risk of incidence and death from pancreatic cancer were examined in a 10‐year prospective cohort study of 446,407 Korean men aged 40 to 65 years who received health insurance from the National Health Insurance Corporation and who had a medical evaluation in 1992. Relative risks (RR) and 95% confidence intervals (CI) were calculated using a Cox proportional hazards model after adjusting for age, body mass index, exercise and alcohol use. Current smoking was associated with an increased risk of incidence (RR = 1.7, 95% CI = 1.6–1.9) and mortality (RR = 1.6, 95% CI = 1.4–1.7) from pancreatic cancer. The RR for pancreatic cancer increased with both duration and amount of smoking. Diabetes was also associated with an increased risk of both incidence (RR = 1.8, 95% CI = 1.5–2.2) and mortality (RR = 1.7, 95% CI = 1.4–2.1) from pancreatic cancer. There was no interaction between smoking and fasting serum glucose in terms of pancreatic cancer risk. Thus, our prospective study has demonstrated that cigarette smoking and elevated fasting serum glucose are independently associated with an increased risk of pancreatic cancer in a large cohort of Korean males. © 2006 Wiley‐Liss, Inc.
Generation of tumoricidal PAX3 peptide antigen specific cytotoxic T lymphocytes
Authors: Rodeberg David A. , Nuss Rebecca A. , Elsawa Sherine F. , Erskine Courtney L. , Celis Esteban 
Published: January 2006

AbstractThe transcription factor PAX3 is expressed during early embryogenesis and in multiple cancer types, including embryonal rhabdomyosarcoma (ERMS), Ewing sarcoma (ES) and malignant melanoma (MEL), suggesting that it could function as a general tumor associated antigen. Major histocompatibility complex (MHC) peptide binding algorithms were used to predict potential epitopes in PAX3 capable of stimulating in vitro naïve HLA‐A0201 restricted cytotoxic T‐lymphocytes (CTLs). Two peptides, PAX3‐282 (QLMAFNHLI) and a modified version of this peptide PAX3‐282.9V (QLMAFNHLV), were capable of inducing antigen‐specific CTLs. Of these peptides, PAX3‐282.9V was the most efficient inducer of primary CTL response. These CTLs were able to lyse HLA‐A0201 expressing target cells that were pulsed with peptide, and more importantly, were effective in killing tumor cells that express PAX3, including ERMS, ES and MEL cell lines. These findings provide compelling evidence that peptide PAX3‐282 is naturally processed by tumors and is presented in the context of HLA‐A0201 in adequate amounts to allow CTL recognition. Also, PAX3‐282.9V is an effective immunogenic peptide able to induce CTL recognition of PAX3‐containing tumors and may be used as an antitumor peptide vaccine. © 2006 Wiley‐Liss, Inc.
Structurally diagnostic ion/molecule reactions: class and functional‐group identification by mass spectrometry
Authors: Eberlin Marcos N. 
Published: January 2006

AbstractThis article discusses the application of gas‐phase ion/molecule reactions for fine structural elucidation in mass spectrometry. This approach is illustrated via a representative collection of class‐ and functional group–selective reactions, a few of historical relevance as well as by more recent and instructive examples, and their applications. The focus is on reactions performed under well‐controlled conditions of sequential mass spectrometry, discussing key mechanistic details and potential applications. Recent and innovative strategies that allow these reactions to be performed under ambient conditions, making this fast, selective and sensitive approach for structural investigation much more generally applicable, are also discussed. Copyright © 2006 John Wiley & Sons, Ltd.
G3139 antisense oligonucleotide directed against antiapoptotic Bcl‐2 enhances doxorubicin cytotoxicity in the FU‐SY‐1 synovial sarcoma cell line
Authors: Joyner David E. , Albritton Karen H. , Bastar Jeffrey D. , Randall R. Lor 
Published: January 2006

AbstractSynovial sarcoma (SS) is a highly aggressive, periarticular soft tissue sarcoma that causes death in more than half of affected children, adolescents, and young adults. Five‐ and 10‐year survival rates are as low as 36 and 20%, respectively. Bcl‐2, a negative regulator of apoptosis, is overexpressed in up to 90% of SS. Increased Bcl‐2 expression not only leads to the development of cancer, but also to resistance of many anticancer chemotherapeutic agents. We hypothesized reducing Bcl‐2 expression in SS should enhance doxorubicin cytotoxicity. Cell cultures representing two human sarcomas (FU‐SY‐1 SS and the pleomorphic SW982) and a primary human dermal fibroblast comparator (NHDF) were exposed in vitro to doxorubicin, or to doxorubicin preceded by Bcl‐2 (G3139) antisense oligonucleotides, and assayed for cell survival, apoptosis, and modulations in Bcl‐2 and Bcl‐xL mRNA and protein content. SW982 sarcoma cells proved most susceptible to doxorubicin, while NHDF mesenchymal cells were least sensitive to doxorubicin. Treatment of FU‐SY‐1 SS with G3139 reduced Bcl‐2 mRNA and protein levels, which enhanced doxorubicin‐induced cell killing. There was a concurrent reduction in Bcl‐xL mRNA following G3139 application in FU‐SY‐1 and NHDF cultures, but not in SW982. G3139 anti‐Bcl‐2 intervention sensitized the FU‐SY‐1 SS to doxorubicin, due to increased apoptosis. G3139 intervention was ineffective in the two non‐SS cell lines. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:474–480, 2006