Miracle-dz/UniFAR-FTUs huggingface dataset:
Fingerprints in the Air: Unique Identification of Wireless Devices Using RF RSS Fingerprints

Recent years have witnessed the proliferation of indoor localization, device identification, and wireless attendance security systems. These solutions typically leverage RF received signal strength fingerprints to locate persons. However, they entail an important albeit commonly ignored issue, i.e., detecting whether an individual is carrying more than one wireless device. In other words, additional devices should be excluded from the analysis. To detect the unique identification problem, bio-assisted methods, such as fingerprint, face, and gait recognition, are deployed near entrances. However, these methods are not only difficult to implement but also entail additional costs. This paper studies the unique identification problem using RF received signal strength fingerprints, which are collected and modeled as time series. The similarity of the time series is calculated to achieve unique identification. Specifically, a naive algorithm based on dynamic time warping is proposed to compute the similarity in the asynchronous time series. Then, an improved two-step algorithm based on feature extraction and spectral clustering is proposed to reduce the computational complexity of the similarity check. In addition, an effectiveness index is proposed to obtain the optimal number of clusters. The results of simulations and experiments show that our algorithms can detect the unique identification problem with moderate computational complexity in typical scenarios.
Body Fat has No Effect on the Maximal Fat Oxidation Rate in Young, Normal, and Overweight Women

Abstract Blaize, AN, Potteiger, JA, Claytor, RP, and Noe, DA. Body fat has no effect on the maximal fat oxidation rate in young normal and overweight women. J Strength Cond Res 28(8): 2121–2126, 2014—The purpose of this study was to examine how fat mass affects the maximal fat oxidation rates of women. Fourteen active, healthy women (age, 21–31 years) with body composition ranging from 18.6 to 30.0% fat were divided into 2 groups (15–24.9% = lower-fat group; 25–35% = higher-fat group). On day 1, subjects performed a graded exercise test on the treadmill to determine maximal oxygen consumption (V[Combining Dot Above]O2max). On day 2, subjects were measured for % fat and performed a maximal fat oxidation test. Fat and carbohydrate oxidation rates were determined using gas exchange analysis. Fat oxidation in absolute (in gram per minute) and relative to fat-free body mass (in milligram per kilogram of fat-free mass per minute) was determined using stoichiometric equations and appropriate energy equivalents. There were no significant differences (p > 0.05) in maximal fat oxidation rates between the women in lower-fat (0.39 ± 0.10 g·min−1, 8.52 ± 2.69 mg·kg−1 FFM·min−1) and higher-fat (0.49 ± 0.13 g·min−1, 10.81 ± 2.80 mg·kg−1 FFM·min−1) groups. Maximal fat oxidation occurred at an exercise intensity of 55.7 ± 11.1% and 59.1 ± 5.4% V[Combining Dot Above]O2max for the lower-fat and higher-fat groups, respectively, with no significant difference between groups (p > 0.05). The maximal fat oxidation rate (g·min−1 and mg·kg−1 FFM·min−1) was not significantly correlated with any of the descriptive variables (fat mass, fat-free mass, percent body fat, or V[Combining Dot Above]O2max). In conclusion, personal trainers and health practitioners can use the exercise intensities that elicited the highest rate of fat oxidation to prescribe exercise programs to women, despite their body composition, that prevent weight gain and/or promote body fat and body weight loss.
Engraftment potential into NOD/SCID mice of CD34+ cells derived from human fetal liver as compared to fetal bone marrow.

