bluuebunny/crossref_metadata_2025_split huggingface dataset:
Infrared thermometry study of nanofluid pool boiling phenomena
Authors: Gerardi Craig , Buongiorno Jacopo , Hu Lin-wen , McKrell Thomas 
Published: March 2011

AbstractInfrared thermometry was used to obtain first-of-a-kind, time- and space-resolved data for pool boiling phenomena in water-based nanofluids with diamond and silica nanoparticles at low concentration (<0.1 vol.%). In addition to macroscopic parameters like the average heat transfer coefficient and critical heat flux [CHF] value, more fundamental parameters such as the bubble departure diameter and frequency, growth and wait times, and nucleation site density [NSD] were directly measured for a thin, resistively heated, indium-tin-oxide surface deposited onto a sapphire substrate. Consistent with other nanofluid studies, the nanoparticles caused deterioration in the nucleate boiling heat transfer (by as much as 50%) and an increase in the CHF (by as much as 100%). The bubble departure frequency and NSD were found to be lower in nanofluids compared with water for the same wall superheat. Furthermore, it was found that a porous layer of nanoparticles built up on the heater surface during nucleate boiling, which improved surface wettability compared with the water-boiled surfaces. Using the prevalent nucleate boiling models, it was possible to correlate this improved surface wettability to the experimentally observed reductions in the bubble departure frequency, NSD, and ultimately to the deterioration in the nucleate boiling heat transfer and the CHF enhancement.
Acute toxicity of second generation HIV protease-inhibitors in combination with radiotherapy: a retrospective case series
Authors: See Alfred P , Zeng Jing , Tran Phuoc T , Lim Michael 
Published: March 2011

AbstractBackgroundThere is little data on the safety of combining radiation therapy and human immunodeficiency virus (HIV) protease inhibitors to treat cancers in HIV-positive patients. We describe acute toxicities observed in a series of HIV-positive patients receiving modern radiation treatments, and compare patients receiving HIV protease inhibitors (PI) with patients not receiving HIV PIs.MethodsBy reviewing the clinical records beginning January 1, 2009 from the radiation oncology department, we identified 29 HIV-positive patients who received radiation therapy to 34 body sites. Baseline information, treatment regimen, and toxicities were documented by review of medical records: patient age, histology and source of the primary tumor, HIV medication regimen, pre-radiation CD4 count, systemic chemotherapy, radiation therapy dose and fractionation, irradiated body region, toxicities, and duration of follow-up. Patients were grouped according to whether they received concurrent HIV PIs and compared using Pearson's chi-square test.ResultsAt baseline, the patients in the two groups were similar with the exception of HIV medication regimens, CD4 count and presence of AIDS-defining malignancy. Patients taking concurrent PIs were more likely to be taking other HIV medications (p = 0.001) and have CD4 count >500 (p = 0.006). Patients taking PIs were borderline less likely to have an AIDS-defining malignancy (p = 0.06). After radiation treatment, 100 acute toxicities were observed and were equally common in both groups (64 [median 3 per patient, IQR 1-7] with PIs; 36 [median 3 per patient, IQR 2-3] without PIs). The observed toxicities were also equally severe in the two groups (Grades I, II, III respectively: 30, 30, 4 with PIs; 23, 13, 0 without PIs: p = 0.38). There were two cases that were stopped early, one in each group; these were not attributable to toxicity.ConclusionsIn this study of recent radiotherapy in HIV-positive patients taking second generation PIs, no difference in toxicities was observed in patients taking PIs compared to patients not taking PIs during radiation therapy. This suggests that it is safe to use unmodified doses of PIs and radiation therapy in HIV cancer patients, and that it is feasible to use PIs as a radiosensitizer in cancer therapy, as has been suggested by pre-clinical results.
Convergence of Logic of Cellular Regulation in Different Premalignant Cells by an Information Theoretic Approach
Authors: Kravchenko-Balasha Nataly , Remacle F , Gross Ayelet , Rotter Varda , Levitzki Alexander , Levine RD 
Published: March 2011

Abstract

Background
Surprisal analysis is a thermodynamic-like molecular level approach that identifies biological constraints that prevents the entropy from reaching its maximum. To examine the significance of altered gene expression levels in tumorigenesis we apply surprisal analysis to the WI-38 model through its precancerous states. The constraints identified by the analysis are transcription patterns underlying the process of transformation. Each pattern highlights the role of a group of genes that act coherently to define a transformed phenotype.

