bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Emerging Role of the COP9 Signalosome in Cancer
Authors: Richardson Katharine S. , Zundel Wayne 
Published: December 2005

AbstractIn the last several years, multiple lines of evidence have suggested that the COP9 signalosome (CSN) plays a significant role in the regulation of multiple cancers and could be an attractive target for therapeutic intervention. First, the CSN plays a key role in the regulation of Cullin-containing ubiquitin E3 ligases that are central mediators of a variety of cellular functions essential during cancer progression. Second, several studies suggest that the individual subunits of the CSN, particularly CSN5, might regulate oncogenic and tumor suppressive functions independently of, or coordinately with, the CSN holocomplex. Thus, deregulation of CSN subunit function can have a dramatic effect on diverse cellular functions, including the maintenance of DNA fidelity, cell cycle control, DNA repair, angiogenesis, and microenvironmental homeostasis that are critical for tumor development. Additionally, clinical studies have suggested that the expression or localization of some CSN subunits correlate to disease progression or clinical outcome in a variety of tumor types. Although the study of CSN function in relation to tumor progression is in its infancy, this review will address current studies in relation to cancer initiation, progression, and potential for therapeutic intervention. (Mol Cancer Res 2005;3(12):645–53)
Mechanisms of Intraseasonal Amplification of the Cold Siberian High
Authors: Takaya Koutarou , Nakamura Hisashi 
Published: January 2006

Abstract
Mechanisms of intraseasonal amplification of the Siberian high are investigated on the basis of composite anomaly evolution for its strongest events at each of the grid points over Siberia. At each location, the amplification of the surface high is associated with formation of a blocking ridge in the upper troposphere. Over central and western Siberia, what may be called “wave-train (Atlantic-origin)” type is common, where a blocking ridge forms as a component of a quasi-stationary Rossby wave train propagating across the Eurasian continent. A cold air outbreak follows once anomalous surface cold air reaches the northeastern slope of the Tibetan Plateau.
It is found through the potential vorticity (PV) inversion technique that interaction between the upper-level stationary Rossby wave train and preexisting surface cold anomalies is essential for the strong amplification of the surface high. Upper-level PV anomalies associated with the wave train reinforce the cold anticyclonic anomalies at the surface by inducing anomalous cold advection that counteracts the tendency of the thermal anomalies themselves to migrate eastward as surface thermal Rossby waves. The surface cold anomalies thus intensified, in turn, act to induce anomalous vorticity advection aloft that reinforces the blocking ridge and cyclonic anomalies downstream of it that constitute the propagating wave train. The baroclinic development of the anomalies through this vertical coupling is manifested as a significant upward flux of wave activity emanating from the surface cold anomalies, which may be interpreted as dissipative destabilization of the incoming external Rossby waves.
AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1
Authors: Nishida Sumiyuki , Hosen Naoki , Shirakata Toshiaki , Kanato Keisuke , Yanagihara Masashi , Nakatsuka Shin-ichi , Hoshida Yoshihiko , Nakazawa Tsutomu , Harada Yukie , Tatsumi Naoya , Tsuboi Akihiro , Kawakami Manabu , Oka Yoshihiro , Oji Yusuke , Aozasa Katsuyuki , Kawase Ichiro , Sugiyama Haruo 
Published: December 2005

Abstract
AML1-ETO, a chimeric gene frequently detected in acute myelogenous leukemia (AML), inhibits the differentiation of myeloid progenitors by suppressing genes associated with myeloid differentiation and increases the replating ability of clonogenic myeloid progenitors. However, AML1-ETO alone cannot induce AML and thus additional genetic events are required for the onset of AML. The Wilms tumor gene (WT1), which has been identified as the gene responsible for Wilms tumor, is expressed at high levels in almost all human leukemias. In this study, we have generated transgenic mice (WT1-Tg) that overexpress WT1 in hematopoietic cells to investigate the effects of WT1 on AML1-ETO-associated leukemogenesis. AML1-ETO-transduced bone marrow (BM) cells from WT1-Tg mice exhibited inhibition of myeloid differentiation at more immature stages and higher in vitro colony-forming ability compared with AML1-ETO-transduced BM cells from wild-type mice. Most importantly, all of the mice that received a transplant of AML1-ETO-transduced BM cells from the WT1-Tg mice rapidly developed AML. These results demonstrate that AML1-ETO may exert its leukemogenic function in cooperation with the expression of WT1.
Epithelial-specific transcription factor ESE-3 is involved in the development of monocyte-derived DCs
Authors: Appel Silke , Bringmann Anita , Grünebach Frank , Weck Markus M. , Bauer Jürgen , Brossart Peter 
Published: December 2005

