bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies reactive to Plasmodium falciparum serine repeat antigen in children with Burkitt lymphoma from Ghana
Authors: Guech‐Ongey Mercy , Yagi Masanori , Palacpac Nirianne Marie Q. , Emmanuel Benjamin , Talisuna Ambrose O. , Bhatia Kishor , Stefan D. Cristina , Biggar Robert J. , Nkrumah Francis , Neequaye Janet , Tougan Takahiro , Horii Toshihiro , Mbulaiteye Sam M. 
Published: May 2011

AbstractThe role of protective immunity to Plasmodium falciparum (Pf) malaria in Burkitt lymphoma (BL) is unknown. We investigated the association between BL and antibodies reactive to SE36 antigen, a recombinant protein based on P. falciparum serine repeat antigen 5 gene, targeted by protective malaria immune responses. Cases were children (0–14 years) enrolled at the Korle‐Bu Teaching Hospital, Accra, Ghana, during 1965–1994 with BL confirmed by histology or cytology (92% of cases). Controls were apparently healthy children enrolled contemporaneous to the cases from the nearest neighbor house to the case house and were age,‐ sex‐frequency‐matched to the cases. Anti‐SE36 IgG antibodies were measured using enzyme‐linked absorbent immunoassays (ELISAs). SE36 titers were estimated by extrapolating ELISA optical density readings to a standard fitting curve. Anti‐SE36 titers were log‐transformed for analysis. Odds ratios (ORs) and two‐sided 95% confidence intervals (95% CIs) were estimated using unconditional logistic regression. The mean log endpoint dilution titers were 0.63 logs lower in cases than in controls (8.26 [SD 1.68] vs. 8.89 [SD 1.75], Student's t‐test, p = 0.019). Lower titers were observed in cases than controls aged 0–4 years (p = 0.05) and in those aged 5–14 years (p = 0.06). Low and medium tertiles of anti‐SE36 IgG antibodies were associated with increased OR for BL ([OR 1.67, 95% CI 1.21–2.31] and [OR 1.33, 95% CI 0.96–1.86], respectively, ptrend = 0.002) in analyses adjusting for age, sex, calendar period and test plate. Our findings suggest that compared to similarly aged children enrolled from the same community, children with BL in Ghana have lower antibodies to SE36 antigen.
Breast cancer prognosis is inherited independently of patient, tumor and treatment characteristics
Authors: Verkooijen Helena M. , Hartman Mikael , Usel Massimo , Benhamou Simone , Neyroud‐Caspar Isabelle , Czene Kamila , Vlastos Georges , Chappuis Pierre O. , Bouchardy Christine , Rapiti Elisabetta 
Published: May 2011

AbstractPopulation‐based studies have shown a concordance of breast cancer survival among first‐degree relatives (FDRs), suggesting a heritable component. Reasons for such heritability remain to be elucidated. We aimed to determine whether association of breast cancer survival among FDRs is linked to shared patient and tumor characteristics or type of treatment. At the population‐based Geneva Breast Cancer Registry, we identified 162 FDR pairs diagnosed with breast cancer. We categorized FDRs into poor, medium and good familial survival risk groups according to breast cancer–specific survival of their proband (mother or sister). We compared patient, tumor and treatment characteristics between categories and calculated standardized mortality ratios (SMRs) and adjusted disease‐specific mortality for each group. Breast cancer patients in the poor familial survival risk group were more likely to be diagnosed at later stages than those in the good familial survival risk group. Similarly, they had higher SMRs than those in the medium and good survival risk groups (18.7, 95% confidence interval [CI]: 9.4–33.5 vs. 16.5, 95% CI: 7.5–31.3 and 9.4, 95% CI: 3.4–20.4, respectively). After adjustment for patient and tumor characteristics and type of treatment, women in the poor familial survival risk group were almost five times more likely to die of breast cancer than those in the good familial survival risk group (adjusted hazard ratio 4.8, 95% CI: 1.4–16.4). Our study shows that breast cancer prognosis clusters within families and suggests that the hereditary component is independent of patient and tumor characteristics and type of treatment.
The neurotensin receptor‐1 promotes tumor development in a sporadic but not an inflammation‐associated mouse model of colon cancer
Authors: Bugni James M. , Rabadi Leina Al‐ , Jubbal Kevin , Karagiannides Iordanis , Lawson Gregory , Pothoulakis Charalabos 
Published: May 2011

