bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased antigen presenting cell‐mediated T cell activation in mice and patients without the autoimmune regulator
Authors: Ramsey Chris , Hässler Signe , Marits Per , Kämpe Olle , Surh Charles D. , Peltonen Leena , Winqvist Ola 
Published: January 2006

AbstractPatients with autoimmune polyendocrine syndrome type I (APS I)suffer from endocrine and non‐endocrine disorders due to mutations in the autoimmune regulator gene (AIRE). Mouse Aire is expressed both in thymic medullary epithelial cells and in peripheral antigen‐presenting cells, suggesting a role in both central and peripheral tolerance. We here report that Aire–/– dendritic cells (DC) activate naive T cells more efficiently than do Aire+/+ DC. Expression array analyses of Aire–/– DC revealed differential regulation of 68 transcripts, among which, the vascular cell adhesion molecule‐1 (VCAM‐1) transcript was up‐regulated in Aire–/– DC. Concurrently, the expression of the VCAM‐1 protein was up‐regulated on both Aire–/– DC and monocytes from APS I patients. Blocking the interaction of VCAM‐1 prevented enhanced Aire–/– DC stimulation of T cell hybridomas. We determined an increased number of DC in spleen and lymph nodes and of monocytes in the blood from Aire–/– mice, and an increased number of blood monocytes in APS I patients. Our findings imply a role for Aire in peripheral DC regulation of T cell activation, and suggest that Aire participates in peripheral tolerance.
Palladium(II) Compounds with Fluorinated Pincer‐Type (SCS) Ligands: X‐ray Structures of C6H4‐1,3‐(CH2SC6H4F‐4)2 and [PdCl(SCS–Rf)] [Rf = C6H4F‐2, C6H4F‐3, C6H4F‐4, C6H4(CF3)‐2, and C6H4(CF3)‐4]
Authors: Cervantes Ruy , Castillejos Sandra , Loeb Stephen J. , Ortiz‐Frade Luis , Tiburcio Jorge , Torrens Hugo 
Published: January 2006

AbstractMetathesis reactions employing lead fluorothiolates and C6H4‐1,3‐(CH2Br)2 afford the corresponding pincer‐type dithioether ligands C6H4‐1,3‐(CH2SRf)2 [Rf = C6H4F‐2 (L1), C6H4F‐3 (L2), C6H4F‐4 (L3), C6H4CF3‐2 (L4), C6H4CF3‐3 (L5), and C6H4CF3‐4 (L6)]. A series of PdII pincer‐type complexes [PdCl(κ3‐Ln)], 1 to 6, were prepared and fully characterized. The X‐ray diffraction molecular structures of C6H4‐1,3‐[CH2S(C6H4F‐4)]2 (L3), [PdCl(SCS–C6H4F‐2)] (1), [PdCl(SCS–C6H4F‐3)] (2), [PdCl(SCS–C6H4F‐4)] (3), [PdCl{SCS–C6H4(CF3)‐2}] (4), and [PdCl{SCS–C6H4(CF3)‐4}] (6) are also reported. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Synthesis, Characterization, and Catalytic Properties of ansa‐Zirconocenes [Zr{1‐Me2Si(3‐η5‐C9H5R)2}Cl2] (R = Me, nPr, nBu, and Bz)
Authors: Alonso‐Moreno Carlos , Antiñolo Antonio , Carrillo‐Hermosilla Fernando , Otero Antonio , Rodríguez Ana M. , Sancho José , Volkis Victoria , Eisen Moris 
Published: January 2006

