bluuebunny/crossref_metadata_2025_split huggingface dataset:
DNA methylation-based biomarkers for early detection of non-small cell lung cancer: an update
Authors: Anglim Paul P , Alonzo Todd A , Laird-Offringa Ite A 
Published: October 2008

Abstract
Lung cancer is the number one cancer killer in the United States. This disease is clinically divided into two sub-types, small cell lung cancer, (10–15% of lung cancer cases), and non-small cell lung cancer (NSCLC; 85–90% of cases). Early detection of NSCLC, which is the more common and less aggressive of the two sub-types, has the highest potential for saving lives. As yet, no routine screening method that enables early detection exists, and this is a key factor in the high mortality rate of this disease. Imaging and cytology-based screening strategies have been employed for early detection, and while some are sensitive, none have been demonstrated to reduce lung cancer mortality. However, mortality might be reduced by developing specific molecular markers that can complement imaging techniques. DNA methylation has emerged as a highly promising biomarker and is being actively studied in multiple cancers. The analysis of DNA methylation-based biomarkers is rapidly advancing, and a large number of potential biomarkers have been identified. Here we present a detailed review of the literature, focusing on DNA methylation-based markers developed using primary NSCLC tissue. Viable markers for clinical diagnosis must be detectable in 'remote media' such as blood, sputum, bronchoalveolar lavage, or even exhaled breath condensate. We discuss progress on their detection in such media and the sensitivity and specificity of the molecular marker panels identified to date. Lastly, we look to future advancements that will be made possible with the interrogation of the epigenome.
Effects on hemodynamics and gas exchange of omega-3 fatty acid-enriched lipid emulsion in acute respiratory distress syndrome (ARDS): a prospective, randomized, double-blind, parallel group study
Authors: Sabater Joan , Masclans Joan Ramon , Sacanell Judit , Chacon Pilar , Sabin Pilar , Planas Merce 
Published: October 2008

AbstractIntroductionWe investigated the effects on hemodynamics and gas exchange of a lipid emulsion enriched with omega-3 fatty acids in patients with ARDS.MethodsThe design was a prospective, randomized, double-blind, parallel group study in our Intensive Medicine Department of Vall d'Hebron University Hospital (Barcelona-Spain). We studied 16 consecutive patients with ARDS and intolerance to enteral nutrition (14 men and 2 women; mean age: 58 ± 13 years; APACHE II score: 17.8 ± 2.3; Lung Injury Score: 3.1 ± 0.5; baseline PaO2/FiO2ratio: 149 ± 40). Patients were randomized into 2 groups: Group A (n = 8) received the study emulsion Lipoplus®20%, B.Braun Medical (50% MCT, 40% LCT, 10% ω-3); Group B (n = 8) received the control emulsion Intralipid®Fresenius Kabi (100% LCT). Lipid emulsions were administered during 12 h at a dose of 0.12 g/kg/h. Measurements of the main hemodynamic and gas exchange parameters were made at baseline (immediately before administration of the lipid emulsions), every hour during the lipid infusion, at the end of administration, and six hours after the end of administration lipid infusion.ResultsNo statistically significant changes were observed in the different hemodynamic values analyzed. Likewise, the gas exchange parameters did not show statistically significant differences during the study. No adverse effect attributable to the lipid emulsions was seen in the patients analyzed.ConclusionThe lipid emulsion enriched with omega-3 fatty acids was safe and well tolerated in short-term administration to patients with ARDS. It did not cause any significant changes in hemodynamic and gas exchange parameters.Trial registrationISRCTN63673813
Toxicity of CdSe Nanoparticles in Caco-2 Cell Cultures
Authors: Wang Lin , Nagesha Dattatri K , Selvarasah Selvapraba , Dokmeci Mehmet R , Carrier Rebecca L 
Published: October 2008

Abstract

Background
Potential routes of nanomaterial exposure include inhalation, dermal contact, and ingestion. Toxicology of inhalation of ultra-fine particles has been extensively studied; however, risks of nanomaterial exposure via ingestion are currently almost unknown. Using enterocyte-like Caco-2 cells as a small intestine epithelial model, the possible toxicity of CdSe quantum dot (QD) exposure via ingestion was investigated. Effect of simulated gastric fluid treatment on CdSe QD cytotoxicity was also studied.

