bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of catastrophic flooding on stream biogeochemistry in a headwater stream in Shenandoah National Park, USA
Authors: Reinhardt K.S. , Furman T. 
Published: January 2008

AbstractThis study examined the stream chemistry changes in Staunton River (a second‐order headwater stream with an average annual discharge 704 m3 ha−1 yr−1, Shenandoah National Park, Virginia) resulting from a catastrophic flood in June 1995. This flood, which followed after 800 mm of rain in a 4‐day period, caused large‐scale debris flows and complete scouring of riparian soils down to bedrock in the lower 2 km of the stream, and has been estimated to be a 1000‐year flood. The flood affected stream chemistry on both short‐ and long‐term time scales. The primary short‐term response was elevations in stream concentration of Ca2+, Mg2+, and K+ by 59%, 87%, and 49%, respectively, for 6 months immediately following the flood. The long‐term impact of decreased concentration of all base cations and SiO2 during summer months (8% average) lasted about 2 years. At the episodic time scale, Ca2+, Mg2+, and K+ flushed from soil sources during pre‐flood storms while Na+ and SiO2 diluted; these trends generally reversed during post‐flood storms for 2 years. Short‐term effects are attributed to the leaching of unconsolidated soil and upturned organic matter that clogged the streambed after the flood. The long‐term and superimposed episodic impacts may have resulted from the loss of riparian soils and vegetation in the flood. Copyright © 2008 John Wiley & Sons, Ltd.
Do nonmelanoma skin cancers develop from extra‐cutaneous stem cells?
Authors: Simka Marian 
Published: January 2008

AbstractA hypothesis is presented that nonmelanoma skin cancers can develop from extra‐cutaneous stem cells, and not exclusively from skin keratinocytes. This idea is supported by recent findings regarding the initiation of cancers in the digestive tract, and by a cancer stem cell model of a neoplasia. It is known that multipotent adult progenitor cells can trans‐differentiate into very diverse cellular lineages and can be recruited to areas of profound tissue injury. In these settings, they might also initiate malignant transformation. Some epidemiological data and recent findings regarding mechanisms of wound healing indicate that skin cancers could also originate from bone marrow‐derived or other extra‐cutaneous stem cells in addition to local stem cells. It can therefore be speculated that the biology of keratinocyte stem cells derived from these sources differs from that of local epidermal stem cells, and consequently, these cells might be poorly controlled within their niches. Furthermore, in chronically inflamed skin, or in an immunodeficient patient, malignant transformation of extra‐cutaneous stem cells is more likely to occur. There is one well‐documented case of basal cell cancer which has arisen from donor cells in a kidney transplant recipient, but it remains unclear if this cancer developed directly from a donor‐derived cell, or via fusion of such cells with premalignant keratinocytes. Hopefully, combining animal models of skin cancer initiation with experiments exploring the role of bone marrow‐derived cells in skin healing will bring to light the exact mechanism of carcinogenesis of nonmelanoma skin cancers. © 2008 Wiley‐Liss, Inc.
Specific imaging of VEGF‐A expression with radiolabeled anti‐VEGF monoclonal antibody
Authors: Stollman Thamar H. , Scheer Marian G.W. , Leenders William P.J. , Verrijp Kiek C.N. , Soede Annemieke C. , Oyen Wim J.G. , Ruers Theo J.M. , Boerman Otto C. 
Published: January 2008

AbstractVascular endothelial growth factor‐A (VEGF‐A) is one of the most important angiogenic factors. Here, we studied in a nude mouse model whether the expression of VEGF‐A in a tumor could be imaged with a radiolabeled anti‐VEGF antibody. The humanized anti‐VEGF‐A antibody A.4.6.1. (bevacizumab), which is reactive with all VEGF‐A isoforms, was radiolabeled with In‐111 or with I‐125. The accumulation of the radiolabeled antibodies in VEGF‐A expressing tumors (LS174T) in nude mice was examined in biodistribution studies and by gamma camera imaging. The uptake of the In‐111‐bevacizumab in the tumor at 3 days p.i. was significantly higher than that of I‐125‐bevacizumab (19.4 ± 7.0 %ID/g vs. 9.6 ± 3.3 %ID/g, p = 0.04). Coinjection of an excess unlabeled antibody resulted in a significant decrease in radioactivity concentration in the tumor (<2.9 ± 1.9 %ID/g, p < 0.005), indicating VEGF‐mediated antibody uptake. Highest uptake in the tumor was observed at relatively low antibody protein doses (<3 μg) (20–25 %ID/g). VEGF‐A‐expressing tumors could be clearly visualized on planar scintigraphic images from 24‐hr post injection onwards. In conclusion, VEGF‐A expression in tumors can be visualized specifically with radiolabeled anti‐VEGF‐A‐mAb. © 2008 Wiley‐Liss, Inc.
The DNA demethylating agent 5‐aza‐2′‐deoxycytidine activates NY‐ESO‐1 antigenicity in orthotopic human glioma
Authors: Natsume Atsushi , Wakabayashi Toshihiko , Tsujimura Kunio , Shimato Shinji , Ito Motokazu , Kuzushima Kiyotaka , Kondo Yutaka , Sekido Yoshitaka , Kawatsura Hitomi , Narita Yuji , Yoshida Jun 
Published: January 2008

