bluuebunny/crossref_metadata_2025_split huggingface dataset:
Parasitism byCuscuta pentagonasequentially induces JA and SA defence pathways in tomato
Authors: RUNYON JUSTIN B. , MESCHER MARK C. , FELTON GARY W. , DE MORAES CONSUELO M. 
Published: November 2009

ABSTRACTWhile plant responses to herbivores and pathogens are well characterized, responses to attack by other plants remain largely unexplored. We measured phytohormones and C18fatty acids in tomato attacked by the parasitic plantCuscuta pentagona, and used transgenic and mutant plants to explore the roles of the defence‐related phytohormones salicylic acid (SA) and jasmonic acid (JA). Parasite attachment to 10‐day‐old tomato plants elicited few biochemical changes, but a second attachment 10 d later elicited a 60‐fold increase in JA, a 30‐fold increase in SA and a hypersensitive‐like response (HLR). Host age also influenced the response: neitherCuscutaseedlings nor established vines elicited a HLR in 10‐day‐old hosts, but both did in 20‐day‐old hosts. Parasites grew larger on hosts deficient in SA (NahG) or insensitive to JA [jasmonic acid‐insensitive1(jai1) ], suggesting that both phytohormones mediate effective defences. Moreover, amounts of JA peaked 12 h before SA, indicating that defences may be coordinated via sequential induction of these hormones. Parasitism also induced increases in free linolenic and linoleic acids and abscisic acid. These findings provide the first documentation of plant hormonal signalling induced by a parasitic plant and show that tomato responses toC. pentagonadisplay characteristics similar to both herbivore‐ and pathogen‐induced responses.
Conserving water in and applying solar power to haemodialysis: ‘Green Dialysis’ through wiser resource utilization
Authors: AGAR JOHN WM 
Published: November 2009

ABSTRACT:Natural resources are under worldwide pressure, water and sustainable energy being the paramount issues. Haemodialysis, a water‐voracious and energy‐hungry healthcare procedure, thoughtlessly wastes water and leaves a heavy carbon footprint. In our service, 100 000 L/week of previously discarded reverse osmosis reject water – water which satisfies all World Health Organisation criteria for potable (drinking) water – no longer drains to waste but is captured for reuse. Reject water from the hospital‐based dialysis unit provides autoclave steam for instrument sterilization, ward toilet flushing, janitor stations and garden maintenance. Satellite centre reject water is tanker‐trucked to community sporting fields, schools and aged‐care gardens. Home‐based nocturnal dialysis patient reuse reject water for home domestic utilities, gardens and animal watering. Although these and other potential water reuse practices should be mandated through legislation for all dialysis services, this is yet to occur. In addition, we now are piloting the use of solar power for the reverse osmosis plant and the dialysis machines in our home dialysis training service. If previously attempted, these have yet to be reported. After measuring the power requirements of both dialytic processes and modelling the projected costs, a programme has begun to solar power all dialysis‐related equipment in a three‐station home haemodialysis training unit. Income‐generation with the national electricity grid via a grid‐share and reimbursement arrangement predicts a revenue stream back to the dialysis service. Dialysis services must no longer ignore the non‐medical aspects of their programmes but plan, trial, implement and embrace ‘green dialysis’ resource management practices.
Lost in translation: barriers to learning in health professional clinical education
Authors: Newton Jennifer M. , Billett Stephen , Jolly Brian , Ockerby Cherene M. 
Published: November 2009

AbstractThe perennial debate concerning the so‐called ‘theory‐practice gap’ pervades health professional education. It is uncertain whether this gap – the notion that knowledge gained in university does not translate well into the workplace – is unavoidable or if it is a manifestation of the learning approaches used and the cultures operative in the two locations. This paper examines how nursing students’ knowledge and skills gained within university clinical laboratories transfer into the reality of the clinical environment. A series of one‐on‐one interviews were conducted over a two year period with second and third year nursing students (n = 28) participating in a preceptorship clinical placement model at one healthcare organisation. This paper focuses on data from the students' first interview. Data were transcribed and imported into NVivo 8 for thematic analysis. Four key themes emerged, including: ‘How I learn’ which focuses on students’ perceptions of their learning preferences; ‘Lack of engagement – it’s not real’ which concerns a perceived lack of authenticity of clinical laboratories; ‘Lack of affordances’ relating to the learning opportunities available in the clinical setting; and ‘Teacher Impact’ which focuses on the influence of individual teachers on student learning. The ‘parallel universes’ of academia and the workplace create dissonance for students as they juxtapose the authenticity of the clinical laboratories with the reality of professional healthcare practice. Transfer is inextricably linked with the individuals’ learning preferences, the affordances the workplace offers to students, and the willingness of staff to provide exciting, engaging learning opportunities. The challenge for health professional education is to provide a model of clinical education that meets not only the needs of university and clinical staff, but most importantly, the needs of students.
The Use of Clinical Scales in Depicting Cerebrovascular Complications in Bacterial Meningitis
Authors: Merkelbach Stefan , König Jochem , Röhn Sonja , Müller Martin 
Published: November 2009

