Miracle-dz/UniFAR-FTUs huggingface dataset:
A widely tunable CMOS Gm-C filter with a negative source degeneration resistor transconductor

We propose a new negative source degeneration resistor (NSDR) transconductor to achieve a wide continuous-tuning range gm-C filter applicable for IEEE802.11a/b/g wireless-LANs and W-CDMA. The NSDR-transconductor using a source degeneration resistor and positive feedback differential amplifier that acts as a negative resistor. This configuration enables the equivalent source degeneration resistance to be drastically increased without degrading linearity, thus resulting in a wide gm tuning. A 6th -order elliptic low-pass filter using this NSDR-transconductor exhibits a cutoff frequency (f/sub c/) tuning range of 1.5-12MHz, which is two times wider than that of conventional filters. Additionally, we introduce a new figure of merit (FoM) evaluating the basic filter performance. This filter shows 0.35 fj (FoM) in the IEEE802.11a mode, which is, to our best knowledge, the best value in the CMOS channel-select filters.
Aspirin-Mediated Acetylation Protects Against Multiple Neurodegenerative Pathologies by Impeding Protein Aggregation.

AIMS Many progressive neurological disorders, including Alzheimer's disease (AD), Huntington's disease, and Parkinson's disease (PD), are characterized by accumulation of insoluble protein aggregates. In prospective trials, the cyclooxygenase inhibitor aspirin (acetylsalicylic acid) reduced the risk of AD and PD, as well as cardiovascular events and many late-onset cancers. Considering the role played by protein hyperphosphorylation in aggregation and neurodegenerative diseases, and aspirin's known ability to donate acetyl groups, we asked whether aspirin might reduce both phosphorylation and aggregation by acetylating protein targets. RESULTS Aspirin was substantially more effective than salicylate in reducing or delaying aggregation in human neuroblastoma cells grown in vitro, and in Caenorhabditis elegans models of human neurodegenerative diseases in vivo. Aspirin acetylates many proteins, while reducing phosphorylation, suggesting that acetylation may oppose phosphorylation. Surprisingly, acetylated proteins were largely excluded from compact aggregates. Molecular-dynamic simulations indicate that acetylation of amyloid peptide energetically disfavors its association into dimers and octamers, and oligomers that do form are less compact and stable than those comprising unacetylated peptides. INNOVATION Hyperphosphorylation predisposes certain proteins to aggregate (e.g., tau, α-synuclein, and transactive response DNA-binding protein 43 [TDP-43]), and it is a critical pathogenic marker in both cardiovascular and neurodegenerative diseases. We present novel evidence that acetylated proteins are underrepresented in protein aggregates, and that aggregation varies inversely with acetylation propensity after diverse genetic and pharmacologic interventions. CONCLUSIONS These results are consistent with the hypothesis that aspirin inhibits protein aggregation and the ensuing toxicity of aggregates through its acetyl-donating activity. This mechanism may contribute to the neuro-protective, cardio-protective, and life-prolonging effects of aspirin. Antioxid. Redox Signal. 27, 1383-1396.
System identification of a small scaled helicopter using simulated annealing algorithm

Developing an autonomous helicopter requires designing of precise controllers, which can be a daunting task if system dynamics are not known accurately. Thus very accurate system dynamics should be available to design controllers. The main idea of this paper is to present Simulated Annealing (SA) algorithm as a tool in time domain parametric system identification of a RC helicopter (Align T-Rex 550L). In addition, Prediction Error Minimization (PEM) and Genetic Algorithm (GA) have been taken as reference identification algorithms for the purpose of comparison. The work includes collecting flight data and pre-processing of the recorded data, and time domain parametric identification of state space system for hovering condition. The rigid body dynamics of the helicopter is represented in the state space form that has 40 parameters. The accuracy of the identified system is verified by comparing estimated and actual responses, by Pearson Correlation Coefficient, also 90% confidence interval is calculated for each of the identified parameters. Results show a high level of correlation of the actual responses and estimated responses of the system identified using SA, because of its ability to jump out of local optima.
Empagliflozin Treatment Is Associated With Improved β-Cell Function in Type 2 Diabetes Mellitus

