bluuebunny/crossref_metadata_2025_split huggingface dataset:
Successful nontransplant resection of POST‐TEXT III and IV hepatoblastoma
Authors: Lautz Timothy B. , Ben‐Ami Tamar , Tantemsapya Niramol , Gosiengfiao Yasmin , Superina Riccardo A. 
Published: November 2010

AbstractBACKGROUND:Liver transplantation is increasingly advocated as primary surgical therapy for children with hepatoblastoma involving 3 or 4 sectors of the liver after neoadjuvant chemotherapy. This study evaluated the results of nontransplant hepatectomy in children who might otherwise have been considered for liver transplantation.METHODS:All children who underwent resection at a single institution from 1998 to 2009 for POST‐TEXT IV or centrally located POST‐TEXT III hepatoblastoma after neoadjuvant chemotherapy were reviewed.RESULTS:Fourteen children (7 boys) with a median age of 8 months at diagnosis met study criteria. Pulmonary metastases in 3 patients were resected in 2 and resolved with chemotherapy in 1 patient. Preoperative grouping after neoadjuvant chemotherapy was POST‐TEXT IV in 3 patients and POST‐TEXT III in 11 patients. Thirteen of 14 (93%) children who underwent aggressive resection despite being potential candidates for primary transplantation were alive and tumor‐free with a median follow‐up of 57 months. Observed survival rates at 1, 2, and 5 years were 93%, 91%, and 88% respectively. Event‐free survival rates at 1, 2, and 5 years were 93%, 91%, and 75%, respectively.CONCLUSIONS:Excellent survival (93%) was obtained with aggressive resection in children with POST‐TEXT III and IV hepatoblastoma meeting criteria for transplant referral. The 1 death occurred in a patient with unfavorable small cell histology. These children should be managed at institutions experienced in both advanced pediatric hepatobiliary surgery and transplantation. Operative exploration was frequently required to ultimately determine which tumors can be resected and which require transplantation. Cancer 2011. © 2010 American Cancer Society.
Disease and host characteristics as predictors of time to first bone metastasis and death in men with progressive castration‐resistant nonmetastatic prostate cancer
Authors: Smith Matthew R. , Cook Richard , Lee Ker‐Ai , Nelson Joel B. 
Published: November 2010

AbstractBACKGROUND:The natural history of castration‐resistant nonmetastatic prostate cancer is poorly defined.METHODS:The authors used data from 331 subjects in the placebo group of a randomized controlled trial to evaluate the relations of disease and host characteristics with time to first bone metastases in men with prostate cancer, rising prostate‐specific antigen (PSA) despite androgen deprivation therapy, and no radiographic evidence of metastases. Relations between baseline covariates and clinical outcomes were assessed by Cox proportional hazard analyses. Covariates in the model were age, body mass index, prior prostatectomy, prior orchiectomy, Gleason score, performance status, PSA, urinary N‐telopeptide, bone alkaline phosphatase, albumin, lactate dehydrogenase, and hemoglobin.RESULTS:At 2 years, 46% of subjects had developed bone metastases, and 20% had died. Median bone metastasis‐free survival was 25 months. In multivariate analyses, baseline PSA ≥13.1 ng/mL was associated with shorter overall survival (relative risk [RR], 2.34; 95% confidence interval [CI], 1.71–3.21; P < .0001), time to first bone metastasis (RR, 1.98; 95% CI, 1.43‐2.74; P < .0001), and bone metastasis‐free survival (RR, 1.98; 95% CI, 1.45–2.70; P < .0001). PSA velocity was significantly associated with overall and bone metastasis‐free survival. Other covariates were not consistently associated with clinical outcomes.CONCLUSIONS:In men with progressive castration‐resistant prostate cancer and no detectable metastases, baseline PSA was significantly associated with time to first bone metastasis, bone metastasis‐free survival, and overall survival. Other disease and host characteristics, including body mass index and bone turnover markers, were not consistently associated with clinical outcomes. Cancer 2011. © 2010 American Cancer Society.
Determinants of Pulmonary Blood Flow Distribution
Authors: Glenny Robb W. , Robertson H. Thomas 
Published: November 2010

AbstractThe primary function of the pulmonary circulation is to deliver blood to the alveolar capillaries to exchange gases. Distributing blood over a vast surface area facilitates gas exchange, yet the pulmonary vascular tree must be constrained to fit within the thoracic cavity. In addition, pressures must remain low within the circulatory system to protect the thin alveolar capillary membranes that allow efficient gas exchange. The pulmonary circulation is engineered for these unique requirements and in turn these special attributes affect the spatial distribution of blood flow. As the largest organ in the body, the physical characteristics of the lung vary regionally, influencing the spatial distribution on large‐, moderate‐, and small‐scale levels. © 2011 American Physiological Society.Compr Physiol1:39‐59, 2011..
Gaseous Therapeutics in Acute Lung Injury
Authors: Ryter Stefan W. , Choi Augustine M. K. 
Published: November 2010

