bluuebunny/crossref_metadata_2025_split huggingface dataset:
Three Novel Functional CdII Dicarboxylates with Nanometer Channels: Hydrothermal Synthesis, Crystal Structures, and Luminescence Properties
Authors: Tian Yu‐Peng , Zhu Yong‐Min , Zhou Hong‐Ping , Wang Peng , Wu Jie‐Ying , Tao Xu‐Tang , Jiang Min‐Hua 
Published: November 2006

AbstractThree novel functional transition‐metal complexes with H2A (H2A = 9‐ethylcarbazole‐3,6‐dicarboxylic acid), Cd(HA)2(H2O)2 (1), [Cd(A)(phen)]·1.5H2O (2) (phen = 1,10‐phenanthroline), and Cd(HA)2(bipy) (3) (bipy = 4,4′‐bipyridine), have been successfully synthesized by a hydrothermal synthetic method and characterized by single‐crystal X‐ray diffraction, infrared spectroscopy, elemental analysis, thermogravimetric analysis, and photoluminescence. The results show that all of the complexes contain nanometer channels, while the coordination modes were changed by the addition of the mixed ligands. The 2D supramolecular open‐framework 1 is constructed through hydrogen‐bond and aromatic π–π interactions. 2D coordination polymer 2 is constructed by π–π interactions between adjacent metal‐organic polymeric coordination chains. Interestingly, the 3D supramolecular architecture of 3 first formed 2D grid layers from 1D chains by intermolecular hydrogen bonds and then extended into a 3D structure through aromatic π–π interactions. Furthermore, strong emissions from these complexes were also changed by the coordination modes in the solid state. However, complexes 1–3 show high thermal stability.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Stereochemical Control of Chirally Flexible Phosphepines
Authors: Zalubovskis Raivis , Fjellander Ester , Szabó Zoltán , Moberg Christina 
Published: November 2006

AbstractThe barriers to interconversion of the two enantiomeric atropisomers of 6‐methoxy‐6,7‐dihydro‐5H‐dibenzo[c,e]phosphepine and that of the diastereomeric forms of 6‐(–)‐menthoxy‐6,7‐dihydro‐3H‐dibenzo[c,e]phosphepine were determined by NMR spectroscopical methods to be 19.3 and 18.5 kcal mol–1, respectively, at 298 K. The ratio of the atropisomers was shown to depend on the group bound to phosphorus. Only complexes with two homochiral ligands bound to the each metal center were obtained upon reaction with [Rh(COD)2]+ BF4–. The Rh complexes catalyzed the hydrogenation of α‐acetamidocinnamate. The major isomer of6‐(–)‐menthoxy‐6,7‐dihydro‐5H‐dibenzo[c,e]phosphepinewas found to exhibit higher activity but to afford a product with lower ee than its diastereomer. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Use of micromolded carbon dual electrodes with a palladium decoupler for amperometric detection in microchip electrophoresis
Authors: Mecker Laura C. , Martin R. Scott 
Published: November 2006

AbstractThe fabrication and evaluation of micromolded dual carbon ink electrodes and their integration with a fabricated palladium decoupler for use in microchip electrophoresis is described. As opposed to previous work involving carbon‐based dual electrodes with microchip electrophoresis, this approach results in electrodes that are amenable to mass production in a manner where the decoupler/electrode alignment is fixed and reproducible. In this work, electrode sizes and spacings were optimized to result in dual carbon electrodes that are 1 µm in height and separated by 100 µm. Fluorescence microscopy was used to investigate leakage around the electrode/channel interface as well as to investigate what effect the dual electrodes have on band broadening phenomena. The performance of the microelectrodes was demonstrated by the separation and selective dual electrode detection of neurotransmitters in the presence of ascorbic acid. It was also found that addition of SDS to the buffer system improved both the LODs and collection efficiencies. This approach, which is the first involving carbon‐based dual electrodes with an on‐chip palladium decoupler, will be useful for separating and detecting neurotransmitters that are either collected by in vivo sampling or released from cells on‐chip.
Kommunikation im Netz der Information
Authors: Hesse Friedrich W. , Buder Jürgen , Bauer Korinna 
Published: November 2006

AbstractWie kann der Wissensaustausch in Computernetzen sinnvoll unterstützt werden? Neue Studien geben Einblick in die Chancen und Risiken netzbasierter Kommunikation in Gruppen, deren Gelingen nicht nur vom Medium abhängt
Unique regulation of long term potentiation in the rat ventral hippocampus
Authors: Maggio Nicola , Segal Menahem 
Published: November 2006

