gebhart/patrepeval huggingface dataset:
FPGA implementation of MD5 hash algorithm (2002)

In information security, message authentication is an essential technique to verify that received messages come from the alleged source and have not been altered. A key element of authentication schemes is the use of a message authentication code (MAC). One technique to produce a MAC is based on using a hash function and is referred to as an HMAC. The Message Digest 5 (MD5) is one of the algorithms, which has been specified for use in Internet Protocol Security (IPSEC), as the basis for an HMAC. The input message may be arbitrarily large and is processed in 512-bit blocks by executing 64 steps involving the manipulation of 128-bit blocks. There is an increasing interest in high-speed cryptographic accelerators for IPSEC applications such as virtual private networks. As we show, it is reasonable to construct cryptographic accelerators using hardware implementations of HMACs based on a hash algorithm such as MD5. Two different architectures, iterative and full loop unrolling, of MD5 have been implemented using field programmable gate arrays (FPGAs). The performance of these implementations is discussed.
A Legged Anchoring Mechanism for Capsule Endoscopes Using Micropatterned Adhesives (2008)

This paper presents a new concept for an anchoring mechanism to enhance existing capsule endoscopes. The mechanism consists of three actuated legs with compliant feet lined with micropillar adhesives to be pressed into the intestine wall to anchor the device at a fixed location. These adhesive systems are inspired by gecko and beetle foot hairs. Single-leg and full capsule mathematical models of the forces generated by the legs are analyzed to understand capsule performance. Empirical friction models for the interaction of the adhesives with an intestinal substrate were experimentally determined in vitro using dry and oil-coated elastomer micropillar arrays with 140 microm pillar diameter, 105 microm spacing between pillars, and an aspect ratio of 1:1 on fresh porcine small intestine specimens. Capsule prototypes were also tested in a simulated intestine environment and compared with predicted peristaltic loads to assess the viability of the proposed design. The experimental results showed that a deployed 10 gr capsule robot can withstand axial peristaltic loads and anchor reliably when actuation forces are greater than 0.27 N using dry micropillars. Required actuation forces may be reduced significantly by using micropillars coated with a thin silicone oil layer.
A network analysis of the dynamics of seizure (2012)

Seizures are events that spread through the brain's network of connections and create pathological activity. To understand what is occurring in the brain during seizure we investigated the time progression of the brain's state from seizure onset to seizure suppression. Knowledge of a seizure's dynamics and the associated spatial structure is important for localizing the seizure foci and determining the optimal location and timing of electrical stimulation to mitigate seizure development. In this study, we analyzed intracranial EEG data recorded in 2 human patients with drug-resistant epilepsy prior to undergoing resection surgery using network analyses. Specifically, we computed a time sequence of connectivity matrices from iEEG (intracranial electroencephalography) recordings that represent network structure over time. For each patient, connectivity between electrodes was measured using the coherence in the band of frequencies with the strongest modulation during seizure. The connectivity matrices' structure was analyzed using an eigen-decomposition. The leading eigenvector was used to estimate each electrode's time dependent centrality (importance to the network's connectivity). The electrode centralities were clustered over the course of each seizure and the cluster centroids were compared across seizures. We found, for each patient, there was a consistent set of centroids that occurred during each seizure. Further, the brain reliably evolved through the same progression of states across multiple seizures including characteristic onset and suppression states.
Exploiting Spatial Redundancy of Image Sensor for Motion Robust rPPG (2014)

Remote photoplethysmography (rPPG) techniques can measure cardiac activity by detecting pulse-induced color variations on human skin using an RGB camera. State-of-the-art rPPG methods are sensitive to subject body motions (e.g., motion-induced color distortions). This study proposes a novel framework to improve the motion robustness of rPPG. The basic idea of this paper originates from the observation that a camera can simultaneously sample multiple skin regions in parallel, and each of them can be treated as an independent sensor for pulse measurement. The spatial redundancy of an image sensor can thus be exploited to distinguish the pulse signal from motion-induced noise. To this end, the pixel-based rPPG sensors are constructed to estimate a robust pulse signal using motion-compensated pixel-to-pixel pulse extraction, spatial pruning, and temporal filtering. The evaluation of this strategy is not based on a full clinical trial, but on 36 challenging benchmark videos consisting of subjects that differ in gender, skin types, and performed motion categories. Experimental results show that the proposed method improves the SNR of the state-of-the-art rPPG technique from 3.34 to 6.76 dB, and the agreement ( ±1.96σ) with instantaneous reference pulse rate from 55% to 80% correct. ANOVA with post hoc comparison shows that the improvement on motion robustness is significant. The rPPG method developed in this study has a performance that is very close to that of the contact-based sensor under realistic situations, while its computational efficiency allows real-time processing on an off-the-shelf computer.
The Detection of Monkeypox in Humans in the Western Hemisphere (2004)