BACKGROUND AND OBJECTIVES We hypothesized that qualitative or quantitative differences in hematopoietic stem cells from fetal liver (FL) and fetal bone marrow (FBM) may be the cause of their organ specificity. DESIGN AND METHODS To analyze possible differences in vivo, we compared the engraftment potential of equal numbers of CD34+ cells isolated from human FL or FBM into immunodeficient NOD/SCID mice. RESULTS Mice showing engraftment following transplantation of CD34+ cells from FL demonstrated 14% (range 2-76%) CD45+ cells of human origin in the bone marrow compared to significantly lower levels of engraftment (4%, range 2-20%, p < 0.04) of FBM CD34+ cells. Likewise, the percentage of CD34+ CD38- cells in FBM was 4 times lower than the percentage in FL (1.4+/-0.9% and 5.6+/-0.7%, respectively). Similar organ distribution of engrafted human cells was found. Subset analysis of human cells in bone marrow of engrafted mice revealed identical distribution of the lymphoid, myeloid and erythroid lineages after transplantation of CD34+ cells from FL or FBM. INTERPRETATION AND CONCLUSIONS The FL CD34+ cells showed a four-fold higher content of the CD34+ CD38- subset coinciding with a four-fold higher engraftment of CD34+ cells into NOD/SCID mice. Since the organ distribution and differentiation potential of the cells engrafted were similar, we concluded that CD34+ hematopoietic cells derived from FL and FBM have quantitatively different, but qualitatively the same potential for engraftment into NOD/SCID mice.
Anti-tumor effects of penfluridol through dysregulation of cholesterol homeostasis.

BACKGROUND Psychiatric patients appear to be at lower risk of cancer. Some antipsychotic drugs might have inhibitory effects on tumor growth, including penfluridol, a strong agent. To test this, we conducted a study to determine whether penfluridol exerts cytotoxic effects on tumor cells and, if so, to explore its anti-tumor mechanisms. METHODS Growth inhibition of mouse cancer cell lines by penfluridol was determined using the 3- (4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Cytotoxic activity was determined by clonogenic cell survival and trypan blue assays. Animal tumor models of these cancer cells were established and to evaluate penfluridol for its anti-tumor efficacy in vivo. Unesterified cholesterol in cancer cells was examined by filipin staining. Serum total cholesterol and tumor total cholesterol were detected using the cholesterol oxidase/p- aminophenazone (CHOD-PAP) method. RESULTS Penfluridol inhibited the proliferation of B16 melanoma (B16/ F10), LL/2 lung carcinoma (LL/2), CT26 colon carcinoma (CT26) and 4T1 breast cancer (4T1) cells in vitro. In vivo penfluridol was particularly effective at inhibiting LL/2 lung tumor growth, and obviously prolonged the survival time of mice bearing LL/2 lung tumors implanted subcutaneously. Accumulated unesterified cholesterol was found in all of the cancer cells treated with penfluridol, and this effect was most evident in LL/2, 4T1 and CT26 cells. No significant difference in serum cholesterol levels was found between the normal saline-treated mice and the penfluridol-treated mice. However, a dose-dependent decrease of total cholesterol in tumor tissues was observed in penfluridol-treated mice, which was most evident in B16/F10-, LL/2-, and 4T1-tumor-bearing mice. CONCLUSION Our results suggested that penfluridol is not only cytotoxic to cancer cells in vitro but can also inhibit tumor growth in vivo. Dysregulation of cholesterol homeostasis by penfluridol may be involved in its anti-tumor mechanisms.
Directional migration of endothelial cells towards angiogenesis using polymer fibres in a 3D co‐culture system

Development of an in vitro prevascularized scaffold is of great importance to produce vascularization in tissue‐engineered devices and for other clinical purposes. To this aim, polymer fibres covered with human umbilical vein endothelial cells (HUVECs) were used to induce directional ‘angiogenesis’ in a 3D co‐culture system. Gelatin or RGD peptides were immobilized on surface‐modified polymer fibres [100 µm diameter poly(ethylene terephthalate) monofilaments] via N‐hepthylamine plasma polymer and carboxy‐methyl‐dextran interlayers. Fibres fully covered with HUVECs were then embedded in a fibrin gel, following a parallel alignment pattern, in the presence of fibroblasts. Tube‐like structures occurred along the fibres and a network was formed between neighbouring fibres. These events were promoted with increased incubation times. Biomolecule‐grafted fibres created a guidance pathway that facilitated coated endothelial cells to form lumens and, from them, sprouting processes. However, there were no significant differences between the different surface modifications on fibres in terms of promoting tube‐like structures. Thus, different stages of angiogenesis can be initiated and guided using HUVECs precovered polymer fibres embedded in a soft supportive matrix, such as fibrin, which can be further applied to the development of in vitro prevascularized tissue‐engineered scaffolds. Copyright © 2010 John Wiley & Sons, Ltd.
Human Galectin-2: Novel Inducer of T Cell Apoptosis with Distinct Profile of Caspase Activation1

