bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metal Complexation by Tripodal N‐Acyl(thio)urea and Picolin(thio)amide Compounds: Synthesis/Extraction and Potentiometric Studies
Authors: Reinoso‐García Marta M. , Dijkman Arjan , Verboom Willem , Reinhoudt David N. , Malinowska Elżbieta , Wojciechowska Dorota , Pietrzak Mariusz , Selucky Pavel 
Published: May 2005

AbstractThe synthesis and binding properties towards different cations of a series of tripodal ligands functionalized with N‐acyl(thio)urea and picolin(thio)amide moieties are described. For the extraction of Am3+ and Eu3+ the compounds are not efficient. However, N‐acylurea derivative 10 exhibit a significant selectivity for Am3+ over Eu3+. Upon addition of the synergistic hexabrominated bis(dicarbollide)cobalt anion (Br6‐COSAN) the distribution coefficients for Am3+ and Eu3+ increase up to 1000 for picolinamide derivative 11. Extraction studies with metal picrates (Pb2+, Cu2+, Ag+, Hg2+, Cd2+, Eu3+, Fe3+, K+, Na+, and Ca2+) or the incorporation in ion selective electrodes (ISEs), show that picolinamide derivative 11 is a very selective and strong ionophore for Hg2+ and that N‐acylthiourea 8 is a very good ionophore for Ag+. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Thermus thermophilus Glycosynthases for the Efficient Synthesis of Galactosyl and Glucosyl β‐(1→3)‐Glycosides
Authors: Drone Jullien , Feng Hui‐yong , Tellier Charles , Hoffmann Lionel , Tran Vinh , Rabiller Claude , Dion Michel 
Published: May 2005

AbstractInverting mutant glycosynthases were designed according to the Withers strategy, starting from wild‐type Thermus thermophilus retaining Tt‐β‐Gly glycosidase. Directed mutagenesis of catalytic nucleophile glutamate 338 by alanine, serine, and glycine afforded the E338A, E338S, and E338G mutant enzymes, respectively. As was to be expected, the mutants were unable to catalyze the hydrolysis of the transglycosidation products. In agreement with previous results, the E338S and E338G catalysts were much more efficient than E338A. Moreover, our results showed that these enzymes were inactive in the hydrolysis of the α‐D‐glycopyranosyl fluorides used as donors, and so suitable experimental conditions, under which the rate of spontaneous hydrolysis of the donor was considerably lower than that of enzymatic transglycosidation, provided galactosyl and glucosyl β‐(1→3)‐glycosides in yields of up to 90 %. The structure of native Tt‐β‐Gly available in the Protein Data Bank offers a good basis for interpretation of our results by means of molecular modeling. Thus, in the case of the E338S mutant, a lower energy of the system was obtained when the donor and the acceptor were in the right position to form the β‐(1→3)‐glycosidic bond. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Nucleophilic Carbenes and Pseudo‐Cross‐Conjugated Mesomeric Betaines of Indazole Starting from Analogues of the Alkaloid‐Betaine Nigellicine
Authors: Schmidt Andreas , Merkel Lars , Eisfeld Wolfgang 
Published: May 2005

AbstractThe alkaloid Nigellicine possesses the indazolium‐3‐carboxylate ring system as electronically relevant partial structure which represents a member of the class of pseudo‐cross‐conjugated mesomeric betaines. Indazolium‐3‐carboxylate, prepared starting from indazole‐3‐carboxylic acid by an esterification–methylation–saponification sequence, can be converted into the isoconjugated phenyl‐ and 4‐(nitrophenyl)amidates and the thiocarboxylate as additional examples of pseudo‐cross‐conjugated systems. In accordance with results of ab initio calculations decarboxylation of indazolium‐3‐carboxylate with formation of the nucleophilic carbene indazol‐3‐ylidene begins at approximately 40 °C as evidenced by temperature‐dependent NMR spectroscopy. The carbene can be trapped with protons as indazolium salts, and carbon dioxide which reconstitutes the pseudo‐cross‐conjugated mesomeric betaine. According to the calculations, the carbene adopts a singlet ground state. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Catalytic Activation of Silylated Nucleophiles Using tBu‐P4 as a Base
Authors: Ueno Masahiro , Hori Chieko , Suzawa Koichi , Ebisawa Masashi , Kondo Yoshinori 
Published: May 2005