Our investigation documents the isolation and identification of monkeypox virus from humans in the Western Hemisphere. Infection of humans was associated with direct contact with ill prairie dogs that were being kept or sold as pets.
Assessment of the antimicrobial effectiveness of a new silver alginate wound dressing: a RCT (2010)

The regression of local signs of infection, local tolerance, acceptability and usefulness were similar for the two dressings. However, Askina Calgitrol Ag improved the bacteriological status of the wounds. Further trials are required to show that it has a positive impact on the healing process.
Suppression of Ongoing T Cell-Mediated Autoimmunity by Peptide-MHC Class II Dimer Vaccination (2009)

Tissue-specific autoimmune diseases such as type 1 diabetes (T1D) are characterized by T cell-driven pathology. Administration of autoantigenic peptides provides a strategy to selectively target the pathogenic T cell response. Indeed, treatment with beta cell peptides effectively prevents T1D in NOD mice. However, the efficacy of peptide immunotherapy generally wanes as beta cell autoimmunity progresses and islet inflammation increases. With the goal of enhancing the efficacy of peptide immunotherapy, soluble (s)IA(g7)-Ig dimers covalently linked to beta cell autoantigen-derived peptides were tested for the capacity to suppress late preclinical T1D. NOD female mice with established beta cell autoimmunity were vaccinated i.v. with a short course of sIA(g7)-Ig dimers tethered to peptides derived from glutamic acid decarboxylase (GAD)65 (sIA(g7)-pGAD65). Treatment with sIA(g7)-pGAD65 dimers and the equivalent of only approximately 7 microg of native peptide effectively blocked the progression of insulitis and the development of diabetes. Furthermore, suppression of T1D was dependent on beta cell-specific IL-10-secreting CD4+ T cells, although the frequency of GAD65-specific FoxP3-expressing CD4+ T cells was also increased in sIA(g7)-pGAD65 dimer vaccinated NOD mice. These results demonstrate that MHC class II-Ig dimer vaccination is a robust approach to suppress ongoing T cell-mediated autoimmunity, and may provide a superior strategy of adjuvant-free peptide-based immunotherapy to induce immunoregulatory T cells.
High-extinction ratio and low-loss silica-based 8×8 strictly nonblocking thermooptic matrix switch (1999)

This paper describes a silica-based 8/spl times/8 strictly nonblocking thermooptic matrix switch with a high-extinction ratio and low loss. We realized this matrix switch by using a configuration which combines a double Mach-Zehnder interferometer (MZI) switching unit and an N/spl times/N matrix arrangement thus reducing the total waveguide length. The 8/spl times/8 matrix switch was fabricated on a 4-in wafer using planar lightwave circuit technology. We obtained an average extinction ratio of 60.3 dB and an average insertion loss of 5.1 dB. The operating wavelength bandwidth completely covers the gain band of practical erbium-doped fiber amplifiers (EDFAs).
Mobilization of CD34+ progenitor cells by granulocyte colony- stimulating factor in human immunodeficiency virus type 1-infected adults (1996)

