Miracle-dz/UniFAR-FTUs huggingface dataset:
An energy efficient QoS routing protocol for cognitive radio ad hoc networks

The explosive growth in the use of real-time applications on mobile devices has resulted in new challenges to the design of routing protocols for cognitive radio ad hoc networks (CRANs). In this paper, we propose a new on-demand Quality-of-Service (QoS) routing, namely an energy efficient QoS routing (EQR) protocol for CRANs using TDMA. It can establish QoS routes with reserved bandwidth on a per flow basis in a multi-hop networks. The objective of this work is to establish bandwidth guaranteed QoS routes in small CRANs whose topologies change at low to medium rate. The protocol is based on DSR, and builds QoS routes only as needed. We assume the application is session-oriented and requires constant bandwidth. A session specifies its QoS requirement as the number of transmission timeslots it needs on its route from a source to a destination. For each session (flow), the QoS routing protocol will find both the route and the channel and timeslots for each link on the route. The simulation results show the effectiveness of our proposed approach with good generalization ability.
Inhibitory effects of antiarrhythmic drugs on phenacetin O-deethylation catalysed by human CYP1A2.

AIMS The aim of the study was to clarify whether the pharmacokinetic interaction between theophylline and mexiletine is mediated by inhibition of CYP1A2 and to assess the possible interaction potential of other antiarrhythmic drugs with drugs metabolized by CYP1A2. METHODS The inhibitory effects of mexiletine and 10 antiarrhythmic drugs on phenacetin O-deethylation, a marker reaction of CYP1A2, were studied using human liver microsomes and cDNA-expressed CYP1A2. RESULTS Propafenone and mexiletine inhibited phenacetin O-deethylation with IC50 values of 29 and 37 microM, respectively. Disopyramide, procainamide and pilsicainide produced negligible inhibition of phenacetin O-deethylation (IC50 >1 mM). Amiodarone, bepridil, aprindine, lignocaine, flecainide and quinidine inhibited phenacetin O-deethylation in a concentration-dependent manner, although the inhibitory effects were relatively weak with IC50 values ranging from 86 to 704 microM. Propafenone and mexiletine selectively abolished the high-affinity component of phenacetin O-deethylation in human liver microsomes. In addition, propafenone and mexiletine inhibited phenacetin O-deethylation catalysed by cDNA-expressed CYP1A2. CONCLUSIONS These data suggest that, among the antiarrhythmic drugs studied, propafenone and mexiletine are relatively potent inhibitors of CYP1A2, which may cause a drug-drug interaction with drugs metabolized by CYP1A2.
Modeling Passive Mode-Locking in Quantum Dot Lasers: A Comparison Between a Finite-Difference Traveling-Wave Model and a Delayed Differential Equation Approach

We present a detailed quantitative comparison between a finite-difference traveling wave (FDTW) model and a delayed differential equation (DDE) approach for the simulation of passive mode-locking in quantum dot lasers with both ring and Fabry-Perot (FP) cavities. Modifications with respect to the standard DDE models available in the literature are proposed. The new DDE approach improves the quantitative agreement with the FDTW model when applied to the simulation of passive mode-locking in FP lasers, preserving a very high computational efficiency. The modifications proposed in the DDE model also apply to the simulation of quantum-well and bulk devices.
Specificity of eicosanoid production depends on the TLR‐4‐stimulated macrophage phenotype

Eicosanoid metabolism differs in profile and quantity between macrophages of different tissue origin and method of elicitation, as well as between primary and immortalized macrophages after activation with inflammatory stimuli. Using a lipidomic approach, we comprehensively analyzed the eicosanoids made by murine RPMs, TGEMs, BMDM, and the macrophage‐like cell line RAW after stimulation with the TLR‐4‐specific agonist KLA. Direct correlation among total COX metabolites, COX side‐products (11‐HETE, 15‐HETE), COX‐2 mRNA, and protein at 8 h was found when comparing each cell type. Comprehensive qPCR analysis was used to compare relative transcript levels between the terminal prostanoid synthases themselves as well as between each cell type. Levels of PGE2, PGD2, and TxB2 generally correlated with enzyme transcript expression of PGES, PGDS, and TBXS, providing evidence of comparable enzyme activities. PGIS transcript was expressed only in RPM and TGEM macrophages and at an exceptionally low level, despite high metabolite production compared with other synthases. Presence of PGIS in RPM and TGEM also lowered the production of PGE2 versus PGD2 by approximately tenfold relative to BMDM and RAW cells, which lacked this enzyme. Our results demonstrate that delayed PG production depends on the maximal level of COX‐2 expression in different macrophages after TLR‐4 stimulation. Also, the same enzymes in each cell largely dictate the profile of eicosanoids produced depending on the ratios of expression between them, with the exception of PGIS, which appears to have much greater synthetic capacity and competes selectively with mPGES‐1.
Cascade control applied to asymmetric multilevel converter based-STATCOM