AbstractCancer/testis antigens (CTAs) are considered to be suitable targets for the immunotherapy of human malignancies. It has been demonstrated that in a variety of tumors, the expression of certain CTAs is activated via the demethylation of their promoter CpG islands. In our study, we have shown that while the composite expression of 13 CTAs in 30 human glioma specimens and newly established cell lines from the Japanese population was nearly imperceptible, the DNA‐demethylating agent 5‐aza‐2′‐deoxycytidine (5‐aza‐CdR) markedly reactivated CTA expression in glioma cells but not in normal human cells. We quantified the diminished methylation status of NY‐ESO‐1‐one of the most immunogenic CTAs‐following 5‐aza‐CdR treatment by using a novel Pyrosequencing™ technology and methylation‐specific PCR. Microarray analysis revealed that 5‐aza‐CdR is capable of signaling the immune system, particularly, human leukocyte antigen (HLA) class I upregulation. 51Cr‐release cytotoxicity assays and cold target inhibition assays using NY‐ESO‐1‐specific cytotoxic T lymphocyte (CTL) lines demonstrated the presentation of de novo NY‐ESO‐1 antigenic peptides on the cell surfaces. In an orthotopic xenograft model, the systemic administration of 5‐aza‐CdR resulted in a significant volume reduction of the transplanted tumors and prolonged the survival of the animals after the adoptive transfer of NY‐ESO‐1‐specific CTLs. These results suggested that 5‐aza‐CdR induces the expression of epigenetically silenced CTAs in poorly immunogenic gliomas and thereby presents a new strategy for tumor immunotherapy targeting 5‐aza‐CdR‐induced CTAs. © 2008 Wiley‐Liss, Inc.
JunD suppresses bone formation and contributes to low bone mass induced by estrogen depletion
Authors: Kawamata Aya , Izu Yayoi , Yokoyama Haruna , Amagasa Teruo , Wagner Erwin F. , Nakashima Kazuhisa , Ezura Yoichi , Hayata Tadayoshi , Noda Masaki 
Published: January 2008

AbstractJunD is an activator protein‐1 (AP‐1) component though its function in skeletal system is still not fully understood. To elucidate the role of JunD in the regulation of bone metabolism, we analyzed JunD‐deficient mice. JunD deficiency significantly increased bone mass and trabecular number. This bone mass enhancement was due to JunD deficiency‐induced increase in bone formation activities in vivo. Such augmentation of bone formation was associated with simultaneous increase in bone resorption while the former was dominant over the latter as accumulation of bone mass occurred in JunD‐deficient mice. In a pathological condition relevant to postmenopausal osteoporosis, ovariectomy reduced bone mass in wild type (WT) mice as known before. Interestingly, JunD deficiency suppressed ovariectomy‐induced increase in bone resorption and kept high bone mass. In addition, JunD deficiency also enhanced new bone formation after bone marrow ablation. Examination of molecular bases for these observations revealed that JunD deficiency enhanced expression levels of c‐jun, fra‐1, and fra‐2 in bone in conjunction with elevated expression levels of runx2, type I collagen, and osteocalcin. Thus, JunD is involved in estrogen depletion‐induced osteopenia via its action to suppress bone formation and to enhance bone resorption. J. Cell. Biochem. 103: 1037–1045, 2008. © 2008 Wiley‐Liss, Inc.
From retroviral vector production to gene transfer: spontaneous inactivation is caused by loss of reverse transcription capacity
Authors: Carmo M. , Panet A. , Carrondo M. J. T. , Alves P. M. , Cruz P. E. 
Published: January 2008

