bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of the dynamics of social queues by quasi-birth-and-death processes (abstract only)
Authors: Toyoizumi Hiroshi , Field Jeremy 
Published: April 2012

A wide variety of animals are known to form simple hierarchical groups called social queues, where individuals inherit resources or social status in a predictable order. Queues are often age-based, so that a new individual joins the end of the queue on reaching adulthood, and must wait for older individuals to die in order to reach the front of the queue. While waiting, an individual may work for her group, in the process often risking her own survival and hence her chance of inheritance. Eventually, she may survive to reach the head of the queue and becomes the dominant of the group.
Queueing has been particularly well-studied in hover wasps (Hymenoptera: Stenogastrinae). In hover wasp social groups, only one female lays eggs, and there is a strict, age-based queue to inherit the reproductive position. While the dominant individual (queen) concentrates on breeding, subordinate helpers risk death by foraging outside the nest, but have a slim chance of eventually inheriting dominance. Some explanations for this altruistic behavior and for the stability of social queues have been proposed and analyzed [1, 2]. Since both the productivity of the nest and the chance to inherit the dominant position depend critically on group size, queueing dynamics are crucial for understanding social queues, but detailed analysis is lacking.

Here, using hover wasps as an example, we demonstrate that the application of Little's formula [3] and quasi-birth-and-death (QBD) processes are useful for analyzing queueing dynamics and the population demographics of social queues. Let (L(t),M(t)) be the number of adults and brood (eggs, larvae and pupae) in a nest at time t. We model the vector (L(t),M(t)) as a QBD process starting from the state (L(0),M(0)) = (1, 0) to analyze the nest history of a social queue. The boundary state {L(t) = 0}, which corresponds to the termination of the nest, is regarded as the taboo state of this QBD process. Let
Q
be the transition rate matrix of the taboo process. By choosing different
Q
, we can set various conditions for the social queue. By using standard technique such as calculating
Q
?1, we can estimate and compare the productivity of the nest in wide variety of social queues in different queueing and environmental conditions.

Our work leads to better understanding of how environmental conditions and strategic decision-making by individuals interact to produce the observed group dynamics; and in turn, how group dynamics affects individual decision-making.
Proteasome Inhibition Blocks NF-κB and ERK1/2 Pathways, Restores Antigen Expression, and Sensitizes Resistant Human Melanoma to TCR-Engineered CTLs
Authors: Jazirehi Ali R. , Economou James S. 
Published: April 2012

AbstractAdoptive cell transfer (ACT) of ex vivo engineered autologous lymphocytes encoding high-affinity MART-1/HLA-A*0201–specific T-cell receptor (TCR)α/β chains (F5 CTL), densely infiltrate into sites of metastatic disease, mediating dramatic but partial clinical responses in patients with melanoma. We hypothesized that MART-1 downmodulation in addition to aberrant apoptotic/survival signaling could confer resistance to death signals delivered by transgenic CTLs. To explore this hypothesis, we established an in vitro model of resistant (R) lines from MART-1+/HLA-A*0201+ F5 CTL–sensitive parental (P) lines under serial F5 CTL–selective pressure. We have recently reported that several melanoma R lines, while retaining MART-1 expression, exhibited constitutive NF-κB activation and overexpression of NF-κB–dependent resistance factors. Another established melanoma cell line M244, otherwise sensitive to F5 CTL, yielded R lines after serial F5 CTL–selective pressure, which had both reduced MART-1 expression levels, thus, could not be recognized, and were resistant to CTL-delivered apoptotic death signals. The proteasome inhibitor bortezomib blocked NF-κB activity, decreased phospho-ERK1/2, increased phospho-c-jun–NH2–kinase (p-JNK) levels, reduced expression of resistance factors, restored MART-1 expression to sufficient levels, which in combination allowed M244R lines be sensitized to F5 CTL killing. These findings suggest that proteasome inhibition in immune resistant tumors can restore proapoptotic signaling and improve tumor antigen expression. Mol Cancer Ther; 11(6); 1332–41. ©2012 AACR.
Inter-rater reliability of the Nottingham Neurological Driving Assessment for people with dementia – a preliminary evaluation
Authors: Lincoln NB , Taylor J , Radford KA 
Published: April 2012