Results
We identify a major transcription pattern that represents a contraction of signaling networks accompanied by induction of cellular proliferation and protein metabolism, which is essential for full transformation. In addition, a more minor, "tumor signature" transcription pattern completes the transformation process. The variation with time of the importance of each transcription pattern is determined. Midway through the transformation, at the stage when cells switch from slow to fast growth rate, the major transcription pattern undergoes a total inversion of its weight while the more minor pattern does not contribute before that stage.

Conclusions
A similar network reorganization occurs in two very different cellular transformation models: WI-38 and the cervical cancer HF1 models. Our results suggest that despite differences in a list of transcripts expressed in different cancer models the rationale of the network reorganization remains essentially the same.
Gene networks associated with conditional fear in mice identified using a systems genetics approach
Authors: Park Christopher C , Gale Greg D , de Jong Simone , Ghazalpour Anatole , Bennett Brian J , Farber Charles R , Langfelder Peter , Lin Andy , Khan Arshad H , Eskin Eleazar , Horvath Steve , Lusis Aldons J , Ophoff Roel A , Smith Desmond J 
Published: March 2011

AbstractBackgroundOur understanding of the genetic basis of learning and memory remains shrouded in mystery. To explore the genetic networks governing the biology of conditional fear, we used a systems genetics approach to analyze a hybrid mouse diversity panel (HMDP) with high mapping resolution.ResultsA total of 27 behavioral quantitative trait loci were mapped with a false discovery rate of 5%. By integrating fear phenotypes, transcript profiling data from hippocampus and striatum and also genotype information, two gene co-expression networks correlated with context-dependent immobility were identified. We prioritized the key markers and genes in these pathways using intramodular connectivity measures and structural equation modeling. Highly connected genes in the context fear modules includedPsmd6,Ube2aandUsp33, suggesting an important role for ubiquitination in learning and memory. In addition, we surveyed the architecture of brain transcript regulation and demonstrated preservation of gene co-expression modules in hippocampus and striatum, while also highlighting important differences.Rps15a, Kif3a, Stard7, 6330503K22RIK, andPlvapwere among the individual genes whose transcript abundance were strongly associated with fear phenotypes.ConclusionApplication of our multi-faceted mapping strategy permits an increasingly detailed characterization of the genetic networks underlying behavior.
Quantitative analysis of polycomb response elements (PREs) at identical genomic locations distinguishes contributions of PRE sequence and genomic environment
Authors: Okulski Helena , Druck Birgit , Bhalerao Sheetal , Ringrose Leonie 
Published: March 2011

Abstract

Background
Polycomb/Trithorax response elements (PREs) are cis-regulatory elements essential for the regulation of several hundred developmentally important genes. However, the precise sequence requirements for PRE function are not fully understood, and it is also unclear whether these elements all function in a similar manner. Drosophila PRE reporter assays typically rely on random integration by P-element insertion, but PREs are extremely sensitive to genomic position.

Results
We adapted the ΦC31 site-specific integration tool to enable systematic quantitative comparison of PREs and sequence variants at identical genomic locations. In this adaptation, a miniwhite (mw) reporter in combination with eye-pigment analysis gives a quantitative readout of PRE function. We compared the Hox PRE Frontabdominal-7 (Fab-7) with a PRE from the vestigial (vg) gene at four landing sites. The analysis revealed that the Fab-7 and vg PREs have fundamentally different properties, both in terms of their interaction with the genomic environment at each site and their inherent silencing abilities. Furthermore, we used the ΦC31 tool to examine the effect of deletions and mutations in the vg PRE, identifying a 106 bp region containing a previously predicted motif (GTGT) that is essential for silencing.

Conclusions
This analysis showed that different PREs have quantifiably different properties, and that changes in as few as four base pairs have profound effects on PRE function, thus illustrating the power and sensitivity of ΦC31 site-specific integration as a tool for the rapid and quantitative dissection of elements of PRE design.
Stem cell factor and granulocyte colony-stimulating factor reduce β-amyloid deposits in the brains of APP/PS1 transgenic mice
Authors: Li Bin , Gonzalez-Toledo Maria E , Piao Chun-Shu , Gu Allen , Kelley Roger E , Zhao Li-Ru 
Published: March 2011

Abstract
Introduction
Alzheimer's disease (AD) is widely recognized as a serious public health problem and heavy financial burden. Currently, there is no treatment that can delay or stop the progressive brain damage in AD. Recently, we demonstrated that stem cell factor (SCF) in combination with granulocyte colony-stimulating factor (G-CSF) (SCF+G-CSF) has therapeutic effects on chronic stroke. The purpose of the present study is to determine whether SCF+G-CSF can reduce the burden of β-amyloid deposits in a mouse model of AD.

