bluuebunny/crossref_metadata_2025_split huggingface dataset:
CC‐chemokine ligand 17 gene therapy induces tumor regression through augmentation of tumor‐infiltrating immune cells in a murine model of preexisting CT26 colon carcinoma
Authors: Kanagawa Naoko , Niwa Masakazu , Hatanaka Yutaka , Tani Yoichi , Nakagawa Shinsaku , Fujita Takuya , Yamamoto Akira , Okada Naoki 
Published: July 2007

AbstractChemokines, which regulate leukocyte trafficking and infiltration of local sites, are attractive candidates for improving the efficacy of cancer immunotherapy by enhancing the accumulation of immune cells in tumor tissue. Herein, we evaluated the antitumor effects of intratumoral injection of RGD fiber‐mutant adenoviral vectors (AdRGDs) encoding the chemokines CCL17, CCL19, CCL20, CCL21, CCL22, CCL27, XCL1 or CX3CL1 in a murine model of preexisting CT26 colon carcinoma. Among these 8 chemokine‐expressing AdRGDs, injection of AdRGD‐CCL17 most effectively induced tumor regression and generated specific immunity in rechallenge experiments. Tumor elimination activity by intratumoral injection of AdRGD‐CCL17 depended on both the vector dose and the number of injections, and mainly required CD8+ CTLs in an effector phase as confirmed by analysis using BALB/c nude mice and an in vivo depletion assay. In addition, CCL17 gene transduction induced significant increases in the number of infiltrating macrophages and CD8+ T cells in CT26 tumors, and changed the tumor microenvironment to an immunologic activation state in which there was enhanced expression of lymphocyte activation markers and cell adhesion molecules. Thus, our data provide evidence that CCL17 gene transduction of local tumor sites is a promising approach for the development of a cancer immunogene therapy that can recruit activated tumor‐infiltrating immune effector cells. © 2007 Wiley‐Liss, Inc.
Overexpression of the paternally expressed gene 10 (PEG10) from the imprinted locus on chromosome 7q21 in high‐risk B‐cell chronic lymphocytic leukemia
Authors: Kainz Birgit , Shehata Medhat , Bilban Martin , Kienle Dirk , Heintel Daniel , Krömer‐Holzinger Elisabeth , Le Trang , Kröber Alexander , Heller Gerwin , Schwarzinger Ilse , Demirtas Dita , Chott Andreas , Döhner Hartmut , Zöchbauer‐Müller Sabine , Fonatsch Christa , Zielinski Christoph , Stilgenbauer Stephan , Gaiger Alexander , Wagner Oswald , Jäger Ulrich 
Published: July 2007

AbstractWe report high expression of the maternally imprinted gene PEG10 in high‐risk B‐CLL defined by high LPL mRNA expression. Differential expression was initially identified by microarray analysis and confirmed by real time PCR in 42 B‐CLL patients. mRNA expression ranged from 0.3‐ to 375.4‐fold compared to normal peripheral blood mononuclear cells (PBMNC). Expression levels in CD19+ B‐CLL cells were 100‐fold higher than in B‐cells from healthy donors. PEG10 expression levels in B‐CLL patient samples remained stable over time even after chemotherapy. High PEG10 expression correlated with high LPL expression (p = 0.001) and a positive Coombs' test (p = 0.04). Interestingly, similar expression patterns were observed for the neighbouring imprinted gene sarcoglycan‐ε (SGCE). Monoallelic expression and maintained imprinting of PEG10 were found by allele‐ or methylation‐specific PCR. The intensity of intracellular staining of PEG10 protein corresponded to mRNA levels as confirmed by immunofluorescence staining. Short term knock‐down of PEG10 in B‐CLL cells and HepG2 cells was not associated with changes in cell survival but resulted in a significant change in the expression of 80 genes. However, long term inhibition of PEG10 led to induction of apoptosis in B‐CLL cells. Our data indicate (i) a prognostic value of PEG10 in B‐CLL patients; (ii) specific deregulation of the imprinted locus at 7q21 in high‐risk B‐CLL; (iii) a potential functional and biological role of PEG10 protein expression. Altogether, PEG10 represents a novel marker in B‐CLL. © 2007 Wiley‐Liss, Inc.
Quantitative hypermethylation of NMDAR2B in human gastric cancer
Authors: Liu Jun‐Wei , Kim Myoung Sook , Nagpal Jatin , Yamashita Keishi , Poeta Luana , Chang Xiaofei , Lee Juna , Park Hannah Lui , Jeronimo Carmen , Westra William H. , Mori Masaki , Moon Chulso , Trink Barry , Sidransky David 
Published: July 2007