AbstractMorphological and electrophysiological evidence has been accumulated in recent years to indicate that a functional gradient exists along the septo‐temporal axis of the hippocampus such that spatial memory is associated primarily with the dorsal (septal) sector while the functions of the ventral sector are not yet clearly defined. Also, the ventral hippocampus (VH) is reported to express a much smaller long term potentiation of responses to afferent stimulation than the dorsal sector. In the present study, we first confirmed that CA1 region of VH slices expresses significantly smaller LTP than the dorsal hippocampus. Strikingly, much larger LTP was obtained in VH slices following low frequency priming stimulation applied prior to the tetanic stimulation. DHPG ((S)‐3,5‐Dihydroxyphenylglycine hydrate) a metabotropic glutamate receptor agonist, produced a similar potentiating effect on LTP as that produced by the priming stimulation. In both cases, the spectral analysis of spontaneous electrical activity recorded from the same location in the slice revealed an increase in peak amplitude around 30 Hz. MCPG, a metabotropic glutamate receptor antagonist, and both thapsigargin and cyclopiazonic acid, inhibitors of Ca2+ release from stores, blocked the potentiating action of both DHPG and the priming stimulation. These results indicate that the ventral hippocampus possesses different network properties compared to the dorsal hippocampus and that its ability to undergo plastic changes is controlled by a metabotropic glutamate receptor. © 2006 Wiley‐Liss, Inc.
Occupational exposure to organochlorine insecticides and cancer incidence in the Agricultural Health Study
Authors: Purdue Mark P. , Hoppin Jane A. , Blair Aaron , Dosemeci Mustafa , Alavanja Michael C.R. 
Published: November 2006

AbstractOrganochlorine (OC) insecticides have been regulated as possible human carcinogens primarily on the basis of animal studies. However, the epidemiologic evidence is inconsistent. We investigated the relationship between cancer incidence and OC insecticide use among pesticide applicators enrolled in the Agricultural Health Study, a prospective cohort study of 57,311 licensed applicators in Iowa and North Carolina enrolled between 1993 and 1997. Information on ever use of 7 OC insecticides (aldrin, chlordane, DDT, dieldrin, heptachlor, lindane, toxaphene) was collected from a self‐administered questionnaire at enrollment. Lifetime exposure‐days to OC insecticides were calculated using additional data from a take‐home questionnaire completed by 25,291 participants (44% of total). We found no clear evidence of an association between use of OC insecticides and incident cancers (N = 1,150) ascertained through December, 2002. When we focused on individual insecticides and structurally similar groups (aldrin and dieldrin; chlordane and heptachlor), significantly increased relative risks of some cancers were observed for use of some chemicals (rectal cancer and chlordane, lung cancer and dieldrin, non‐Hodgkin lymphoma (NHL) and lindane, melanoma and toxaphene, leukemia and chlordane/heptachlor). Some significant decreased relative risks were also observed (colon cancer and aldrin; overall cancer and heptachlor). In conclusion, we did not observe any clear relationship between cancer risk and the use of OC insecticides. Our chemical‐specific findings are based on small numbers and multiple comparisons, and should be interpreted with caution; however, some observed associations (lindane and NHL, chlordane/heptachlor and leukemia) are supported by previous evidence. © 2006 Wiley‐Liss, Inc.
Identification of an HLA‐A24‐restricted cytotoxic T lymphocyte epitope from human papillomavirus type‐16 E6: The combined effects of bortezomib and interferon‐γ on the presentation of a cryptic epitope
Authors: Morishima Satoko , Akatsuka Yoshiki , Nawa Akihiro , Kondo Eisei , Kiyono Tohru , Torikai Hiroki , Nakanishi Toru , Ito Yoshinori , Tsujimura Kunio , Iwata Kosuke , Ito Koji , Kodera Yoshihisa , Morishima Yasuo , Kuzushima Kiyotaka , Takahashi Toshitada 
Published: November 2006