This paper shows how a single phase STATCOM model can be seen as a two block series connection. In this way, it is suitable to use a cascade control in order to regulate both DC links voltages and reactive power needed by AC main. This last is achieved through control strategy consisting in two parts: one of them is a cascade multi-loop control which delivers only one average control signal and the other part consists of adjustment mechanism which calculates the deviations from average control signal allowing generating the control signals for each cell. Tuning of cascade control is treated. In this case STATCOM is based on an asymmetrical multilevel converter. In order to verify the control strategy simulation and experimental results are presented.
Molecular architecture of bacterial flagellum

1. INTRODUCTION 2 2. OVERALL STRUCTURE AND SUBSTRUCTURES 5 2.1 Overall structure and components 5 2.2 Bidirectional rotary motor 5 2.3 Drive shaft 8 2.4 Bushing 8 2.5 Universal joint 9 2.6 Helical propeller 9 2.7 Axial junction 10 2.8 Capping structure 11 3. ASSEMBLY PROCESS OF THE FLAGELLUM 11 3.1 Step by step assembly 11 3.2 Flagellum-specific export apparatus and the channel 12 4. UNIQUE CHARACTERISTICS OF THE FLAGELLAR MOTOR DYNAMICS 13 5. STRUCTURAL DESIGN OF FLAGELLIN FOR ASSEMBLY REGULATION AND POLYMORPHISM 14 5.1 Domain organization and terminal disorder of flagellin 15 5.2 The role of terminal disorder in filament formation and polymorphism 17 5.3 Common structural motif for regulation of self-assembly 21 6. STRUCTURAL DESIGN OF FLAGELLAR FILAMENTS FOR POLYMORPHISM 22 6.1 Polymorphic mechanism 23 6.2 Structures of the filaments deduced by electron microscopy 25 6.2.1 Overview of the electron microscopic studies 25 6.2.2 Helical image reconstruction procedure 27 6.2.3 Structural details of the filament 28 6.3 X-ray fibre diffraction studies 32 6.3.1 Overview of the X-ray studies 32 6.3.2 Orientation of liquid crystalline sols and diffraction patterns 33 6.3. 3 Equatorial analysis 35 6.3. 4 A preliminary map refined at 11 resolution 37 6.4 Overall chain folding of the subunit in the filament 38 6.4. 1 Mapping out the terminal and central regions 38 6.4. 2 The chain folding and role of each domain 42 6.5 Polymorphic nature of flagellar filament 43 6.5.1 Comparison of the L- and R-type 43 6.5.2 New helical symmetry Lt-type 46 6.5.3 Direct comparison of the Lt-type lattice to the other two 48 6.5. 4 Plausible conformational changes involved in polymorphism 51 7. PERSPECTIVE 55 8. ACKNOWLEDGEMENTS 55 9. REFERENCES 55
Hepatocellular nodules in cirrhosis: Focus on diagnostic criteria on liver biopsy. A Western experience

The spectrum of so‐called space‐occupying small (0.5–2.5 cm) sizable nodules arising in the cirrhotic liver includes a series of hyperplastic (large regenerative), dysplastic (low‐ and high‐grade dysplastic), and malignant hepatocellular (well‐differentiated hepatocellular carcinoma, HCC) nodules. Major progress in their classification and understanding was achieved through image analysis techniques and careful histological dissection of explanted native livers. Needless to say, the actual understanding of their natural history is crucial to a proper histological classification. The differential diagnosis of these hepatocellular nodules is difficult, particularly on biopsy specimens of focal liver lesions revealed by ultrasound (US), taken during the follow‐up of cirrhotic patients. In this study we attempted to summarize, on the basis of our experience, essential clinicopathological features useful to distinguish the different nodules on needle biopsy. Synoptic tables of differential diagnosis and figures of elementar lesions, which have to be looked for, are provided. Only the continuous integration of clinical features, image analysis information of pathological findings, and follow‐up data allows establishing the autonomy of these polymorphic and controversial entities and the boundaries between them. (Liver Transpl 2004;10:S9–S15.)
Deletion of autophagy inducer RB1CC1 results in degeneration of the retinal pigment epithelium