We conducted a clinical trial to determine the feasibility of growth factor mobilization of CD34+ progenitor cells in human immunodeficiency virus type 1 (HIV-1)-infected individuals. Eight asymptomatic, HIV-1-infected adults (median CD4+ T-cell count, 415 cells/microL), received 480 micrograms/d of granulocyte colony-stimulating factor (G-CSF) for 6 days without evidence of viral activation. Despite concerns that HIV-1 might inhibit hematopoiesis, CD34+ cells were successfully mobilized to the periphery of all donors, independent of the baseline CD4+ T-cell count, and the status of antiretroviral therapy. Leukapheresis was performed on day 6, and yielded a median of 194 x 10(6) CD34+ cells per leukapheresis (n = 7). CD34-enriched cells from the leukapheresis were predominantly myeloid-committed, but between 0.2% and 1.7% were primitive CD34+/CD38- progenitors. A median of 21.7% of the mobilized CD34+ cells were dimly positive for CD4. Consequently, CD34(+)-enriched cells were purified on the cell sorter (mean purity, 97.7% +/- 2.4%; n = 7), and examined for HIV-1 DNA. Purified CD34+ cells from two of seven donors were polymerase chain reaction (PCR)-positive for HIV-1, but only from one of three samples from each donor. We conclude that G-CSF can safely mobilize CD34+ progenitor cells in HIV-1-infected subjects, and that these cells are suitable for consideration in gene-transfer strategies.
Converting Your Thoughts to Texts: Enabling Brain Typing via Deep Feature Learning of EEG Signals (2017)

An electroencephalography (EEG) based Brain Computer Interface (BCI) enables people to communicate with the outside world by interpreting the EEG signals of their brains to interact with devices such as wheelchairs and intelligent robots. More specifically, motor imagery EEG (MI-EEG), which reflects a subjects active intent, is attracting increasing attention for a variety of BCI applications. Accurate classification of MI-EEG signals while essential for effective operation of BCI systems, is challenging due to the significant noise inherent in the signals and the lack of informative correlation between the signals and brain activities. In this paper, we propose a novel deep neural network based learning framework that affords perceptive insights into the relationship between the MI-EEG data and brain activities. We design a joint convolutional recurrent neural network that simultaneously learns robust high-level feature presentations through low-dimensional dense embeddings from raw MI-EEG signals. We also employ an Autoencoder layer to eliminate various artifacts such as background activities. The proposed approach has been evaluated extensively on a large- scale public MI-EEG dataset and a limited but easy-to-deploy dataset collected in our lab. The results show that our approach outperforms a series of baselines and the competitive state-of-the- art methods, yielding a classification accuracy of 95.53%. The applicability of our proposed approach is further demonstrated with a practical BCI system for typing.
Using node merging to enhance graph coloring (1999)

A Chaitin-style register allocator often blocks during its simplification phase because no node in the interference graph has a degree that is sufficiently small. Typically, this is handled by node-splitting, or by optimistically continuing---and hoping that a legal N-coloring will still be found. We observe that the merging of two nodes in a graph causes a reduction in the degree of any node that had been adjacent to both. We have enhanced Chaitin's coloring algorithm so that it attempts node-merging during graph simplification; this often allows simplification to continue, while still guaranteeing a coloring for the graph. We have tested this algorithm using Appel's database of register-coloring graphs, and have compared it with Chaitin's algorithm. The merge-enhanced algorithm yields a better coloring about 8% of the time, and a worse coloring less than 0.1% of the time.
The Substrate Recognition Domains of the N-end Rule Pathway (2008)

The N-end rule pathway is a ubiquitin-dependent system where E3 ligases called N-recognins, including UBR1 and UBR2, recognize type-1 (basic) and type-2 (bulky hydrophobic) N-terminal residues as part of N-degrons. We have recently reported an E3 family (termed UBR1 through UBR7) characterized by the 70-residue UBR box, among which UBR1, UBR2, UBR4, and UBR5 were captured during affinity-based proteomics with synthetic degrons. Here we characterized substrate binding specificity and recognition domains of UBR proteins. Pull-down assays with recombinant UBR proteins suggest that 570-kDa UBR4 and 300-kDa UBR5 bind N-degron, whereas UBR3, UBR6, and UBR7 do not. Binding assays with 24 UBR1 deletion mutants and 31 site-directed UBR1 mutations narrow down the degron-binding activity to a 72-residue UBR box-only fragment that recognizes type-1 but not type-2 residues. A surface plasmon resonance assay shows that the UBR box binds to the type-1 substrate Arg-peptide with Kd of approximately 3.4 microm. Downstream from the UBR box, we identify a second substrate recognition domain, termed the N-domain, required for type-2 substrate recognition. The approximately 80-residue N-domain shows structural and functional similarity to 106-residue Escherichia coli ClpS, a bacterial N-recognin. We propose a model where the 70-residue UBR box functions as a common structural element essential for binding to all known destabilizing N-terminal residues, whereas specific residues localized in the UBR box (for type 1) or the N-domain (for type 2) provide substrate selectivity through interaction with the side group of an N-terminal amino acid. Our work provides new insights into substrate recognition in the N-end rule pathway.
Structural Requirements of Ceramide and Sphingosine Based Inhibitors of Mitochondrial Ceramidase (2001)