AbstractTrialkylsilyl groups play an important role as effective protecting groups in organic synthesis. Various O, N, and C nucleophilic sites can be protected by trialkylsilyl groups to control the selectivity of reactions. The nucleophilic attack of a fluoride anion on a silyl group is recognized as one of the most useful methods for desilylation. The activation of the nucleophile–silicon bond is important not only for desilylation but also for the generation of a reactive nucleophilic anion to achieve a new bond formation. The phosphazene bases developed by Schwesinger are known to be strong non‐metallic organic bases. Among them, the tBu‐P4 base has been used for various selective deprotonative transformations, although the ability of tBu‐P4 base to activate silylated nucleophiles has not yet been shown. A novel catalytic activation of various O, N, and C nucleophile–silicon bonds using tBu‐P4 base was investigated to perform nucleophilic reactions with various electrophiles. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
A Metathesis Approach to Aromatic Heterocycles
Authors: Donohoe Timothy J. , Orr Allan J. , Gosby Katherine , Bingham Matilda 
Published: May 2005

AbstractThe ring closing metathesis (RCM) reaction can be used to prepare substituted furans and pyrroles. By utilising a Pd‐catalysed coupling reaction with methoxyallene, allylic alcohols and sulfonamides can be converted into substrates that are ideal precursors to ring closing metathesis. After the RCM reaction is complete, the addition of acid promotes an elimination of methanol to form the fully aromatised system. A range of different substitution patterns and functional groups are compatible with this sequence. Double allene coupling, RCM and elimination reactions are also possible and allow the formation of biaryl systems. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2005)
Cover Picture: Thermus thermophilus Glycosynthases for the Efficient Synthesis of Galactosyl and Glucosyl β‐(1→3)‐Glycosides (Eur. J. Org. Chem. 10/2005)
Authors: Drone Jullien , Feng Hui‐yong , Tellier Charles , Hoffmann Lionel , Tran Vinh , Rabiller Claude , Dion Michel 
Published: May 2005

AbstractThe cover picture shows the molecular modeling of the active site of a “glycosynthase” mutant obtained by directed mutagenesis (E338S) of the native thermostable Tt‐β‐Glyglycosidase from Thermus thermophilus. The relative orientations of the donor (α‐D‐glucopyranosyl fluoride) and of the acceptor (phenyl β‐D‐glucopyranoside), which corresponded to an energy minimum, were in agreement with the β‐(1→3) regioselectivity exhibited by this E338S mutant enzyme. The stabilization of the initial ligands in this state, particularly due to stacking between the phenyl aglycon group of the acceptor and W312, gives an explanation for the very good transglycosydation yields (95%) obtained by using phenyl β‐D‐glucopyranoside. Details are discussed in the article by M. Dion et al. on p. 1977 ff.
Light‐dependent mutagenesis by benzo[a]pyrene is mediated via oxidative DNA damage
Authors: Kim Su‐Ryang , Kokubo Kiyoko , Matsui Keiko , Yamada Noriyo , Kanke Yusuke , Fukuoka Masamichi , Yamada Masami , Nohmi Takehiko 
Published: May 2005

AbstractBenzo[a]pyrene (B[a]P) is an environmental carcinogenic polycyclic aromatic hydrocarbon (PAH). Mammalian enzymes such as cytochrome P‐450s and epoxide hydrase convert B[a]P to reactive metabolites that can covalently bind to DNA. However, some carcinogenic compounds that normally require metabolic activation can also be directly photoactivated to mutagens. To examine whether B[a]P is directly mutagenic in the presence of light, we exposed Salmonella typhimurium strains with different DNA repair capacities to B[a]P and white fluorescent light at wavelengths of 370–750 nm. B[a]P plus light significantly enhanced the number of His+ revertants. Mutagenesis was completely light‐dependent and required no exogenous metabolic activation. The order of mutability of strains with different DNA repair capacities was strain YG3001 (uvrB, mutMST) ≫ strain TA1535 (uvrB) > strain YG3002 (mutMST) > strain TA1975. The uvrB gene product is involved in the excision repair of bulky DNA adducts, and the mutMST gene encodes 8‐oxoguanine (8‐oxoG) DNA glycosylase, which removes 8‐oxoG from DNA. Introduction of a plasmid carrying the mOgg1 gene that is the mouse counterpart of mutMST substantially reduced the light‐mediated mutagenicity of B[a]P in strain YG3001. B[a]P plus light induced predominantly G:C → T:A and G:C → C:G transversions. We propose that B[a]P can directly induce bulky DNA adducts if light is present, and that the DNA adducts induce oxidative DNA damage, such as 8‐oxoG, when exposed to light. These findings have implications for the photocarcinogenicity of PAHs. Environ. Mol. Mutagen., 2005. © 2005 Wiley‐Liss, Inc.
Localization of a putative low‐penetrance ependymoma susceptibility locus to 22q11 using a chromosome 22 tiling‐path genomic microarray
Authors: Ammerlaan Anneke C. J. , de Bustos Cecilia , Ararou Abdelhay , Buckley Patrick G. , Mantripragada Kiran K. , Verstegen Marco J. , Hulsebos Theo J. M. , Dumanski Jan P. 
Published: May 2005