Objective: The purpose was to examine the inter-rater reliability of the Nottingham Neurological Driving Assessment. Participants: Six drivers with dementia (mean age 78 years, 5 men). Interventions: Participants were assessed for their safety to drive on a set route while being observed by two driving assessors, who were experienced in assessing safety to drive in people with dementia. Main measures: Performance was rated in terms of overall safety to drive and 25 items were recorded as correct, minor error (not compromising safety) and major error (compromising safety). Results: Four drivers were found to be probably safe to drive and two definitely unsafe to drive. There was perfect agreement in the overall decisions about safety to drive. There were significant discrepancies between correct or minor error and major error on six of the 25 items of the road test involving three participants. Conclusions: Two experienced driving assessors agreed on the overall safety to drive of six participants with dementia. There were discrepancies about safety on six out of 150 observations (4%).
Synthesis and characterization of ZnS:Mn/ZnS core/shell nanoparticles for tumor targeting and imaging in vivo
Authors: Yu Zhangsen , Ma Xiying , Yu Bin , Pan Yuefang , Liu Zhaogang 
Published: April 2012

Fluorescence imaging technique has been used for imaging of biological cells and tissues in vivo. The Cd-free luminescent quantum dots conjugating with a cancer targeting ligand has been taken as a promising biocompatibility and low cytotoxicity system for targeted cancer imaging. This work reports the synthesis of fluorescent-doped core/shell quantum dots of water-soluble manganese-doped zinc sulfide. Quantum dots of manganese-doped zinc sulfide were prepared by nucleation doping strategy, with 3-mercaptopropionic acid as stabilizer at 90℃ in aqueous solution. The manganese-doped zinc sulfide nanoparticles exhibit strong orange fluorescence under UV irradiation, resistance to photo-bleaching, and low-cytotoxicity to HeLa cells. The structure and optical properties of nanoparticles were characterized by scanning electron microscope, X-ray diffraction, dynamic light scattering, and photoluminescence emission spectroscopy. Manganese-doped zinc sulfide nanoparticles conjugated with folic acid using 2,2′-(ethylenedioxy)-bis-(ethylamine) as the linker. The covalent binding of both 2,2′-(ethylenedioxy)-bis-(ethylamine) and folic acid on the surface of manganese-doped zinc sulfide nanoparticles probed by Fourier transform infrared spectroscopy detection. Furthermore, in vitro cytotoxicity assessment of manganese-doped zinc sulfide–folic acid probes use HeLa cells. The obtained fluorescent probes (manganese-doped zinc sulfide) were used for tumor targeting and imaging in vivo. The manganese-doped zinc sulfide–folic acid fluorescent probes which targeting the tumor cells in the body of nude mouse tumor model would emit orange fluorescence, when exposed to a 365 nm lamp. We investigate the biodistribution of the manganese-doped zinc sulfide–folic acid fluorescent probes in tumor mouse model by measuring zinc concentration in tissues. These studies demonstrate the practicality of manganese-doped zinc sulfide–folic acid fluorescent probes as promising platform for tumor targeting and imaging in vivo.
Genome-wide host responses against infectious laryngotracheitis virus vaccine infection in chicken embryo lung cells
Authors: Lee Jeongyoon , Bottje Walter G , Kong Byung-Whi 
Published: April 2012

Abstract

Background
Infectious laryngotracheitis virus (ILTV; gallid herpesvirus 1) infection causes high mortality and huge economic losses in the poultry industry. To protect chickens against ILTV infection, chicken-embryo origin (CEO) and tissue-culture origin (TCO) vaccines have been used. However, the transmission of vaccine ILTV from vaccinated- to unvaccinated chickens can cause severe respiratory disease. Previously, host cell responses against virulent ILTV infections were determined by microarray analysis. In this study, a microarray analysis was performed to understand host-vaccine ILTV interactions at the host gene transcription level.

Results
The 44 K chicken oligo microarrays were used, and the results were compared to those found in virulent ILTV infection. Total RNAs extracted from vaccine ILTV infected chicken embryo lung cells at 1, 2, 3 and 4 days post infection (dpi), compared to 0 dpi, were subjected to microarray assay using the two color hybridization method. Data analysis using JMP Genomics 5.0 and the Ingenuity Pathway Analysis (IPA) program showed that 213 differentially expressed genes could be grouped into a number of functional categories including tissue development, cellular growth and proliferation, cellular movement, and inflammatory responses. Moreover, 10 possible gene networks were created by the IPA program to show intermolecular connections. Interestingly, of 213 differentially expressed genes, BMP2, C8orf79, F10, and NPY were expressed distinctly in vaccine ILTV infection when compared to virulent ILTV infection.

