Miracle-dz/UniFAR-FTUs huggingface dataset:
New generation cardiac troponin I assay for the access immunoassay system.

The measurement of troponins in blood has rapidly become an alternative to conventional methods of detecting myocardial damage (1)(2)(3)(4)(5)(6)(7)(8), particularly in unstable angina, and several studies have indicated the prognostic importance of increased troponins in various clinical settings (9)(10)(11)(12)(13)(14). These studies, however, have also pointed out the need for more sensitive methods because patients with even small increases of troponin seem to be at increased risk of cardiac events. Currently, cardiac troponin I (cTnI) can be quantified by assays from several manufacturers (15)(16)(17)(18)(19), whereas only one company currently commercializes a cardiac troponin T assay (2)(20)(21). The aim of this work was to evaluate the analytical performance of a new generation of the Access cTnI assay. We also provide data on values in apparently healthy subjects. Venous blood was drawn from 70 patients admitted to our Coronary Care Unit because of suspicion of an acute coronary syndrome. Only patients found to have increased myocardial markers such as creatine kinase-MB and troponin I were included. The study was approved by the ethics committee of the Medical Faculty of Uppsala University. Serum samples were also obtained from 122 apparently healthy subjects (70 women and 52 men; median age, 41 years; range, 26–73 years) as part of a health-screening program. The new ACCESS cTnI assay (Beckman Coulter, Inc., Chaska, MN) is a two-site immunoenzymatic (sandwich) immunoassay. Paramagnetic particles coated with mouse monoclonal anti-cTnI, mouse monoclonal anti-cTnI-alkaline phosphatase conjugate, and sample are added to a reaction vessel to form a particle-cTnI-conjugate sandwich. The …
Lymphoblastic Lymphoma in Childhood and Adolescence

Lymphoblastic lymphoma (LBL) are thought to derive from immature precursor T-cells or B-cells. LBL are the second most common subtype of Non-Hodgkin Lymphoma (NHL) in children and adolescents. LBL are closely related to acute lymphoblastic leukemia (ALL), the most common type of cancer in children. Using ALL-type treatment regimen to treat children with LBL was an important development in the treatment of LBL. During the last decades, several systematic clinical trials contributed to the controlled optimization of treatment. Today event-free survival (EFS) can be achieved for 75–90% of patients. However, acute and long-term toxicity, the lack of prognostic parameters and the poor outcome for patients who suffer from refractory or relapsed LBL remain highly relevant subjects for improvement. To date, the pathogenesis of LBL is poorly understood. Learning more about the biology and pathogenesis of LBL might pave the way for targeted treatment to improve survival especially in relapsed and refractory patients.
Local Softening of Information Geometric Indicators of Chaos in Statistical Modeling in the Presence of Quantum-Like Considerations

In a previous paper (C. Cafaro et al., 2012), we compared an uncorrelated 3D Gaussian statistical model to an uncorrelated 2D Gaussian statistical model obtained from the former model by introducing a constraint that resembles the quantum mechanical canonical minimum uncertainty relation. Analysis was completed by way of the information geometry and the entropic dynamics of each system. This analysis revealed that the chaoticity of the 2D Gaussian statistical model, quantified by means of the Information Geometric Entropy (IGE), is softened or weakened with respect to the chaoticity of the 3D Gaussian statistical model, due to the accessibility of more information. In this companion work, we further constrain the system in the context of a correlation constraint among the system’s micro-variables and show that the chaoticity is further weakened, but only locally. Finally, the physicality of the constraints is briefly discussed, particularly in the context of quantum entanglement.
Effects of river damming on ground‐dwelling arthropods along riparian–upland habitats