AbstractNMDA receptor Type 2B (NMDAR2B) is a candidate TSG first identified in esophageal squamous cell carcinoma (ESCC). To evaluate NMDAR2B methylation in gastric cancer progression, we performed quantitative methylation‐specific PCR (MSP), RT‐PCR and immnunohistochemistry (IHC) in primary gastric tissues and colony formation assays in gastric cancer cell lines. We found that the expression of NMDAR2B was reactivated by the demethylating agent, 5‐aza‐2′‐deoxycytidine, with or without trichostatin A in gastric cancer cell lines. Moreover, inactivation of NMDAR2B was found to be closely correlated with promoter methylation status in gastric cell lines and primary gastric tumors. IHC data also showed that NMDAR2B was specifically expressed in gastric epithelial cells and its expression was diminished or absent in gastric cancer epithelium. Quantitative analysis of NMDAR2B promoter methylation showed 61% (17/28) hypermethylation in primary gastric tumors versus 5% (1/20) in normal gastric tissues from nongastric cancer patients. Forced over‐expression of NMDAR2B in gastric cancer cell lines significantly inhibited cell colony formation. Taken together, the above results suggest that NMDAR2B methylation is a common and important biologically relevant event in gastric cancer progression. © 2007 Wiley‐Liss, Inc.
Formation of CaTiO3/TiO2 composite coating on titanium alloy for biomedical applications
Authors: Wei Daqing , Zhou Yu , Jia Dechang , Wang Yaming 
Published: July 2007

AbstractPlasma electrochemical oxidation (PEO) was used to prepare TiO2‐based coating containing Ca and P on titanium alloy. After alkali‐ and then heat‐treatment at 800°C of the PEO coating, a CaTiO3/TiO2 composite (CTC) coating was obtained. The current results indicate that the apatite‐forming ability of the CTC coating is higher than that of the PEO coating. During the simulated body fluid (SBF) incubation, Ca of the CTC coating is released into the SBF. An ionic exchange between Ca2+ ions of the CTC coating and H3O+ ions of the SBF may take place during the SBF incubation. As a result, the abundant TiOH groups are formed on the surface of the CTC coating. The hydroxyl functionalized surface greatly enhances the nucleation and growth of apatite, leading to the high apatite‐forming ability of the CTC coating. The apatite induced by the CTC coating exhibits a porous and carbonated structure. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2008
Prevalence of IgG autoantibody against F‐actin in patients suspected of having autoimmune or acute viral hepatitis
Authors: Jaskowski Troy D. , Konnick Eric Q. , Ashwood Edward R. , Litwin Christine M. , Hill Harry R. 
Published: July 2007