AbstractAcute lung injury (ALI) and acute respiratory distress syndrome (ARDS) remain major causes of morbidity and mortality in critical care medicine despite advances in therapeutic modalities. ALI can be associated with sepsis, trauma, pharmaceutical or xenobiotic exposures, high oxygen therapy (hyperoxia), and mechanical ventilation. Of the small gas molecules (NO, CO, H2S) that arise in human beings from endogenous enzymatic activities, the physiological significance of NO is well established, whereas that of CO or H2S remains controversial. Recent studies have explored the potential efficacy of inhalation therapies using these small gas molecules in animal models of ALI. NO has vasoregulatory and redox‐active properties and can function as a selective pulmonary vasodilator. Inhaled NO (iNO) has shown promise as a therapy in animal models of ALI including endotoxin challenge, ischemia/reperfusion (I/R) injury, and lung transplantation. CO, another diatomic gas, can exert cellular tissue protection through antiapoptotic, anti‐inflammatory, and antiproliferative effects. CO has shown therapeutic potential in animal models of endotoxin challenge, oxidative lung injury, I/R injury, pulmonary fibrosis, ventilator‐induced lung injury, and lung transplantation. H2S, a third potential therapeutic gas, can induce hypometabolic states in mice and can confer both pro‐ and anti‐inflammatory effects in rodent models of ALI and sepsis. Clinical studies have shown variable results for the efficacy of iNO in lung transplantation and failure for this therapy to improve mortality in ARDS patients. No clinical studies have been conducted with H2S. The clinical efficacy of CO remains unclear and awaits further controlled clinical studies in transplantation and sepsis. © 2011 American Physiological Society.Compr Physiol1:105‐121, 2011.
Pulmonary Vascular Disease Related to Hemodynamic Stress in the Pulmonary Circulation
Authors: Chan Stephen Y , Loscalzo Joseph 
Published: November 2010

AbstractHemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension. Recently, some advances have been made in our molecular understanding of the exogenous upstream stimuli that initiate hemodynamic pertubations as well as the downstream vasoactive effectors that control these responses. However, much still remains unknown regarding how these complex signaling pathways connect in order to result in these characteristic pathophysiological changes. This chapter will describe our current understanding of and needed areas of research into the clinical, physiological, and molecular changes associated with pressure/volume overload in the pulmonary circulation. © 2011 American Physiological Society.Compr Physiol1:123‐139, 2011.
Hypoxic Pulmonary Hypertension of the Newborn
Authors: Gao Yuansheng , Raj J Usha 
Published: November 2010

AbstractHypoxic pulmonary hypertension of the newborn is characterized by elevated pulmonary vascular resistance and pressure due to vascular remodeling and increased vessel tension secondary to chronic hypoxia during the fetal and newborn period. In comparison to the adult, the pulmonary vasculature of the fetus and the newborn undergoes tremendous developmental changes that increase susceptibility to a hypoxic insult. Substantial evidence indicates that chronic hypoxia alters the production and responsiveness of various vasoactive agents such as endothelium‐derived nitric oxide, endothelin‐1, prostanoids, platelet‐activating factor, and reactive oxygen species, resulting in sustained vasoconstriction and vascular remodeling. These changes occur in most cell types within the vascular wall, particularly endothelial and smooth muscle cells. At the cellular level, suppressed nitric oxide‐cGMP signaling and augmented RhoA‐Rho kinase signaling appear to be critical to the development of hypoxic pulmonary hypertension of the newborn. © 2011 American Physiological Society.Compr Physiol1:61‐79, 2011.
The Adventitia: Essential Role in Pulmonary Vascular Remodeling
Authors: Stenmark Kurt R. , Nozik‐Grayck Eva , Gerasimovskaya Evgenia , Anwar Adil , Li Min , Riddle Suzette , Frid Maria 
Published: November 2010