Autophagy regulates cellular homeostasis and response to environmental stress. Within the retinal pigment epithelium (RPE) of the eye, the level of autophagy can change with both age and disease. The purpose of this study is to determine the relationship between reduced autophagy and age-related degeneration of the RPE. The gene encoding RB1CC1/FIP200 (RB1-inducible coiled-coil 1), a protein essential for induction of autophagy, was selectively knocked out in the RPE by crossing Best1-Cre mice with mice in which the Rb1cc1 gene was flanked with Lox-P sites (Rb1cc1flox/flox). Ex vivo and in vivo analyses, including western blot, immunohistochemistry, transmission electron microscopy, fundus photography, optical coherence tomography, fluorescein angiography, and electroretinography were performed to assess the structure and function of the retina as a function of age. Deletion of Rb1cc1 resulted in multiple autophagy defects within the RPE including decreased conversion of LC3-I to LC3-II, accumulation of autophagy-targeted precursors, and increased numbers of mitochondria. Age-dependent degeneration of the RPE occurred, with formation of atrophic patches, subretinal migration of activated microglial cells, subRPE deposition of inflammatory and oxidatively damaged proteins, subretinal drusenoid deposits, and occasional foci of choroidal neovascularization. There was secondary loss of photoreceptors overlying the degenerated RPE and reduction in the electroretinogram. These observations are consistent with a critical role of autophagy in the maintenance of normal homeostasis in the aging RPE, and indicate that disruption of autophagy leads to retinal phenotypes associated with age-related degeneration.
Genetic and physiologic analysis of a formyl-tetrahydrofolate synthetase mutant of Streptococcus mutans

Previously we reported that transposon Tn917 mutagenesis of Streptococcus mutans JH1005 yielded an isolate detective in its normal ability to produce a mutacin (P. J. Crowley, J. D. Hillman, and A. S. Bleiweis, abstr. D55, p. 258 in Abstracts of the 95th General Meeting of the American Society for Microbiology 1995, 1995). In this report we describe the recovery of the mutated gene by shotgun cloning. Sequence analysis of insert DNA adjacent to Tn917 revealed homology to the gene encoding formyl-tetrahydrofolate synthetase (Fhs) from both prokaryotic and eukaryotic sources. In many bacteria, Fhs catalyzes the formation of 10-formyl-tetrahydrofolate, which is used directly in purine biosynthesis and formylation of Met-tRNA and indirectly in the biosynthesis of methionine, serine, glycine, and thymine. Analysis of the fhs mutant grown anaerobically in a minimal medium demonstrated that the mutant had an absolute dependency only for adenine, although addition of methionine was necessary for normal growth. Coincidently it was discovered that the mutant was sensitive to acidic pH; it grew more slowly than the parent strain on complex medium at pH 5. Complementation of the mutant with an integration vector harboring a copy of fhs restored its ability to grow in minimal medium and at acidic pH as well as to produce mutacin. This represents the first characterization of Fhs in Streptococcus.
iFACE: A 3D Synthetic Talking Face

We present the iFACE system, a visual speech synthesizer that provides a form of virtual face-to-face communication. The system provides an interactive tool for the user to customize a graphic head model for the virtual agent of a person based on his/her range data. The texture is mapped onto the customized model to achieve a realistic appearance. Face animations are produced by using text stream or speech stream to drive the model. A set of basic facial shapes and head action is manually built and used to synthesize expressive visual speech based on rules.
The mdx Mutation in the 129/Sv Background Results in a Milder Phenotype: Transcriptome Comparative Analysis Searching for the Protective Factors

The mdx mouse is a good genetic and molecular murine model for Duchenne Muscular Dystrophy (DMD), a progressive and devastating muscle disease. However, this model is inappropriate for testing new therapies due to its mild phenotype. Here, we transferred the mdx mutation to the 129/Sv strain with the aim to create a more severe model for DMD. Unexpectedly, functional analysis of the first three generations of mdx129 showed a progressive amelioration of the phenotype, associated to less connective tissue replacement, and more regeneration than the original mdxC57BL. Transcriptome comparative analysis was performed to identify what is protecting this new model from the dystrophic characteristics. The mdxC57BL presents three times more differentially expressed genes (DEGs) than the mdx129 (371 and 137 DEGs respectively). However, both models present more overexpressed genes than underexpressed, indicating that the dystrophic and regenerative alterations are associated with the activation rather than repression of genes. As to functional categories, the DEGs of both mdx models showed a predominance of immune system genes. Excluding this category, the mdx129 model showed a decreased participation of the endo/exocytic pathway and homeostasis categories, and an increased participation of the extracellular matrix and enzymatic activity categories. Spp1 gene overexpression was the most significant DEG exclusively expressed in the mdx129 strain. This was confirmed through relative mRNA analysis and osteopontin protein quantification. The amount of the 66 kDa band of the protein, representing the post-translational product of the gene, was about 4,8 times higher on western blotting. Spp1 is a known DMD prognostic biomarker, and our data indicate that its upregulation can benefit phenotype. Modeling the expression of the DEGs involved in the mdx mutation with a benign course should be tested as a possible therapeutic target for the dystrophic process.
RAS transformation causes sustained activation of epidermal growth factor receptor and elevation of mitogen‐activated protein kinase in human mammary epithelial cells