Results
Commercially available CdSe QDs, which have a ZnS shell and poly-ethylene glycol (PEG) coating, and in-house prepared surfactant coated CdSe QDs were dosed to Caco-2 cells. Cell viability and attachment were studied after 24 hours of incubation. It was found that cytotoxicity of CdSe QDs was modulated by surface coating, as PEG coated CdSe QDs had less of an effect on Caco-2 cell viability and attachment. Acid treatment increased the toxicity of PEG coated QDs, most likely due to damage or removal of the surface coating and exposure of CdSe core material. Incubation with un-dialyzed in-house prepared CdSe QD preparations, which contained an excess amount of free Cd2+, resulted in dramatically reduced cell viability.

Conclusion
Exposure to CdSe QDs resulted in cultured intestinal cell detachment and death; cytotoxicity depended largely, however, on the QD coating and treatment (e.g. acid treatment, dialysis). Experimental results generally indicated that Caco-2 cell viability correlated with concentration of free Cd2+ ions present in cell culture medium. Exposure to low (gastric) pH affected cytotoxicity of CdSe QDs, indicating that route of exposure may be an important factor in QD cytotoxicity.
Enhanced A3 adenosine receptor selectivity of multivalent nucleoside-dendrimer conjugates
Authors: Klutz Athena M , Gao Zhan-Guo , Lloyd John , Shainberg Asher , Jacobson Kenneth A 
Published: October 2008

AbstractBackgroundAn approach to use multivalent dendrimer carriers for delivery of nucleoside signaling molecules to their cell surface G protein-coupled receptors (GPCRs) was recently introduced.ResultsA known adenosine receptor (AR) agonist was conjugated to polyamidoamine (PAMAM) dendrimer carriers for delivery of the intact covalent conjugate to on the cell surface. Depending on the linking moiety, multivalent conjugates of theN6-chain elongated functionalized congener ADAC (N6-[4-[[[4-[[[(2-aminoethyl)amino]carbonyl]methyl]anilino]carbonyl]methyl]phenyl]-adenosine) achieved unanticipated high selectivity in binding to the cytoprotective human A3AR, a class A GPCR. The key to this selectivity of > 100-fold in both radioreceptor binding (Ki app= 2.4 nM) and functional assays (EC50= 1.6 nM in inhibition of adenylate cyclase) was maintaining a free amino group (secondary) in an amide-linked chain. Attachment of neutral amide-linked chains or thiourea-containing chains preserved the moderate affinity and efficacy at the A1AR subtype, but there was no selectivity for the A3AR. Since residual amino groups on dendrimers are associated with cytotoxicity, the unreacted terminal positions of this A3AR-selective G2.5 dendrimer were present as carboxylate groups, which had the further benefit of increasing water-solubility. The A3AR selective G2.5 dendrimer was also visualized binding the membrane of cells expressing the A3receptor but did not bind cells that did not express the receptor.ConclusionThis is the first example showing that it is feasible to modulate and even enhance the pharmacological profile of a ligand of a GPCR based on conjugation to a nanocarrier and the precise structure of the linking group, which was designed to interact with distal extracellular regions of the 7 transmembrane-spanning receptor. This ligand tool can now be used in pharmacological models of tissue rescue from ischemia and to probe the existence of A3AR dimers.
Interleukin-1beta and tumor necrosis factor-alpha are expressed by different subsets of microglia and macrophages after ischemic stroke in mice
Authors: Clausen Bettina H , Lambertsen Kate L , Babcock Alicia A , Holm Thomas H , Dagnaes-Hansen Frederik , Finsen Bente 
Published: October 2008

AbstractBackgroundInterleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) are expressed by microglia and infiltrating macrophages following ischemic stroke. Whereas IL-1β is primarily neurotoxic in ischemic stroke, TNF-α may have neurotoxic and/or neuroprotective effects. We investigated whether IL-1β and TNF-α are synthesized by overlapping or segregated populations of cells after ischemic stroke in mice.MethodsWe used flow cytometry and immunohistochemistry to examine cellular co-expression of IL-1β and TNF-α at 6, 12 and 24 hours after permanent middle cerebral artery occlusion in mice, validating the results by the use of bone marrow chimeric mice.ResultsWe found that IL-1β and TNF-α were expressed in largely segregated populations of CD11b+CD45dimmicroglia and CD11b+CD45highmacrophages, with cells expressing both cytokines only rarely. The number of Gr1+granulocytes producing IL-1β or TNF-α was very low, and we observed no IL-1β- or TNF-α-expressing T cells or astrocytes.ConclusionTaken together, the results show that IL-1β and TNF-α are produced by largely segregated populations of microglia and macrophages after ischemic stroke in mice. Our findings provide evidence of a functional diversity among different subsets of microglia and macrophages that is potentially relevant to future design of anti-inflammatory therapies in stroke.
Partitioning the population attributable fraction for a sequential chain of effects
Authors: Mason Craig A , Tu Shihfen 
Published: October 2008