AbstractA rapidly emerging concept is that the vascular adventitia acts as a biological processing center for the retrieval, integration, storage, and release of key regulators of vessel wall function. It is the most complex compartment of the vessel wall and comprises a variety of cells including fibroblasts, immunomodulatory cells, resident progenitor cells, vasa vasorum endothelial cells, and adrenergic nerves. In response to vascular stress or injury, resident adventitial cells are often the first to be activated and reprogrammed to then influence tone and structure of the vessel wall. Experimental data indicate that the adventitial fibroblast, the most abundant cellular constituent of adventitia, is a critical regulator of vascular wall function. In response to vascular stresses such as overdistension, hypoxia, or infection, the adventitial fibroblast is activated and undergoes phenotypic changes that include proliferation, differentiation, and production of extracellular matrix proteins and adhesion molecules, release of reactive oxygen species, chemokines, cytokines, growth factors, and metalloproteinases that, collectively, affect medial smooth muscle cell tone and growth directly and that stimulate recruitment and retention of circulating inflammatory and progenitor cells to the vessel wall. Resident dendritic cells also participate in “sensing” vascular stress and actively communicate with fibroblasts and progenitor cells to simulate repair processes that involve expansion of the vasa vasorum, which acts as a conduit for further delivery of inflammatory/progenitor cells. This review presents the current evidence demonstrating that the adventitia acts as a key regulator of pulmonary vascular wall function and structure from the “outside in.” © 2011 American Physiological Society.Compr Physiol1:141‐161, 2011.
Asymptotical Theory of Runaway Electron Diffusion Due to Magnetic Turbulence in Tokamak Plasmas
Authors: Abdullaev S. S. , Finken K. H. , Kudyakov T. , Lehnen M. 
Published: November 2010

AbstractAsymptotic theory of transport of runaway electrons in a toroidal plasma in the presence of small‐scale magnetic turbulence is proposed. It is based on relativistic Hamiltonian guiding center equations for runaway electrons in toroidal plasmas. Using the asymptotical analysis the explicit relation between the spectral (m, n)‐ components of perturbation Hamiltonian and the corresponding spectrum of the magnetic turbulence is found. This relation depends only on a few parameters of runaway orbits and magnetic surfaces. The radial profiles of runaway diffusion coefficients are found employing two methods, the quasilinear approximation and the direct calculations using a fast running mapping. The dependence of the shielding factor of the runaway electron parameters and the turbulence spectra is discussed (© 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Temperature of Particulates in Low‐Pressure rf‐Plasmas in Ar, Ar/H2 and Ar/N2 Mixtures
Authors: Maurer H. R. , Basner R. , Kersten H. 
Published: November 2010

AbstractThe temperature of micro‐particles, confined in the sheath of a capacitively coupled low‐pressure rf‐discharge in front of an Adaptive Electrode, has been measured for different plasma conditions and in different gas mixtures by using temperature‐dependent optical features of the particles. In the range from 10 to 50 Pa, the temperature increase with rising discharge power is found to be more pronounced at low pressures than at higher pressures. Addition of molecular gases to the argon‐plasma may either result in a temperature decrease (as in the case of nitrogen) or in additional heating of the particles (when hydrogen is added). The measured particle temperature is discussed with respect to appearing plasma‐particle interactions which contribute to the particle's energy balance (© 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Degradation of urine samples and its influence on the 13C/12C ratios of excreted steroids
Authors: Piper Thomas , Geyer Hans , Schänzer Wilhelm 
Published: November 2010

AbstractThe degradation processes in deficiently stored urine samples are well investigated regarding steroid concentrations and diagnostic ratios, such as the quotient of testosterone divided by epitestosterone. In contrast, nothing is known about the influence on carbon isotope ratios (CIR) by inappropriate storage conditions. In general, it is assumed that degradation, i.e. deconjugation or dehydrogenation, does not change CIR and thus CIR can be used in cases where the steroid profile turns out to be invalid.Therefore, the CIR of urinary steroids was investigated in different urine samples during the course of degradation over a time period of six months. Several steroids excreted as glucuronides (androsterone (A), etiocholanolone (E), testosterone, pregnanediol (PD) and 5α‐ and 5β‐androstane‐3α,17β‐diol) or sulfo‐conjugated (A, E and androst‐5‐ene‐3β,17β‐diol (5EN17b)) were investigated together with their unconjugated correspondents (A, E, PD and 5EN17b) and the main dehydrogenation products (5α‐ and 5β‐androstane‐3,17‐dion and androst‐4‐ene‐3,17‐dion). For this purpose, the exiting methods for CIR determination were extended and validated. In addition, the urinary concentrations of all investigated steroids were monitored.Particular attention was paid to dehydroepiandrosterone conjugated and unconjugated together with its degradation product 3α,5‐cyclo‐5α‐androstan‐6β‐ol‐17‐one as here the strongest influence on CIR was expected. Copyright © 2010 John Wiley & Sons, Ltd.
Efficient Asymmetric Synthesis of 4H‐Chromene Derivatives through a Tandem Michael Addition–Cyclization Reaction Catalyzed by a Salen–Cobalt(II) Complex
Authors: Dong Zhenhua , Liu Xiaohua , Feng Juhua , Wang Min , Lin Lili , Feng Xiaoming 
Published: November 2010