AbstractNeurotensin receptor‐1 (NTR‐1) is overexpressed in colon cancers and colon cancer cell lines. Signaling through this receptor stimulates proliferation of colonocyte‐derived cell lines and promotes inflammation and mucosal healing in animal models of colitis. Given the causal role of this signaling pathway in mediating colitis and the importance of inflammation in cancer development, we tested the effects of NTR‐1 in mouse models of inflammation‐associated and sporadic colon cancer using NTR‐1‐deficient (Ntsr1−/−) and wild‐type (Ntsr1+/+) mice. In mice treated with azoxymethane (AOM) to model sporadic cancer, NTR‐1 had a significant effect on tumor development with Ntsr1+/+ mice developing over twofold more tumors than Ntsr1−/− mice (p = 0.04). There was no effect of NTR‐1 on the number of aberrant crypt foci or tumor size, suggesting that NT/NTR‐1 signaling promotes the conversion of precancerous cells to adenomas. Interestingly, NTR‐1 status did not affect tumor development in an inflammation‐associated cancer model where mice were treated with AOM followed by two cycles of 5% dextran sulfate sodium (DSS). In addition, colonic molecular and histopathologic analyses were performed shortly after a single cycle of DSS. NTR‐1 status did not affect colonic myeloperoxidase activity or histopathologic scores for damage and inflammation. However, Ntsr1−/− mice were more resistant to DSS‐induced mortality (p = 0.01) and had over twofold higher colonic expression levels of Il6 and Cxcl2 (p < 0.04), cytokines known to promote tumor development. These results represent the first direct demonstration that targeted disruption of the Ntsr1 gene reduces susceptibility to colon tumorigenesis.
T cells raised against allogeneic HLA‐A2/CD20 kill primary follicular lymphoma and acute lymphoblastic leukemia cells
Authors: Abrahamsen Ingerid Weum , Kjellevoll Synneva , Greve‐Isdahl Margrethe , Mensali Nadia , Wälchli Sébastien , Kumari Shraddha , Loland Beate Fossum , Egeland Torstein , Kolstad Arne , Olweus Johanna 
Published: May 2011

AbstractT cells mediating a graft‐versus‐leukemia/lymphoma effects without causing graft‐versus‐host disease would greatly improve the safety and applicability of hematopoietic stem cell transplantation. We recently demonstrated that highly peptide‐ and HLA‐specific T cells can readily be generated against allogeneic HLA‐A*02:01 in complex with a peptide from the B cell‐restricted protein CD20. Here, we show that such CD20‐specific T cells can easily be induced from naïve precursors in cord blood, demonstrating that they do not represent cross‐reactive memory cells. The cells displayed high avidity and mediated potent cytotoxic effects on cells from patients with the CD20pos B cell malignancies follicular lymphoma (FL) and acute lymphoblastic leukemia (ALL). However, the cytotoxicity was consistently lower for cells from two of the ALL patients. The ALL cells that were less efficiently killed did not display lower surface expression of CD20 or HLA‐A*02:01, or mutations in the CD20 sequence. Peptide pulsing fully restored the levels of cytotoxicity, indicating that they are indeed susceptible to T cell‐mediated killing. Adoptive transfer of CD20‐specific T cells to an HLA‐A*02:01pos patient requires an HLA‐A*02:01neg, but otherwise HLA identical, donor. A search clarified that donors meeting these criteria can be readily identified even for patients with rare haplotypes. The results bear further promise for the clinical utility of CD20‐specific T cells in B cell malignancies.
The age‐specific prevalence of human papillomavirus and risk of cytologic abnormalities in rural Nigeria: Implications for screen‐and‐treat strategies
Authors: Gage Julia C. , Ajenifuja Kayode O. , Wentzensen Nicolas A. , Adepiti Akinfolarin C. , Eklund Claire , Reilly Mary , Hutchinson Martha , Wacholder Sholom , Harford Joe , Soliman Amr S. , Burk Robert D. , Schiffman Mark 
Published: May 2011