AbstractOur objectives in this study were to compare results obtained by an enzyme immunoassay (EIA) for F‐actin antibody (FAA) immunoglobulin G (IgG) to those determined by an indirect fluorescent antibody (IFA) assay for smooth muscle antibody (SMA) IgG, and to determine the prevalence of FAA in patient sera having serologic evidence of acute viral hepatitis. Sera from 415 patients suspected of having autoimmune hepatitis (AIH), 208 patients suspected of having acute viral hepatitis A, B, or C, and 100 healthy blood donors (HBD) were included in the study. Only one of 100 HBD showed low levels (20–30 Units) of F‐actin IgG. In patients suspected of having AIH, the prevalence of FAA increased as SMA titers increased and all sera with SMA titers of ≥1:160 were FAA‐positive. In contrast, there were many sera with negative (<1:20) or low (1:20–1:40) SMA titers that contained moderate to high levels (>30 Units) of FAA; many exceeding 80 Units. Moreover, 51.4% of these sera were also positive for anti‐nuclear antibody (ANA), which is also utilized in diagnosing type 1 AIH. FAA was detected in 25% of viral hepatitis antibody–positive sera, with the majority (59.3%) containing low levels, and all were ANA‐negative. J. Clin. Lab. Anal. 21:249–253, 2007. © 2007 Wiley‐Liss, Inc.
Measurement of gp210 autoantibodies in sera of patients with primary biliary cirrhosis
Authors: Bauer Alicja , Habior Andrzej 
Published: July 2007

AbstractPrimary biliary cirrhosis (PBC) is an autoimmune liver disease with unknown etiology. Patients with PBC have antimitochondrial autoantibodies (AMA) and additionally 50% of them have antinuclear antibodies (ANA). A 15–amino acid fragment (DRKASPPSGLWSPAY) from the C‐terminal part of the nuclear envelope glycoprotein gp210 has been proposed as one of the antigenic targets for ANA. The aim of this work was to develop an immunoenzymatic assay for determination of gp210 autoantibodies using for its binding a synthetic pentadecapeptide derived from the gp210 amino acid sequence and to determine level of these autoantibodies in sera of patients with PBC and other autoimmune liver diseases from Poland. Polystyrene microtitration plates coated with the synthetic peptide were consecutively incubated with diluted sera, anti‐human immunoglobulin G (IgG) antibodies conjugated with horseradish peroxidase, and with tetramethylobenzidine. Optical density (OD) was read at 450 nm. The mean values of the intra‐ and interassay of variation coefficients of the test were 4.1 and 10.2%, respectively. Anti‐gp210 was detected in 44% of PBC patients and in 6% of patients with PSC. The results were negative for healthy blood donors and other controls. The specificity of the test was 99%, so the anti‐gp‐210 autoantibodies estimated on DRKASPPSGLWSPAY can be a reliable marker of PBC. J. Clin. Lab. Anal. 21:227–231, 2007. © 2007 Wiley‐Liss, Inc.
Evaluation of PorB variable region typing of Neisseria gonorrhoeae using PCR‐ELISA in samples collected from men who have sex with men
Authors: Ling A.E. , Bash M.C. , Lynn F. , Lister N.A. , Zhu P. , Garland S.M. , Fairley C.K. , Tabrizi S.N. 
Published: July 2007

AbstractA polymerase chain reaction (PCR)‐based enzyme‐linked immunosorbent assay (ELISA) methodology was developed to characterize Neisseria gonorrhoeae porB gene variable regions (VR); the methodology was evaluated in comparison to porB VR typing by checkerboard hybridization. Clinical noncultured samples from 35 men who have sex with men (MSM), positive by nucleic amplification assays for N. gonorrhoeae, were typed using a panel of 40 oligonucleotide probes to porB VRs and compared to checkerboard hybridization. Complete concordance was observed between the two methods at PIB VRs 1, 3, and 7. At the more degenerate VRs 5 and 6, PCR ELISA resulted in obtaining more typeable VRs than checkerboard hybridization due to single nucleotide mismatches. By PCR ELISA, two predominant PIB porB types were identified in 58% of the samples and the remaining 16 samples had one of six other porB types. Both PCR ELISA and checkerboard hybridization methods of porB VR typing allowed characterization of N. gonorrhoeae from noncultured clinical samples including throat and rectal swabs and discriminated N. gonorrhoeae from N. meningitidis present in some of the samples. PCR ELISA is a rapid, relatively inexpensive and alternative molecular typing method for N. gonorrhoeae, suitable for use in conjunction with molecular diagnostic tests. J. Clin. Lab. Anal. 21:237–243, 2007. © 2007 Wiley‐Liss, Inc.
Activin receptor‐like kinase 1 inhibits human microvascular endothelial cell migration: Potential roles for JNK and ERK
Authors: David Laurent , Mallet Christine , Vailhé Bruno , Lamouille Samy , Feige Jean‐Jacques , Bailly Sabine 
Published: July 2007