AbstractAbout 50% of cervical cancers are associated with human papillomavirus type 16 (HPV‐16), and since the HPV‐16 E6 and E7 oncoproteins are constitutively expressed in the tumor cells, they are attractive targets for cytotoxic T lymphocyte (CTL)‐mediated immunotherapy. Nevertheless, only a limited number of HPV‐16 E6 epitopes have been identified to date. Using reverse immunological methods, we have generated a CTL clone against the HPV‐16 E649–57 epitope restricted by HLA‐A*2402, which is the most common allele in Japan and relatively frequent worldwide, capable of lysing 293T cells transduced with HLA‐A*2402 and HPV‐16 E6. Although it was unable to recognize the SiHa cervical cancer cell line positive for HPV‐16 and HLA‐A*2402, the cells became susceptible to lysis when transduced with E6‐E7 genes, which was unexpectedly offset by pretreatment with interferon (IFN)‐γ alone. Interestingly, however, combined pretreatment with a proteasome inhibitor, bortezomib and IFN‐γ fully restored CTL‐mediated lysis of the original SiHa cells. Furthermore, such intervention of 2 of 4 other cervical cancer cell lines expressing HPV‐16 E6 and HLA‐A*2402 was found to induce IFN‐γ production by specific CTLs. Tetramer analysis further revealed that induction of E649–57‐specific T cells was possible in 5 of 7 patients with HPV‐16‐positive high grade cervical intraepithelial neoplasia or cervical cancer by in vitro stimulation with E649–57 peptide. Thus, these findings together indicate that E649–57 is a candidate epitope for immunotherapy and immunological monitoring of such patients. © 2006 Wiley‐Liss, Inc.
Risk of cervical cancer associated with Chlamydia trachomatis antibodies by histology, HPV type and HPV cofactors
Authors: Madeleine Margaret M. , Anttila Tarja , Schwartz Stephen M. , Saikku Pekka , Leinonen Maija , Carter Joseph J. , Wurscher Michelle , Johnson Lisa G. , Galloway Denise A. , Daling Janet R. 
Published: November 2006

AbstractHuman papillomavirus (HPV) is the central etiologic factor for cervical cancer, and prior studies suggested C. trachomatis may act as an HPV cofactor. We examined the C. trachomatis‐cervical cancer association by serotype, histology, HPV type in the tumor, and other HPV cofactors. We conducted a population‐based study in the Seattle‐Puget Sound area of 302 women with invasive squamous cell carcinomas (SCC), 185 women with adenocarcinomas of the cervix (AC), and 318 HPV seropositive control women. The risk of SCC associated with antibodies to C. trachomatis was increased (OR 1.6, 95% CI 1.1–2.2) but not for AC (OR 1.0, 95% CI 0.6–1.5). This association was independent of HPV type in the SCC tumor tissue. There was an association between specific serotypes of C. trachomatis and SCC for 6 of the 10 serotypes: B (OR 3.6, 95% CI 1.5–8.4), D (OR 2.1, 95% CI, 1.2–3.5), E (OR 2.4, 95% CI, 1.4–3.9), G (OR 3.0, 95% CI, 1.1–7.9), I (OR 4.2, 95% CI, 1.5–11.7), and J (OR 2.3, 95% CI, 1.0–5.1), but not for the 4 types (C, F, H, and K) that were present at very low prevalence in this population. There was an increased risk of SCC, but not AC, associated with antibodies to C. trachomatis that was not serotype specific. © 2006 Wiley‐Liss, Inc.
Inflammation and IGF‐I activate the Akt pathway in breast cancer
Authors: Prueitt Robyn L. , Boersma Brenda J. , Howe Tiffany M. , Goodman Julie E. , Thomas Douglas D. , Ying Lei , Pfiester Candice M. , Yfantis Harris G. , Cottrell John R. , Lee Dong H. , Remaley Alan T. , Hofseth Lorne J. , Wink David A. , Ambs Stefan 
Published: November 2006