Galectin-2 is structurally closely related to galectin-1, but has a distinct expression profile primarily confined to the gastrointestinal tract. Prominent differences in the proximal promoter regions between galectins-2 and -1 concern Sp1-, hepatocyte NF-3, and T cell-specific factor-1 binding sites. Of note, these sequence elements are positioned equally in the respective regions for human and rat galectins-2. Labeled galectin-2 binds to T cells in a β-galactoside-specific manner. In contrast to galectin-1, the glycoproteins CD3 and CD7 are not ligands, while the shared affinity to β1 integrin (or a closely associated glycoprotein) accounts for a substantial extent of cell surface binding. The carbohydrate-dependent binding of galectin-2 induces apoptosis in activated T cells. Fluorogenic substrate and inhibitor assays reveal involvement of caspases-3 and -9, in accordance with cleavage of the DNA fragmentation factor. Enhanced cytochrome c release, disruption of the mitochondrial membrane potential, and an increase of the Bax/Bcl-2 ratio by opposite regulation of expression of both proteins add to the evidence that the intrinsic apoptotic pathway is triggered. Cell cycle distribution and expression of regulatory proteins remained unaffected. Notably, galectins-1 and -7 reduce cyclin B1 expression, defining functional differences between the structurally closely related galectins. Cytokine secretion of activated T cells was significantly shifted to the Th2 profile. Our study thus classifies galectin-2 as proapoptotic effector for activated T cells, raising a therapeutic perspective. Of importance for understanding the complex galectin network, it teaches the lesson that selection of cell surface ligands, route of signaling, and effects on regulators of cell cycle progression are markedly different between structurally closely related galectins.
A model‐based reconstruction for undersampled radial spin‐echo DTI with variational penalties on the diffusion tensor

Radial spin‐echo diffusion imaging allows motion‐robust imaging of tissues with very low T2 values like articular cartilage with high spatial resolution and signal‐to‐noise ratio (SNR). However, in vivo measurements are challenging, due to the significantly slower data acquisition speed of spin‐echo sequences and the less efficient k‐space coverage of radial sampling, which raises the demand for accelerated protocols by means of undersampling. This work introduces a new reconstruction approach for undersampled diffusion‐tensor imaging (DTI). A model‐based reconstruction implicitly exploits redundancies in the diffusion‐weighted images by reducing the number of unknowns in the optimization problem and compressed sensing is performed directly in the target quantitative domain by imposing a total variation (TV) constraint on the elements of the diffusion tensor. Experiments were performed for an anisotropic phantom and the knee and brain of healthy volunteers (three and two volunteers, respectively). Evaluation of the new approach was conducted by comparing the results with reconstructions performed with gridding, combined parallel imaging and compressed sensing and a recently proposed model‐based approach. The experiments demonstrated improvements in terms of reduction of noise and streaking artifacts in the quantitative parameter maps, as well as a reduction of angular dispersion of the primary eigenvector when using the proposed method, without introducing systematic errors into the maps. This may enable an essential reduction of the acquisition time in radial spin‐echo diffusion‐tensor imaging without degrading parameter quantification and/or SNR. Copyright © 2015 John Wiley & Sons, Ltd.
Structural and functional studies of enzymes in nucleotide metabolism