River damming is one of the most serious anthropogenic disturbances impacting river ecosystems. Little is known about the consequences of river damming on ground‐dwelling arthropods, although they represent a functionally important component of riverine ecosystems because they provide an essential link between aquatic and terrestrial ecosystems. We investigated the effects of river damming on the composition and structure of arthropod communities in the Baijia Stream located in the centre of the Three Gorges Reservoir. Our results revealed that (a) river damming modified the community composition of riparian arthropods, as 24 taxa disappeared and 11 taxa colonized the new habitat after damming; (b) river damming altered the community structure of arthropods because higher richness and abundance of arthropods were recorded in the regulated section, especially for predators, detritivores, and herbivores; and (c) river damming altered the lateral distribution along riparian–upland gradients and the temporal dynamics of arthropod communities. Interestingly, upland habitats of streams supported more species than the riparian habitat in the regulated section, suggesting that uplands may become an important habitat for riparian species after river damming. Although higher total abundance and richness and higher abundance of some feeding guilds of arthropods were observed in the regulated section, the negative effects of river damming on biodiversity are addressed in this paper. Thus, ground‐dwelling arthropods appear to be sensitive indicators of the ecological effects of river damming. Assessment of the consequences of river damming and dam management plans should consider ground‐dwelling arthropod communities in associated riparian and upland habitats.
Integrative Genomic Analysis of Small-Cell Lung Carcinoma Reveals Correlates of Sensitivity to Bcl-2 Antagonists and Uncovers Novel Chromosomal Gains

Cancer is a highly heterogeneous disease in terms of the genetic profile and the response to therapeutics. An early identification of a genomic marker in drug discovery may help select patients that would respond to treatment in clinical trials. Here we suggest coupling compound screening with comparative genomic hybridization analysis of the model systems for early discovery of genomic biomarkers. A Bcl-2 antagonist, ABT-737, has recently been discovered and shown to induce regression of solid tumors, but its activity is limited to a fraction of small-cell lung carcinoma (SCLC) models tested. We used comparative genomic hybridization on high-density single-nucleotide polymorphism genotyping arrays to carry out a genome-wide analysis of 23 SCLC cell lines sensitive and resistant to ABT-737. The screen revealed a number of novel recurrent gene copy number abnormalities, which were also found in an independent data set of 19 SCLC tumors and confirmed by real-time quantitative PCR. A previously unknown amplification was identified on 18q and associated with the sensitivity of SCLC cell lines to ABT-737 and another Bcl-2 antagonist. The region of gain contains Bcl-2 and NOXA, two apoptosis-related genes. Expression microarray profiling showed that the genes residing in the amplified region of 18q are also overexpressed in the sensitive lines relative to the resistant lines. Fluorescence in situ hybridization analysis of tumors revealed that Bcl-2 gain is a frequent event in SCLC. Our findings suggest that 18q21-23 copy number will be a clinically relevant predictor for sensitivity of SCLC to Bcl-2 family inhibitors. The 18q21-23 genomic marker may have a broader application in cancer because Bcl-2 is associated with apoptosis evasion and chemoresistance. (Mol Cancer Res 2007;5(4):331–39)
The Role of Thrombelastography in Multiple Trauma

Hemorrhage and traumatic coagulopathyis are major causes of early death in multiply injured patients. Thrombelastography (TEG) seems to be a fast and accurate coagulation test in trauma care. We suggest that multiply injured trauma patients would benefit the most from an early assessment of coagulation by TEG, mainly RapidTEG, to detect an acute traumatic coagulopathy and especially primary fibrinolysis, which is related with high mortality. This review gives an overview on TEG and its clinical applications.
Interrelated two-way clustering: an unsupervised approach for gene expression data analysis

DNA arrays can be used to measure the expression levels of thousands of genes simultaneously. Most research is focusing on interpretation of the meaning of the data. However, the majority of methods are supervised, with less attention having been paid to unsupervised approaches which are important when domain knowledge is incomplete or hard to obtain. In this paper we present a new framework for unsupervised analysis of gene expression data which applies an interrelated two-way clustering approach to the gene expression matrices. The goal of clustering is to find important gene patterns and perform cluster discovery on samples. The advantage of this approach is that we can dynamically use the relationships between the groups of genes and samples while iteratively clustering through both gene-dimension and sample-dimension. We illustrate the method on gene expression data from a study of multiple sclerosis patients. The experiments demonstrate the effectiveness of this approach.
Apoptosis in UV-exposed Rabbit Corneas