AbstractThe ansa‐indene ligands {1‐Me2Si(3‐C9H6R)2} [R = Me (1), nPr (2), nBu (3), and Bz (4)] were prepared by alkylation of the unsubstituted ansa‐indene. These ligands were converted, by reaction with nBuLi, to the di‐lithium compounds [Li2{1‐Me2Si(3‐C9H5R)2}] [R = Me (5), nPr (6), nBu (7), and Bz (8)]. ansa‐Zirconocenes, [Zr{1‐Me2Si(3‐η5‐C9H5R)2}Cl2] [R = Me (9), nPr (10), nBu (11), and Bz (12)], have been prepared by the reaction of ZrCl4 with 5–8 in diethyl ether/toluene at–78 °C. The molecular structure of meso‐[Zr{1‐Me2Si[3‐η5‐C9H5(CH3)]2}Cl2] (9) and rac‐[Zr{1‐Me2Si[3‐η5‐C9H5(CH2CH2CH3)]2}Cl2] (10) have been determined by single‐crystal X‐ray diffraction studies. Ethylene polymerization catalysis has been studied for complexes 9–12 as a mixture of meso and rac isomers in the presence of methylaluminoxane (MAO) as cocatalyst. Complexes 9–12 exhibit high activities and give rise to polyethylene with low molecular weights without the introduction of molecular hydrogen. In addition, active species from these complexes were found to be very stable in comparison with unsubstituted analogues.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Reassignment, Isolation, Spectral and X‐ray Characterization of Diastereoisomers of the Macrocyclic Ligand 3,10‐meso‐3,5,7,7,10,12,14,14‐Octamethyl‐1,4,8,11‐tetraazacyclotetradecane and their NiII and CuII Complexes
Authors: Lin Yung‐Chan , Misra Tarun Kumar , Lu Tian‐Huey , Joseph Maddirala Shambabu , Chung Chung‐Sun 
Published: January 2006

AbstractReduction of the macrocyclic ligand, 3,10‐meso‐3,5,7,7,10,12,14,14‐octamethyl‐1,4,8,11‐tetraazacyclotetradecane‐4,11‐diene dihydroperchlorate (L), with sodium borohydride yielded three [Lb (1), Lc (2), and Ld (3)] of four possible diastereoisomers. The diastereoisomeric macrocycles and their NiII and CuII complexes have been characterized and confirmed by IR, UV/Vis, and NMR spectroscopy as well as X‐ray crystallography. The chiral carbon centers and methyl groups at the 5 and 12 positions of 1, 2 and 3 have the 5S,12R‐C‐meso, 5S,12S‐C‐racemic, and 5R,12R‐C‐racemic configurations, respectively. In accordance with the X‐ray structure determination, the geometry around the NiII ion in the complexes is approximately square‐planar and the CuII ion has an octahedral geometry. The N–H configuration of [NiLc](ClO4)2(H2O)0.5 (5) is trans‐II, different from the most thermodynamically stable trans‐III configuration that is found in [NiLb](ClO4)2 (4), [CuLb(H2O)2](ClO4)2 (7), and [CuLd(ClO4)2] (8). UV/Vis spectra reveal that NiII complexes exhibit almost 100 % planar species in aqueous solution resulting from steric effects produced by numerous methyl groups, especially axial orientations and distorted structures. In six coordinate CuII complexes, acetonitrile acts as a better axial donor than the water molecule; the weaker axial bonding is a result of steric interactions that lead to stronger in‐plane coordinations. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
A Simple and Efficient Synthetic Route to Enantiopure Scorpionate Ligands
Authors: Otero Antonio , Fernández‐Baeza Juan , Antiñolo Antonio , Tejeda Juan , Lara‐Sánchez Agustín , Sánchez‐Barba Luis , Sánchez‐Molina Margarita , Franco Sonia , López‐Solera Isabel , Rodríguez Ana M. 
Published: January 2006

AbstractA simple and efficient synthetic route for the preparation of enantiopure scorpionate ligands is described that allows the optimization and rapid access to ligands with diverse chiral environments. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Advances in the enantioseparation of second‐generation antidepressant drugs by electrodriven methods
Authors: Mandrioli Roberto , Raggi Maria A. 
Published: January 2006