Abstract
Background
While the population attributable fraction (PAF) provides potentially valuable information regarding the community-level effect of risk factors, significant limitations exist with current strategies for estimating a PAF in multiple risk factor models. These strategies can result in paradoxical or ambiguous measures of effect, or require unrealistic assumptions regarding variables in the model. A method is proposed in which an overall or total PAF across multiple risk factors is partitioned into components based upon a sequential ordering of effects. This method is applied to several hypothetical data sets in order to demonstrate its application and interpretation in diverse analytic situations.

Results
The proposed method is demonstrated to provide clear and interpretable measures of effect, even when risk factors are related/correlated and/or when risk factors interact. Furthermore, this strategy not only addresses, but also quantifies issues raised by other researchers who have noted the potential impact of population-shifts on population-level effects in multiple risk factor models.

Conclusion
Combined with simple, unadjusted PAF estimates and an aggregate PAF based on all risk factors under consideration, the sequentially partitioned PAF provides valuable additional information regarding the
process
through which population rates of a disorder may be impacted. In addition, the approach can also be used to statistically control for confounding by other variables, while avoiding the potential pitfalls of attempting to separately differentiate direct and indirect effects.
DNA damage in preserved specimens and tissue samples: a molecular assessment
Authors: Zimmermann Juergen , Hajibabaei Mehrdad , Blackburn David C , Hanken James , Cantin Elizabeth , Posfai Janos , Evans Thomas C 
Published: October 2008

Abstract
The extraction of genetic information from preserved tissue samples or museum specimens is a fundamental component of many fields of research, including the Barcode of Life initiative, forensic investigations, biological studies using scat sample analysis, and cancer research utilizing formaldehyde-fixed, paraffin-embedded tissue. Efforts to obtain genetic information from these sources are often hampered by an inability to amplify the desired DNA as a consequence of DNA damage.
Previous studies have described techniques for improved DNA extraction from such samples or focused on the effect of damaging agents – such as light, oxygen or formaldehyde – on free nucleotides.
We present ongoing work to characterize lesions in DNA samples extracted from preserved specimens. The extracted DNA is digested to single nucleosides with a combination of DNase I, Snake Venom Phosphodiesterase, and Antarctic Phosphatase and then analyzed by HPLC-ESI-TOF-MS.
We present data for moth specimens that were preserved dried and pinned with no additional preservative and for frog tissue samples that were preserved in either ethanol, or formaldehyde, or fixed in formaldehyde and then preserved in ethanol. These preservation methods represent the most common methods of preserving animal specimens in museum collections. We observe changes in the nucleoside content of these samples over time, especially a loss of deoxyguanosine. We characterize the fragmentation state of the DNA and aim to identify abundant nucleoside lesions. Finally, simple models are introduced to describe the DNA fragmentation based on nicks and double-strand breaks.
Prescription profile of potentially aristolochic acid containing Chinese herbal products: an analysis of National Health Insurance data in Taiwan between 1997 and 2003
Authors: Hsieh Shu-Ching , Lin I-Hsin , Tseng Wei-Lum , Lee Chang-Hsing , Wang Jung-Der 
Published: October 2008

Abstract

Background
Some Chinese herbal products (CHPs) may contain aristolochic acid (AA) or may be adulterated by the herbs suspected of containing AA which is nephrotoxic and carcinogenic. This study aims to identify the risk and the prescription profile of AA-containing CHPs (AA-CHPs) in Taiwan.

Methods
A longitudinal analysis was conducted on a randomly sampled cohort of 200,000 patients using the data from the National Health Insurance (NHI) in Taiwan between 1997 and 2003.

Results
During the 7-year study period, 78,644 patients were prescribed with AA-CHPs; most patients were females, or middle-aged, or both. A total of 526,867 prescriptions were made to use 1,218 licensed AA-CHPs. Over 85% of the AA-exposed patients took less than 60 g of AA-herbs; however, about 7% were exposed to a cumulated dose of over 100 g of Radix et Rhizoma Asari (Xixin), Caulis Akebiae (Mutong) or Fructus Aristolochiae (Madouling). Patients of respiratory and musculoskeletal diseases received most of the AA-CHP prescriptions. The most frequently prescribed AA-CHPs Shujing Huoxie Tang, Chuanqiong Chadiao San and Longdan Xiegan Tang, containing Radix Stephaniae Tetrandrae, Radix et Rhizoma Asari and Caulis Akebiae, respectively.