Abstract Objective To examine whether lowering plasma glucose concentration with the sodium-glucose transporter-2 inhibitor empagliflozin improves β-cell function in patients with type 2 diabetes mellitus (T2DM). Methods Patients with T2DM (N = 15) received empagliflozin (25 mg/d) for 2 weeks. β-Cell function was measured with a nine-step hyperglycemic clamp (each step, 40 mg/dL) before and at 48 hours and at 14 days after initiating empagliflozin. Results Glucosuria was recorded on days 1 and 14 [mean ± standard error of the mean (SEM), 101 ± 10 g and 117 ± 11 g, respectively] after initiating empagliflozin, as were reductions in fasting plasma glucose levels (25 ± 6 mg/dL and 38 ± 8 mg/dL, respectively; both P < 0.05). After initiating empagliflozin and during the stepped hyperglycemic clamp, the incremental area under the plasma C-peptide concentration curve increased by 48% ± 12% at 48 hours and 61% ± 10% at 14 days (both P < 0.01); glucose infusion rate increased by 15% on day 3 and 16% on day 14, compared with baseline (both P < 0.05); and β-cell function, measured with the insulin secretion/insulin resistance index, increased by 73% ± 21% at 48 hours and 112% ± 20% at 14 days (both P < 0.01). β-cell glucose sensitivity during the hyperglycemic clamp was enhanced by 42% at 14 hours and 54% at 14 days after initiating empagliflozin (both P < 0.01). Conclusion Lowering the plasma glucose concentration with empagliflozin in patients with T2DM augmented β-cell glucose sensitivity and improved β-cell function.
Nonthermal Dielectric Barrier Discharge (DBD) Plasma Suppresses Herpes Simplex Virus Type 1 (HSV-1) Replication in Corneal Epithelium.

PURPOSE Herpes keratitis (HK) is the leading cause of cornea-derived and infection-associated blindness in the developed world. Despite the availability of effective antivirals, some patients develop refractory disease, drug-resistant infection, and topical toxicity. A nonpharmaceutical treatment modality may offer a unique advantage in the management of such cases. This study investigated the antiviral effect of nonthermal dielectric barrier discharge (DBD) plasma, a partially ionized gas that can be applied to organic substances to produce various biological effects. METHODS Human corneal epithelial cells and explanted corneas were infected with herpes simplex virus type 1 (HSV-1) and exposed to culture medium treated with nonthermal DBD plasma. The extent of infection was measured by plaque assay, quantitative PCR, and Western blot. Corneal toxicity assessment was performed with fluorescein staining, histologic examination, and 8-OHdG detection. RESULTS Application of DBD plasma-treated medium to human corneal epithelial cells and explanted corneas produced a dose-dependent reduction of the cytopathic effect, viral genome replication, and the overall production of infectious viral progeny. Toxicity studies showed lack of detrimental effects in explanted human corneas. CONCLUSIONS Nonthermal DBD plasma substantially suppresses corneal HSV-1 infection in vitro and ex vivo without causing pronounced toxicity. TRANSLATIONAL RELEVANCE Nonthermal plasma is a versatile tool that holds great biomedical potential for ophthalmology, where it is being investigated for wound healing and sterilization and is already in use for ocular microsurgery. The anti-HSV-1 activity of DBD plasma demonstrated here could be directly translated to the clinic for use against drug-resistant herpes keratitis.
Shared Active Site Architecture between the Large Subunit of Eukaryotic Primase and DNA Photolyase

Background DNA synthesis during replication relies on RNA primers synthesised by the primase, a specialised DNA-dependent RNA polymerase that can initiate nucleic acid synthesis de novo. In archaeal and eukaryotic organisms, the primase is a heterodimeric enzyme resulting from the constitutive association of a small (PriS) and large (PriL) subunit. The ability of the primase to initiate synthesis of an RNA primer depends on a conserved Fe-S domain at the C-terminus of PriL (PriL-CTD). However, the critical role of the PriL-CTD in the catalytic mechanism of initiation is not understood. Methodology/Principal Findings Here we report the crystal structure of the yeast PriL-CTD at 1.55 Å resolution. The structure reveals that the PriL-CTD folds in two largely independent alpha-helical domains joined at their interface by a [4Fe-4S] cluster. The larger N-terminal domain represents the most conserved portion of the PriL-CTD, whereas the smaller C-terminal domain is largely absent in archaeal PriL. Unexpectedly, the N-terminal domain reveals a striking structural similarity with the active site region of the DNA photolyase/cryptochrome family of flavoproteins. The region of similarity includes PriL-CTD residues that are known to be essential for initiation of RNA primer synthesis by the primase. Conclusion/Significance Our study reports the first crystallographic model of the conserved Fe-S domain of the archaeal/eukaryotic primase. The structural comparison with a cryptochrome protein bound to flavin adenine dinucleotide and single-stranded DNA provides important insight into the mechanism of RNA primer synthesis by the primase.
Potential for transcriptional upregulation of cochlin in glaucomatous trabecular meshwork: a combinatorial bioinformatic and biochemical analytical approach.