AbstractBackgroundThe loss of gene transfer capacity in retroviral vectors constitutes a major disadvantage in the development of retroviral vectors for gene therapy applications. In the present work the loss of a vector's capacity to perform reverse transcription was studied as a possible explanation for the low stability of retroviral vectors from the production stage to the target cell gene transfer event.MethodsInactivation studies were performed with murine leukemia virus vectors at 37 °C and several residual activities were tested, including viral infectivity, reverse transcription capacity, reverse transcriptase (RT) activities and viral RNA stability.ResultsThe results indicate a high correlation between loss of infectivity and the capacity of the virus to perform the initial steps of reverse transcription. To further understand the thermosensitivity of the reverse transcription process, the two enzyme activities of RT were investigated. The results indicate that, although the inactivation rate of the DNA polymerase is faster than that of RNase H, the decline of these two enzyme activities is significantly slower than that of reverse transcription. Also, viral RNA stability is not implicated in the loss of the virus capacity to perform reverse transcription as the rate of viral RNA degradation was very slow. Furthermore, it was observed that the amount of viral RNA that entered the cells decreased slowly due to viral inactivation at 37 °C.ConclusionsThe reverse transcription process is thermolabile and this sensitivity determines the rate of retroviral inactivation. Strategies targeting stabilization of the reverse transcription complex should be pursued to improve the applicability of retroviral vectors in gene therapy studies. Copyright © 2008 John Wiley & Sons, Ltd.
An integrative approach of organic matter stabilization in temperate soils: Linking chemistry, physics, and biology
Authors: Kögel‐Knabner Ingrid , Ekschmitt Klemens , Flessa Heinz , Guggenberger Georg , Matzner Egbert , Marschner Bernd , von Lützow Margit 
Published: January 2008

AbstractWith this topical issue, we present the work of the Priority Program 1090 of the German Research Foundation (“Deutsche Forschungsgemeinschaft DFG”): “Soils as a source and sink for CO2 – mechanisms and regulation of organic matter stabilisation in soils”. This introduction gives an overview on the sites investigated and the major research approaches, including a glossary of major terms used in the field of soil organic matter research. We point out the advantages of integration of data from a broad field of different soil‐science disciplines and the progress achieved by application and combination of new analytical methods describing the quality and turnover of soil organic matter.
Elevation of XPA protein level in testis tumor cells without increasing resistance to cisplatin or UV radiation
Authors: Köberle Beate , Roginskaya Vera , Zima Karen S. , Masters John R.W. , Wood Richard D. 
Published: January 2008

AbstractMost testicular germ cell tumors are curable using cisplatin‐based chemotherapy, and cell lines from these tumors are unusually sensitive to cisplatin and other DNA‐damaging agents. It has been suggested that this might be caused by a lower‐than normal nucleotide excision repair (NER) activity. Previous studies found that cell lines from testicular germ cell tumors have on average about one‐third the level of the NER protein XPA in comparison to cell lines from other tumors. We asked whether over‐expression of XPA protein would alleviate the cellular sensitivity and increase the DNA repair capacity of a testis tumor cell line. Increasing XPA levels in 833K cells by 10‐fold did not increase resistance to UV irradiation. XPA was localized to the cell nucleus in all cell lines, before and after exposure to UV‐radiation. 833K cells were proficient in removing UV radiation‐induced photoproducts from the genome and increased XPA did not enhance the rate of removal. Further, over‐expressing functional XPA protein did not correlate with increased resistance of 833K testis tumor cells to cisplatin. Thus, although the amount of XPA in this testis tumor cell line is lower than normal, it is sufficient for NER in vivo. The relative sensitivity of testis tumor cells to cisplatin, UV radiation, and other DNA damaging agents is likely related not to NER capacity, but to other factors such as the integrity of the p53 pathway in these cells. © 2008 Wiley‐Liss, Inc.
The boundary integral equation approach for numerical solution of the one‐dimensional Sine‐Gordon equation
Authors: Dehghan Mehdi , Mirzaei Davoud 
Published: January 2008