Purpose. Apoptosis was studied in rabbit corneas as a possible mechanism of cell death after photokeratitis induced by different UV wavelengths. Method. Fourteen albino rabbit corneas were exposed to 280-and 310-nm UV radiation (UVR) in 10-nm full wavebands at doses that cause biomicroscopically significant keratitis (0.12 J/cm2 for 280 nm and 0.47 J/cm2 for 310 nm). Animals were killed 24 and 76 h after exposure. Corneas were processed for light and transmission electron microscopy and in situ end labeling of fragmented DNA by using a modification of the TUNEL technique. Results. Corneas exposed to 280-nm UVR showed TUNEL-positive staining only in epithelial cells and superficial keratocytes at 24 and 76 h after irradiation. Twenty-four hours after 310-nm UVR exposure, TUNEL-positive staining was present in the epithelial cells, keratocytes throughout the entire thickness of the central stroma, and in endothelial cells. Seventy-six hours after exposure to 310-nm UVR, keratocytes disappeared throughout the whole thickness of the damaged stroma. Only a few epithelial cells were TUNEL positive at that time. Transmission electron microscopy (TEM) verified the occurrence of apoptotic nuclei and cells. Conclusion. Apoptosis appears to be a mechanism of corneal cell death after UVR. The 310-nm UVR caused more extensive damage to the corneal stroma and endothelium than did the 280-nm UVR.
Personal Use of Hair Dyes and Hematolymphopoietic Malignancies

In the context of a population-based case-control study in Italy, the authors investigated the possible association between the personal use of hair dyes and non-Hodgkin's lymphoma (NHL), leukemia, multiple myeloma, and Hodgkin's disease. They collected all incident cases of hematolymphopoietic malignancies; the control group was formed with a random sample of the general population. Overall, the authors interviewed 2,737 research subjects and 1,779 control subjects. Among women, the authors found no association between ever using hair dyes and the risk of hematolymphopoietic malignancies. However, for permanent hair dyes, the authors observed a slightly increased risk of lymphocytic leukemia (odds ratio [OR] = 1.3; 95% confidence interval [CI] = 0.8-2.2) and of follicular subtypes of NHL (OR = 1.3; 95% CI = 0.8-2.0). Women who used black hair dye colors were at an increased risk of developing leukemia (OR = 1.9; 95% CI = 1.0-3.4), in particular chronic lymphocytic leukemia (OR = 3.0; 95% CI = 1.1-7.5). In spite of the lack of information on the timing and frequency of hair dye use and the imprecision of the ORs, associations were suggested between leukemia and permanent black hair dye use and follicular NHL and the use of permanent hair dyes.
Flow and transport from a stream to a well in an unconfined aquifer

Flow, stream depletion rate (SDR), and transport are evaluated with three analytical models for wells installed in a semi-infinite, homogeneous, anisotropic, unconfined aquifer near a fully penetrating stream with a streambed with reduced conductivity. The first model, presented in Maroney and Rehmann (2017), involves re-evaluating the calculations of Huang et al. (2012) for the SDR of a radial collector well. The present solution for SDR has a single integral that requires numerical evaluation, while the previous model has five. Analytical results show that at steady state the flow through the streambed equals the pumping rate of the well. That is, the steady SDR is one, and it does not depend on streambed or aquifer properties or the well design. Before the SDR reaches steady state, streambed conductance, aquifer anisotropy, and the position of the well relative to the stream affect SDR much more than the orientation, length, and depth of the lateral well screens. The second model builds on the method developed for SDR for a radial collector well. It provides flow and SDR for a partially penetrating vertical well installed in a semiinfinite, homogeneous, unconfined aquifer adjacent to a stream with a reduced conductivity streambed. Like the model for SDR of a radial collector well, the SDR for this case has only one improper integral that must be evaluated numerically. Steady drawdown is symmetric across the horizontal plane at the center of the aquifer for a well centered in the aquifer. The supply of water from the stream decreases hydraulic gradients at the top and bottom of the aquifer. The model for a partially penetrating well provides quantitative guidance for practical applications. For example, for removing contaminants, a well with small degree of penetration should be placed near the level of the contamination, and for dewatering—which
Human scFvs That Counteract Bioactivities of Staphylococcus aureus TSST-1