PURPOSE To determine the existence of a relatively higher abundance of potential TFs in glaucomatous trabecular meshwork (TM) that may bind putative promoter regions and affect cochlin protein expression in glaucomatous compared to normal TM. METHODS Combinatorial bioinformatics and biochemical analyses, using human glaucomatous and normal donor tissue (n = 4 each). Biochemical analysis included electrophoretic mobility shift assays (EMSAs), filter binding assays (FBAs), coupled in vitro transcription-translation (TNT) assays and promoter mutation analysis. RESULTS Combinatorial bioinformatics and biochemical analyses revealed the existence of a higher abundance of TFs in glaucomatous than in normal TM nuclear extracts. The evidence of a relatively high abundance of TFs, leading to increased expression of cochlin predicted by bioinformatic and biochemical analyses (EMSA and FBA), was further supported by TNT and promoter mutation TNT assays. CONCLUSIONS These results support the finding that the observed increased cochlin expression in glaucomatous TM is due to relative elevated abundance of TFs. The results also demonstrate the utility of combinatorial bioinformatic and biochemical analyses for genes with uncharacterized promoter regions.
Efficient Clustering with Limited Distance Information

Given a point set S and an unknown metric d on S, we study the problem of efficiently partitioning S into k clusters while querying few distances between the points. In our model we assume that we have access to one versus all queries that given a point s in S return the distances between s and all other points. We show that given a natural assumption about the structure of the instance, we can efficiently find an accurate clustering using only O(k) distance queries. Our algorithm uses an active selection strategy to choose a small set of points that we call landmarks, and considers only the distances between landmarks and other points to produce a clustering. We use our algorithm to cluster proteins by sequence similarity. This setting nicely fits our model because we can use a fast sequence database search program to query a sequence against an entire dataset. We conduct an empirical study that shows that even though we query a small fraction of the distances between the points, we produce clusterings that are close to a desired clustering given by manual classification.
Entropy Coding Aided Adaptive Subcarrier-Index Modulated OFDM

We propose entropy coding-aided adaptive subcarrier-index-modulated orthogonal frequency division multiplexing (SIM-OFDM). In conventional SIM-OFDM, the indices of the subcarriers activated are capable of conveying extra information. We propose the novel concept of compressing the index information bits by employing the Huffman coding. The probabilities of the different subcarrier activation patterns are obtained from an optimization procedure, which improves the performance of the scheme. Both the maximum-likelihood as well as the logarithmic-likelihood ratio-based soft detector may be employed for detecting the subcarriers activated as well as the information mapped to the classic constellation symbols. As an additional advantage of employing the variable-length Huffman codebook, all the legitimate subcarrier activation patterns may be employed, whereas the conventional SIM-OFDM is capable of using only a subset of the patterns. Our simulation results show that an improved performance is attainable by the proposed system.
Effects of bromopride on expression of metalloproteinases and interleukins in left colonic anastomoses: an experimental study