AbstractThis article describes a numerical method based on the boundary integral equation and dual reciprocity method for solving the one‐dimensional Sine‐Gordon (SG) equation. The time derivative is approximated by the time‐stepping method and a predictor–corrector scheme is employed to deal with the nonlinearity which appears in the problem. Numerical results are presented for some problems to demonstrate the usefulness and accuracy of this approach. In addition, the conservation of energy in SG equation is investigated. © 2008 Wiley Periodicals, Inc. Numer Methods Partial Differential Eq 2008
Differential expression of SOX17 and SOX2 in germ cells and stem cells has biological and clinical implications
Authors: de Jong J , Stoop H , Gillis AJM , van Gurp RJHLM , van de Geijn G‐JM , Boer M de , Hersmus R , Saunders PTK , Anderson RA , Oosterhuis JW , Looijenga LHJ 
Published: February 2008

AbstractCombined action of SOX and POU families of transcription factors plays major roles in embryonic development. In embryonic stem cells, the combination of SOX2 and POU5F1 (OCT3/4) is essential for maintaining the undifferentiated state by activating pluripotency‐linked genes, and inhibition of genes involved in differentiation. Besides embryonic stem cells, POU5F1 is also present in early germ cells, primordial germ cells, and gonocytes, where it has a role in suppression of apoptosis. Here we demonstrate that SOX2 is absent in germ cells of human fetal gonads, and as expected carcinoma in situ (CIS), ie the precursor lesion of testicular germ cell tumours of adolescents and adults (TGCTs), and seminoma. Based on genome‐wide expression profiling, SOX17 was found to be present, instead of SOX2, in early germ cells and their malignant counterparts, CIS and seminoma. Immunohistochemistry, western blot analysis, and quantitative RT‐PCR showed that SOX17 is a suitable marker to distinguish seminoma from embryonal carcinoma, confirmed in representative cell lines. Aberrant SOX2 expression can be present in Sertoli cells when associated with CIS, which can be misdiagnosed as embryonal carcinoma. In conclusion, this study demonstrates the absence of SOX2 in human embryonic and malignant germ cells, which express SOX17 in conjunction with POU5F1. This finding has both diagnostic and developmental biological implications. It allows the identification of seminoma‐like cells from embryonal carcinoma based on a positive marker and might be the explanation for the different function of POU5F1 in normal and malignant germ cells versus embryonic stem cells. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
A survey of public transport use by immunocompromised children in the United Kingdom
Authors: Manley Sue , Selwood Karen , Pizer Barry 
Published: January 2008

AbstractBackgroundThe advice given to immunocompromised children and their families on the use of public transport at our oncology unit has been inconsistent, with a lack of written or evidence based guidelines. We therefore carried out two surveys, one national and one local on this issue, to determine what advice is given to families. We also undertook an extensive literature search on this subject.MethodsThe first survey was completed by the Paediatric Oncology Nurses Forum link member at each of the 22 United Kingdom Childrens' Cancer Study Group (UKCCSG) centres. We asked their current practice for use of public transport for hospital visits, school attendance, regular weekly use and holidays. We looked at recommendations for travel on holiday in the UK and abroad with reference to neutrophil and platelet counts. The second survey was completed by parents of 64 children attending our outpatient clinic over a 2‐week period to ascertain whether the families comply with our verbal recommendations.ResultsThere was a 100% response from UKCCSG centres. None of the centres had any written or evidence based guidelines. 55% of centres allowed public transport for hospital visits, 82% for school and 90% for holidays. Sixty‐eight percent of centres allowed UK travel with a neutrophil count of 0.5–1 × 109/L and 18% if neutrophils <0.5 × 109/L. Eighteen percent of centres allowed foreign travel with a neutrophil count of 0.5–1 × 109/L but only 9% if <0.5 × 109/L. The second survey showed 2% used public transport to attend hospital, 5% for school, 17% for regular use and 50% travelled by plane for holidays. A Pubmed literature search revealed a lack of studies on immunocompromised patients.ConclusionA certain use of public transport is necessary for patients to engage in as normal a life as possible. There is a need for further studies to produce sensible and consistent advice on this issue. Pediatr Blood Cancer 2008;50:988–991. © 2008 Wiley‐Liss, Inc.
Congenital amegakaryocytic thrombocytopenia: The diagnostic importance of combining pathology with molecular genetics
Authors: Rose Melissa J. , Nicol Kathleen K. , Skeens Micah A. , Gross Thomas G. , Kerlin Bryce A. 
Published: January 2008