Some Staphylococcus aureus isolates produced toxic shock syndrome toxin-1 (TSST-1) which is a pyrogenic toxin superantigen (PTSAg). The toxin activates a large fraction of peripheral blood T lymphocytes causing the cells to proliferate and release massive amounts of pro-inflammatory cytokines leading to a life-threatening multisystem disorder: toxic shock syndrome (TSS). PTSAg-mediated-T cell stimulation circumvents the conventional antigenic peptide presentation to T cell receptor (TCR) by the antigen-presenting cell (APC). Instead, intact PTSAg binds directly to MHC-II molecule outside peptide binding cleft and simultaneously cross-links TCR-Vβ region. Currently, there is neither specific TSS treatment nor drug that directly inactivates TSST-1. In this study, human single chain antibodies (HuscFvs) that bound to and neutralized bioactivities of the TSST-1 were generated using phage display technology. Three E. coli clones transfected with TSST-1-bound phages fished-out from the human scFv library using recombinant TSST-1 as bait expressed TSST-1-bound-HuscFvs that inhibited the TSST-1-mediated T cell activation and pro-inflammatory cytokine gene expressions and productions.Computerized simulation, verified by mutations of the residues of HuscFv complementarity determining regions (CDRs),predicted to involve in target binding indicated that the HuscFvs formed interface contact with the toxin residues important for immunopathogenesis. The HuscFvs have high potential for future therapeutic application.
The global burden of rheumatoid arthritis: estimates from the Global Burden of Disease 2010 study

Objectives To estimate the global burden of rheumatoid arthritis (RA), as part of the Global Burden of Disease 2010 study of 291 conditions and how the burden of RA compares with other conditions. Methods The optimum case definition of RA for the study was the American College of Rheumatology 1987 criteria. A series of systematic reviews were conducted to gather age-sex-specific epidemiological data for RA prevalence, incidence and mortality. Cause-specific mortality data were also included. Data were entered into DisMod-MR, a tool to pool available data, making use of study-level covariates to adjust for country, region and super-region random effects to estimate prevalence for every country and over time. The epidemiological data, in addition to disability weights, were used to calculate years of life lived with disability (YLDs). YLDs were added to the years of life lost due to premature mortality to estimate the overall burden (disability-adjusted life years (DALYs)) for RA for the years 1990, 2005 and 2010. Results The global prevalence of RA was 0.24% (95% CI 0.23% to 0.25%), with no discernible change from 1990 to 2010. DALYs increased from 3.3 million (M) (95% CI 2.6 M to 4.1 M) in 1990 to 4.8 M (95% CI 3.7 M to 6.1 M) in 2010. This increase was due to a growth in population and increase in aging. Globally, of the 291 conditions studied, RA was ranked as the 42nd highest contributor to global disability, just below malaria and just above iodine deficiency (measured in YLDs). Conclusions RA continues to cause modest global disability, with severe consequences in the individuals affected.
Transcriptional Dynamics of the Embryonic Stem Cell Switch

Recent ChIP experiments of human and mouse embryonic stem cells have elucidated the architecture of the transcriptional regulatory circuitry responsible for cell determination, which involves the transcription factors OCT4, SOX2, and NANOG. In addition to regulating each other through feedback loops, these genes also regulate downstream target genes involved in the maintenance and differentiation of embryonic stem cells. A search for the OCT4–SOX2–NANOG network motif in other species reveals that it is unique to mammals. With a kinetic modeling approach, we ascribe function to the observed OCT4–SOX2–NANOG network by making plausible assumptions about the interactions between the transcription factors at the gene promoter binding sites and RNA polymerase (RNAP), at each of the three genes as well as at the target genes. We identify a bistable switch in the network, which arises due to several positive feedback loops, and is switched on/off by input environmental signals. The switch stabilizes the expression levels of the three genes, and through their regulatory roles on the downstream target genes, leads to a binary decision: when OCT4, SOX2, and NANOG are expressed and the switch is on, the self-renewal genes are on and the differentiation genes are off. The opposite holds when the switch is off. The model is extremely robust to parameter changes. In addition to providing a self-consistent picture of the transcriptional circuit, the model generates several predictions. Increasing the binding strength of NANOG to OCT4 and SOX2, or increasing its basal transcriptional rate, leads to an irreversible bistable switch: the switch remains on even when the activating signal is removed. Hence, the stem cell can be manipulated to be self-renewing without the requirement of input signals. We also suggest tests that could discriminate between a variety of feedforward regulation architectures of the target genes by OCT4, SOX2, and NANOG.
Task-priority formulations for the kinematic control of highly redundant articulated structures