AbstractThe asymmetric synthesis of 2‐amino‐5‐oxo‐5,6,7,8‐tetrahydro‐4H‐chromene derivatives was achieved through a tandem Michael addition–cyclization reaction of easily available cyclohexane‐1,3‐dione and ethyl 2‐cyano‐3‐phenylacrylates. Moderate to good yields (up to 81 %) and high enantioselectivities (up to 89 % ee) were obtained with a chiral salen–cobalt(II) complex. This process was air tolerant and easily performed, which provides an efficient method for the synthesis of chiral 4H‐chromene derivatives.
Detection of immunogenic parasite and host‐specific proteins in the sera of active and chronic individuals infected with Toxoplasma gondii
Authors: Yeng Chen , Osman Emelia , Mohamed Zeehaida , Noordin Rahmah 
Published: November 2010

AbstractToxoplasma gondii infection in pregnant women may result in abortion and foetal abnormalities, and may be life‐threatening in immunocompromised hosts. To identify the potential infection markers of this disease, 2‐DE and Western blot methods were employed to study the parasite circulating antigens and host‐specific proteins in the sera of T. gondii‐infected individuals. The comparisons were made between serum protein profiles of infected (n=31) and normal (n=10) subjects. Antigenic proteins were identified by immunoblotting using pooled sera and monoclonal anti‐human IgM‐HRP. Selected protein spots were characterised using mass spectrometry. Prominent differences were observed when serum samples of T. gondii‐infected individuals and normal controls were compared. A significant up‐regulation of host‐specific proteins, α2‐HS glycoprotein and α1‐B glycoprotein, was also observed in the silver‐stained gels of both active and chronic infections. However, only α2‐HS glycoprotein and α1‐B glycoprotein in the active infection showed immunoreactivity in Western blots. In addition, three spots of T. gondii proteins were detected, namely (i) hypothetical protein chrXII: 3984434‐3 TGME 49, (ii) dual specificity protein phosphatase, catalytic domain TGME 49 and (iii) NADPH‐cytochrome p450 reductase TGME 49. Thus, 2‐DE approach followed by Western blotting has enabled the identification of five potential infection markers for the diagnosis of toxoplasmosis: three are parasite‐specific proteins and two are host‐specific proteins.
Comprehensive analysis of low‐abundance proteins in human urinary exosomes using peptide ligand library technology, peptide OFFGEL fractionation and nanoHPLC‐chip‐MS/MS
Authors: Zhang Yuan , Li Yanyan , Qiu Feng , Qiu Zongyin 
Published: November 2010

AbstractHuman urinary exosomes are 30–100 nm vesicles that originate as the internal vesicles in multivesicular bodies from every renal epithelial cell type facing the urinary track and may serve as a suitable noninvasive starting material for biomarker discovery relevant to a variety of renal disease. To comprehensively explore the low‐abundance proteome, combinatorial peptide ligand libraries, combined with peptide OFFGEL electrophoresis were employed for the enrichment and separation of relatively low‐abundant proteins in urinary exosomes. After analysis by nanoHPLC‐chip‐MS/MS, 512 proteins were identified, including a large number of proteins with extreme molecular weight or extreme pI value, which could not be well mapped by using traditional 2‐D‐gel‐based separation methods. This in‐depth analysis of low‐abundant proteins in urinary exosomes led to an increased understanding of molecular composition of these little vesicles and may be helpful for the discovery of novel biomarker. Our work also provides an effective strategy of concentration and identification of low‐abundance proteome from complex bio‐samples.
Monitoring the tidal Delaware River for ambient toxicity
Authors: MacGillivray A Ronald , Russell David E , Brown Steven S , Fikslin Thomas J , Greene Richard , Hoke Robert A , Nally Christopher , O'Donnell Linda 
Published: November 2010