AbstractCervical screening for carcinogenic human papillomavirus (HPV) infection is being considered for low‐income countries. Effectiveness requires targeted screening in older women in whom prevalent infections are more likely to be persistent and predictive of precancer. Some studies in West Africa have found unusually high HPV prevalences across all adult ages, which may reduce the positive predictive value (PPV) of HPV‐based screening, if positivity in older women does not sufficiently predict elevated risk. We conducted a population‐based study in rural Nigeria to identify HPV prevalence and associated cervical abnormalities. Using stratified random sampling, we enrolled women age 15+. Nonvirgins had a cervical exam including liquid‐based cytology and PCR HPV DNA testing from residual cytology specimens. Two‐thirds of invited women participated, and 14.7% had detectable carcinogenic HPV, a proportion that did not decline with age (p‐trend = 0.36) and showed slight peaks in the 15–29 and 60–69 age groups. Among women of the age typically considered for screen‐and‐treat programs (30–49 years), 12.8% were HPV positive, and the PPV for high‐grade or worse cytology was 16.4%. Comparatively, women age < 30 were more likely to be HPV positive (18.9%, p = 0.03) with a lower PPV (4.2% p = 0.05). Among women age 50+ (typically excluded from screening in resource‐poor settings because inexpensive treatment is not available), HPV positivity was 14.2% with a PPV of 13.9%. In Irun and similar settings where HPV does not decline with age, HPV‐based screen‐and‐treat programs might be feasible for mid‐adult women because prevalence is sufficiently low and positivity predicts elevated risk of more easily treated precancer.
The interplay between lipid profiles, glucose, BMI and risk of kidney cancer in the Swedish AMORIS study
Authors: Van Hemelrijck Mieke , Garmo Hans , Hammar Niklas , Jungner Ingmar , Walldius Göran , Lambe Mats , Holmberg Lars 
Published: May 2011

AbstractWith exception of cholesterol and total fat intake, associations between lipid biomarkers and kidney cancer have not often been researched. We aimed to assess possible links between lipid profiles and kidney cancer risk in a large prospective cohort study, while also taking into account glucose levels and BMI. A cohort based on 542,924 persons with baseline information on glucose, triglycerides (TGs), total cholesterol (TC) and creatinine was selected from the Swedish Apolipoprotein Mortality Risk study. A subgroup of 85,621 also had baseline measurements of HDL, LDL, apolipoprotein A‐I and apoB. Multivariate Cox proportional hazard models were used to analyze associations between quartiles and dichotomized values of these lipid components and kidney cancer risk. During a mean follow‐up of 13 years, 958 persons developed kidney cancer. TGs were the only lipid component for which a statistically significant association was found with kidney cancer risk when using both quartiles and a clinical cutoff (hazard ratio: 1.25 (95% CI: 0.99–1.60), 1.29 (1.01–1.66) and 1.66 (1.30–2.13) for the 2nd, 3rd and 4th quartile, compared to the 1st, with p‐value for trend: <0.001). The association remained after exclusion of the 95% percentile of TG. Quartiles of glucose were also positively associated with kidney cancer risk, whereas quartiles of TC were negatively associated with kidney cancer risk. This detailed analysis of lipid components only showed a consistent relation between TG levels and kidney cancer risk. Further mechanistic studies are required to assess links between lipid abnormalities and kidney cancer.
Integrin targeted oncolytic adenoviruses Ad5‐D24‐RGD and Ad5‐RGD‐D24‐GMCSF for treatment of patients with advanced chemotherapy refractory solid tumors
Authors: Pesonen Sari , Diaconu Iulia , Cerullo Vincenzo , Escutenaire Sophie , Raki Mari , Kangasniemi Lotta , Nokisalmi Petri , Dotti Gianpietro , Guse Kilian , Laasonen Leena , Partanen Kaarina , Karli Eerika , Haavisto Elina , Oksanen Minna , Karioja‐Kallio Aila , Hannuksela Päivi , Holm Sirkka‐Liisa , Kauppinen Satu , Joensuu Timo , Kanerva Anna , Hemminki Akseli 
Published: May 2011