Conclusions
Comprehensive knowledge of gene expression and biological functionalities of host factors during vaccine ILTV infection can provide insight into host cellular defense mechanisms compared to those of virulent ILTV.
Identification and expression analysis of methyl jasmonate responsive ESTs in paclitaxel producing Taxus cuspidata suspension culture cells
Authors: Lenka Sangram K , Boutaoui Nadia , Paulose Bibin , Vongpaseuth Kham , Normanly Jennifer , Roberts Susan C , Walker Elsbeth L 
Published: April 2012

Abstract

Background
Taxol® (paclitaxel) promotes microtubule assembly and stabilization and therefore is a potent chemotherapeutic agent against wide range of cancers. Methyl jasmonate (MJ) elicited Taxus cell cultures provide a sustainable option to meet the growing market demand for paclitaxel. Despite its increasing pharmaceutical importance, the molecular genetics of paclitaxel biosynthesis is not fully elucidated. This study focuses on identification of MJ responsive transcripts in cultured Taxus cells using PCR-based suppression subtractive hybridization (SSH) to identify genes involved in global pathway control.

Results
Six separate SSH cDNA libraries of paclitaxel-accumulating Taxus cuspidata P991 cell lines were constructed at three different post-elicitation time points (6h, 18h and 5 day) to identify genes that are either induced or suppressed in response to MJ. Sequencing of 576 differentially screened clones from the SSH libraries resulted in 331 unigenes. Functional annotation and Gene Ontology (GO) analysis of up-regulated EST libraries showed enrichment of several known paclitaxel biosynthetic genes and novel transcripts that may be involved in MJ-signaling, taxane transport, or taxane degradation. Macroarray analysis of these identified genes unravelled global regulatory expression of these transcripts. Semi-quantitative RT-PCR analysis of a set of 12 candidate genes further confirmed the MJ-induced gene expression in a high paclitaxel accumulating Taxus cuspidata P93AF cell line.

Conclusions
This study elucidates the global temporal expression kinetics of MJ responsive genes in Taxus suspension cell culture. Functional characterization of the novel genes identified in this study will further enhance the understanding of paclitaxel biosynthesis, taxane transport and degradation.
Lidocaine Patch (5%) is No More Potent than Placebo in Treating Chronic Back Pain When Tested in a Randomised Double Blind Placebo Controlled Brain Imaging Study
Authors: Hashmi Javeria A , Baliki Marwan N , Huang Lejian , Parks Elle L , Chanda Mona L , Schnitzer Thomas , Apkarian A Vania 
Published: April 2012

Background: The 5% Lidocaine patch is used for treating chronic neuropathic pain conditions such as chronic back pain (CBP), diabetic neuropathy and complex regional pain syndrome, but is effective in a variable proportion of patients. Our lab has reported that this treatment reduces CBP intensity and associated brain activations when tested in an open labelled preliminary study. Notably, effectiveness of the 5% Lidocaine patch has not been tested against placebo for treating CBP. In this study, effectiveness of the 5% Lidocaine patch was compared with placebo in 30 CBP patients in a randomised double-blind study where 15 patients received 5% Lidocaine patches and the remaining patients received placebo patches. Functional MRI was used to identify brain activity for fluctuations of spontaneous pain, at baseline and at two time points after start of treatment (6 hours and 2 weeks). Results: There was no significant difference between the treatment groups in either pain intensity, sensory and affective qualities of pain or in pain related brain activation at any time point. However, 50% patients in both the Lidocaine and placebo arms reported a greater than 50% decrease in pain suggesting a marked placebo effect. When tested against an untreated CBP group at similar time points, the patch treated subjects showed significantly greater decrease in pain compared to the untreated group (n = 15). Conclusions: These findings suggest that although the 5% Lidocaine is not better than placebo in its effectiveness for treating pain, the patch itself induces a potent placebo effect in a significant proportion of CBP patients.
The Emergence of Adolescent Onset Pain Hypersensitivity following Neonatal Nerve Injury
Authors: Vega-Avelaira David , McKelvey Rebecca , Hathway Gareth , Fitzgerald Maria 
Published: April 2012