AbstractEpendymomas frequently display allelic loss of chromosome 22 in the absence of mutations in the known tumor‐suppressor genes on chromosome 22, suggesting the role of an alternative predisposing gene or genes from this chromosome. In an effort to localize these genes, 37 ependymomas derived from 33 patients were analyzed for the presence of copy number changes by use of a high‐resolution chromosome 22 genomic microarray. Eighteen ependymomas (49%) displayed an array‐CGH profile consistent with monosomy of chromosome 22. However, in 10 of these tumors, the fluorescence ratios for 22q clones scored as deleted were different from those at the single gene copy level. This suggests either analysis of mixed populations of tumor and normal stromal cells or analysis of mixed tumor cell populations with different genetic profiles. Four ependymomas derived from two patients showed overlapping interstitial deletions of 2.2 Mb and ∼510 kb. Further analyses revealed that these deletions were present in the constitutional DNA of these two patients as well as in some of their unaffected relatives. Detailed microsatellite analysis of these families refined the commonly deleted segment to a region of 320 kb between markers RH13801 and D22S419. Our results provide additional evidence for the involvement of genes on chromosome 22 in the development of ependymoma and suggest the presence of a low‐penetrance ependymoma susceptibility locus at 22q11. © 2005 Wiley‐Liss, Inc.
Identification of recurrent chromosomal aberrations in germ cell tumors of neonates and infants using genomewide array‐based comparative genomic hybridization
Authors: Veltman Imke , Veltman Joris , Janssen Irene , Hulsbergen‐van de Kaa Christina , Oosterhuis Wolter , Schneider Dominik , Stoop Hans , Gillis Ad , Zahn Susanne , Looijenga Leendert , Göbel Ulrich , van Kessel Ad Geurts 
Published: May 2005

AbstractHuman germ cell tumors (GCTs) of neonates and infants comprise a heterogeneous group of neoplasms, including teratomas and yolk sac tumors with distinct clinical and epidemiologic features. As yet, little is known about the cytogenetic constitution of these tumors. We applied the recently developed genomewide array‐based comparative genomic hybridization (array CGH) technology to 24 GCTs derived from patients under the age of 5 years. In addition, we included seven tumors derived from children and adolescents older than 5 years. In the series from those under the age of 5 years, most teratomas displayed normal profiles, except for some minor recurrent aberrations. In contrast, the yolk sac tumors displayed recurrent losses of 1p35–pter and gains of 3p21–pter and of 20q13. In the GCTs of patients older than 5 years, the main recurrent anomalies included gains of 12p and of whole chromosomes 7 and 8. In addition, gains of the 1q32–qter region and losses of the 6q24–qter and 18q21–qter regions were frequent in GCTs of varied histology, independent of age. We concluded that array CGH is a highly suitable method for identifying recurrent chromosomal anomalies in GCTs of neonates and infants. The recurrent anomalies observed point to chromosomal regions that may harbor novel diagnostic/prognostic identifiers and genes relevant to the development of these neoplasms. © 2005 Wiley‐Liss, Inc.
Prevalence estimates of recurrent balanced cytogenetic aberrations and gene fusions in unselected patients with neoplastic disorders
Authors: Mitelman Felix , Mertens Fredrik , Johansson Bertil 
Published: May 2005