AbstractThe safety of oncolytic viruses for treatment of cancer has been shown in clinical trials while antitumor efficacy has often remained modest. As expression of the coxsackie‐adenovirus receptor may be variable in advanced tumors, we developed Ad5‐D24‐RGD, a p16/Rb pathway selective oncolytic adenovirus featuring RGD‐4C modification of the fiber. This allows viral entry through alpha‐v‐beta integrins frequently highly expressed in advanced tumors. Advanced tumors are often immunosuppressive which results in lack of tumor eradication despite abnormal epitopes being present. Granulocyte‐macrophage colony stimulating factor (GMCSF) is a potent activator of immune system with established antitumor properties. To stimulate antitumor immunity and break tumor associated immunotolerance, we constructed Ad5‐RGD‐D24‐GMCSF, featuring GMCSF controlled by the adenoviral E3 promoter. Preliminary safety of Ad5‐D24‐RGD and Ad5‐RGD‐D24‐GMCSF for treatment of human cancer was established. Treatments with Ad5‐D24‐RGD (N = 9) and Ad5‐RGD‐D24‐GMCSF (N = 7) were well tolerated. Typical side effects were grade 1‐2 fatigue, fever and injection site pain. 77% (10/13) of evaluable patients showed virus in circulation for at least 2 weeks. In 3 out of 6 evaluable patients, disease previously progressing stabilized after a single treatment with Ad5‐RGD‐D24‐GMCSF. In addition, 2/3 patients had stabilization or reduction in tumor marker levels. All patients treated with Ad5‐D24‐RGD showed disease progression in radiological analysis, although 3/6 had temporary reduction or stabilization of marker levels. Induction of tumor and adenovirus specific immunity was demonstrated with ELISPOT in Ad5‐RGD‐D24‐GMCSF treated patients. RGD modified oncolytic adenoviruses with or without GMCSF seem safe for further clinical development.
Role of exosomes released by chronic myelogenous leukemia cells in angiogenesis
Authors: Taverna Simona , Flugy Anna , Saieva Laura , Kohn Elise C , Santoro Alessandra , Meraviglia Serena , De Leo Giacomo , Alessandro Riccardo 
Published: May 2011

AbstractOur study is designed to assess if exosomes released from chronic myelogenous leukemia (CML) cells may modulate angiogenesis. We have isolated and characterized the exosomes generated from LAMA84 CML cells and demonstrated that addition of exosomes to human vascular endothelial cells (HUVEC) induces an increase of both ICAM‐1 and VCAM‐1 cell adhesion molecules and interleukin‐8 expression. The stimulation of cell‐cell adhesion molecules was paralleled by a dose‐dependent increase of adhesion of CML cells to a HUVEC monolayer. We further showed that the treatment with exosomes from CML cells caused an increase in endothelial cell motility accompanied by a loss of VE‐cadherin and β‐catenin from the endothelial cell surface. Functional characterization of exosomes isolated from CML patients confirmed the data obtained with exosomes derived from CML cell line. CML exosomes caused reorganization into tubes of HUVEC cells cultured on Matrigel. When added to Matrigel plugs in vivo, exosomes induced ingrowth of murine endothelial cells and vascularization of the Matrigel plugs. Our results suggest for the first time that exosomes released from CML cells directly affect endothelial cells modulating the process of neovascularization.
On the Chiral Homogeneity of Nature: From Atoms to Small Molecules
Authors: Viedma Cristóbal , Cintas Pedro 
Published: May 2011