Methods
APP/PS1 transgenic mice were used as the model of AD. To track bone marrow-derived cells in the brain, the bone marrow of the APP/PS1 mice was replaced with the bone marrow from mice expressing green fluorescent protein (GFP). Six weeks after bone marrow transplantation, mice were randomly divided into a saline control group and a SCF+G-CSF-treated group. SCF in combination with G-CSF was administered subcutaneously for 12 days. Circulating bone marrow stem cells (CD117+ cells) were quantified 1 day after the final injection. Nine months after treatment, at the age of 18 months, mice were sacrificed. Brain sections were processed for immunohistochemistry to identify β-amyloid deposits and GFP expressing bone marrow-derived microglia in the brain.

Results
Systemic administration of SCF+G-CSF to APP/PS1 transgenic mice leads to long-term reduction of β-amyloid deposition in the brain. In addition, we have also observed that the SCF+G-CSF treatment increases circulating bone marrow stem cells and augments bone marrow-derived microglial cells in the brains of APP/PS1 mice. Moreover, SCF+G-CSF treatment results in enhancement of the co-localization of bone marrow-derived microglia and β-amyloid deposits in the brain.

Conclusions
These data suggest that bone marrow-derived microglia play a role in SCF+G-CSF-induced long-term effects to reduce β-amyloid deposits. This study provides insights into the contribution of the hematopoeitic growth factors, SCF and G-CSF, to limit β-amyloid accumulation in AD and may offer a new therapeutic approach for AD.
Improving RNA-Seq expression estimates by correcting for fragment bias
Authors: Roberts Adam , Trapnell Cole , Donaghey Julie , Rinn John L , Pachter Lior 
Published: March 2011

AbstractThe biochemistry of RNA-Seq library preparation results in cDNA fragments that are not uniformly distributed within the transcripts they represent. This non-uniformity must be accounted for when estimating expression levels, and we show how to perform the needed corrections using a likelihood based approach. We find improvements in expression estimates as measured by correlation with independently performed qRT-PCR and show that correction of bias leads to improved replicability of results across libraries and sequencing technologies.
Modeling the cumulative genetic risk for multiple sclerosis from genome-wide association data
Authors: Wang Joanne H , Pappas Derek , De Jager Philip L , Pelletier Daniel , de Bakker Paul IW , Kappos Ludwig , Polman Chris H ,   Australian and New Zealand Multiple Sclerosis Genetics Consortium (ANZgene), Chibnik Lori B , Hafler David A , Matthews Paul M , Hauser Stephen L , Baranzini Sergio E , Oksenberg Jorge R 
Published: March 2011

Abstract
Background
Multiple sclerosis (MS) is the most common cause of chronic neurologic disability beginning in early to middle adult life. Results from recent genome-wide association studies (GWAS) have substantially lengthened the list of disease loci and provide convincing evidence supporting a multifactorial and polygenic model of inheritance. Nevertheless, the knowledge of MS genetics remains incomplete, with many risk alleles still to be revealed.

Methods
We used a discovery GWAS dataset (8,844 samples, 2,124 cases and 6,720 controls) and a multi-step logistic regression protocol to identify novel genetic associations. The emerging genetic profile included 350 independent markers and was used to calculate and estimate the cumulative genetic risk in an independent validation dataset (3,606 samples). Analysis of covariance (ANCOVA) was implemented to compare clinical characteristics of individuals with various degrees of genetic risk. Gene ontology and pathway enrichment analysis was done using the DAVID functional annotation tool, the GO Tree Machine, and the Pathway-Express profiling tool.