AbstractStereochemistry is steadily increasing in importance in the development of new drugs, and the availability of pure enantiomer drugs can make therapy safer and more efficacious. In particular, almost all second‐generation antidepressant drugs possess one or more chiral centres; however, only some of them are administered as single enantiomers. A fundamental part of the quality control of pharmaceutical formulations is the determination of enantiomeric excess and enantiomeric purity; this is also important for the therapeutic drug monitoring of depressed patients. For this purpose, efficient and reliable analytical methods are needed and electrodriven techniques (most of all CE, CEC and MEKC) are very efficient and inexpensive candidates for the role. In this review, the enantioselective electrodriven methods available for the analysis of second‐generation antidepressant are presented and discussed. In particular, the following pharmacological classes of antidepressants will be considered: selective serotonin reuptake inhibitors (fluoxetine, citalopram, paroxetine, sertraline); norepinephrine reuptake inhibitors (reboxetine); serotonin and norepinephrine reuptake inhibitors (venlafaxine, milnacipran, duloxetine); and noradrenergic and specific serotonergic antidepressants (mirtazapine).
Sensitive chiral analysis by capillary electrophoresis
Authors: García‐Ruiz Carmen , Marina María Luisa 
Published: January 2006

AbstractIn this review, an updated view of the different strategies used up to now to enhance the sensitivity of detection in chiral analysis by CE will be provided to the readers. With this aim, it will include a brief description of the fundamentals and most of the recent applications performed in sensitive chiral analysis by CE using offline and online sample treatment techniques (SPE, liquid–liquid extraction, microdialysis, etc.), on‐column preconcentration techniques based on electrophoretic principles (ITP, stacking, and sweeping), and alternative detection systems (spectroscopic, spectrometric, and electrochemical) to the widely used UV‐Vis absorption detection.
Capillary electrophoresis at the omics level: Towards systems biology
Authors: Babu C. V. Suresh , Song Eun Joo , Babar Sheikh Md. Enayetul , Wi Mun Hyung , Yoo Young Sook 
Published: January 2006

AbstractEmerging systems biology aims at integrating the enormous amount of existing omics data in order to better understand their functional relationships at a whole systems level. These huge datasets can be obtained through advances in high‐throughput, sensitive, precise, and accurate analytical instrumentation and technological innovation. Separation sciences play an important role in revealing biological processes at various omic levels. From the perspective of systems biology, CE is a strong candidate for high‐throughput, sensitive data generation which is capable of tackling the challenges in acquiring qualitative and quantitative knowledge through a system‐level study. This review focuses on the applicability of CE to systems‐based analytical data at the genomic, transcriptomic, proteomic, and metabolomic levels.
Polymorphic amino acids at codons 9 and 37 of HLA‐DQB1 alleles may confer susceptibility to cervical cancer among Chinese women
Authors: Wu Yuping , Chen Yulong , Li Longyu , Cao Yicheng , Liu Zehuan , Liu Benrong , Du Zhengping , Zhang Yanling , Chen Shangwu , Lin Zhongqiu , Xu Anlong 
Published: January 2006

AbstractCervical cancer is strongly associated with the infection by oncogenic forms of human papillomavirus (HPV). Although most women are able to clear HPV infection, some develop persistent infections that may lead to cancer, implying genetic susceptibility factors for malignant progression. To verify whether HLA class II DQB1 polymorphism is related to cervical cancer in Chinese population, HLA‐DQB typing was carried out by PCR‐SBT for 258 patients with cervical cancer and 284 healthy controls, and the allele frequencies were calculated. In this study, HLA‐DQB1*060101 and DQB1*0602 alleles were significantly higher in the HPV16 infected patients with cervical cancer compared with healthy controls (χ2 = 31.7452, p < 0.0001; χ2 = 12.7838, pc = 0.0066), but DQB1*050201 allele was significantly lower (χ2 = 26.2187, p < 0.0001). This result indicates that HLA‐DQB1*060101 and DQB1*0602 may confer susceptibility to cervical cancer, and DQB1*050201 may contribute to the resistance to the development of cervical cancer among Chinese women. Sequence analysis reveals that DQB1*060101 allele encodes Leu at position 9 and Asp at position 37, unique to the susceptibility to cervical cancer, whereas the other DQB1 alleles encode Phe or Tyr and Ile or Tyr at the same two positions, respectively. This finding implies that polymorphic amino acids at the putative antigen binding residues 9 and 37 of HLA‐DQB1 alleles may play an important role in the development of cervical cancer. © 2006 Wiley‐Liss, Inc.
Upregulation of mortalin/mthsp70/Grp75 contributes to human carcinogenesis
Authors: Wadhwa Renu , Takano Syuichi , Kaur Kamaljit , Deocaris Custer C. , Pereira‐Smith Olivia M. , Reddel Roger R. , Kaul Sunil C. 
Published: January 2006