Abstract
Dendritic cells (DCs) are recognized as the most potent antigen-presenting cells of the immune system with the unique ability to initiate and maintain primary immune responses. In order to better characterize the functional and phenotypic features of DCs, a subtractive cDNA library to identify differentially expressed genes in monocyte-derived DCs (MDCs) was constructed. Using this approach, we found that the epithelial transcription factor ESE-3, which was previously shown to be exclusively expressed in cells of epithelial origin, is differentially expressed in MDCs. This was further confirmed by reverse transcriptase–polymerase chain reaction (RT-PCR) and Western blot analyses. The expression of ESE-3 is up-regulated upon maturation of MDCs and inhibited by treating the cells with IL-10 or IFN-γ. Knockdown experiments using siRNA suggest that ESE-3 plays an important role during MDC development. Our results might help to improve the phenotypic characterization of DCs and lead to a better understanding of the cellular mechanisms involved in antigen presentation and T-cell stimulation.
Polymorphisms in the IL10 but not in the IL1beta and IL4 genes are associated with inhibitor development in patients with hemophilia A
Authors: Astermark Jan , Oldenburg Johannes , Pavlova Anna , Berntorp Erik , Lefvert Ann-Kari ,   for the MIBS Study Group
Published: December 2005

Abstract
The aim of the Malmö International Brother Study (MIBS) is to evaluate host genetic factors associated with the development of inhibitory antibodies in patients with hemophilia. Factor VIII gene mutations and genetic polymorphisms of the IL1beta, IL4, and IL10 genes, known to influence antibody production in autoimmune diseases, were analyzed in 164 patients (124 with severe, 26 with moderate, and 14 with mild disease) in 78 unrelated families with hemophilia A. Seventy-seven (47%) patients in 54 families had a history of inhibitors (57 high responding, 20 low responding). Inversions were found in 36 families (75 patients). There was no association between the development of inhibitor and the IL1beta Taq I RFLP alleles in exon 5 or the –590 C/T single nucleotide polymorphism (SNP) in the promoter region of IL4. There was, however, a strong association between an allele with 134 bp in one of the CA repeat microsatellites, IL10G, located in the promoter region of the IL10 gene, and the development of inhibitor (odds ratio [OR], 4.4; 95% confidence interval [95% CI], 2.1-9.5; P < .001). The association was consistent in the subgroup of families with severe hemophilia and inversions. IL10 is the first gene located outside the causative factor VIII gene mutation to be associated with inhibitor development.
Parkin-deficient mice are not more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicity
Authors: Perez Francisco A , Curtis Wendy R , Palmiter Richard D 
Published: December 2005

AbstractBackgroundAutosomal recessive juvenile parkinsonism (AR-JP) is caused by mutations in theparkingene which encodes an E3 ubiquitin-protein ligase. Parkin is thought to be critical for protecting dopaminergic neurons from toxic insults by targeting misfolded or oxidatively damaged proteins for proteasomal degradation. Surprisingly, mice with targeted deletions ofparkindo not recapitulate robust behavioral or pathological signs of parkinsonism. Since Parkin is thought to protect against neurotoxic insults, we hypothesized that the reason Parkin-deficient mice do not develop parkinsonism is because they are not exposed to appropriate environmental triggers. To test this possibility, we challenged Parkin-deficient mice with neurotoxic regimens of either methamphetamine (METH) or 6-hydroxydopamine (6-OHDA). Because Parkin function has been linked to many of the pathways involved in METH and 6-OHDA toxicity, we predicted that Parkin-deficient mice would be more sensitive to the neurotoxic effects of these agents.ResultsWe found no signs consistent with oxidative stress, ubiquitin dysfunction, or degeneration of striatal dopamine neuron terminals in aged Parkin-deficient mice. Moreover, results from behavioral, neurochemical, and immunoblot analyses indicate that Parkin-deficient mice are not more sensitive to dopaminergic neurotoxicity following treatment with METH or 6-OHDA.ConclusionOur results suggest that the absence of a robust parkinsonian phenotype in Parkin-deficient mice is not due to the lack of exposure to environmental triggers with mechanisms of action similar to METH or 6-OHDA. Nevertheless, Parkin-deficient mice could be more sensitive to other neurotoxins, such as rotenone or MPTP, which have different mechanisms of action; therefore, identifying conditions that precipitate parkinsonism specifically in Parkin-deficient mice would increase the utility of this model and could provide insight into the mechanism of AR-JP. Alternatively, it remains possible that the absence of parkinsonism in Parkin-deficient mice could reflect fundamental differences between the function of human and mouse Parkin, or the existence of a redundant E3 ubiquitin-protein ligase in mouse that is not found in humans. Therefore, additional studies are necessary to understand why Parkin-deficient mice do not display robust signs of parkinsonism.
Work factors and smoking cessation in nurses' aides: a prospective cohort study
Authors: Eriksen Willy 
Published: December 2005