Results
In the discovery dataset, the median cumulative genetic risk (P-Hat) was 0.903 and 0.007 in the case and control groups, respectively, together with 79.9% classification sensitivity and 95.8% specificity. The identified profile shows a significant enrichment of genes involved in the immune response, cell adhesion, cell communication/signaling, nervous system development, and neuronal signaling, including ionotropic glutamate receptors, which have been implicated in the pathological mechanism driving neurodegeneration. In the validation dataset, the median cumulative genetic risk was 0.59 and 0.32 in the case and control groups, respectively, with classification sensitivity 62.3% and specificity 75.9%. No differences in disease progression or T2-lesion volumes were observed among four levels of predicted genetic risk groups (high, medium, low, misclassified). On the other hand, a significant difference (F = 2.75, P = 0.04) was detected for age of disease onset between the affected misclassified as controls (mean = 36 years) and the other three groups (high, 33.5 years; medium, 33.4 years; low, 33.1 years).

Conclusions
The results are consistent with the polygenic model of inheritance. The cumulative genetic risk established using currently available genome-wide association data provides important insights into disease heterogeneity and completeness of current knowledge in MS genetics.
High Growth Rate of Benign Thyroid Nodules Bearing RET/PTC Rearrangements
Authors: Sapio Maria Rosaria , Guerra Anna , Marotta Vincenzo , Campanile Elisabetta , Formisano Raffaele , Deandrea Maurilio , Motta Manuela , Limone Paolo Piero , Fenzi Gianfranco , Rossi Guido , Vitale Mario 
Published: March 2011

Context:
Benign thyroid nodules display a broad range of behaviors from a stationary size to a progressive growth. The RET/PTC oncogene has been documented in a fraction of benign thyroid nodules, besides papillary thyroid carcinomas, and it might therefore influence their growth.

Objective:
The aim of the present work was to evaluate whether RET/PTC in benign thyroid nodules associates with a different nodular growth rate.

Study Design:
In this prospective multicentric study, 125 subjects with benign nodules were included. RET rearrangements were analyzed in cytology samples; clinical and ultrasonographic nodule characteristics were assessed at the start and at the end of the study.

Results:
RET/PTC was present in 19 nodules. The difference between the mean baseline nodular volume of the RET/PTC− and RET/PTC+ nodules was not significant. After 36 months of follow-up, the RET/PTC+ group (n = 16) reached a volume higher than the RET/PTC− group (n = 90) (5.04 ± 2.67 vs. 3.04 ± 2.26 ml; P = 0.0028). We calculated the monthly change of nodule volumes as a percentage of baseline. After a mean follow-up of 36.6 months, the monthly volume increase of nodules bearing a RET rearrangement was 4.3-fold that of nodules with wild-type RET (1.83 ± 1.2 vs. 0.43 ± 1.0% of baseline volume; P &lt; 0.0001).

Conclusions:
Benign thyroid nodules bearing RET rearrangements grow more rapidly than those with wild-type RET. Searching for RET rearrangements in benign thyroid nodules might be useful to the clinician in choosing the more appropriate and timely therapeutic option.
Effect of Exenatide on Splanchnic and Peripheral Glucose Metabolism in Type 2 Diabetic Subjects
Authors: Cersosimo E. , Gastaldelli A. , Cervera A. , Wajcberg E. , Sriwijilkamol A. , Fernandez M. , Zuo P. , Petz R. , Triplitt C. , Musi N. , DeFronzo R. A. 
Published: March 2011

Objective:
Our objective was to examine the mechanisms via which exenatide attenuates postprandial hyperglycemia in type 2 diabetes mellitus (T2DM).

Study Design:
Seventeen T2DM patients (44 yr; seven females, 10 males; body mass index = 33.6 kg/m2; glycosylated hemoglobin = 7.9%) received a mixed meal followed for 6 h with double-tracer technique ([1-14C]glucose orally; [3-3H]glucose iv) before and after 2 wk of exenatide. In protocol II (n = 5), but not in protocol I (n = 12), exenatide was given in the morning of the repeat meal. Total and oral glucose appearance rates (RaT and RaO, respectively), endogenous glucose production (EGP), splanchnic glucose uptake (75 g − RaO), and hepatic insulin resistance (basal EGP × fasting plasma insulin) were determined.