ABSTRACTTo evaluate the utility of different scales for clinical assessment, over time, in acute bacterial meningitis, the authors investigated 53 consecutive patients (mean age 53 ± 17 years). Clinical status on days 1, 3, 5, 8, and 14 after admission was determined by the Scandinavian Stroke Scale (SSS), Glasgow Coma Scale (GCS), and Hunt and Hess Scale (HH), and, on day 21, by the Glasgow Outcome Scale (GOS). Transcranial Doppler examinations were performed serially to assess for disease‐related arterial narrowing. This was observed in 27 patients (51%) within 2 weeks of admission. All scales were observed to correlate with the 21‐day GOS. Patients with cerebral arterial narrowing had significantly decreased SSS scores between days 1 and 8 and worse GCS and HH scores between days 3 and 5. Mean blood flow velocity in the middle cerebral artery on days 5 and 8 significantly correlated with GOS (r= 0.268, P < .008; r=−0.324, P < .003, respectively). The use of such clinical scales allows standardized assessment of patients with bacterial meningitis and provides prognostic information. Cerebral arterial narrowing was observed to correlate with neurologic impairment.
Middle Cerebral Artery Flow Velocity Correlates With Common Carotid Artery Volume Flow Rate After CO2 Inhalation
Authors: Ratanakorn Disya , Greenberg Jason P. , Meads Dana B. , Tegeler Charles H. 
Published: November 2009

ABSTRACTCerebral vasoreactivity can be studied with transcranial Doppler (TCD) by monitoring CO2‐induced middle cerebral artery (MCA) velocity changes. Expected MCA mean velocity (Vm) changes due to changes in end‐expiratory CO2(EE‐CO2) are established, but reactivity of common carotid artery (CCA) volume flow rate (VFR) has not been extensively reported. The authors assess the relationship between MCA Vm, CCA VFR, and EE‐CO2. Ten normal individuals without cerebrovascular disease and with CCA diameters of more than 3.0 mm were studied. CCA VFR was obtained by Color Velocity Imaging Quantification and ipsilateral MCA Vm by standard TCD methods. Each side was studied before, during, and after inhalation of 5% CO2. EE‐CO2, blood pressure, and pulse rate were monitored. Four women and 6 men with mean age of 36 years were included. Significant correlations between MCA Vm and EE‐CO2, CCA VFR and EE‐CO2, and MCA Vm and CCA VFR were found. MCA Vm and CCA VFR increased 5.2% and 4.3% per mm Hg increase in EE‐CO2, respectively. MCA Vm increased 0.3 cm/s per ml/min increase in CCA VFR. In normal individuals, there is a direct correlation between MCA Vm, CCA VFR, and EE‐CO2. Measurement of CCA VFR changes during CO2inhalation may be an alternative method to estimate cerebral vasoreactivity when the MCA velocity cannot be obtained because of inadequate acoustic temporal windows.
Can blood components with age‐related changes influence the ageing of endothelial cells?
Authors: Noh Ji Yeon , Oh Sang Ho , Lee Ju Hee , Kwon Yeon Sook , Ryu Dong Jin , Lee Kwang Hoon 
Published: November 2009