We compare two formulations for the kinematic control of redundant manipulators, based on task prioritization. We also propose an incremental method to speed up the evaluation of the solution. This is especially interesting when dealing with multiple task-priority levels and with highly redundant structures. Finally, the effectiveness of the approach in the context of posture control of human-like articulated figures is illustrated.
A new role of the Rac-GAP β2-chimaerin in cell adhesion reveals opposite functions in breast cancer initiation and tumor progression

β2-chimaerin is a Rac1-specific negative regulator and a candidate tumor suppressor in breast cancer but its precise function in mammary tumorigenesis in vivo is unknown. Here, we study for the first time the role of β2-chimaerin in breast cancer using a mouse model and describe an unforeseen role for this protein in epithelial cell-cell adhesion. We demonstrate that expression of β2-chimaerin in breast cancer epithelial cells reduces E-cadherin protein levels, thus loosening cell-cell contacts. In vivo, genetic ablation of β2-chimaerin in the MMTV-Neu/ErbB2 mice accelerates tumor onset, but delays tumor progression. Finally, analysis of clinical databases revealed an inverse correlation between β2-chimaerin and E-cadherin gene expressions in Her2+ breast tumors. Furthermore, breast cancer patients with low β2-chimaerin expression have reduced relapse free survival but develop metastasis at similar times. Overall, our data redefine the role of β2-chimaerin as tumor suppressor and provide the first in vivo evidence of a dual function in breast cancer, suppressing tumor initiation but favoring tumor progression.
Natural selection, plasticity and the emergence of a behavioural syndrome in the wild.

Individuals often show consistent behavioural differences where behaviours can form integrated units across functionally different contexts. However, the factors causing and maintaining behavioural syndromes in natural populations remain poorly understood. In this study, we provide evidence for the emergence of a behavioural syndrome during the first months of life in wild brown trout (Salmo trutta). Behavioural traits of trout were scored before and after a 2-month interval covering a major survival bottleneck, whereupon the consistency and covariance of behaviours were analysed. We found that selection favoured individuals with high activity levels in an open-field context, a personality trait consistent throughout the duration of the experiment. In addition, a behavioural syndrome emerged over the 2 months in the wild, linking activity to aggressiveness and exploration tendency. These novel results suggest that behavioural syndromes can emerge rapidly in nature from interaction between natural selection and behavioural plasticity affecting single behaviours.
A Prospective, Randomized, Controlled Trial of Preoperative Transarterial Chemoembolization for Resectable Large Hepatocellular Carcinoma

Objective:To evaluate the effect of preoperative transarterial chemoembolization (TACE) for resectable large hepatocellular carcinoma (HCC). Summary Background Data:Resection of HCC is potentially curative, but local recurrence is very common. There is currently no effective neoadjuvant or adjuvant therapy. Methods:From July 2001 to December 2003, 108 patients (hepatitis B carrier = 98.1%) with resectable HCC (≥5 cm) was randomly assigned to preoperative TACE treatment (n = 52) or no preoperative treatment (control group) (n = 56). Results:Five patients (9.6%) in the preoperative TACE group did not receive surgical therapy because of extrahepatic metastasis or liver failure. The preoperative TACE group had a lower resection rate (n = 47, 90.4% vs. n = 56, 100%; P= 0.017), and longer operative time (mean, 176.5 minutes vs. 149.3 minutes; P= 0.042). No significant difference was found between the 2 groups in operative blood loss, surgical morbidity, and hospital mortality. At a median follow-up of 57 months, 41 (78.8%) of 52 patients in the preoperative TACE group and 51 (91.1%) of 56 patients in the control group had recurrent disease (P= 0.087). The 1-, 3-, and 5-year disease-free survival rates were 48.9%, 25.5%, and 12.8%, respectively, for the preoperative TACE group and 39.2%, 21.4%, and 8.9%, respectively, for the control group (P= 0.372). The 1-, 3-, and 5-year overall survival rates were 73.1%, 40.4%, and 30.7%, respectively, for the preoperative TACE group and 69.6%, 32.1%, and 21.1%, respectively, for the control group (P= 0.679). Conclusions:Preoperative TACE did not improve surgical outcome. It resulted in drop-out from definitive surgery because of progression of disease and liver failure.