Anastomotic dehiscence is the most severe complication of colorectal surgery. Metalloproteinases (MMPs) and interleukins (ILs) can be used to analyze the healing process of anastomosis. To evaluate the effects of bromopride on MMP and cytokine gene expression in left colonic anastomoses in rats with or without induced abdominal sepsis, 80 rats were divided into two groups for euthanasia on the third or seventh postoperative day (POD). They were then divided into subgroups of 20 rats for sepsis induction or not, and then into subgroups of 10 rats for administration of bromopride or saline. Left colonic anastomosis was performed and abdominal sepsis was induced by cecal ligation and puncture. A colonic segment containing the anastomosis was removed for analysis of gene expression of MMP-1α, MMP-8, MMP-13, IL-β, IL-6, IL-10, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). On the third POD, bromopride was associated with increased MMP-1α, MMP-13, IL-6, IFN-γ, and IL-10 gene expression. On the seventh POD, all MMP transcripts became negatively modulated and all IL transcripts became positively modulated. In the presence of sepsis, bromopride administration increased MMP-8 and IFN-γ gene expression and decreased MMP-1, TNF-α, IL-6, and IL-10 gene expression on the third POD. On the seventh POD, we observed increased expression of MMP-13 and all cytokines, except for TNF-α. In conclusion, bromopride interferes with MMP and IL gene expression during anastomotic healing. Further studies are needed to correlate these changes with the healing process.
Cultured Alveolar Epithelial Cells From Septic Rats Mimic In Vivo Septic Lung

Sepsis results in the formation of pulmonary edema by increasing in epithelial permeability. Therefore we hypothesized that alveolar epithelial cells isolated from septic animals develop tight junctions with different protein composition and reduced barrier function relative to alveolar epithelial cells from healthy animals. Male rats (200–300g) were sacrificed 24 hours after cecal ligation and double puncture (2CLP) or sham surgery. Alveolar epithelial cells were isolated and plated on fibronectin-coated flexible membranes or permeable, non-flexible transwell substrates. After a 5 day culture period, cells were either lysed for western analysis of tight junction protein expressin (claudin 3, 4, 5, 7, 8, and 18, occludin, ZO-1, and JAM-A) and MAPk (JNK, ERK, an p38) signaling activation, or barrier function was examined by measuring transepithelial resistance (TER) or the flux of two molecular tracers (5 and 20 Å). Inhibitors of JNK (SP600125, 20 µM) and ERK (U0126, 10 µM) were used to determine the role of these pathways in sepsis induced epithelial barrier dysfunction. Expression of claudin 4, claudin 18, and occludin was significantly lower, and activation of JNK and ERK signaling pathways was significantly increased in 2CLP monolayers, relative to sham monolayers. Transepithelial resistance of the 2CLP monolayers was reduced significantly compared to sham (769 and 1234 ohm-cm2, respectively), however no significant difference in the flux of either tracer was observed. Inhibition of ERK, not JNK, significantly increased TER and expression of claudin 4 in 2CLP monolayers, and prevented significant differences in claudin 18 expression between 2CLP and sham monolayers. We conclude that alveolar epithelial cells isolated from septic animals form confluent monolayers with impaired barrier function compared to healthy monolayers, and inhibition of ERK signaling partially reverses differences between these monolayers. This model provides a unique preparation for probing the mechanisms by which sepsis alters alveolar epithelium.
Compliance with Guidelines-Recommended Processes in Pneumonia: Impact of Health Status and Initial Signs

Initial care has been associated with improved survival of community-acquired pneumonia (CAP). We aimed to investigate patient comorbidities and health status measured by the Charlson index and clinical signs at diagnosis associated with adherence to recommended processes of care in CAP. We studied 3844 patients hospitalized with CAP. The evaluated recommendations were antibiotic adherence to Spanish guidelines, first antibiotic dose <6 hours and oxygen assessment. Antibiotic adherence was 72.6%, first dose <6 h was 73.4% and oxygen assessment was 90.2%. Antibiotic adherence was negatively associated with a high Charlson score (Odds ratio [OR], 0.91), confusion (OR, 0.66) and tachycardia ≥100 bpm (OR, 0.77). Delayed first dose was significantly lower in those with tachycardia (OR, 0.75). Initial oxygen assessment was negatively associated with fever (OR, 0.61), whereas tachypnea ≥30 (OR, 1.58), tachycardia (OR, 1.39), age >65 (OR, 1.51) and COPD (OR, 1.80) were protective factors. The combination of antibiotic adherence and timing <6 hours was negatively associated with confusion (OR, 0.69) and a high Charlson score (OR, 0.92) adjusting for severity and hospital effect, whereas age was not an independent factor. Deficient health status and confusion, rather than age, are associated with lower compliance with antibiotic therapy recommendations and timing, thus identifying a subpopulation more prone to receiving lower quality care.
Mannose-binding lectin genotypes and outcome in end-stage renal disease: a prospective cohort study