AbstractActivin receptor‐like kinase 1 (ALK1) is an endothelial‐specific type I receptor of the TGFβ receptor family that is implicated in angiogenesis and in the pathogenesis of the vascular disease, hereditary hemorrhagic telangiectasia (HHT). In the absence of a specific ligand, ALK1 cellular functions have been mainly studied through the use of a constitutively active form of this receptor (ALK1ca) and are still debated. We previously reported that ALK1ca inhibits proliferation and migration of human endothelial cells suggesting that ALK1 plays an important role in the maturation phase of angiogenesis (Lamouille et al., 2002, Blood 100: 4495–4501). In the present work, we further analyzed the role of ALK1 in the migration of human dermal microvascular endothelial cell (HMVEC‐d) and observed that silencing endogenous ALK1 expression with siRNAs accelerates endothelial cell migration in the wound assay. Further, we demonstrate that ALK1‐induced inhibition of migration is Smad‐independent. Using a panel of kinase inhibitors, we found that HMVEC‐d wound closure was completely inhibited by a JNK inhibitor and to a lower degree by an ERK kinase inhibitor. Further, HMVEC‐d wounding induced activation of both JNK and ERK, and these were inhibited by ALK1ca expression. Taken together, these results support a significant role for ALK1 as a negative regulator of endothelial cell migration and suggest the implication of JNK and ERK as mediators of this effect. J. Cell. Physiol. 213: 484–489, 2007. © 2007 Wiley‐Liss, Inc.
TRAIL inhibits osteoclastic differentiation by counteracting RANKL‐dependent p27Kip1 accumulation in pre‐osteoclast precursors
Authors: Zauli Giorgio , Rimondi Erika , Stea Susanna , Baruffaldi Fabio , Stebel Marco , Zerbinati Carlotta , Corallini Federica , Secchiero Paola 
Published: July 2007

AbstractExperimental evidences indicate that the TNF family member TNF‐related apoptosis inducing ligand (TRAIL) might be involved in modulating osteoclastic differentiation. The ability of recombinant soluble TRAIL to affect bone density in vivo was evaluated by using 4‐week‐old mice subcutaneously (s.c.) injected with TRAIL for 8 days. TRAIL injection induced a significant increase of tibia trabecular thickness and total bone mass in 4‐week‐old mice, accompanied by a significant decrease of TRAP serum levels, without modulation of osteocalcin and osteoprotegerin (OPG). Parallel experiments performed in vitro showed that inhibition of osteoclastic differentiation, induced by treatment of human peripheral blood osteoclast precursors with TRAIL, was associated to inhibition of receptor activator of nuclear factor kappa B ligand (RANKL)‐induced accumulation of p27Kip1. The potential role of p27Kip1 pathway in mediating the anti‐osteoclastic activity of TRAIL was further suggested by in vitro gene knock‐down experiments performed in osteoclast precursor cultures. Taken together, our data strongly suggest that recombinant TRAIL inhibits osteoclastogenesis by inducing the ubiquitin‐mediated degradation of p27Kip1. J. Cell. Physiol. 214:117–125, 2008. © 2007 Wiley‐Liss, Inc.
Adult mesenchymal stem cells for tissue engineering versus regenerative medicine
Authors: Caplan Arnold I. 
Published: July 2007