Please cite this paper as:Can blood components with age‐related changes influence the ageing of endothelial cells? Experimental Dermatology 2009.Abstract: Research on vascular endothelial cell ageing helps elucidate the pathogenesis of diseases associated with cell ageing. To investigate endothelial senescence, we used 2‐DE coupled with MS to perform a proteomic analysis of: (i) peripheral blood mononuclear cells (PBMCs) from donors in their 20 s (‘young’) or 60 s (‘old’) and (ii) human dermal microvascular endothelial cells (HDMECs) treated with sera from young and old donors. Identified proteins could be classified into several functional categories: (i) cytoskeletal regulators: CapG and cofilin 1; (ii) stress response and signal pathway proteins: TXNDC5 and RSU‐1; and (iii) apoptosis proteins: Annexin V. We confirmed by Western blot a decrease of RSU‐1, CapG and TXNDC5 in PBMCs from old donors. RSU‐1, which regulates signal transduction of the downstream Ras, showed decreased mRNA and protein levels in PBMCs from old donors and decreased mRNA levels in HDMECs treated with sera from old donors. In addition, Ras protein levels were increased in PBMCs from old donors. These data indicate that reduced RSU‐1 might induce Ras expression, which subsequently could provoke Ras‐induced senescence. In conclusion, our data suggest that blood components that exhibit age‐related changes, such as alterations in cytoskeletal regulators and stress proteins, may be associated with endothelial cell ageing.
Variability of Cloud‐free Ultraviolet Dose Rates on Global Scale Due to Modeled Scenarios of Future Ozone Recovery
Authors: Kazantzidis Andreas , Tourpali Kleareti , Bais Alkiviadis F. 
Published: November 2009

AbstractSimulations of the total ozone content and vertical ozone and temperature profiles during the period 1980–2080 from three chemistry climate models (CCMs) were used and the future variability of five UV dose rate types in global scale was simulated. For each CCM, radiative transfer calculations for cloud‐free skies and constant values of aerosol optical properties and surface reflectivity were performed and the percentage difference, relative to the mean over the period 1996–2005, was calculated. The potential biological consequences of ozone recovery are quantified due to the different influence of ozone‐absorbing wavelengths on the selected UV action spectra: average percentage differences between a few and 60% are revealed during the 2070s, depending on the latitude zone and the season. Although the research into the prediction of UV radiation levels is ongoing, due to the possible future changes in cloudiness, aerosols or surface reflectivity, the long‐term changes in ozone, as projected by the CCMs in a similar way, will affect strongly some of the selected UV dose rates in the future.
Human neuroblastoma cell line SNU‐NB1 loses sensitivity to brain‐derived neurotrophic factor during establishment
Authors: Yun Woong Jae , Kim Soo Hee , Shin Eun , Jang Ja June , Lee Kyoungbun 
Published: November 2009

ABSTRACTBackground and aims:The expression pattern of high affinity neurotrophin receptors dichotomizes the clinicopathologic characteristics of neuroblastoma (NB). The effects mediated by trkA have been documented in many experimental systems, whereas the effects mediated by trkB have only been investigated in limited studies.Methods:We established a new cell line of NB, “SNU‐NB1”, by primary culture and the effects mediated by trkB were addressed in this cell line.Results:NB cells in primary culture showed amplification of N‐myc and expression of trkB. Activation of trkB in primary culture by brain‐derived neurotrophic factor (BDNF) was followed by activation of extracellular signal‐regulated kinase1/2 (ERK1/2), growth inhibition, neuronal differentiation, and N‐myc down‐regulation. However, fully transformed SNU‐NB1 cells lost BDNF sensitivity while being tumorigenicin vivo. Restoration of trkB expression in SNU‐NB1 cells, by retroviral infection of trkB, induced differentiation and inhibition of growth in the cells following BDNF treatment. Although the prognosis of neuroblastomas is different according to the status of trkA and trkB mRNA expressions, the cytologic effects mediated by trkB per se are similar to those by trkA in NB.Conclusion:The patterns of trkA and trkB mRNA expression were markers for different lineages of transformed cells but were inconsistent with the clinical behavior.
A Novel Paradigm to Trigger Apoptosis in Chronic Lymphocytic Leukemia
Authors: Loeder Sandra , Zenz Thorsten , Schnaiter Andrea , Mertens Daniel , Winkler Dirk , Döhner Hartmut , Debatin Klaus-Michael , Stilgenbauer Stephan , Fulda Simone 
Published: November 2009