AbstractMortalin, also known as mthsp70/GRP75/PBP74, interacts with the tumor suppressor protein p53 and inactivates its transcriptional activation and apoptotic functions. Here, we examined the level of mortalin expression in a large variety of tumor tissues, tumor‐derived and in vitro immortalized human cells. It was elevated in many human tumors, and in all of the tumor‐derived and in vitro immortalized cells. In human embryonic fibroblasts immortalized with an expression plasmid for hTERT, the telomerase catalytic subunit, with or without human papillomavirus E6 and E7 genes, we found that subclones with spontaneously increased mortalin expression levels became anchorage‐independent and acquired the ability to form tumors in nude mice. Furthermore, overexpression of mortalin was sufficient to increase the malignancy of breast carcinoma cells. The study demonstrates that upregulation of mortalin contributes significantly to tumorigenesis, and thus is a good candidate target for cancer therapy. © 2006 Wiley‐Liss, Inc.
EMMPRIN‐induced MMP‐2 activation cascade in human cervical squamous cell carcinoma
Authors: Sier Cornelis F.M. , Zuidwijk Kim , Zijlmans Henry J.M.A.A. , Hanemaaijer Roeland , Mulder‐Stapel Adri A. , Prins Frans A. , Dreef Enno J. , Kenter Gemma G. , Fleuren Gert Jan , Gorter Arko 
Published: January 2006

AbstractTumor progression and recurrence of cervical cancer is associated with upregulation of matrix metalloproteinase 2 (MMP‐2). We evaluated the location, origin and activity of MMP‐2 in cervical squamous cell carcinomas in comparison with MT1‐MMP (MMP‐14), TIMP‐2 and extracellular matrix metalloproteinase inducer (EMMPRIN). Positive immunostaining for MMP‐2 in malignant cells was detected in 83% of the patients. Two patterns of tumor cell MMP‐2 staining were observed: either homogenous in all tumor cells or confined to the cells neighboring the stroma (tumor‐border staining pattern, TBS). Fluorescence in situ zymography showed active MMP‐2 mainly around tumor nodules displaying TBS. The MMP‐2 staining of TBS tumors correlated significantly with the presence of TIMP‐2 and MT1‐MMP, proteins involved in docking MMP‐2 to the cell surface and essential for MMP‐2 activation. In situ mRNA hybridization in TBS tumors demonstrated more abundant presence of MMP‐2 mRNA in neighboring myofibroblasts than in the adjacent tumor cells. Moreover, the TBS MMP‐2 pattern correlated with the presence of EMMPRIN (p = 0.023), suggesting that tumor cells induce MMP‐2 production in nearby stromal cells. This pro‐MMP‐2 could subsequently be activated on tumor cells via the presence of MT1‐MMP and TIMP‐2. The biological relevance of this locally activated MMP‐2 was underscored by the observation that only the TBS pattern of MMP‐2 significantly correlated with decreased survival. In conclusion, the colocalization of EMMPRIN, MT1‐MMP and TIMP‐2 in human cervical carcinomas seems to be involved in a specific distribution pattern of tumor cell bound MMP‐2, which is related with local proteolytic activity and therefore might be associated with worse prognosis of the patients. © 2006 Wiley‐Liss, Inc.
Combined prophylactic and therapeutic cancer vaccine: Enhancing CTL responses to HPV16 E2 using a chimeric VLP in HLA‐A2 mice
Authors: Qian Jiahua , Dong Yujun , Pang Yuk‐Ying S. , Ibrahim Ramy , Berzofsky Jay A. , Schiller John T. , Khleif Samir N. 
Published: January 2006