Abstract

Background
The prevalence of smoking in nursing personnel remains high. The aim of this study was to identify work factors that predict smoking cessation among nurses' aides.

Methods
Of 2720 randomly selected, Norwegian nurses' aides, who were smoking at least one cigarette per day when they completed a questionnaire in 1999, 2275 (83.6 %) completed a second questionnaire 15 months later. A wide spectrum of work factors were assessed at baseline. Respondents who reported smoking 0 cigarettes per day at follow-up were considered having stopped smoking. The odds ratios and 95 % confidence intervals of stopping smoking were derived from logistic regression models.

Results
Compared with working 1–9 hours per week, working 19–36 hours per week (odds ratio (OR) = 0.35; 95 % confidence interval (CI) = 0.13 – 0.91), and working more than 36 hours per week (i.e. more than full-time job) (OR = 0.27; CI = 0.09 – 0.78) were associated with reduced odds of smoking cessation, after adjustments for daily consumption of cigarettes at baseline, age, gender, marital status, and having preschool children. Adjusting also for chronic health problems gave similar results.

Conclusion
There seems to be a negative association between hours of work per week and the odds of smoking cessation in nurses' aides. It is important that health institutions offer workplace-based services with documented effects on nicotine dependence, such as smoking cessation courses, so that healthcare workers who want to stop smoking, especially those with long working hours, do not have to travel to the programme or to dedicate their leisure time to it.
Cystathionine β-synthase T833C/844INS68 polymorphism: a family-based study on mentally retarded children
Authors: Dutta Samikshan , Sinha Swagata , Chattopadhyay Anindita , Gangopadhyay Prasanta Kumar , Mukhopadhyay Jotideb , Singh Manoranjan , Mukhopadhyay Kanchan 
Published: December 2005

Abstract

Background
Cystathionine β-synthase (CBS) mediates conversion of homocysteine to cystathionine and deficiency in enzyme activity may lead to hyperhomocysteinemia/homocystinuria, which are often associated with mental retardation (MR). A large number of polymorphisms have been reported in the CBS gene, some of which impair its activity and among these, a T833C polymorphism in cis with a 68 bp insertion at 844 in the exon 8 is found to be associated with mild hyperhomocysteinemia in different ethnic groups.

Methods
The present study is aimed at investigating the association between T833C/844ins68 polymorphism and MR. One hundred and ninety MR cases were recruited after psychometric evaluation. Hundred and thirty-eight control subjects, two hundred and sixty-seven parents of MR probands and thirty cardiovascular disorder (CVD) patients were included for comparison. Peripheral blood was collected after obtaining informed written consent. The T833C/844ins68 polymorphism was investigated by PCR amplification of genomic DNA and restriction fragment length polymorphism analysis, followed by statistical analysis.

Results
The genotypic distribution of the polymorphism was within the Hardy-Weinberg equilibrium. A slightly increased genotypic frequency was observed in the Indian control population as compared to other Asian populations. Both haplotype-based haplotype relative risk analysis and transmission disequilibrium test reveled lack of association of the T833C/844ins68 polymorphism with MR; nevertheless, the relative risk calculated was higher (>1) and in a limited number of informative MR families, preferential transmission of the double mutant from heterozygous mothers to the MR probands was noticed (χ2 = 4.00, P < 0.05).

Conclusion
This is the first molecular genetic study of CBS gene dealing with T833C/844ins68 double mutation in MR subjects. Our preliminary data indicate lack of association between T833C/844ins68 polymorphism with MR. However, higher relative risk and biased transmission of the double mutation from heterozygous mothers to MR probands are indicative of a risk of association between this polymorphism with mental retardation.
Peroxisome proliferator-activated receptor γ contributes to T lymphocyte apoptosis during sepsis
Authors: Soller Mathias , Tautenhahn Anja , Brüne Bernhard , Zacharowski Kai , John Stefan , Link Hartmut , von Knethen Andreas 
Published: December 2005