AbstractAdult mesenchymal stem cells (MSCs) can be isolated from bone marrow or marrow aspirates and because they are culture‐dish adherent, they can be expanded in culture while maintaining their multipotency. The MSCs have been used in preclinical models for tissue engineering of bone, cartilage, muscle, marrow stroma, tendon, fat, and other connective tissues. These tissue‐engineered materials show considerable promise for use in rebuilding damaged or diseased mesenchymal tissues. Unanticipated is the realization that the MSCs secrete a large spectrum of bioactive molecules. These molecules are immunosuppressive, especially for T‐cells and, thus, allogeneic MSCs can be considered for therapeutic use. In this context, the secreted bioactive molecules provide a regenerative microenvironment for a variety of injured adult tissues to limit the area of damage and to mount a self‐regulated regenerative response. This regenerative microenvironment is referred to as trophic activity and, therefore, MSCs appear to be valuable mediators for tissue repair and regeneration. The natural titers of MSCs that are drawn to sites of tissue injury can be augmented by allogeneic MSCs delivered via the bloodstream. Indeed, human clinical trials are now under way to use allogeneic MSCs for treatment of myocardial infarcts, graft‐versus‐host disease, Crohn's Disease, cartilage and meniscus repair, stroke, and spinal cord injury. This review summarizes the biological basis for the in vivo functioning of MSCs through development and aging. J. Cell. Physiol. 213: 341–347, 2007. © 2007 Wiley‐Liss, Inc.
Molecular mechanisms of the antiproliferative effect of beraprost, a prostacyclin agonist, in murine vascular smooth muscle cells
Authors: Lin Heng , Lee Ja‐Ling , Hou Hsin‐Han , Chung Chih‐Peng , Hsu Sung‐Po , Juan Shu‐Hui 
Published: July 2007

AbstractProstacyclin (PGI2) has been shown to inhibit proliferation in vascular smooth muscle cells. To clarify the underlying molecular mechanism, we investigated the vasoprotection of beraprost (a PGI2 agonist) both in vivo and in vitro. Beraprost eliminated increases in proliferation of rat aortic smooth muscle cells (RASMCs) by 12‐O‐tetradecanoylphorbol 13‐acetate, and enhanced the peroxisome proliferator‐activated receptor‐delta (PPARδ) and inducible nitric oxide synthetase (iNOS) expressions, which were associated with the antiproliferative action of beraprost according to inhibition experiments by [3H]thymidine incorporation. Additionally, elimination of iNOS activity by PPARδ antagonists suggested that iNOS is the downstream target of PPARδ. Furthermore, beraprost increased both consensus PPARδ‐responsive element (PPRE)‐driven luciferase activity and the binding activity of the PPARδ to the putative PPRE in the iNOS promoter; nevertheless, it was abolished by PPARδ antagonists. Deletion of PPRE (−1,349/−1,330) in the iNOS promoter region (−1,359/+2) strongly reduced promoter‐driven activity, representing a novel mechanism of iNOS induction by beraprost. Consistent with this, PPARδ and the concomitant iNOS induction by beraprost were also evident in vivo. Beraprost‐mediated protection in a murine model of balloon angioplasty was significantly attenuated by 13S‐HODE, a PPARδ antagonist. Taken together, the results suggest that the causal relationship between PPARδ and iNOS contributes to the vasoprotective action of beraprost in RASMCs. J. Cell. Physiol. 214: 434–441, 2008. © 2007 Wiley‐Liss, Inc.
Compensating for a bad start: catch‐up growth in juvenile lizards (Amphibolurus muricatus, agamidae)
Authors: Radder Rajkumar S. , Warner Daniel A. , Shine Richard 
Published: July 2007

AbstractIn most natural environments, food availability varies unpredictably through space and time, and growth rates of individual organisms respond accordingly. However, growth rates are not necessarily a simple function of current nutritional conditions: growth rates can be affected by earlier nutritional experience as well as current circumstances. Thus, even a brief period of dietary restriction early in life might influence growth rates later on: either reducing them (if early experience sets subsequent rates, as in the “silver spoon” effect) or increasing them (if underfed individuals can compensate by growing more rapidly to cancel out the early decrement). Alternatively, later growth may be unaffected by earlier rates of growth. We experimentally manipulated food supply (and thus, growth rates) of hatchling lizards (Amphibolurus muricatus) for 1 month post‐hatching, then maintained both high‐food and low‐food animals under identical nutritional conditions in outdoor enclosures for another 6 months. Low food abundance early in life significantly reduced juvenile growth, but these previously underfed animals exploited the subsequent (common garden) conditions to grow much faster than their larger (initially better‐fed) siblings. Thus, the two groups were indistinguishable in body size at 6 months of age. Intriguingly, the compensatory growth occurred in winter, a period that is generally unsuitable for rapid growth in ectotherms. J. Exp. Zool. 307A:500–508, 2007. © 2007 Wiley‐Liss, Inc.
Daily and annual variations of the hepatic Glucose 6‐phosphate dehydrogenase activity and seasonal changes in the body fats of the gilthead seabream Sparus aurata
Authors: Gómez‐Milán Encarnación , Lozano Maria José Sánchez‐Muros 
Published: July 2007