Abstract
This study assessed ambient waters in an urbanized area of the Delaware River, to determine whether river water samples exhibited chronic lethal or sublethal toxicity when measured in laboratory experiments. Toxicity was assessed at 16 fixed stations in the main-stem river and 29 stations in tributaries of the tidal Delaware River with salinities from 0 to 15 parts per 1000 (ppt) using Pimephales promelas, Americamysis bahia, Menidia beryllina, and Ceriodaphnia dubia in 7-d tests; Pseudokirchneriella subcapitata in a 96-h test; and Hyalella azteca in a 10-d water-only test. The toxicity tests measured organism survival, growth, and reproduction. Results from testing water samples collected in 4 different y indicated that the samples from sites tested in the main-stem of the Delaware River and from the majority of its tributaries did not produce chronic toxicity. The surveys identified tributaries that warrant further assessment for toxicity. Integr Environ Assess Manag 2011;7:466–477. © 2011 SETAC
The NP9 protein encoded by the human endogenous retrovirus HERV‐K(HML‐2) negatively regulates gene activation of the Epstein‐Barr virus nuclear antigen 2 (EBNA2)
Authors: Gross Henrik , Barth Stephanie , Pfuhl Thorsten , Willnecker Vivienne , Spurk Andreas , Gurtsevitch Vladimir , Sauter Marlies , Hu Bin , Noessner Elfriede , Mueller‐Lantzsch Nikolaus , Kremmer Elisabeth , Grässer Friedrich A. 
Published: November 2010

AbstractEpstein‐Barr virus (EBV) is a human tumour virus that efficiently growth‐transforms primary human B‐lymphocytes in vitro. The viral nuclear antigen 2 (EBNA2) is essential for immortalisation of B‐cells and stimulates viral and cellular gene expression through interaction with DNA‐bound transcription factors. Like its cellular homologue Notch, it associates with the DNA‐bound repressor RBPJκ (CSL/CBF1) thereby converting RBPJκ into the active state. For instance, both EBNA2 and Notch activate the cellular HES1 promoter. In EBV‐transformed lymphocytes, the RNA of the NP9 protein encoded by human endogenous retrovirus HERV‐K(HML‐2) Type 1 is strongly up‐regulated. The NP9 protein is detectable both in EBV‐positive Raji cells, a Burkitt's lymphoma cell line, and in IB4, an EBV‐transformed human lymphoblastoid cell line. NP9 binds to LNX that forms a complex with the Notch regulator Numb. Therefore, the function of NP9 vis‐à‐vis Notch and EBNA2 was analysed. Here, we show that NP9 binds to EBNA2 and negatively affects the EBNA2‐mediated activation of the viral C‐ and LMP2A promoters. In contrast, NP9 did neither interfere in the activation of the HES1 promoter by Notch nor the induction of the viral LMP1 promoter by EBNA2. In an electrophoretic mobility shift analysis, NP9 reduced the binding of EBNA2 to DNA‐bound RBPJκ by about 50%. The down‐regulation of EBNA2‐activity by NP9 might represent a cellular defence mechanism against viral infection or could, alternatively, represent an adaptation of the virus to prevent excessive viral protein production that might otherwise be harmful for the infected cell.
Exposure to professional pest control treatments and the risk of childhood acute lymphoblastic leukemia
Authors: Bailey Helen D. , Armstrong Bruce K. , de Klerk Nicholas H. , Fritschi Lin , Attia John , Scott Rodney J. , Smibert Elizabeth , Milne Elizabeth ,   for the Aus‐ALL Consortium
Published: November 2010

AbstractPrevious studies suggest that exposure to pesticides increases the risk of childhood acute lymphoblastic leukemia (ALL). The aim of this analysis was to investigate whether professional pest treatments in or around the home before birth or during childhood increased the risk of childhood ALL. Data from 388 cases and 870 frequency‐matched controls were analyzed using unconditional logistic regression, adjusting for study matching variables and potential confounders, to calculate odds ratios (ORs). A meta‐analysis of our findings with the published findings of previous studies was also conducted. The ORs for any professional pest control treatments were 1.19 (95% CI 0.83, 1.69) in the year before pregnancy, 1.30 (95% CI 0.86, 1.97) during pregnancy and 1.24 (95% CI 0.93, 1.65) for those done after the child's birth. The ORs for exposure after birth were highest when it occurred between the ages of two and three years. ORs were elevated for termite treatments before birth. ORs were higher for pre‐B than T cell ALL and for t(12;21) (ETV6‐Runx‐1) than other cytogenetic sub‐types. The pooled OR from a meta‐analysis of our study with three previous studies of professional pest control treatments during pregnancy was 1.37 (95% CI 1.00, 1.88). Our results, and those of our meta‐analysis, provide some evidence of a modestly increased risk of ALL for professional pest control treatments done during the index pregnancy and possibly in the child's early years. The analysis of pooled data from international collaborations may provide more certainty regarding these potentially important associations.