AbstractChromosome abnormalities have been reported in more than 46,000 benign and malignant neoplastic disorders, leading to the identification of numerous recurrent abnormalities. A substantial number of recurrent balanced aberrations (RBAs), in particular, reciprocal translocations, occur with remarkable specificity in association with clinical and tumor characteristics. This information has become increasingly important both in basic cancer research, as a means to identify pathogenetically important genes, and clinically, as a diagnostic and prognostic instrument. Knowledge of the frequencies of such aberrations thus is of theoretical as well as practical value. However, it is unknown to what extent the data available in the literature reflect reality. A large proportion of the published cases, at least 40%, are biased, in the sense that they were reported because of a specific or unusual karyotypic feature. We have systematically ascertained all RBAs and present data on the frequencies of these abnormalities and their molecular genetic consequences among unselected patients, that is, those studied as part of investigations of consecutive series of individuals with a particular neoplastic disorder. The salient features of the present study are: (1) published data clearly overestimate the prevalence of individual RBAs in most tumor types as well as the proportion of patients having such aberrations. In fact, several well‐known published RBAs are not recurrent or have not even been seen among unselected patients, and in no tumor entity, except for chronic myeloid leukemia, does the frequency of unselected cytogenetically abnormal neoplasms with RBAs exceed 35%; (2) the proportions of unselected cases characterized by RBAs among those tumor entities in which at least one RBA has been identified vary considerably both within and among hematologic malignancies, malignant lymphomas, and solid tumors; and (3) the molecular consequences of a substantial proportion, ranging from 19% in hematologic malignancies to 65% in epithelial tumors, of the most common RBAs in unselected patients remain to be clarified. © 2005 Wiley‐Liss, Inc.
New stool tests for colorectal cancer screening: A systematic review focusing on performance characteristics and practicalness
Authors: Haug Ulrike , Brenner Hermann 
Published: May 2005

AbstractNew stool tests may be promising tools for future colorectal cancer (CRC) screening. The aim of this review was to summarize current evidence of performance characteristics and practicalness in a population‐based screening setting of recently developed stool tests. The MEDLINE database was searched for relevant articles published until July 2004. Studies were included if they comprised more than 10 cases and more than 10 controls. Details on study population, performance characteristics and stool collection procedure were taken into account. Overall, 29 studies, mostly retrospective, were included, investigating 17 different stool markers or marker combinations. Underlying study populations were very heterogeneous and mostly very small. Half of the studies reported sensitivity for adenomas in addition to sensitivity for CRC, and fewer than half reported sensitivity by tumor stage or location. Performance characteristics of stool tests varied to a large extent. For most DNA‐based markers, specificity was about 95% or higher, but sensitivity was mostly low even for invasive CRC. More studies with larger sample sizes were done for protein‐based markers, which typically had lower specificity. In most studies, stool samples were frozen within a rather short time period after defecation. While promising performance characteristics have been reported for some tests, more pervasive evidence from larger, prospectively designed studies, which also consider aspects of practicalness, e.g., the possibility of mailing the samples, is needed. © 2005 Wiley‐Liss, Inc.
Thyroid cancer and multiple primary tumors in the SEER cancer registries1
Authors: Ronckers Cécile M. , McCarron Peter , Ron Elaine 
Published: May 2005

AbstractThyroid cancer incidence rates have increased steadily in the United States and elsewhere. Radiation exposure at a young age is a strong risk factor, but otherwise the etiology is unclear. To explore etiologic clues, we studied the risk of thyroid cancer after an earlier primary cancer, as well as the risk of developing multiple primaries after an earlier thyroid cancer in the U.S. Surveillance, Epidemiology and End‐Results (SEER) cancer registries program (1973–2000). In 2,036,597 patients diagnosed with any invasive cancer who survived for a minimum of 2 months, we observed a 42% increased risk compared to the general population for second thyroid cancer based on 1,366 cases (95% confidence interval (CI) = 35–50%; excess absolute risk (EAR) = 0.38/10,000 person‐years (PY)). Elevated risks were observed after most cancer sites studied. The most pronounced excess (observed/expected (O/E) = 2.86) was seen for second thyroid cancers detected in the year after diagnosis of the first cancer. Among 29,456 2‐month thyroid cancer survivors, 2,214 second cancers occurred (O/E = 1.11, 95% CI = 1.06–1.15; EAR = 7.64/10,000 PY). Again, the highest risk was seen in the first year (O/E = 1.26). Patients <40 years of age at diagnosis of thyroid cancer had a 39% increased risk of a second cancer, whereas for older patients the risk was elevated 6%. We observed consistently increased risks for cancers of the breast, prostate, and kidney, and a likely radiation treatment‐related excess of leukemia. Based on small numbers of cases, cancers of the salivary glands, trachea, scrotum, adrenal glands, and brain and central nervous system (CNS) also occurred in excess. A decreased risk was observed for smoking‐related malignancies. Thyroid cancer is associated with primary cancers of many different organs. Although enhanced medical surveillance likely plays a role, 2‐way, positive associations between thyroid cancer and cancers of the breast, prostate, kidney, salivary glands, brain and CNS, scrotum, and leukemia suggest etiologic similarities and possible treatment effects. © 2005 Wiley‐Liss, Inc.
Black tea induces tumor cell apoptosis by Bax translocation, loss in mitochondrial transmembrane potential, cytochrome c release and caspase activation
Authors: Bhattacharyya Arindam , Lahiry Lakshmishri , Mandal Debaprasad , Sa Gaurisankar , Das Tanya 
Published: May 2005