Enzymes in nucleotide metabolism serve as the producers of the building blocks for DNA and RNA. From a medical perspective, nucleotide metabolism, and in particular salvage pathway enzymes, have attracted special interest, as nucleoside prodrugs given in the treatment of cancer and HIV are converted into their active metabolite forms by these enzymes. In this thesis, two enzymes; uridine monophosphate kinase (UMPK) from Ureaplasma parvum (Up) and human phosphoribosyltransferase domain containing protein 1 (PRTFDC1), have been investigated. Furthermore, a nucleoside analog library (NAL) consisting of 45 FDA-approved nucleoside analogs has been developed. The structure of Up-UMPK revealed that it was a hexamer. Kinetic constants were determined for UMP and ATP. UTP was a competitive inhibitor of UMP, and a non-competitive inhibitor of ATP. In contrast to other bacterial UMPKs, Up-UMPK was not activated by GTP. PRTFDC1 is a homolog of hypoxanthine-guanine phosphoribosyltransferase (HPRT). Mutations in HPRT are associated with Lesch-Nyhan syndrome. The three-dimensional structures of PRTFDC1 and HRPT are very similar. Even though PRTFDC1 recognizes guanine and hypoxanthine as substrates, the functional turnover rates are less than 1% of the activity of HPRT. NAL was screened using the high-throughput method, differential static light scattering (DSLS). An interaction profile of 23 enzymes involved in nucleotide metabolism and NAL was revealed. Interactions were detected for uridine phosphorylase 1 (UPP1) and guanine deaminase (GDA) with eight and six nucleoside prodrugs, respectively. The knowledge gained from this study can be important in the future search for drug lead candidates for UPP1 and GDA.
Emerging monoclonal antibodies as targeted innovative therapeutic approaches to asthma

Asthma is characterized by discordant responses among cells of the adaptive and innate immune systems. This interplay involves a complex pattern of cytokine‐driven processes resulting in cell migration and recruitment, inflammation, and proliferative states. The significant majority of asthmatic patients respond well to conventional inhaled treatments. However, about 5% of asthmatics have severe refractory asthma and account for 50% of the health expenditure on asthma. Human(ized) monoclonal antibodies (hMabs) targeting inflammatory pathways are promising therapeutic agents in asthma management. The anti‐IgE hMab omalizumab was the first biologic treatment approved for the treatment of allergic asthma. Potential future strategies and targets include interleukin (IL)‐5, IL‐4, and IL‐13, anti‐TSLP, IL‐25, and IL‐33. hMabs targeting IL‐5 have shown great promise in severe refractory asthma with a persisting eosinophilia, and clinical trials with hMabs against IL‐13 and IL4Rα have also shown clinical benefit. Studies of hMabs against other cytokines in severe asthma are under way.
In vitro and in vivo expression of alpha 7 integrin and desmin define the primary and secondary myogenic lineages.

Skeletal muscle fibers form during two periods of development and differ biochemically, functionally and in their morphology. Primary fibers develop in the rat hindlimb during Days 14 to 16 of embryogenesis. These fibers are subsequently surrounded by secondary fibers that eventually constitute the bulk of muscle mass in the limbs. We have used the expression of the alpha 7 muscle laminin binding integrin (Song et al., J. Cell Biol. 117, 643-657, 1992) and the intermediate filament protein desmin to identify myogenic cells at distinct stages of development both in vitro and in vivo. The phenotypes of these cells, determined by immunofluorescence microscopy, discriminate two lineages and indicate that the development of primary and secondary muscle fibers is regulated by multiple mechanisms. The cells which compose the primary myogenic lineage are derived from a population of precursor cells that is in part present in the Day 12 embryo limb bud and which do not express either alpha 7 integrin or desmin. These precursor cells develop into cells that express desmin, but not alpha 7, and which subsequently mature into replicating myoblasts that are competent to undergo terminal differentiation. This maturation process requires the in vivo environment of the Day 13 embryo limb. The alpha 7 integrin and slow myosin heavy chain are first expressed in primary muscle cells well after the onset of terminal differentiation. Some cells that give rise to secondary muscle fibers also are present in the Day 12 embryo hindlimb. The precursors of secondary fibers will develop into cells which express either alpha 7 integrin or desmin and subsequently into replicating myoblasts that express both proteins. Upon terminal differentiation of secondary myoblasts there is an increase in the expression of both alpha 7 integrin and desmin. The temporal regulation of expression of these proteins indicates that the environment of the limb plays a role in the maturation of precursors of both lineages. At least two roles of alpha 7 integrin during myogenesis are related to its association with beta 1 integrin and its function as a laminin receptor. Laminin selectively maintains the proliferation of secondary myoblasts and modulates their shape and mobility in vitro. This responsiveness of secondary myoblasts to laminin corresponds to the time when laminin is a major component of the extracellular matrix, when there is an expansion of the population of secondary myoblasts, and when the alpha 7 integrin is expressed on secondary myoblasts in vivo. (ABSTRACT TRUNCATED AT 400 WORDS)
Lysine 43 Is Trimethylated in Subunit c from Bovine Mitochondrial ATP Synthase and in Storage Bodies Associated with Batten Disease*