AbstractAkt signaling may promote breast cancer progression and poor disease outcome. We hypothesized that serum insulin‐like growth factor I (IGF‐I) and a proinflammatory tumor environment induce phosphorylation of Akt and downstream targets of Akt in breast cancer. We studied the relationship between Akt pathway activation, IGF‐I and markers of inflammation, e.g., nitric oxide synthase‐2 (NOS2), cyclooxygenase‐2 (COX2) and tumor phagocyte density, in 248 breast tumors. We also examined the association of Akt phosphorylation with breast cancer survival. We observed that phosphorylation of Akt, BAD and caspase‐9 correlated strongly with the expression of the 2 proinflammatory enzymes, NOS2 and COX2, in breast tumors (p < 0.001; Spearman rank correlation). Both NOS2 and COX2 expression were independently associated with Akt phosphorylation in the multivariate analysis. Serum IGF‐I concentrations and the IGF‐I/IGFBP3 ratio correlated with Akt phosphorylation at Thr308 and Ser473 in breast tumors (p ≤ 0.05; Spearman rank correlation). The association with Akt phosphorylation at Thr308 remained statistically significant in the multivariate analysis. Akt pathway activation was not associated with overall survival in the unstratified analysis, but we observed a statistical interaction between Akt phosphorylation and tumor phagocyte density on breast cancer survival (pinteraction < 0.05). We further corroborated our findings in cell culture models by demonstrating that ANA‐1 macrophages, nitric oxide and prostaglandin E2 induce Akt phosphorylation in human breast cancer cells. In summary, a proinflammatory environment was found to activate the Akt pathway in breast cancer, and may modify the association between the Akt phosphorylation status and breast cancer survival. © 2006 Wiley‐Liss, Inc.
Aberrant promoter methylation of insulin‐like growth factor binding protein‐3 gene in human cancers
Authors: Tomii Kunitoshi , Tsukuda Kazunori , Toyooka Shinichi , Dote Hideaki , Hanafusa Tadashi , Asano Hiroaki , Naitou Minoru , Doihara Hiroyoshi , Kisimoto Takumi , Katayama Hideki , Pass Harvery I. , Date Hiroshi , Shimizu Nobuyoshi 
Published: November 2006

AbstractInsulin‐like growth factor binding protein‐3 (IGFBP‐3) is postulated to be a mediator of growth suppression signals. Here, we examined the methylation status of IGFBP‐3 to correlate to clinicopathological factors in human cancers. The methylation status of IGFBP‐3 was determined by bisulfite DNA sequencing and was correlated with expression semi‐quantified by real‐time RT‐PCR to develop a methylation‐specific PCR (MSP) assay for IGFBP‐3. Using the MSP assay, we examined the methylation status of IGFBP‐3 in gastric cancer (GC), colorectal cancer (CRC), breast cancer (BC) and malignant mesothelioma (MM). IGFBP‐3 methylation was detected in 6 of 13 (46%) and 16 of 24 (67%) GC cell lines and tumors, respectively; 4 of 8 (50%) and 15 of 26 (58%) CRC cell lines and tumors, respectively; 3 of 11 (27%) and 7 of 39 (18%) BC cell lines and tumors, respectively and 1 of 5 (20%) and 18 of 56 (32%) MM cell lines and tumors, respectively. Interestingly, the methylation status of MM specimens from Japanese patients (75%, 12 out of 16 patients) was significantly higher than those from the USA (15%, 6 out of 40 patients) (p < 0.0001), suggesting the presence of ethnic differences in the IGFBP‐3 methylation status. We also found that IGFBP‐3 methylation was preferentially present in GCs arising in the lower‐third of the stomach (p = 0.079). In summary, our results showed that IGFBP‐3 methylation played an important role in the silencing of its expression, suggesting that IGFBP‐3 may act as a tumor suppressor gene in several human cancers examined. © 2006 Wiley‐Liss, Inc.
Allelotyping analyses of synchronous primary and metastasis CIN colon cancers identified different subtypes
Authors: Weber Jean‐Christophe , Meyer Nicolas , Pencreach Erwan , Schneider Anne , Guérin Eric , Neuville Agnès , Stemmer Christine , Brigand Cécile , Bachellier Philippe , Rohr Serge , Kedinger Michèle , Meyer Christian , Guenot Dominique , Oudet Pierre , Jaeck Daniel , Gaub Marie‐Pierre 
Published: November 2006

AbstractIn colorectal cancer, the molecular alterations that lead to metastasis are not clearly established, probably because of their high genetic complexity. To identify combinations of genetic changes involved in tumor progression and metastasis, we focused on chromosome instable (CIN) colon cancers. We compared by allelotyping of 33 microsatellites, the genomic alterations of 38 primary colon tumors with the synchronously resected matched liver metastases (CLM). We observed that (i) the number of patients with alterations at certain loci did not differ significantly between the whole primary tumor and the paired CLM, (ii) a group of patients had fewer alterations in the metastasis when compared with the matched primary tumor. A 2‐way hierarchical unsupervised clustering of the allelotyping data revealed 2 tumor subtypes that have different levels of CIN (CIN‐High, CIN‐Low). Both subtypes have a minimal common set of alterations at chromosomes 8p, 17p and 18q, but does not include alteration at 5q or mutation at K‐Ras. These 2 subtypes were also observed using a collection of 104 independent primary CIN colon tumors. In addition, we found a third subtype, consisting of tumors with a very low number of alterations not associated with specific loci (CIN‐Very Low). We found that colon carcinogenesis may require a minimal set of alterations and that, in contrast to the current hypothesis, the level of CIN does not correlate with tumor progression. Therefore, our results suggest that metastasis potential could be present at very early stages of tumor development. © 2006 Wiley‐Liss, Inc.
Expression and differential signaling of heregulins in pancreatic cancer cells
Authors: Kolb Armin , Kleeff Jörg , Arnold Nichole , Giese Nathalia A. , Giese Thomas , Korc Murray , Friess Helmut 
Published: November 2006