Activation of the ras oncogene is an important step in carcinogenesis. Human MCF‐10A mammary epithelial cells were transformed with a point‐mutated form of the Ha‐ras oncogene. Epidermal growth factor receptor (EGFR) phosphorylation levels were chronically elevated after EGF induction and the EGFR ligand–driven internalization rate was slower in Ha‐ras transformed MCF‐10A cells. Additionally, basal levels of p42/44 mitogen‐activated protein kinase (MAPK) expression and enzyme activity were significantly higher in Ha‐ras transformed cells, localized predominantly in the nucleus. The anti‐EGFR monoclonal antibody (MAb) 225 and the EGFR tyrosine kinase inhibitor PD153035 blocked anchorage‐independent growth of Ha‐ras transformed cells in soft agar and were more effective when used in combination. The MEK inhibitor PD98059 and anti‐erbB‐2 MAb L26 also suppressed colony formation of Ha‐ras transformed cells in soft agar. Therefore, Ha‐ras transformation leads to an augmentation in signaling through the EGFR as a result of an increase in ligand‐dependent phosphorylation, a decrease in its internalization and an up‐regulation in basal p44/42 MAPK levels. These effects may contribute to uncontrolled growth of Ha‐ras–transformed human mammary epithelial cells. Int. J. Cancer 88:44–52, 2000. © 2000 Wiley‐Liss, Inc.
A 9b 100MS/s 1.46mW SAR ADC in 65nm CMOS

A 9b 100MS/s successive approximation register (SAR) ADC has been implemented in 65nm CMOS, with an active area of 0.012mm2. A tri-level based charge redistribution technique improves DAC switching energy efficiency and settling time, which is achieved by connecting bottom plates of differential capacitor arrays. The ADC achieves an SNDR of 53.1dB (8.53 ENOB) and consumes 1.46mW from a 1.2V supply, resulting in an FOM of 39fJ/conversion-step.
Modeling and measurements of parasitic parameters for integrated power electronics modules

In this paper, the parasitic inductance and capacitance of integrated power electronics modules (IPEMs) were modeled using Maxwell Q3D extractor. The IPEMs were then measured using impedance analyzer. A set of impedance curves was obtained under different measurement conditions, such as different DC bias voltages. Together with the device model, the Maxwell Q3D extractor results were simulated in Saber to get the impedance curves, which were compared with impedance measurement results. The comparison showed good agreement between simulation and measurement results.
Dynamic Contrast-Enhanced Magnetic Resonance Imaging of Breast Tumors at 3 and 7 T: A Comparison

ObjectivesThe objective of this study was to compare the image quality, contrast enhancement behavior, and diagnostic value of bilateral 3-dimensional dynamic contrast-enhanced breast magnetic resonance imaging (MRI), with high spatial and temporal resolution, at 3 and 7 T, in the same patient group. Materials and MethodsTwenty-four consecutive patients (mean [SD] age, 57 [17] years) were included in this prospective institutional review board–approved study. Written informed consent was obtained from all patients. T1-weighted 3-dimensional sequences (time-resolved angiography with stochastic trajectories) were optimized at 3 and 7 T, with high temporal (both 14 seconds) and spatial resolution (1.1 × 1.1 × 1.1 mm3 [3 T], 0.7 × 0.7 × 0.7 mm3 [7 T]): echo time/repetition time, 2.84/6.01 milliseconds (3 T) and 2.5/4.75 milliseconds (7 T); acquisition time, 9 minutes (3 T/7 T). Dotarem® (gadoterate meglumine, Guerbet, Roissy CdG, France) contrast agent was injected intravenously as a bolus (0.2 mL/kg of body weight) after 3 baseline images. The images were rated according to breast imaging-reporting and data system by 2 radiologists in consensus. Signal-to-noise ratio and average enhancement ratios were measured quantitatively by means of region of interest analysis. In addition, B1 mapping was done in the same 5 healthy subjects at both field strengths. ResultsTwenty-eight enhancing lesions were detected in the 24 patients at both field strengths (16 malignant, 12 benign). At 7 T, higher contrast than that at 3 T and good image quality were achieved. With the high spatial isotropic resolution of 0.7 mm at 7 T, images with more detailed information could be acquired when compared with those acquired at 3 T. Sensitivity was 93.75% and 100%, at 3 and 7 T, respectively. Specificity was 91.67% at both field strengths. The signal-to-noise ratio at both field strengths was comparable, but at 7 T, the spatial resolution was 3.2-times higher than that at 3 T. A signal-to-noise ratio decrease toward prepectoral breast regions due to B1 inhomogeneities was observed at both field strengths but was stronger at 7 T (51%) than at 3 T (19%)(P = 0.0002). At 7 T, B1+ dropped by 20.7% and 32.8% in the prepectoral and lateral region of the breast in healthy subjects. ConclusionsOur comparison study shows that 7-T DCE-MRI provides simultaneous high temporal and spatial resolution that is significantly improved compared with lower field strengths, but further technical improvements are necessary to overcome B1 inhomogeneity problems at 7 T to fully unfold the potential of breast MRI at 7 T.
The Lactobacillus plantarum ftsH Gene Is a Novel Member of the CtsR Stress Response Regulon