AbstractWe identified the strategies to induce a CTL response to human papillomavirus (HPV) 16 E2 in HLA‐A2 transgenic mice (AAD). A chimeric HPV16 virus‐like particle (VLP) that includes full length HPV16 E7 and E2 (VLP‐E7E2) was generated. The combination of E2 and E7 has the advantage that E2 is expressed in early dysplasia and neoplasia lesions, where E7 is expressed in more advance lesions. Since T cell response to E2 is less defined, we first evaluated the strategies to enhancing CD8+ T cell responses to HPV E7, using different combinations of immune‐modulators with VLP‐E7E2. Data showed that the CTL response to E7 could be significantly enhanced by coinjection of GM‐CSF and antiCD40 antibodies with chimeric VLP‐E7E2 without adjuvant. However, using the same combination, a low level of CD8+ T cell response to E2 was detected. To enhance the CD8+ T cell response to E2, we analyzed T cell epitopes from E2 sequence. A heterogonous prime‐boost with chimeric VLP‐E7E2 and E2 peptides was performed. The data showed that the priming with chimeric VLP‐E7E2, followed by boosting with E2 peptides, gave a better CTL response than 2 immunizations with E2 peptides. The enhanced immunity is due to the increase of CD11c+ and CD11c+ CD40+ double positive dendritic cells in mice that received immune‐modulators, GM‐CSF and antiCD40. Furthermore, the level of anti‐L1 antibodies remains similar in mice immunized with chimeric VLP with/without immune‐modulators. Thus, the data suggested that the chimeric VLP‐E7E2 has a therapeutic potential for the treatment of HPV‐associated CINs and cancer without diminishing VLPs potential as a prophylactic vaccine by inducing anti‐L1 antibodies against free virus. © 2006 Wiley‐Liss, Inc.
Associations between vitamin D, vitamin D receptor gene and the androgen receptor gene with colon and rectal cancer
Authors: Slattery Martha L. , Sweeney Carol , Murtaugh Maureen , Ma Khe‐Ni , Caan Bette J. , Potter John D. , Wolff Roger 
Published: January 2006

AbstractThe transcriptional activity of the vitamin D receptor (VDR) gene is regulated, at least in part, by the androgen receptor (AR) gene. We evaluate how the number of polyglutamine (CAG) repeats of the AR gene influence colorectal cancer in conjunction with vitamin D, sunshine exposure and VDR. Studies of colon (1,580 cases and 1,968 controls) and rectal (797 cases and 1,016 controls) cancer were used. Vitamin D intake and average hours of sunshine exposure interacted with AR genotype in men. Men with low vitamin D intake or low levels of sunshine exposure who had 23+ CAG repeats of the AR gene had the greatest risk of colon cancer. ORs for men with 23 or more CAG repeats of the AR gene and in the lowest tertile of vitamin D intake or sunshine exposure were 1.71 (95% CI 1.14, 2.56) and 1.51 (95% CI 1.09, 2.09). Men with high levels of sunshine exposure were at reduced risk of developing rectal cancer if they had 23 or more CAG repeats (OR 0.62 95% CI 0.39, 0.97) than if they had fewer than 23 CAG repeats. The FF genotype of the Fok1 VDR gene was associated with reduced risk of colon cancer among women with any allele of 23+ CAG repeats (OR 0.62 95% CI 0.44, 0.88), whereas men with the LL/bb VDR genotypes were at reduced risk of rectal cancer if they also had 23+ CAG repeats (OR 0.71 95% CI 0.48, 1.05) relative to men with fewer than 23 CAG repeats of the AR gene. These data provide support for the role of vitamin D and sunshine exposure in the etiology of colorectal cancer and suggest that AR gene may modulate the association. © 2006 Wiley‐Liss, Inc.
HSP70 vaccine in combination with gene therapy with plasmid DNA encoding sPD‐1 overcomes immune resistance and suppresses the progression of pulmonary metastatic melanoma
Authors: Geng Hui , Zhang Gui‐Mei , Xiao Han , Yuan Ye , Li Dong , Zhang Hui , Qiu Hui , He Yu‐Fei , Feng Zuo‐Hua 
Published: January 2006

