gebhart/patrepeval huggingface dataset:
New Slide Attacks on Almost Self-Similar Ciphers. (2019)

The slide attack is a powerful cryptanalytic tool which can break iterated block ciphers with a complexity that does not depend on their number of rounds. However, it requires complete self similarity in the sense that all the rounds must be identical. While this can be the case in Feistel structures, this rarely happens in SP networks since the last round must end with an additional post-whitening subkey. In addition, in many SP networks the final round has additional asymmetries – for example, in AES the last round omits the MixColumns operation. Such asymmetry in the last round can make it difficult to utilize most of the advanced tools which were developed for slide attacks, such as deriving from one slid pair additional slid pairs by repeatedly re-encrypting their ciphertexts. Consequently, almost all the successful applications of slide attacks against real cryptosystems (e.g., FF3, GOST, SHACAL-1) had targeted Feistel structures rather than SP networks.
Differential Regulation of the PGC Family of Genes in a Mouse Model of Staphylococcus aureus Sepsis (2010)

The PGC family of transcriptional co-activators (PGC-1alpha [Ppargc1a], PGC-1beta [Ppargc1b], and PRC [Pprc]) coordinates the upregulation of mitochondrial biogenesis, and Ppargc1a is known to be activated in response to mitochondrial damage in sepsis. Therefore, we postulated that the PGC family is regulated by the innate immune system. We investigated whether mitochondrial biogenesis and PGC gene expression are disrupted in an established model of Staphylococcus aureus sepsis both in mice with impaired innate immune function (TLR2-/- and TLR4-/-) and in wild-type controls. We found an early up-regulation of Ppargc1a and Ppargc1b post-infection (at 6 h) in WT mice, but the expression of both genes was concordantly dysregulated in TLR2-/- mice (no increase at 6 h) and in TLR4-/- mice (amplified at 6 h). However, the third family member, PRC, was regulated differently, and its expression increased significantly at 24 h in all three mouse strains (WT, TLR2-/-, and TLR4-/-). In silico analyses showed that Ppargc1a and Ppargc1b share binding sites for microRNA mmu-mir-202-3p. Thus, miRNA-mediated post-transcriptional mRNA degradation could account for the failure to increase the expression of both genes in TLR2-/- mice. The expression of mmu-mir-202-3p was measured by real-time PCR and found to be significantly increased in TLR2-/- but not in WT or TLR4-/- mice. In addition, it was found that mir-202-3p functionally decreases Ppargc1a mRNA in vitro. Thus, both innate immune signaling through the TLRs and mir-202-3p-mediated mRNA degradation are implicated in the co-regulation of Ppargc1a and Ppargc1b during inflammation. Moreover, the identification of mir-202-3p as a potential factor for Ppargc1a and Ppargc1b repression in acute inflammation may open new avenues for mitochondrial research and, potentially, therapy.
Capacity Analysis of MIMO Systems Using Limited Feedback Transmit Precoding Schemes (2008)

This paper employs a high resolution quantization framework to study the effects of finite-rate feedback of the channel state information (CSI) on the performance of multiple-input-multiple-output (MIMO) systems over independently and identically distributed (i.i.d.) Rayleigh flat fading channels. The contributions of this paper are twofold. First, we extend the general distortion analysis of vector quantizers to deal with complex source variables. Necessary and sufficient conditions that guarantee a concise high-resolution distortion analysis in the complex domain is presented. Second, as an application of the proposed complex distortion analysis, tight lower bounds on the capacity loss due to the finite-rate channel quantization are provided for MIMO systems employing a fixed number of equal power spatial beams. Based on the obtained closed-form analytical results, it is shown that the system capacity loss decreases exponentially as the ratio of the quantization rate to the total degrees of freedom of the channel state information to be quantized. Moreover, MIMO CSI-quantizers using mismatched codebooks that are only optimized for high-signal-to-noise ratio (SNR) and low-SNR regimes are also investigated to quantify the penalties incurred by the use of mismatched codebooks. In addition, the analysis is extended to deal with MIMO systems using multi-mode spatial multiplexing transmission schemes with finite-rate CSI feedback. Finally, numerical and simulation results are presented which confirm the tightness of the derived theoretical distortion bounds.
Reduction of calcification of carbodiimide-processed heart valve tissue by prior blocking of amine groups with monoaldehydes. (2006)

Amine blocking and cross-linking technology appears promising in the design of the next generation of tissue valves. Calcification was significantly reduced compared to GA cross-linking. The mechanistic insight of decreased wall calcification is still unknown, and research investigations are ongoing.
Table S1 from Human CD4<sup>+</sup> T Cells Specific for Merkel Cell Polyomavirus Localize to Merkel Cell Carcinomas and Target a Required Oncogenic Domain (2023)

&lt;p&gt;20mer peptides spanning the MCPyV T antigen space&lt;/p&gt;
Detecting the performance impact of upgrades in large operational networks (2010)

Networks continue to change to support new applications, improve reliability and performance and reduce the operational cost. The changes are made to the network in the form of upgrades such as software or hardware upgrades, new network or service features and network configuration changes. It is crucial to monitor the network when upgrades are made because they can have a significant impact on network performance and if not monitored may lead to unexpected consequences in operational networks. This can be achieved manually for a small number of devices, but does not scale to large networks with hundreds or thousands of routers and extremely large number of different upgrades made on a regular basis.
ISG15 deficiency and increased viral resistance in humans but not mice (2016)