The effects of structural analogues of ceramide on rat brain mitochondrial ceramidase (mt-CDase) were investigated. Design of target compounds was mainly based on modifications of the key elements in ceramide and sphingosine, including stereochemistry, the primary and secondary hydroxyl groups, the trans double bond in the sphingosine backbone, and the amide bond. Mt-CDase was inhibited by (1) all stereoisomers of D-erythro-ceramide (D-e-Cer) with an IC50 of 0.11, 0.21, and 0.26 mol % for the L-threo, D-threo, and L-erythro isomers, respectively; (2) all stereoisomers of sphingosine with IC50 ranging from 0.04 to 0.14 mol %, N-methyl-D-erythro-sphingosine (N-Me-Sph, IC50 0.13 mol %); and (3) D-erythro-urea-C16-ceramide (C16-urea-Cer IC50 0.33 mol %). The enzyme was not inhibited by N-methyl ceramide (N-Me-C16-Cer), 1-O-methyl ceramide (1-O-Me-C16-Cer), 3-O-methyl ceramide (3-O-Me-C16-Cer), cis-D-erythro ceramide (cis-D-e-C16-Cer) and 3-O-methyl-D-erythro-sphingosine (3-O-Me-Sph). It was less potently inhibited by D-erythro-sphinganine (D-e-dh-Sph, IC50 0.20 mol %), D-erythro-dehydro sphingosine (D-e-deh-Sph, IC50 0.25 mol %), (2S)-3-keto-sphinganine (3-keto-dh-Sph, IC50 0.34 mol %), (2S) 3-keto-ceramide (3-keto-C16-Cer, IC50 0.60 mol %), and ceramine (C18-ceramine, IC50 0.62 mol %), 1-O-methyl-D-erythro-sphingosine (1-O-Me-Sph), cis-D-erythro-sphingosine (cis-D-e-Sph), (2S)-3-ketosphingosine (3-keto-Sph), (2S)-3-keto-dehyrosphingosine (3-keto-deh-Sph), and N,N-dimethyl-D-erythrosphingosine (N,N-diMe-Sph) were weak inhibitors whereas ceramide-1-phosphate (Cer-1-P) and sphingosine-1-phosphate (Sph-1-P) stimulated the enzyme. Thus, for inhibition, the enzyme requires the primary and secondary hydroxyl groups, the C4-C5 double bond, the trans configuration of this double bond, and the NH-protons from either the amide of ceramide or the amine of sphingosine. Therefore, these results provide important information on the requirements for ceramide-enzyme interaction, and they suggest that ligand interaction with the enzyme occurs in a high affinity low specificity manner, in contrast to catalysis which is highly specific for D-erythro-ceramide (D-e-Cer) but occurs with a lower affinity. In addition, this study identifies two competitive inhibitors of mt-CDase; urea-ceramide (C16-urea-Cer) and ceramine (C18-ceramine) that may be further developed and used to understand the mechanism of mt-CDase in vitro and in biologic responses.
Human platelets express heat shock protein receptors and regulate dendritic cell maturation (2002)