AbstractCongenital Amegakaryocytic Thrombocytopenia (CAMT) is a rare bone marrow failure syndrome that presents with isolated thrombocytopenia within the first year of life. Classic diagnostic bone marrow findings reveal absent or significantly decreased megakaryocytes with otherwise normal marrow cellularity. We present a newborn with thrombocytopenia whose initial bone marrow aspirate showed an appropriate number of megakaryocytes. CAMT was subsequently diagnosed after molecular testing demonstrated a mutation in the thrombopoietin receptor. The presence of a normal number of megakaryocytes on an initial bone marrow aspirate should not exclude CAMT from the differential diagnosis of thrombocytopenia within the first year of life. Pediatr Blood Cancer 2008;50:1263–1265. © 2008 Wiley‐Liss, Inc.
Sevelamer hydrochloride: A novel treatment of hyperphosphatemia associated with tumor lysis syndrome in children
Authors: Abdullah Shaker , Diezi Manuel , Sung Lillian , Dupuis L. Lee , Geary Denis , Abla Oussama 
Published: January 2008

AbstractBackgroundSevelamer is a phosphate‐binder used effectively for the treatment of hyperphosphatemia in patients treated with dialysis.ObjectivesTo describe the safety of sevelamer in children with hyperphosphatemia secondary to tumor lysis syndrome and the serum phosphate concentrations observed following its administration.ProcedureA retrospective chart review of all children with leukemia/lymphoma diagnosed between November 2002 and April 2004 who received sevelamer during their initial admission was conducted. We monitored the effects of sevelamer on serum phosphate concentration, calcium/phosphate product and renal function at hours 24, 48, and 72 from sevelamer initiation.ResultsThirteen patients received sevelamer during the study period. Their median age was 13 years (range 2.7–17.9) and eight were boys. Nine children had acute lymphoblastic leukemia, one had acute myeloid leukemia and 3 had non‐Hodgkin's lymphoma. The most frequently used dose of sevelamer was 400 mg orally twice daily. The median duration of sevelamer therapy was 2 days (range 1–7). Two children were excluded from the efficacy analysis due to concurrent use of dialysis. Mean serum phosphate levels decreased after sevelamer administration, in eleven patients, from a baseline 2.2 mmol/L ± 0.4 (95% CI, 1.7–3.1) to 1.1 mmol/L ± 0.2 at hour 72 (95%CI, 0.6–1.5). The only toxicity attributed to sevelamer was mild vomiting in three patients.ConclusionsSevelamer appears to be effective and tolerable for the treatment of hyperphosphatemia associated with tumor lysis syndrome. Pediatr Blood Cancer 2008;51:59–61. © 2008 Wiley‐Liss, Inc.
Discontinuity and failures of therapy with bisphosphonates: joint assessment of predictors with multi‐state models
Authors: Zambon Antonella , Baio Gianluca , Mazzaglia Giampiero , Merlino Luca , Corrao Giovanni 
Published: January 2008

AbstractBackgroundData from a cohort of women treated with bisphosphonates were used to illustrate that multi‐state models may be the useful tools of analysis where two causes of treatment failure are the ultimate outcome of interest, and the sequence of recurrent episodes of treatment starting and discontinuing is also of concern.MethodsAll the 11 863 women resident in the Italian Region of Lombardy, aged 45 years or over and who received bisphosphonates for the first time during 2003 entered into the study and were followed up until December 2005. Multi‐state models with in‐treatment and treatment‐free periods as transient states, and fractures and gastrointestinal‐related events as competing causes of failure, were fitted to the data. The effect of several covariates on transition rates between states was estimated.ResultsOne half of the women was treated with bisphosphonates for less than 27% of the period of observation. Negative prognostic factors for treatment discontinuation were younger age and the use of alendronate at once‐daily dosing, with low refill compliance during follow‐up. The risk of fracture was higher for older women who experienced fracture before entry in the cohort, and for those who switched between drugs, had low refill compliance, experienced episodes of treatment discontinuation and used corticosteroids during follow‐up.ConclusionsThe use of multi‐state models in pharmacoepidemiology provides non‐biased estimates of the effect of covariates in predicting treatment discontinuation, restarting and failures. Our analyses emphasize the importance of maximising compliance in order to reduce the risks of both treatment discontinuation and fracture. Copyright © 2008 John Wiley & Sons, Ltd.