AbstractThe genesis of enantiopurity in nature, as exemplified by terrestrial amino acids and sugars, has fascinated scientists for more than 150 years. This is a field where we know what we do not know. Starting from theoretical treatments postulated more than 50 years ago, numerous hypotheses, theories, and experiments have been formulated to claim niches of logic and truth. Such arguments vary from purely speculative, often bizarre, to sound enough in terms of reproducibility and feasible generation of mirror symmetry breaking. Although we cannot exclude a biotic origin (i.e,. homochirality was an a posteriori event where one enantiomer tripped and the other survived and evolved, in close resemblance to a Darwinian‐like process), most data and models available are consistent with an abiotic origin that amplified small and stochastic imbalances to produce enantiopure homogeneity prior to life. This analysis revisits recent theoretical background and experiments, which appear to be prebiotically credible, and focuses on primordial molecules such as amino acids. This by no means implies a recreation of the origin of life on Earth, as this task will likely be a surmise forever. These strategies reveal a high degree of robustness and prove how home‐made enantiopurity can be accomplished. Such routes should, in addition, be of enormous practical interest for the production of chiral materials and drugs.
Vascular endothelial growth factor and fibroblast growth factor 2 delivery from spinal cord bridges to enhance angiogenesis following injury
Authors: De Laporte Laura , des Rieux Anne , Tuinstra Hannah M. , Zelivyanskaya Marina L. , De Clerck Nora M. , Postnov Andrei A. , Préat Véronique , Shea Lonnie D. 
Published: May 2011

AbstractThe host response to spinal cord injury can lead to an ischemic environment that can induce cell death and limits cell transplantation approaches to promote spinal cord regeneration. Spinal cord bridges that provide a localized and sustained release of vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF‐2) were investigated for their ability to promote angiogenesis and nerve growth within the injury. Bridges were fabricated by fusion of poly(lactide‐co‐glycolide) microspheres using a gas foaming/particulate leaching technique, and proteins were incorporated by encapsulation into the microspheres and/or mixing with the microspheres before foaming. Compared to the mixing method, encapsulation reduced the losses during leaching and had a slower protein release, while VEGF was released more rapidly than FGF‐2. In vivo implantation of bridges loaded with VEGF enhanced the levels of VEGF within the injury at 1 week, and bridges releasing VEGF and FGF‐2 increased the infiltration of endothelial cells and the formation of blood vessel at 6 weeks postimplantation. Additionally, substantial neurofilament staining was observed within the bridge; however, no significant difference was observed between bridges with or without protein. Bridges releasing angiogenic factors may provide an approach to overcome an ischemic environment that limits regeneration and cell transplantation‐based approaches. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2011.
Osteoinductivity of partially purified bovine, ostrich and emu bone morphogenetic proteins in vitro
Authors: Hu ZhenMing , Peel Sean A.F. , Lindholm Tom C. , Sàndor George K.B. , Clokie Cameron M. L. , Su Yan 
Published: May 2011