AbstractRecently the anti‐cancer role of black tea has gained immense importance. Nevertheless, the signaling pathways underlying black tea‐induced tumor cell death are still unknown. Previously we reported that black tea induces Ehrlich's ascites carcinoma (EAC) cell apoptosis by changing the balance between pro‐and anti‐apoptotic proteins. It is now well accepted that many cell death pathways converge at the mitochondria to decrease mitochondrial transmembrane potential (MTP) thereby releasing apoptogenic proteins and resulting in the activation of effecter caspases responsible for the biochemical and morphological alterations associated with apoptosis. The role of pro‐apoptotic protein, Bax, in initiating mitochondrial death cascade has also been established. Here we demonstrate that in culture black tea extract induces EAC apoptosis in a dose‐dependent manner – with IC50 at 100 μg/ml. At this dose, intracellular Bax level increases in EAC followed by its translocation from cytosol to mitochondria resulting in loss in MTP. A search for the downstream pathway further reveals that black tea induces mitochondrial cytochrome c release and activates caspases 9 and 3 by 2 pathways, a) independent of and b) dependent on MTP loss. Interestingly, Black tea‐induced death signal might probably be amplified through mitochondrial membrane depolarization via a feedback activation loop from caspase 3. All these findings indicate that black tea initiates mitochondrial death cascade in EAC cells and thereby results in EAC apoptosis. © 2005 Wiley‐Liss, Inc.
4‐Aminobiphenyl induces liver DNA adducts in both neonatal and adult mice but induces liver mutations only in neonatal mice
Authors: Chen Tao , Mittelstaedt Roberta A. , Beland Frederick A. , Heflich Robert H. , Moore Martha M. , Parsons Barbara L. 
Published: May 2005

AbstractThe mechanisms underlying the susceptibility of neonatal mice to genotoxic carcinogens were investigated by analyzing the DNA adducts and mutations induced in the livers of neonatal and adult Big Blue transgenic mice by 4‐aminobiphenyl (4‐ABP), a potent human and rodent carcinogen. Neonatal and adult mice were treated with a regimen of 4‐ABP known to induce tumors in neonatal mice. Animals were sacrificed 1 day after the last treatment for DNA adduct analysis and 8 weeks after the last treatment for analysis of lacI and cII mutant frequency (MF). N‐(Deoxyguanosin‐8‐yl)‐4‐ABP was the major DNA adduct identified in the livers of the 4‐ABP‐treated mice and levels of this adduct were significantly higher in treated animals than in the controls for both the neonates and adults. Adduct levels for adult females (44.0 ± 4.8 adducts/106 nucleotides) were higher than in neonatal females (25.9 ± 2.2 adducts/106 nucleotides), while adduct levels in adult males (13.5 ± 2.0 adducts/106 nucleotides) were lower than in neonatal males (33.8 ± 4.1 adducts/106 nucleotides). 4‐ABP treatment significantly increased the liver cII MFs in both sexes of neonatal mice but not in adult mice. Sequence analysis of cII mutant DNA revealed that 4‐ABP induced a unique spectrum of mutations in neonatal mice, characterized by a high frequency of G:C→T:A transversion, while the mutation spectrum in 4‐ABP‐treated adults was similar to that of control mice. Our results indicate that DNA adduct formation by 4‐ABP depends as much on sex as it does on age, whereas the conversion of DNA adducts into mutations differed with animal age. These observations suggest that neonates are more sensitive than adults to genotoxic carcinogens because the relatively high levels of cell division in the developing animal facilitate the conversion of DNA damage into mutation. Supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020‐7136/suppmat/index.html © 2005 Wiley‐Liss, Inc.