Conclusion
About one-third of people in Taiwan have been prescribed with AA-CHPs between 1997 and 2003. Although the cumulated doses were not large, further actions should be carried out to ensure the safe use of AA-CHPs.
Laparoscopic pyeloplasty for ureteropelvic junction obstruction of the lower moiety in a completely duplicated collecting system: a case report
Authors: Stravodimos Konstantinos G. , Anastasiou Ioannis , Adamakis Ioannis , Kapetanakis Theodoros , Koritsiadis Georgios , Constantinides Constantinos 
Published: October 2008

Abstract

Introduction
There are only a few reports on laparoscopic pyeloplasty in kidney abnormalities and only one case for laparoscopic pyeloplasty in a duplicated system. Increasing experience in laparoscopic techniques allows proper treatment of such anomalies. However, its feasibility in difficult cases with altered kidney anatomy such as that of duplicated renal pelvis still needs to be addressed.

Case presentation
We present a case of a 22-year-old white Caucasian female patient with ureteropelvic junction obstruction of the lower ureter of a completely duplicated system that was managed with laparoscopic pyeloplasty. Crossing vessels were identified and transposed. The procedure was carried out successfully and the patient's symptoms subsided. Follow-up studies demonstrated complete resolution of the obstruction.

Conclusion
Since laparoscopic pyeloplasty is still an evolving procedure, its feasibility in complex cases of kidney anatomic abnormalities is herein further justified.
Comparing the xylose reductase/xylitol dehydrogenase and xylose isomerase pathways in arabinose and xylose fermenting Saccharomyces cerevisiae strains
Authors: Bettiga Maurizio , Hahn-Hägerdal Bärbel , Gorwa-Grauslund Marie F 
Published: October 2008

Abstract

Background
Ethanolic fermentation of lignocellulosic biomass is a sustainable option for the production of bioethanol. This process would greatly benefit from recombinant Saccharomyces cerevisiae strains also able to ferment, besides the hexose sugar fraction, the pentose sugars, arabinose and xylose. Different pathways can be introduced in S. cerevisiae to provide arabinose and xylose utilisation. In this study, the bacterial arabinose isomerase pathway was combined with two different xylose utilisation pathways: the xylose reductase/xylitol dehydrogenase and xylose isomerase pathways, respectively, in genetically identical strains. The strains were compared with respect to aerobic growth in arabinose and xylose batch culture and in anaerobic batch fermentation of a mixture of glucose, arabinose and xylose.

Results
The specific aerobic arabinose growth rate was identical, 0.03 h-1, for the xylose reductase/xylitol dehydrogenase and xylose isomerase strain. The xylose reductase/xylitol dehydrogenase strain displayed higher aerobic growth rate on xylose, 0.14 h-1, and higher specific xylose consumption rate in anaerobic batch fermentation, 0.09 g (g cells)-1 h-1 than the xylose isomerase strain, which only reached 0.03 h-1 and 0.02 g (g cells)-1h-1, respectively. Whereas the xylose reductase/xylitol dehydrogenase strain produced higher ethanol yield on total sugars, 0.23 g g-1 compared with 0.18 g g-1 for the xylose isomerase strain, the xylose isomerase strain achieved higher ethanol yield on consumed sugars, 0.41 g g-1 compared with 0.32 g g-1 for the xylose reductase/xylitol dehydrogenase strain. Anaerobic fermentation of a mixture of glucose, arabinose and xylose resulted in higher final ethanol concentration, 14.7 g l-1 for the xylose reductase/xylitol dehydrogenase strain compared with 11.8 g l-1 for the xylose isomerase strain, and in higher specific ethanol productivity, 0.024 g (g cells)-1 h-1 compared with 0.01 g (g cells)-1 h-1 for the xylose reductase/xylitol dehydrogenase strain and the xylose isomerase strain, respectively.