Results:
After 2 wk of exenatide (protocol I), fasting plasma glucose decreased (from 10.2 to 7.6 mm) and mean postmeal plasma glucose decreased (from 13.2 to 11.3 mm) (P &lt; 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.9 to 10.8 μmol/kg · min, P &lt; 0.05), and hepatic insulin resistance declined (both P &lt; 0.05). RaO, gastric emptying (acetaminophen area under the curve), and splanchnic glucose uptake did not change. In protocol II (exenatide given before repeat meal), fasting plasma glucose decreased (from 11.1 to 8.9 mm) and mean postmeal plasma glucose decreased (from 14.2 to 10.1 mm) (P &lt; 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.4 to 10.7 μmol/kg · min, P = 0.05). RaT and RaO decreased markedly from 0–180 min after meal ingestion, consistent with exenatide's action to delay gastric emptying.

Conclusions:
Exenatide improves 1) fasting hyperglycemia by reducing basal EGP and 2) postmeal hyperglycemia by reducing the appearance of oral glucose in the systemic circulation.
Fetal Thyroid Hormone Level at Birth Is Associated with Fetal Growth
Authors: Shields Beverley M. , Knight Beatrice A. , Hill Anita , Hattersley Andrew T. , Vaidya Bijay 
Published: March 2011

Context:
Thyroid function is known to play an important role in fetal neurological development, but its role in regulating fetal growth is not well established. Overt maternal and fetal thyroid disorders are associated with reduced birth weight. We hypothesized that, even in the absence of overt thyroid dysfunction, maternal and fetal thyroid function influence fetal growth.

Aim:
In normal, healthy pregnancies, we aimed to assess whether fetal thyroid hormone at birth (as measured in cord blood) is associated with fetal growth. We also aimed to study whether fetal thyroid hormone at birth is associated with maternal thyroid hormone in the third trimester.

Methods:
In 616 healthy mother-child pairs, TSH, free T4 (FT4), and free T3 (FT3) were measured in mothers at 28 wk gestation and in umbilical cord blood at birth. Birth weight, length, head circumference, and tricep and bicep skinfold thicknesses were measured on the babies.

Results:
Cord FT4 was associated with birth weight (r = 0.25; P &lt; 0.001), length (r = 0.17; P &lt; 0.001), and sum of skinfolds (r = 0.19; P &lt; 0.001). There were no associations between birth measurements and either cord TSH or cord FT3. Maternal FT4 and cord FT4 were correlated (r = 0.14; P = 0.0004), and there were weaker negative associations between maternal TSH and cord FT4 (r = −0.08; P = 0.04) and FT3 (r = −0.10; P = 0.01).

Conclusion:
Associations between cord FT4 and birth size suggest that fetal thyroid function may be important in regulating fetal growth, both of skeletal size and fat. The correlation between third-trimester maternal FT4 and cord FT4 supports the belief that maternal T4 crosses the placenta even in late gestation.
Investigation on the Effects of Depth-to-Span Ratio of Tensegrity Flat Grids on Their Seismic Behavior
Authors: Valipour Masoud , Sadeghi Arjang 
Published: March 2011

Tensegrity state is a stable self-equilibrated state of a spatial system that contains a non-continuous set of compressive elements (struts) inside a continuous set of self-tensioned elements (cables). At the present study, the seismic behavior of double layer flat tensegrity grids consisted of quadrangular tensegrity prisms, have been investigated by carrying out nonlinear full transient time-history dynamic analysis. In order to determine the effects of depth-to-span ratio on seismic behavior of flat tensegrity grids, several non-linear time history analyses have been performed by ANSYS finite element program. Three 1/10, 1/12 & 1/15 grid depth-to-span ratios have been considered for investigation. Then the effects of depth-to-span ratio on seismic behavior of tensegrity flat grids have been determined. It is shown that these systems are sensitive and vulnerable against seismic excitations. Based on the obtained results, some design recommendations have been presented regarding to the seismic behavior of these systems.
Parametric Structural Design and beyond
Authors: Rolvink Anke , van de Straat Roel , Coenders Jeroen 
Published: March 2011

In order to directly make insightful which implications follow from structural design changes and to be able to adapt a structural design quickly to geometrical design changes made by the architect, the structural engineer may embed a parametric and associative design approach in the structural design process. This approach focuses on parametric modelling and the development of parametric tools which serve specific needs in the structural design process, allowing designers for instance to quickly communicate and discuss alternatives or to inform design team members of structural results of changing design parameters. The paper presents multiple projects within these categories of parametric approaches. They are concentrated on design and analysis with the goal of presenting practical examples of these approaches in structural design which were integrated in the full design process in order to benefit from the qualities of a multi-disciplinary parametric and associative design process.