Background: Peripheral nerve injuries can trigger neuropathic pain in adults but cause little or no pain when they are sustained in infancy or early childhood. This is confirmed in rodent models where neonatal nerve injury causes no pain behaviour. However, delayed pain can arise in man some considerable time after nerve damage and to examine this following early life nerve injury we have carried out a longer term follow up of rat pain behaviour into adolescence and adulthood. Results: Spared nerve injury (SNI) or sham surgery was performed on 10 day old (P10) rat pups and mechanical nociceptive reflex thresholds were analysed 3, 7, 14, 21, 28, 38 and 44 days post surgery. While mechanical thresholds on the ipsilateral side are not significantly different from controls for the first 2–3 weeks post P10 surgery, after that time period, beginning at 21 days post surgery (P31), the SNI group developed following early life nerve injury significant hypersensitivity compared to the other groups. Ipsilateral mechanical nociceptive threshold was 2-fold below that of the contralateral and sham thresholds at 21 days post surgery (SNI-ipsilateral 28 (±5) g control groups 69 (±9) g, p<0.001, 3-way ANOVA, n = 6 per group). Importantly, no effect was observed on thermal thresholds. This hypersensivity was accompanied by macrophage, microglial and astrocyte activation in the DRG and dorsal horn, but no significant change in dorsal horn p38 or JNK expression. Preemptive minocycline (daily 40 mg/kg, s.c) did not prevent the effect. Ketamine (20 mg/kg, s.c), on the other hand, produced a dose-dependent reversal of mechanical nociceptive thresholds ipsilateral to the nerve injury such that thresholds return to control levels at the highest doses of 20 mg/Kg. Conclusions: We report a novel consequence of early life nerve injury whereby mechanical hypersensitivity only emerges later in life. This delayed adolescent onset in mechanical pain thresholds is accompanied by neuroimmune activation and NMDA dependent central sensitization of spinal nociceptive circuits. This delayed onset in mechanical pain sensitivity may provide clues to understand the long term effects of early injury such as late onset phantom pain and the emergence of complex adolescent chronic pain syndromes.
A multicenter study confirms CD226gene association with systemic sclerosis-related pulmonary fibrosis
Authors: Bossini-Castillo Lara , Simeon Carmen P , Beretta Lorenzo , Broen Jasper C , Vonk Madelon C , Ríos-Fernández Raquel , Espinosa Gerard , Carreira Patricia , Camps María T , Castillo Maria J , González-Gay Miguel A , Beltrán Emma , Carmen Freire María del , Narváez Javier , Tolosa Carlos , Witte Torsten , Kreuter Alexander , Schuerwegh Annemie J , Hoffmann-Vold Anna-Maria , Hesselstrand Roger , Lunardi Claudio , van Laar Jacob M , Chee Meng May , Herrick Ariane , Koeleman Bobby PC , Denton Christopher P , Fonseca Carmen , Radstake Timothy RDJ , Martin Javier ,   the Spanish Scleroderma Group
Published: April 2012

Abstract

Introduction

CD226 genetic variants have been associated with a number of autoimmune diseases and recently with systemic sclerosis (SSc). The aim of this study was to test the influence of CD226 loci in SSc susceptibility, clinical phenotypes and autoantibody status in a large multicenter European population.

Methods

A total of seven European populations of Caucasian ancestry were included, comprising 2,131 patients with SSc and 3,966 healthy controls. Three CD226 single nucleotide polymorphisms (SNPs), rs763361, rs3479968 and rs727088, were genotyped using Taqman 5'allelic discrimination assays.

Results

Pooled analyses showed no evidence of association of the three SNPs, neither with the global disease nor with the analyzed subphenotypes. However, haplotype block analysis revealed a significant association for the TCG haplotype (SNP order: rs763361, rs34794968, rs727088) with lung fibrosis positive patients (PBonf = 3.18E-02 OR 1.27 (1.05 to 1.54)).

Conclusion

Our data suggest that the tested genetic variants do not individually influence SSc susceptibility but a CD226 three-variant haplotype is related with genetic predisposition to SSc-related pulmonary fibrosis.
Early vascular deficits are correlated with delayed mammary tumorigenesis in the MMTV-PyMT transgenic mouse following genetic ablation of the NG2 proteoglycan
Authors: Gibby Krissa , You Weon-Kyoo , Kadoya Kuniko , Helgadottir Hildur , Young Lawrence JT , Ellies Lesley G , Chang Yunchao , Cardiff Robert D , Stallcup William B 
Published: April 2012

Abstract
Introduction
The neuron-glial antigen 2 (NG2) proteoglycan promotes pericyte recruitment and mediates pericyte interaction with endothelial cells. In the absence of NG2, blood vessel development is negatively impacted in several pathological models. Our goal in this study was to determine the effect of NG2 ablation on the early development and function of blood vessels in mammary tumors in the mammary tumor virus-driven polyoma middle T (MMTV-PyMT) transgenic mouse, and to correlate these vascular changes with alterations in mammary tumor growth.