ABSTRACT FtsH proteins have dual chaperone-protease activities and are involved in protein quality control under stress conditions. Although the functional role of FtsH proteins has been clearly established, the regulatory mechanisms controlling ftsH expression in gram-positive bacteria remain largely unknown. Here we show that ftsH of Lactobacillus plantarum WCFS1 is transiently induced at the transcriptional level upon a temperature upshift. In addition, disruption of ftsH negatively affected the growth of L. plantarum at high temperatures. Sequence analysis and mapping of the ftsH transcriptional start site revealed a potential operator sequence for the CtsR repressor, partially overlapping the −35 sequence of the ftsH promoter. In order to verify whether CtsR is able to recognize and bind the ftsH promoter, CtsR proteins of Bacillus subtilis and L. plantarum were overproduced, purified, and used in DNA binding assays. CtsR from both species bound specifically to the ftsH promoter, generating a single protein-DNA complex, suggesting that CtsR may control the expression of L. plantarum ftsH. In order to confirm this hypothesis, a ΔctsR mutant strain of L. plantarum was generated. Expression of ftsH in the ΔctsR mutant strain was strongly upregulated, indicating that ftsH of L. plantarum is negatively controlled by CtsR. This is the first example of an ftsH gene controlled by the CtsR repressor, and the first of the low-G+C gram-positive bacteria where the regulatory mechanism has been identified.
Right ventricular systolic function assessment: rank of echocardiographic methods vs. cardiac magnetic resonance imaging.

AIMS Right ventricular (RV) systolic function is prognostically important, but its assessment by echocardiography remains challenging, in part because of the multitude of available measurement methods. The purpose of this prospective study was to rank these methods against the reference of RV ejection fraction (EF) as obtained in a broad clinical population by magnetic resonance imaging (MRI). METHODS AND RESULTS Two hundred and twenty-three individuals were included in the study. The following seven Doppler echocardiographic parameters were tested using receiver operating characteristic (ROC) analysis for their accuracy to distinguish between normal and moderately impaired RVEF by MRI (RVEF cut-off 50%), respectively, between moderately and severely reduced RVEF (cut-off 30%): RV fractional area and fractional long-axis change (FLC), RV myocardial performance index (MPI), tricuspid annular peak systolic excursion, Doppler tissue imaging-derived isovolumic acceleration and peak systolic velocity (S') at the lateral tricuspid annulus, and strain at the lateral free wall as obtained by speckle-tracking echocardiography. Survival analysis was performed. All seven Doppler echocardiographic parameters correlated significantly with RVEF by MRI (range between 5 and 85%). RVEF <50% was best detected by S' < 11 cm/s: area under the ROC curve 0.779 (95% confidence interval 0.716-0.843), sensitivity 0.740, and specificity 0.753. RVEF ≤30% was best detected by MPI > 0.50: area under the ROC curve 0.948 (95% confidence interval 0.906-0.991), sensitivity 0.947, and specificity 0.852. The Kaplan-Meier analysis revealed reduced cumulative survival among patients with RVEF ≤30% (P = 0.0003). CONCLUSION A systolic long-axis peak velocity of <11 cm/s at the lateral tricuspid annulus most accurately detects moderately impaired RVEF as obtained by MRI; severely reduced RVEF ≤30% is best detected by RV MPI at a value of >0.50.