AbstractThe aim of this study was to observe the osteogenic activity of native bone morphogenetic proteins (BMPs) obtained from different species including bovine, ostrich and emu sources in order to compare mammalian and avian BMPs. Rat mesenchymal progenitor marrow stromal cells and pre‐osteoblastic C2C12 cell cultures, were exposed to the native BMPs and alkaline phosphatase (ALP) and creatine kinase (CK) levels were determined by assay. The results showed that the ALP activity in C2C12 cultures was elevated by bovine BMP by 2‐ to 10‐fold (p < 0.05‐0.001) from day 3 during 14 days. There were no significant differences in avian BMP related elevations of ALP activity except with ostrich BMPs at day 14 (p < 0.05). However, exposure of MSCs cultures to BMPs derived from bovine, ostrich or emu sources resulted in elevated ALP from day 3 (p < 0.05). Bovine BMP resulted in more ALP elevation than with either of the avian BMPs. All of BMPs elevated Creatine kinase (CK) activity from day 1 and climbed until peaking at day 7. Compared with control cultures, CK was elevated more with exposure to emu BMP and was more elevated with greater statistical significance than with bovine and ostrich BMP before day 5. These higher levels remained until day 14 (p < 0.05). The results of this study suggest that both bovine and avian BMPs are able to stimulate osteogenesis in mature osteoblasts in vitro. The strongest synergistic effect on osteogenesis was detected in cells stimulated with bovine BMP. Avian BMPs had lower effects on ALP and CK activity, emu BMP being more effective than ostrich BMP. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2011.
Structural surface changes and inflammatory responses against alginate‐based microcapsules after exposure to human peritoneal fluid
Authors: de Haan Bart J. , Rossi Alessandra , Faas Marijke M. , Smelt Maaike J. , Sonvico Fabio , Colombo Paolo , de Vos Paul 
Published: May 2011

AbstractMicroencapsulation of cells is a promising approach to prevent rejection in the absence of immunosuppression. Clinical application, however, is hampered by insufficient insight in factors influencing biocompatibility of the capsules in humans. In the present study we exposed alginate‐based capsules prepared of different types of alginate to human peritoneal fluid. Subsequently we studied the physicochemical changes of the capsule's surface by applying micro‐Fourier Transform Infrared Spectroscopy. We did test alginate‐beads and alginate‐poly‐L‐lysine capsules prepared of different types of alginate. In all tested capsule formulations we found adsorption of components from human peritoneal fluid and clear physicochemical changes of the surface. These changes were alginate‐dependent. The adsorption had no significant effects on the permselective properties of the capsule but we found a strong increase of TNFα production by human peripheral blood mononuclear cells when exposed to alginate‐beads treated with human peritoneal fluid. This elevated responsiveness was not observed with alginate‐PLL capsules. The results show that alginate‐based capsule surfaces always undergo physicochemical changes of the surface when exposed to human peritoneal fluid. This adsorption may lead to enhancement of the inflammatory responses against the microcapsules. Our result implicate that biocompatibility measurements should not only been done with freshly prepared capsules but also with capsules that have been exposed to fluid from the implantation site in order to predict thein vivoresponses. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2011.
Inhibition of hydrogen embrittlement of Ni–Ti superelastic alloy in acid fluoride solution by hydrogen peroxide addition
Authors: Yokoyama Ken'ichi , Yazaki Yushin , Sakai Jun'ichi 
Published: May 2011

AbstractInhibition of the hydrogen embrittlement of Ni–Ti superelastic alloy in an acidulated phosphate fluoride (APF) solution has been attempted by adding various amounts of H2O2. In a 0.2% APF solution, hydrogen absorption is markedly inhibited by adding H2O2, although corrosion is slightly enhanced by increasing the amount of added H2O2. By adding a small amount of H2O2 (0.001M), in the early stage of immersion, hydrogen embrittlement is inhibited and corrosion is only slightly enhanced. Upon adding H2O2, it appears that the dominant cathodic reactions change from hydrogen evolution to H2O2 reduction reactions, or the surface conditions of the alloy are changed by H2O2 with a high oxidation capability, thereby inhibiting hydrogen absorption. The present study clearly indicates that infinitesimal addition of H2O2 into acid fluoride solutions is effective for the inhibition of the hydrogen embrittlement of the alloy. © 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2011.