Conclusion
The combination of the xylose reductase/xylitol dehydrogenase pathway and the bacterial arabinose isomerase pathway resulted in both higher pentose sugar uptake and higher overall ethanol production than the combination of the xylose isomerase pathway and the bacterial arabinose isomerase pathway. Moreover, the flux through the bacterial arabinose pathway did not increase when combined with the xylose isomerase pathway. This suggests that the low activity of the bacterial arabinose pathway cannot be ascribed to arabitol formation via the xylose reductase enzyme.
A global transcriptional view of apoptosis in human T-cell activation
Authors: Wang Min , Windgassen Dirk , Papoutsakis Eleftherios T 
Published: October 2008

AbstractBackgroundT-cell activation is an essential step of immune response. The process of proper T-cell activation is strictly monitored and regulated by apoptosis signaling. Yet, regulation of apoptosis, an integral and crucial facet during the process of T-cell activation, is not well understood.MethodsIn this study, a Gene-Ontology driven global gene expression analysis coupled with protein abundance and activity assays identified genes and pathways associated with regulation of apoptosis in primary human CD3+ T cells and separately CD4+ and CD8+ T cells.ResultsWe identified significantly regulated apoptotic genes in several protein families, such as BCL2 proteins, CASPASE proteins, and TNF receptors, and detailed their transcriptional kinetics during the T-cell activation process. Transcriptional patterns of a few select genes (BCL2A1, BBC3 and CASP3) were validated at the protein level. Many of these apoptotic genes are involved in NF-κB signaling pathway, including TNFRSF10A, TNFRSF10B, TRAF4, TRAF1, TRAF3, and TRAF6. Upregulation of NF-κB and IκB family genes (REL, RELA, and RELB, NFKBIA, NFKBIE and NFKB1) at 48 to 96 hours, supported by the increase of phosphorylated RELA (p65), suggests that the involvement of the NF-κB complex in the process of T-cell proliferation is not only regulated at the protein level but also at the transcriptional level. Examination of genes involved in MAP kinase signalling pathway, important in apoptosis, suggests an induction of p38 and ERK1 cascades in T-cell proliferation (at 48 to 96 hours), which was explored using phosphorylation assays for p38 (MAPK14) and ERK1 (MAPK3). An immediate and short-lived increase of AP-1 activity measured by DNA-binding activity suggests a rapid and transient activation of p38 and/or JNK cascades upon T-cell activation.ConclusionThis comparative genome-scale, transcriptional analysis of T-cell activation in the CD4+ and CD8+ subsets and the mixed CD3+ population identified many apoptosis genes not previously identified in the context of T-cell activation. Furthermore, it provided a comprehensive temporal analysis of the transcriptional program of apoptosis associated with T-cell activation.
A role of p38 mitogen-activated protein kinase in adenosine A1 receptor-mediated synaptic depotentiation in area CA1 of the rat hippocampus
Authors: Liang Ying-Ching , Huang Chiung-Chun , Hsu Kuei-Sen 
Published: October 2008

Abstract

Background
Although long-term potentiation (LTP) of synaptic strength is very persistent, current studies have provided evidence that various manipulations or pharmacological treatment when applied shortly after LTP induction can reverse it. This kind of reversal of synaptic strength is termed as depotentiation and may have a function to increase the flexibility and storage capacity of neuronal networks. Our previous studies have demonstrated that an increase in extracellular levels of adenosine and subsequent activation of adenosine A1 receptors are important for the induction of depotentiation; however, the signaling downstream of adenosine A1 receptors to mediate depotentiation induction remains elusive.

Results
We confirm that depotentiation induced by low-frequency stimulation (LFS) (2 Hz, 10 min, 1200 pulses) was dependent on adenosine A1 receptor activation, because it was mimicked by bath-applied adenosine A1 receptor agonist N
6-cyclopentyladenosine (CPA) and was inhibited by the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Pretreatment of the hippocampal slices with the selective p38 mitogen-activated protein kinase (MAPK) inhibitors, 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl]-5-(4-pyrudyl)-1H-imidazole (SB203580) or trans-1-(4-hydroxycyclohexyl)-4-(fluorophenyl)-5-(2-methoxypyrimidin-4-yl)imidazole (SB239063), prevented the induction of depotentiation by LFS and CPA. In agreement with electrophysiological observation, both LFS- and CPA-induced depotentiation are associated with an increase in p38 MAPK activation, which are blocked by DPCPX or SB203580 application.

Conclusion
These results suggest that activation of adenosine A1 receptor and in turn triggering p38 MAPK signaling may contribute to the LFS-induced depotentiation at hippocampal CA1 synapses.