AbstractIn mammalians, Glucose 6‐phosphate dehydrogenase (G6PDH) is clearly related with the daily cycle lipogenesis/lipolysis and therefore with the photoperiod and activity. In fish the temporally changes on the activity of this enzyme have not been described. In this work, annual and diurnal activity of G6PDH was investigated in the liver of Sparus aurata in different seasonal conditions of temperature and photoperiod. During experiment the fish were kept in cages under natural temperature and photoperiod while consuming a commercial diet. The months studied were chosen to establish if there is any influence on the G6PDH activity, because of the change in temperature and photoperiod (equal photoperiod and different temperature, March and October; different photoperiod and equal temperature, May and November; and different photoperiod and temperature, June and January). To study the enzyme activity along the day, the livers of six fish were removed every 3 hr during 24 hr. Annual activity was determined as the average activity during 1 day. Also the annual changes on fat content in muscle and digestive system were studied. The Vmax (maximum velocity) showed seasonal changes in period and phase of the rhythms and for the Km (Michaelis–Menten constant) a period of 24 hr was found in all sampled months, except March, the phase time moves depending on the month. In addition, the annual variations in muscular fat and G6PDH‐specific activity seem to be more related to the reproductive stage than any other variable considered. J. Exp. Zool. 307A:516–526, 2007. © 2007 Wiley‐Liss, Inc.
Is the Friedman Method Applicable to Transformations with Temperature Dependent Reaction Heat?
Authors: Sbirrazzuoli Nicolas 
Published: July 2007

AbstractIn the case of chemical reactions with temperature dependent reaction heat, differences in the activation energy values are obtained using the Friedman (FR) and the advanced non‐linear (NLN) isoconversional methods. The FR method leads to systematic errors when the reaction heat significantly changes with the heating rate (from 7 to 16%), while the advanced NLN isoconversional method that uses integrated values is not subject to these systematic errors. An explanation of this is given. For long time predictions, the FR method can lead to inaccurate results.magnified image
Optically Active Methacrylic Copolymers Bearing Side‐Chain Bisazoaromatic and Bulky Achiral Moieties
Authors: Angiolini Luigi , Benelli Tiziana , Giorgini Loris , Mauriello Francesco , Salatelli Elisabetta 
Published: July 2007

AbstractThe synthesis of two novel series of optically active methacrylic copolymers that contain a side‐chain chiral moiety linked to a photochromic bisazoaromatic chromophore has been carried out by radical copolymerization of the monomer (S)‐3‐methacryloyloxy‐1‐[4′‐phenylazo‐(4‐azobenzene)]pyrrolidine with highly sterically hindered monomers such as tert‐butyl methacrylate or triphenylmethyl methacrylate with the aim to investigate the effect on the optical activity of the resulting derivatives. The copolymeric products have been fully characterized and their spectroscopic and thermal properties compared to those of the related optically active homopolymer and the copolymers with methyl methacrylate, previously reported.The optical activity displayed by the polymers is discussed in terms of extent of chiral conformations assumed by the macromolecules as a consequence of the insertion of co‐monomers capable of affecting the dipole‐dipole interactions that occur in these derivatives between the side‐chain bisazoaromatic chromophores disposed according to a mutual chiral arrangement.magnified image