AbstractThe EGF family of ligands and receptors plays an important role in the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) and contributes to its aggressiveness. A number of molecular approaches have been developed to block these pathways, and studies have already proven the clinical benefit of this concept in PDAC. In the present study, we sought to determine the potential role of heregulins (HRGs), a family of EGF‐like growth factors, in PDAC. Quantitative RT‐PCR analysis revealed that HRGs as well as its signaling ErbB receptors were present in 4 of 4 human pancreatic cancer cell lines (PCCL). HRG‐β1 stimulated the growth of 3 of 4 PCCL, whereas HRG‐α1 inhibited cell growth in 3 of 4 cell lines. Responses towards HRGs could in part be predicted by ErbB2 and ErbB3 expression levels. HRGs induced phosphorylation of different ErbB receptors as well as activation of MAPK, p38MAPK, JNK and PI3K in a cell‐ and ligand‐specific manner. In vivo, HRG was upregulated in pancreatic cancer tissues and localized predominantly in the cancer cells. High HRG‐β levels but not HRG‐α levels were associated with decreased patient survival. In conclusion, HRG is expressed by pancreatic cancer cells and influences pancreatic cancer cell growth and patient survival. © 2006 Wiley‐Liss, Inc.
In between worlds: G.N. Lewis, the shared pair bond and its multifarious contexts
Authors: Simões Ana 
Published: November 2006

AbstractIn this paper, I will look at the rather convoluted discovery process which gave birth to the concept of the shared electron pair bond as developed by G.N. Lewis, to be subsequently appropriated by the American founders of quantum chemistry, and highlight the complex relations between conceptual development and the different contexts in which ideas are created and presented. I will show how the successive installments of Lewis's model of the chemical bond were supported by and gained credence from an epistemological background in which Lewis explored the relations of chemistry to physics. Furthermore, they were shaped by the changing public contexts in which the successive metamorphoses of the ideas took place and their epistemological background was outlined and explored. The complexities which are always associated with a discovery process can therefore be illuminated if one pays attention to different interactive realms—the conceptual, epistemological, and the presentational one. © 2006 Wiley Periodicals, Inc. J Comput Chem, 2007
Lipid‐protein cargo transfer: A mode of direct cell‐to‐cell communication for lipids and their associated proteins
Authors: Laffafian Iraj , Hallett Maurice B. 
Published: November 2006

AbstractCells in tissues or in experimental cell colonies respond to stimuli in a co‐ordinated manner when they are electrically and chemically coupled by gap junctions. These junctions permit the cell‐to‐cell passage of small molecules, such as inositol tris phosphate (IP3) within the colony and are important in co‐ordinating tissue activity. This is the only recognised mechanism of direct chemical signalling that does not involve the release of an extracellular messenger between cells. However, the data in this article demonstrates a new mode of intercellular communication. Two potentially important signalling lipids, PIP2 and ganglioside G‐M1 were shown to move between cells in colonies by tracking (i) fluorescent lipids loaded into the plasma membranes of individual cells in a cell colony using a novel micropipette technique and (ii) movement of fluorescent lipids after localised photobleaching. Furthermore, a large protein molecule, cholera toxin B subunit bound to extracellularly facing ganglioside G‐M1 was also shown to transfer between cells. The transfer was inhibited by pre‐treatment with poly‐L‐lysine and polyethylenimine, suggesting a role for tight junctions, perhaps by permitting diffusion of lipids and their protein “cargo” across these cell‐to‐cell contact points. This is a hitherto unsuspected form of molecular signalling within cell colonies and tissues which may have implications for understanding co‐ordinated cell colony behaviour. J. Cell. Physiol. 210: 336–342, 2007. © 2006 Wiley‐Liss, Inc.