Abstract
In the last two decades, extensive research failed to significantly improve the outcome of patients with sepsis. In part, this drawback is based on a gap in our knowledge about molecular mechanisms understanding the pathogenesis of sepsis. During sepsis, T cells are usually depleted. Recent studies in mice and human cells suggested a role of the peroxisome proliferator-activated receptor γ (PPARγ) in provoking apoptosis in activated T lymphocytes. Therefore, we studied whether expression/activation of PPARγ might contribute to T cell death during sepsis. We observed PPARγ up-regulation in T cells of septic patients. In contrast to controls, PPARγ expressing cells from septic patients responded with apoptosis when exposed to PPARγ agonists. Cell demise was attenuated by SR-202, a synthetic PPARγ antagonist, and specificity was further verified by excluding a proapoptotic response to a PPARα agonist. We propose that up-regulation of PPARγ sensitizes T cells of septic patients to undergo apoptosis. PPARγ activation in T cells requires an exogenous PPARγ agonist, which we identified in sera of septic patients. Septic sera were used to study reporter gene expression containing a PPAR-responsive element. We conclude that PPARγ plays a significant role in T cell apoptosis, contributing to lymphocyte loss in sepsis. Thus, inhibition of PPARγ may turn out to be beneficial for patients suffering from lymphopenia during sepsis.
A study of CD33 (SIGLEC-3) antigen expression and function on activated human T and NK cells: two isoforms of CD33 are generated by alternative splicing
Authors: Hernández-Caselles Trinidad , Martínez-Esparza María , Pérez-Oliva Ana B , Quintanilla-Cecconi Ana M , García-Alonso Ana , Alvarez-López D María Rocío , García-Peñarrubia Pilar 
Published: December 2005

Abstract
The expression of CD33, a restricted leukocyte antigen considered specific for myeloid lineage, has been studied extensively on lymphoid cells. We demonstrated that wide subsets of mitogen- or alloantigen-activated human T and natural killer (NK) cells express CD33 at protein and nucleic acid levels. CD33+ and CD33– T and NK cell populations showed identical surface expression of activation markers such as CD25, CD28, CD38, CD45RO, or CD95. Myeloid and lymphoid CD33 cDNA were identical. However, lymphoid CD33 protein had lower molecular weight, suggesting cell type-specific, post-translational modifications. Additionally, reverse transcriptase-polymerase chain reaction and Northern blot analysis showed an unknown CD33 isoform (CD33m) expressed on all CD33+ cell lines or T cell clones tested. CD33m was identical to CD33 (CD33M) in the signal peptide, the immunoglobulin (Ig) domain C2, the transmembrane, and the cytoplasmic regions but lacked the extracellular ligand-binding variable Ig-like domain encoded by the second exon. CD33m mRNA was mostly detected on NKL and myeloid cell lines but poorly expressed on B cell lines and T lymphocytes. The CD33m extracellular portion was successfully expressed as a soluble fusion protein on transfected human cells, suggesting a functional role on cell membranes. Cross-linking of CD33 diminished the cytotoxic activity of NKL cells against K562 and P815 target cells, working as an inhibitory receptor on NK cells. These data demonstrate that CD33 expression is not restricted to the myeloid lineage and could exist as two different splicing variants, which could play an important role in the regulation of human lymphoid and myeloid cells.
Heterolytic Dissociation of C–H Bond of Methane over Ag+-exchanged Zeolites and Conversion of Methane into Higher Hydrocarbons in the Presence of Ethene or Benzene
Authors: Baba Toshihide , Inazu Koji 
Published: December 2005

Abstract
The heterolytic dissociation of CH4 over silver cationic clusters (Agn+) in Ag+-exchanged zeolites leads to the formation of silver hydride (Agn–H) and methyl cations, which then reacts with C2H4 to form C3H6. This process provides methane conversion of 13.2% at 673 K to afford higher hydrocarbons, such as toluene. Under these reaction conditions, H–ZSM-5 only catalyzes ethene conversion to higher hydrocarbons, such as butenes, and no methane conversion occurs. The reaction of CH4 with benzene also proceeds to form toluene and xylenes over Ag–ZSM-5 at 673 K. Zeolites prepared by exchange with other metal cations, including In and Ga, also activate CH4 in the presence of C2H4. Using 13C-labeled methane (13CH4) as a tracer, propene is shown to be a primary product for the ethene reaction based on the observation of a significant proportion of singly 13C-labeled propene (13CC2H6). In–ZSM-5 catalyzes the formation of not only propene, but also benzene and toluene. 13C label atoms are not found in the benzene thus produced, indicating that benzene originates entirely from C2H4. However, the occurrence of singly 13C-labeled toluene (13CC6H8) implies that toluene is formed by the reaction of benzene with 13CH4. The alternative reaction path, involving 13CC6H8 formation by reaction of propene with n-butenes generated by ethene dimerization, can be refuted by confirmation of the toluene origin through direct reaction of 13CH4 with benzene.
Syntheses and Characterization of Palladium(II) Complexes with Tridentate N-Heterocyclic Carbene Ligands Containing Aryloxy Groups and Their Application to Heck Reaction
Authors: Yagyu Takeyoshi , Oya Shoko , Maeda Masunobu , Jitsukawa Koichiro 
Published: December 2005