AbstractMany tumor immunotherapy efforts are focused on the generation of strong T‐cell response against tumor antigens. However, strong T‐cell response does not always coincide with tumor rejection, for which upregulated expression of immunoinhibitory molecules may be responsible. In this study, the treatment with heat shock protein 70 (HSP70) vaccine induced an infiltration of T cells into the tumor site as well as the expression of IFN‐γ and IL‐2, and delayed lung metastases of tumor, but the tumor progression nonetheless occur finally. We demonstrated that B7‐H1 expressed by residual tumor cells was responsible for the resistance of tumor to the therapy with HSP70 vaccine. Blockade of B7‐H1 by i.v. injection pPD‐1A, a plasmid encoding the extracellular domain of PD‐1 (sPD‐1), could reverse this resistance and enhance the therapeutic efficacy. To complement these findings, we investigated the gene expression of tumor‐infiltrating lymphocytes (TILs) by Real‐time PCR analysis, which revealed that the expression of TH1 cytokines IFN‐γ and IL‐2 by TIL in the mice treated with HSP70 vaccine in combination with sPD‐1 was increased and the expression of negative regulatory molecules IL‐10, TGF‐β and foxp3 was decreased, demonstrating that multifunctional properties afforded by the combination therapy can effectively overcome tumor resistance and promote effective antitumor immunity. The in vivo transfection with pPD‐1A could be performed as infrequently as once a week and still produce a significant antitumor effect. These findings suggest that the treatment with HSP70 vaccine followed by blockade of tumor‐B7‐H1 with sPD‐1 may provide a promising approach for tumor immunotherapy. © 2006 Wiley‐Liss, Inc.
Increased PTEN expression due to transcriptional activation of PPARγ by Lovastatin and Rosiglitazone
Authors: Teresi Rosemary E. , Shaiu Chung‐Wai , Chen Ching‐Shih , Chatterjee V. Krishna , Waite Kristin A. , Eng Charis 
Published: January 2006

AbstractGermline mutations in the tumor suppressor genePTEN(protein phosphatase and tensin homolog located on chromosome ten) predispose to heritable breast cancer. The transcription factor PPARγ has also been implicated as a tumor suppressor pertinent to a range of neoplasias, including breast cancer. A putative PPARγ binding site in thePTENpromoter indicates that PPARγ may regulatePTENexpression. We show here that the PPARγ agonist Rosiglitazone, along with Lovastatin, induce PTEN in a dose‐ and time‐dependent manner. Lovastatin‐ or Rosiglitazone‐induced PTEN expression was accompanied by a decrease in phosphorylated‐AKT and phosphorylated‐MAPK and an increase in G1 arrest. We demonstrate that the mechanism of Lovastatin‐ and Rosiglitazone‐associated PTEN expression was a result of an increase inPTENmRNA, suggesting that this increase was transcriptionally‐mediated. Compound‐66, an inactive form of Rosiglitazone, which is incapable of activating PPARγ, was unable to elicit the same response as Rosiglitazone, signifying that the Rosiglitazone response is PPARγ‐mediated. To support this, we show, using reporter assays including dominant‐negative constructs of PPARγ, that both Lovastatin and Rosiglitazone specifically mediate PPARγ activation. Additionally, we demonstrated that cells lacking PTEN or PPARγ were unable to induce PTEN mediated cellular events in the presence of Lovastatin or Rosiglitazone. These data are the first to demonstrate that Lovastatin can signal through PPARγ and directly demonstrate that PPARγ can upregulate PTEN at the transcriptional level. Since PTEN is constitutively active, our data indicates it may be worthwhile to examine Rosiglitazone and Lovastatin stimulation as mechanisms to increase PTEN expression for therapeutic and preventative strategies including cancer, diabetes mellitus and cardiovascular disease. © 2006 Wiley‐Liss, Inc.