The hydrophobic membrane protein, subunit c, has been isolated from ATP synthase purified from bovine heart mitochondria. It has also been obtained from lysosomal storage bodies associated with ceroid lipofuscinosis from ovine liver and from human brain tissue of a victim of Batten disease. It is likely that the lysosomal protein has originated from the mitochondrion. These samples have been characterized by mass spectrometric methods. Irrespective of its source, subunit c has an intact molecular mass of 7650 Da, 42 Da greater than the value calculated from the amino acid sequence, and the protein has been modified post-translationally. In all three samples, the modification is associated with lysine 43, which lies in a polar loop region linking the two transmembrane α-helices of the protein. This residue is conserved throughout vertebrate sequences. The additional mass arises from trimethylation and not acetylation at the ϵ-N-position of the residue. These experiments show that the post-translational modification of subunit c is not, as has been suggested, an abnormal phenomenon associated with the etiology of Batten disease and ceroid lipofucinoses. Evidently, it occurs either before or during import of the protein into mitochondria or at a mitochondrial location after completion of the import process. The function of the trimethyllysine residue in the assembled ATP synthase complex is obscure. The residue and the modification are not conserved in all ATP synthases, and their role in the assembly and (or) functioning of the enzyme appear to be confined to higher organisms.
Laser-based direct-write techniques for cell printing

Fabrication of cellular constructs with spatial control of cell location (±5 µm) is essential to the advancement of a wide range of applications including tissue engineering, stem cell and cancer research. Precise cell placement, especially of multiple cell types in co- or multi-cultures and in three dimensions, can enable research possibilities otherwise impossible, such as the cell-by-cell assembly of complex cellular constructs. Laser-based direct writing, a printing technique first utilized in electronics applications, has been adapted to transfer living cells and other biological materials (e.g., enzymes, proteins and bioceramics). Many different cell types have been printed using laser-based direct writing, and this technique offers significant improvements when compared to conventional cell patterning techniques. The predominance of work to date has not been in application of the technique, but rather focused on demonstrating the ability of direct writing to pattern living cells, in a spatially precise manner, while maintaining cellular viability. This paper reviews laser-based additive direct-write techniques for cell printing, and the various cell types successfully laser direct-written that have applications in tissue engineering, stem cell and cancer research are highlighted. A particular focus is paid to process dynamics modeling and process-induced cell injury during laser-based cell direct writing.
Assessing the Effects of Removing User Fees in Zambia and Niger

Objectives This study aims to overcome some of the limitations of previous studies investigating the effects of fee removal, by looking at heterogeneity of effects within countries and over time, as well as the existence of spillover effects on groups not targeted by the policy change. Methods Using routine district health services data before and after recent abolitions of user charges in Zambia and Niger, we examine the effects of the policy change on the use of health services by different groups and over time, using an interrupted timeseries design. Results Removing user fees for primary health care services in rural districts in Zambia and for children over five years old in Niger increased use of services by the targeted groups. The impact of the policy change differed widely across districts, ranging from 112% and 1194% in Niger to 239% and 1108% in Zambia. Eighteen months after the policy change, some of these effects had been eroded. There was evidence that abolishing user fees can both have positive and negative spillover effects. Conclusion These results highlight the importance of paying attention to implementation challenges and monitoring the effects of policy reforms which are often more mixed and complicated that they appear. The comparison of these reforms in two countries also sheds light on the potentially different ways in which free care can be used as a tool to improve access.