Methods
Three different tumor paradigms (spontaneous tumors, transplanted tumors, and orthotopic allografts of tumor cell lines) were used to investigate the effects of NG2 ablation on breast cancer progression in the MMTV-PyMT transgenic mouse. In addition to examining effects of NG2 ablation on mammary tumor growth, we also investigated effects on the structure and function of tumor vasculature.

Results
Ablation of NG2 led to reduced early progression of spontaneous, transplanted, and orthotopic allograft mammary tumors. NG2 was not expressed by the mammary tumor cells themselves, but instead was found on three components of the tumor stroma. Microvascular pericytes, myeloid cells, and adipocytes were NG2-positive in both mouse and human mammary tumor stroma. The effect of NG2 on tumor progression therefore must be stromal in nature. Ablation of NG2 had several negative effects on early development of the mammary tumor vasculature. In the absence of NG2, pericyte ensheathment of endothelial cells was reduced, along with reduced pericyte maturation, reduced sprouting of endothelial cells, reduced assembly of the vascular basal lamina, and reduced tumor vessel diameter. These early deficits in vessel structure are accompanied by increased vessel leakiness, increased tumor hypoxia, and decreased tumor growth. NG2 ablation also diminishes the number of tumor-associated and TEK tyrosine kinase endothelial (Tie2) expressing macrophages in mammary tumors, providing another possible mechanism for reducing tumor vascularization and growth.

Conclusions
These results emphasize the importance of NG2 in mediating pericyte/endothelial cell communication that is required for proper vessel maturation and function. In the absence of normal pericyte/endothelial cell interaction, poor vascular function results in diminished early progression of mammary tumors.
Induction Chemotherapy and Dose Intensification of the Radiation Boost in Locally Advanced Anal Canal Carcinoma: Final Analysis of the Randomized UNICANCER ACCORD 03 Trial
Authors: Peiffert Didier , Tournier-Rangeard Laetitia , Gérard Jean-Pierre , Lemanski Claire , François Eric , Giovannini Marc , Cvitkovic Frédérique , Mirabel Xavier , Bouché Olivier , Luporsi Elisabeth , Conroy Thierry , Montoto-Grillot Christine , Mornex Françoise , Lusinchi Antoine , Hannoun-Lévi Jean-Michel , Seitz Jean-François , Adenis Antoine , Hennequin Christophe , Denis Bernard , Ducreux Michel 
Published: April 2012

Purpose Concomitant radiochemotherapy (RCT) is the standard for locally advanced anal canal carcinoma (LAACC). Questions regarding the role of induction chemotherapy (ICT) and a higher radiation dose in LAACC are pending. Our trial was designed to determine whether dose escalation of the radiation boost or two cycles of ICT before concomitant RCT lead to an improvement in colostomy-free survival (CFS). Patients and Methods Patients with tumors ≥ 40 mm, or < 40 mm and N1-3M0 were randomly assigned to one of four treatment arms: (A) two ICT cycles (fluorouracil 800 mg/m2/d intravenous [IV] infusion, days 1 through 4 and 29 to 32; and cisplatin 80 mg/m2 IV, on days 1 and 29), RCT (45 Gy in 25 fractions over 5 weeks, fluorouracil and cisplatin during weeks 1 and 5), and standard-dose boost (SD; 15 Gy); (B) two ICT cycles, RCT, and high-dose boost (HD; 20-25 Gy); (C): RCT and SD boost (reference arm); and (D) RCT and HD boost. Results Two hundred eighty-three of 307 patients achieved full treatment. With a median follow-up period of 50 months, the 5-year CFS rates were 69.6%, 82.4%, 77.1%, and 72.7% in arms A, B, C, and D, respectively. Considering the 2 × 2 factorial analysis, the 5-year CFS was 76.5% versus 75.0% (P = .37) in groups A and B versus C and D, respectively (ICT effect), and 73.7% versus 77.8% in groups A and C versus B and D, respectively (RT-dose effect; P = .067). Conclusion Using CFS as our main end point, we did not find an advantage for either ICT or HD radiation boost in LAACC. Nevertheless, the results of the most treatment-intense arm B should prompt the design of further intensification studies.