Background Patients with end-stage renal disease (ESRD) have high morbidity and mortality rates, with cardiovascular diseases and infections being the major causes of death. Mannose-binding lectin (MBL) has been suggested to play a protective role in this regard. The aim of this study was to investigate a possible clinical association of MBL genotypes (MBL2) with outcome among patients on dialysis or with a functioning graft. Methods A total of 98 patients with ESRD accepted for living-donor renal transplantation or on the waiting list for transplantation were included and prospectively followed for an average of 9 years (range 7.5-9.9). Medical records were evaluated regarding transplantation status, diabetes mellitus, vascular parameters and infections for all the patients. Cox regression models and logistic regression analysis were used for statistical analyses. The cohort was divided into two groups according to the MBL2 genotype (normal A/A versus variant A/O or O/O). Results We found no evidence for an association between the MBL2 genotype and all-cause mortality, cardiovascular events or bacterial infections (pneumonia, urinary tract infection, fistula infection or other infections). Conclusion In this cohort, the MBL2 genotype did not seem to be associated with any long-term clinical effects in ESRD patients on dialysis or with a functioning graft.
Performance analysis of an improved hierarchical droop-based control scheme under topological, parametric and communication uncertainties: Towards a resilient microgrid

In this paper, an improved hierarchical droop-based control structure is presented. This improved control structure can resolve the limitation/drawbacks of the previously-reported droop-based control techniques and enhance microgrid stability margin and improve its performance. The conventional hierarchical droop-based structure is re-implemented and some modifications are done. Then, based on the previous researches of the authors, the performance of the proposed control structure is evaluated under topological and parametric uncertainties and delay in communication system. Some special notes and recommendations are provided to draw a picture of realizing a resilient microgrid including a robust hierarchical control system having enough robustness against small and large-signal disturbances, nonlinearities comes from nonlinear loads and nonlinear dynamics of the resources and moreover, the mentioned uncertainties. To demonstrate the effectiveness of the proposed hierarchical controller, time-domain simulation studies have been performed on a microgrid included four units of distributed generation with local loads and in presence of main grid using MATLAB/Simulink software and the results are presneted.
A common‐mode replica compensated inductor–capacitor voltage‐controlled oscillator for mixed‐signal system‐on‐chip applications

A novel 1.57 GHz complementary metal–oxide semiconductor inductor–capacitor voltage‐controlled oscillator with the common‐mode replica compensation is introduced for mixed‐signal system‐on‐chip applications. In order to alleviate power line disturbances, the center tap node of differential symmetric inductor and the replica biasing circuit are adopted in the differential voltage regulating unit to reduce power supply sensitivity. In addition, this proposed design also leads to low tuning gain and low power dissipation. The post‐layout simulation results under the Taiwan Semiconductor Manufacturing Company's mixed‐signal 0.18 µm 1P6M process show that the proposed design achieves power supply rejection of −68.6 dB at low frequencies and 1.2 MHz/V pushing sensitivity. It exhibits phase noise of −130.6 dBc/Hz at a 1 MHz offset from a 1.57 GHz carrier yet dissipates only 5.58 mW under a 1.8 V power supply. Copyright © 2011 John Wiley & Sons, Ltd.
Mesh-based Autoencoders for Localized Deformation Component Analysis

Spatially localized deformation components are very useful for shape analysis and synthesis in 3D geometry processing. Several methods have recently been developed, with an aim to extract intuitive and interpretable deformation components. However, these techniques suffer from fundamental limitations especially for meshes with noise or large-scale deformations, and may not always be able to identify important deformation components.In this paper we propose a novel mesh-based autoencoder architecture that is able to cope with meshes with irregular topology. We introduce sparse regularization in this framework, which along with convolutional operations, helps localize deformations.Our framework is capable of extracting localized deformation components from mesh data sets with large-scale deformations and is robust to noise. It also provides a nonlinear approach to reconstruction of meshes using the extracted basis, which is more effective than the current linear combination approach. Extensive experiments show that our method outperforms state-of-the-art methods in both qualitative and quantitative evaluations.