Abstract
Evasion of apoptosis is a hallmark of chronic lymphocytic leukemia (CLL), calling for new strategies to bypass resistance. Here, we provide first evidence that small-molecule X-linked inhibitor of apoptosis (XIAP) inhibitors in combination with the death receptor ligand tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) present a novel approach to trigger apoptosis in CLL, including subgroups with resistant disease or unfavorable prognosis. XIAP, cellular IAP (cIAP) 1, and cIAP2 are expressed at high levels in primary CLL samples. Proof-of-concept studies in CLL cell lines show that subtoxic concentrations of XIAP inhibitors significantly enhance TRAIL-induced apoptosis and also sensitize for CD95-mediated apoptosis. Importantly also in primary CLL samples, XIAP inhibitor acts in concert with TRAIL to trigger apoptosis in 18 of 27 (67%) cases. This XIAP inhibitor–induced and TRAIL-induced apoptosis involves caspase-3 activation and is blocked by the caspase inhibitor zVAD.fmk. The cooperative interaction of XIAP inhibitor and TRAIL is even evident in distinct subgroups of patients with poor prognostic features (i.e., with 17p deletion, TP53 mutation, chemotherapy-refractory disease, or unmutated VH genes). Interestingly, cases with unmutated VH genes were significantly more sensitive to XIAP inhibitor–induced and TRAIL-induced apoptosis compared with VH gene–mutated samples, pointing to a role of B-cell receptor signaling in apoptosis regulation. By showing that XIAP inhibitors in combination with TRAIL present a new strategy to trigger apoptosis even in resistant forms and poor prognostic subgroups of CLL, our findings have important implications for the development of apoptosis-based therapies in CLL. [Cancer Res 2009;69(23):8977–86]
Inositol Hexaphosphate Suppresses Growth and Induces Apoptosis in Prostate Carcinoma Cells in Culture and Nude Mouse Xenograft: PI3K-Akt Pathway as Potential Target
Authors: Gu Mallikarjuna , Roy Srirupa , Raina Komal , Agarwal Chapla , Agarwal Rajesh 
Published: November 2009

Abstract
Constitutive activation of phosphoinositide 3-kinase (PI3K)-Akt pathway transmits growth-regulatory signals that play a central role in promoting survival, proliferation, and angiogenesis in human prostate cancer cells. Here, we assessed the efficacy of inositol hexaphosphate (IP6) against invasive human prostate cancer PC-3 and C4-2B cells and regulation of PI3K-Akt pathway. IP6 treatment of cells suppressed proliferation, induced apoptosis along with caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of Akt and its upstream regulators PI3K, phosphoinositide-dependent kinase-1 and integrin-linked kinase-1 (ILK1). Downstream of Akt, IP6 inhibited the phosphorylation of glycogen synthase kinase-3α/β at Ser21/9 and consequently reduced cyclin D1 expression. Efficacy studies employing PC-3 tumor xenograft growth in nude mice showed that 2% (w/v) IP6 feeding in drinking water inhibits tumor growth and weight by 52% to 59% (P &lt; 0.001). Immunohistochemical analysis of xenografts showed that IP6 significantly reduces the expression of molecules associated with cell survival/proliferation (ILK1, phosphorylated Akt, cyclin D1, and proliferating cell nuclear antigen) and angiogenesis (platelet endothelial cell adhesion molecule-1 or CD31, vascular endothelial growth factor, endothelial nitric oxide synthase, and hypoxia-inducible factor-1α) together with an increase in apoptotic markers (cleaved caspase-3 and PARP). These findings suggest that, by targeting the PI3K-ILK1-Akt pathway, IP6 suppresses cell survival, proliferation, and angiogenesis but induces death in prostate cancer cells, which might have translational potential in preventing and controlling the growth of advanced and aggressive prostate cancer for which conventional chemotherapy is not effective. [Cancer Res 2009;69(24):9465–72]
L1 Cell Adhesion Molecule Is a Novel Independent Poor Prognostic Factor of Extrahepatic Cholangiocarcinoma
Authors: Li Shengjin , Jo Young Suk , Lee Jae-Hyek , Min Jeong-Ki , Lee Eung Seuk , Park Taewoo , Kim Jin-Man , Hong Hyo Jeong 
Published: November 2009

AbstractPurpose: Cholangiocarcinomas (CC) are associated with poor survival, but diagnostic markers and therapeutic targets have not yet been elucidated. We previously found aberrant expression of L1 cell adhesion molecule in intrahepatic CC and a role for L1 in the progression of intrahepatic CC. Here, we analyzed L1 expression in extrahepatic CC (ECC) and evaluated its prognostic significance.Experimental Design: We examined L1 expression in tumors from 75 ECC patients by immunohistochemistry. We analyzed the correlations between L1 expression and clinicopathologic factors as well as patient survival.Results: L1 was not expressed in normal extrahepatic bile duct epithelium but was aberrantly expressed in 42.7% of ECC tumors. High expression of L1 was detected at the invasive front of tumors and was significantly associated with perineural invasion (P &lt; 0.01). Univariate analysis indicated that various prognostic factors such as histologic grade 3, advanced pathologic T stage and clinical stage, perineural invasion, nodal metastasis, and high expression of L1 were risk factors predicting patient survival. Multivariate analyses done by Cox's proportional hazards model showed that high expression of L1 (hazard ratio, 2.171; 95% confidence interval, 1.162-4.055; P = 0.015) and nodal metastasis (hazard ratio, 2.088; 95% confidence interval, 1.159-3.764; P = 0.014) were independent risk factors for patient death.Conclusions: L1 was highly expressed in 42.7% of ECC and its expression was significantly associated with perineural invasion. High expression of L1 and nodal metastasis were independent poor prognostic factors predicting overall survival in patients with ECC. (Clin Cancer Res 2009;15(23):7345–51)
Pharmacologically Increased Tumor Hypoxia Can Be Measured by 18F-Fluoroazomycin Arabinoside Positron Emission Tomography and Enhances Tumor Response to Hypoxic Cytotoxin PR-104
Authors: Cairns Rob A. , Bennewith Kevin L. , Graves Edward E. , Giaccia Amato J. , Chang Daniel T. , Denko Nicholas C. 
Published: November 2009