Abstract
Two palladium(II) complexes with tridentate N-heterocyclic carbene ligands containing aryloxy groups were prepared and characterized by X-ray crystallographic method. They showed good performance for Heck reaction.
Anomalous 13C NMR Chemical Shifts of High-spin Saddle Shaped Manganese(III) Octaethyltetraphenylporphyrin Complexes
Authors: Ikezaki Akira , Nakamura Mikio , Cheng Ru-Jen 
Published: December 2005

Abstract
NMR spectra of highly saddled Mn(III) porphyrinates such as Mn(OETPP)(CD3OD)2+ have been measured. The extraordinarily upfield shifted meso-13C signals, which reach as much as −492 ppm at 298 K, are ascribed to the dx2−y2–a2u, dxy–a1u, and dπ–3eg interactions, the former two of which occur only when the porphyrin ring is saddled.
An Efficient Energy Transfer Found in Triphenylene/Hexaazatriphenylene System with Electronic Complimentarity and Structural Similarity
Authors: Ishi-i Tsutomu , Tashiro Hiroshi , Kuwahara Rempei , Mataka Shuntaro , Yoshihara Toshitada , Tobita Seiji 
Published: December 2005

Abstract
In a donor–acceptor system with structural similarity and electronic complimentarity, an efficient energy transfer was observed from energy-donor triphenylenes to energy-acceptor hexaazatriphenylenes in a film state.
Synthesis of Single-crystal BaMo2O7 Nanowire Bundles: A General, Low-temperature Hydrothermal Approach to 1D Molybdenum Oxide-based Nanostructures
Authors: Gao Peng , Xie Yi , Ye Lina , Chen Ying , Li Zhen 
Published: December 2005

Abstract
Multicomponent BaMo2O7 single-crystalline nanowire bundles were synthesized by a hydrothermal crystallization process under mild conditions using cheap and simple bulky oxide and fluoride as precursors. This new strategy has been extended to prepare other 1D molybdenum oxide-based nanomaterials including alkaline earth metal molybdate compounds (such as BaMo3O10), transition-metal molybdate compounds (e.g., CdMoO4, PbMoO4, Ag6Mo10O33, etc.) and metal molybdenum oxide fluoride compounds (e.g., Ba2MoO3F4). Our experiments have also proved that this facile hydrothermal route is a general method for the synthesis of various multicomponent nanomaterials (such as tungstate, chromate, phosphate compounds).
Repetitive Two-step Method for Oligoarene Synthesis through Rapid Cross-coupling of Hydroxyphenylboronic Acids and Anhydrides
Authors: Ishikawa Shunpei , Manabe Kei 
Published: December 2005

Abstract
A two-step Suzuki–Miyaura coupling–triflation procedure, which features the use of hydroxyphenylboronic acids or anhydrides in the palladium-catalyzed cross-coupling step, has been developed for the synthesis of oligoarenes.
Book Reviews
Authors: Lev Benjamin 
Published: December 2005

The range of books reviewed is wide, covering theory and applications in operations research, statistics, management science, econometrics, mathematics, computers, and information systems (no software is reviewed). In addition, we include books in other fields that emphasize technical applications. Publishers who wish to have their books reviewed should send them to Professor Benjamin Lev. We list the books received; not all books received can be reviewed because space is limited. Those who would like to review books are urged to send me their names, addresses, and specific areas of expertise. We commission all reviews and do not accept unsolicited book reviews. Readers are encouraged to suggest books that might be reviewed or to ask publishers to send me copies of such books. The authors or editors of the books reviewed in this issue are H. Thomas Bank, Carlos Castillo-Chavez, Wade D. Cook, Joe Zhu, Jaime Gil-Aluja, Abhijit Gosavi, Marc J. Schniederjans, Jamie L. Hamaker, and Ashlyn M. Schniederjans.