Immunizations using the endoplasmic reticulum-resident heat shock protein Gp96 induce specific immune responses. Specificity is based on the major histocompatibility complex class I-restricted cross-presentation of Gp96-associated peptides derived from endogenous proteins. Initiation of the immune response depends on the ability of Gp96 to induce the production of proinflammatory cytokines by macrophages and dendritic cells (DCs) and of their maturation in a fashion presumably independent of associated peptide. Both events are mediated by Gp96 receptors on antigen-presenting cells. It is known that Gp96 is released from cells at necrosis induced, for example, by virus infection. Although this event supports the efficient induction of immune responses, it might also interfere with processes that are susceptible to chronic inflammation, such as wound healing after tissue damage. Therefore, Gp96-mediated stimulation of the immune system requires tight regulation. Here we show that human thrombocytes specifically interact with Gp96 and that binding of Gp96 to platelets is enhanced more than 10-fold on activation by thrombin. Gp96 interferes with neither thrombin-induced platelet activation nor platelet aggregation. However, the presence of platelets during Gp96-mediated DC activation reduces the secretion of proinflammatory cytokines and the activation of DCs. This effect is independent of soluble platelet factors and cell-to-cell contact between DCs and thrombocytes. Thus, we provide evidence for a regulatory mechanism that neutralizes Gp96 molecules systemically, especially in the blood. This effect might be of significance in wounds in which chronic inflammation and immune responses against autoantigens have to be prevented.
Ca 2+ /Calmodulin-Dependent Protein Kinase II δ Mediates Myocardial Ischemia/Reperfusion Injury Through Nuclear Factor-κB (2013)

This is the first study demonstrating that CaMKIIδ mediates NF-κB activation in cardiomyocytes after in vivo I/R and suggests that CaMKIIδ serves to trigger, as well as to sustain subsequent changes in inflammatory gene expression that contribute to myocardial I/R damage.
The physiological significance of β-actin mRNA localization in determining cell polarity and directional motility (2001)

beta-actin mRNA is localized near the leading edge in several cell types, where actin polymerization is actively promoting forward protrusion. The localization of the beta-actin mRNA near the leading edge is facilitated by a short sequence in the 3' untranslated region, the "zip code." Localization of the mRNA at this region is important physiologically. Treatment of chicken embryo fibroblasts with antisense oligonucleotides complementary to the localization sequence (zip code) in the 3' untranslated region leads to delocalization of beta-actin mRNA, alteration of cell phenotype, and a decrease in cell motility. To determine the components of this process responsible for the change in cell behavior after beta-actin mRNA delocalization, the Dynamic Image Analysis System was used to quantify movement of cells in the presence of sense and antisense oligonucleotides to the zip code. It was found that net path length and average speed of antisense-treated cells were significantly lower than in sense-treated cells. Total path length and the velocity of protrusion of antisense-treated cells were not affected compared with those of control cells. These results suggest that a decrease in persistence of direction of movement and not in velocity results from treatment of cells with zip code-directed antisense oligonucleotides. To test this, direct analysis of directionality was performed on antisense-treated cells and showed a decrease in directionality (net path/total path) and persistence of movement. Less directional movement of antisense-treated cells correlated with a unpolarized and discontinuous distribution of free barbed ends of actin filaments and of beta-actin protein. These results indicate that delocalization of beta-actin mRNA results in delocalization of nucleation sites and beta-actin protein from the leading edge followed by loss of cell polarity and directional movement.
End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival (1989)

The effectiveness of ongoing cardiopulmonary resuscitation efforts is difficult to evaluate. Recent studies suggest that carbon dioxide excretion may be a useful noninvasive indicator of resuscitation from cardiac arrest. A prospective clinical study was done to determine whether end-tidal carbon dioxide monitoring during cardiopulmonary resuscitation could be used as a prognostic indicator of resuscitation and survival. Thirty-five cardiac arrests in 34 patients were monitored with capnometry during cardiopulmonary resuscitation during a 1-year period. Nine patients who were successfully resuscitated had higher average end-tidal carbon dioxide partial pressures during cardiopulmonary resuscitation than 26 patients who could not be resuscitated (15±4 vs 7±5 mm Hg). The 3 patients who survived to leave the hospital had a higher average end-tidal carbon dioxide partial pressure than the 32 nonsurvivors (17 ± 6 vs 8 ± 5 mm Hg). All 9 patients who were successfully resuscitated had an average end-tidal carbon dioxide partial pressure of 10 mm Hg or greater. No patient with an average end-tidal carbon dioxide partial pressure of less than 10 mm Hg was resuscitated. Data from this prospective clinical trial indicate that findings from end-tidal carbon dioxide monitoring during cardiopulmonary resuscitation are correlated with resuscitation from and survival of cardiac arrest. (<i>JAMA</i>. 1989;262:1347-1351)