Abstract
Purpose: Solid tumors contain microenvironmental regions of hypoxia that present a barrier to traditional radiotherapy and chemotherapy, and this work describes a novel approach to circumvent hypoxia. We propose to overcome hypoxia by augmenting the effectiveness of drugs that are designed to specifically kill hypoxic tumor cells.
Experimental Design: We have constructed RKO colorectal tumor cells that express a small RNA hairpin that specifically knocks down the hypoxia-inducible factor 1a (HIF1a) transcription factor. We have used these cells in vitro to determine the effect of HIF1 on cellular sensitivity to the hypoxic cytotoxin PR-104, and its role in cellular oxygen consumption in response to the pyruvate dehydrogenase kinase inhibitor dichloroacetate (DCA). We have further used these cells in vivo in xenografted tumors to determine the role of HIF1 in regulating tumor hypoxia in response to DCA using 18F-fluoroazomycin arabinoside positron emission tomography, and its role in regulating tumor sensitivity to the combination of DCA and PR-104.
Results: HIF1 does not affect cellular sensitivity to PR-104 in vitro. DCA transiently increases cellular oxygen consumption in vitro and increases the extent of tumor hypoxia in vivo as measured with 18F-fluoroazomycin arabinoside positron emission tomography. Furthermore, we show that DCA-dependent alterations in hypoxia increase the antitumor activity of the next-generation hypoxic cytotoxin PR-104.
Conclusions: DCA interferes with the HIF-dependent “adaptive response,” which limits mitochondrial oxygen consumption. This approach transiently increases tumor hypoxia and represents an important method to improve antitumor efficacy of hypoxia-targeted agents, without increasing toxicity to oxygenated normal tissue. (Clin Cancer Res 2009;15(23):7170–4)
Therapeutic Potential of Adult Bone Marrow–Derived Mesenchymal Stem Cells in Prostate Cancer Bone Metastasis
Authors: Chanda Diptiman , Isayeva Tatyana , Kumar Sanjay , Hensel Jonathan A. , Sawant Anandi , Ramaswamy Girish , Siegal Gene P. , Beatty Matthew S. , Ponnazhagan Selvarangan 
Published: November 2009

Abstract
Purpose: Current evidence indicates that an osteoblast lesion in prostate cancer is preceded by osteolysis. Thus, prevention of osteolysis would reduce complications of bone metastasis. Bone marrow–derived mesenchymal stem cells have the ability to differentiate into osteoblast and produce osteoprotegerin, a decoy receptor for the receptor activator for nuclear factor κB ligand, naturally. The present study examined the potential of unmodified mesenchymal stem cells to prevent osteolytic bone lesions in a preclinical mouse model of prostate cancer.
Experimental Design: The human prostate cancer cell line PC3 was implanted in tibiae of severe combined immunodeficient mice. After establishment of the tumor, either unmodified or genetically engineered mesenchymal stem cells overexpressing osteoprotegerin was injected at the site of tumor growth. The effects of therapy were monitored by bioluminescence imaging, micro–computed tomography, immunohistochemistry, and histomorphometry.
Results: Data indicated significant (P &lt; 0.001) inhibition of tumor growth and restoration of bone in mice treated with unmodified and modified mesenchymal stem cells. Detailed analysis suggested that the donor mesenchymal stem cell inhibited tumor progression by producing woven bone around the growing tumor cells in the tibiae and by preventing osteoclastogenesis.
Conclusions: Overcoming the limitation of the number of mesenchymal stem cells available in the bone can provide significant amelioration for osteolytic damage without further modification. (Clin Cancer Res 2009;15(23):7175–85)