ISG15 is an interferon (IFN)-α/β-induced ubiquitin-like protein. It exists as a free molecule, intracellularly and extracellularly, and conjugated to target proteins. Studies in mice have demonstrated a role for Isg15 in antiviral immunity. By contrast, human ISG15 was shown to have critical immune functions, but not in antiviral immunity. Namely, free extracellular ISG15 is crucial in IFN-γ-dependent antimycobacterial immunity, while free intracellular ISG15 is crucial for USP18-mediated downregulation of IFN-α/β signalling. Here we describe ISG15-deficient patients who display no enhanced susceptibility to viruses in vivo, in stark contrast to Isg15-deficient mice. Furthermore, fibroblasts derived from ISG15-deficient patients display enhanced antiviral protection, and expression of ISG15 attenuates viral resistance to WT control levels. The species-specific gain-of-function in antiviral immunity observed in ISG15 deficiency is explained by the requirement of ISG15 to sustain USP18 levels in humans, a mechanism not operating in mice.
Clinico-genomic profiling and clonal dynamic modeling of TP53-aberrant myelodysplastic syndrome and acute myeloid leukemia (2021)

<i>TP53</i>-aberrant myelodysplastic syndrome and acute myeloid leukemia have dismal outcomes. Here, we define the clinico-genomic landscape of <i>TP53</i> disruptions in 40 patients and employ clonal dynamic modeling to map the mutational hierarchy against clinical outcomes. Most <i>TP53</i> mutations (45.2%) localized to the L3 loop or LSH motif of the DNA-binding domain. <i>TP53</i> disruptions had high co-occurrence with mutations in epigenetic regulators, spliceosome machinery, and cohesin complex and low co-occurrence with mutations in proliferative signaling genes. Ancestral and descendant <i>TP53</i> mutations constituted measurable residual disease and fueled relapse. High mutant <i>TP53</i> gene dosage predicted low durability of remission. The median overall survival (OS) was 280 days. Hypomethylating agent-based therapy served as an effective bridge to transplant, leading to improved median OS compared to patients who did not receive a transplant (14.7 <i>vs.</i> 5.1 months). OS was independent of the genomic location of <i>TP53</i> disruption, which has implications for rational therapeutic design.
Polymer‐Based White‐Light‐Emitting Electrochemical Cells with Very High Color‐Rendering Index Based on Blue‐Green Fluorescent Polyfluorenes and Red‐Phosphorescent Iridium Complexes (2018)

Application of the concept of three-color (red (R), green (G), and blue (B)) light-mixing to obtain white light is the most suitable way to realize white-light-emitting devices with very high color-rendering indices (CRI). White-light-emitting devices based on the three-color-mixing method could be used to create lighting and display technologies. Here, white-light-emitting electrochemical cells (LECs) with very high CRIs are reported, which were fabricated by using blend films composed of a fluorescent π-conjugated polymer (FCP), poly(9,9-dioctylfluorene-co-benzothiadiazole) (PFBT), and a phosphorescent iridium complex, [Ir(ppy)<sub>2</sub> (biq)]<sup>+</sup> (PF<sub>6</sub> )<sup>-</sup> (where (ppy)<sup>-</sup> =2-phenylpyridinate and biq=2,2'-biquinoline). The LECs fabricated with PFBT, the benzothiadiazole content of which is 0.01 mol %, showed blue electroluminescence (EL) emission originating from the fluorene segments and green EL emission from the benzothiadiazole units simultaneously. White LECs were then realized by adding red-emitting Ir complexes as guest molecules to the blue-green-emitting PFBT. By optimizing the proportions of the PFBT and Ir complexes in the active layers (PFBT/[Ir(ppy)<sub>2</sub> (biq)]<sup>+</sup> (PF<sub>6</sub> )<sup>-</sup> =1:0.2 (mass ratio)), white-light emission with Commission Internationale de l'Eclairage (CIE) coordinates of (0.29, 0.34) and a very high CRI value of 91.5 was achieved through RGB color-mixing. It was noted that the emission mechanism was based on Förster resonance energy transfer and Dexter energy transfer from excited PFBT to [Ir(ppy)<sub>2</sub> (biq)]<sup>+</sup> (PF<sub>6</sub> )<sup>-</sup> . The utilization of LECs based on blue-green FCPs and red Ir complexes looks very promising for the prospect of realizing white-light-emitting devices with very high CRIs.
Modulation instability of incoherent waves (2000)

Summary form only given. Modulation instability (MI) is a common phenomenon in coherent non-linear wave systems; it can be typically observed on top of a broad pulse or an optical beam. In this case, small noise perturbations grow exponentially as the pulse propagates, transferring energy from large wavelengths into smaller wavelengths. In a sense, MI phenomena can be regarded as a precursor of bright optical solitons. The recent demonstration of existence of incoherent solitons led us to wander whether MI can be observed with incoherent waves as well. Here, we demonstrate analytically and numerically that MI can exist in nonlinear incoherent systems.
The ABNL-MARRO 001 study: a phase 1–2 study of randomly allocated active myeloid target compound combinations in MDS/MPN overlap syndromes (2022)

This trial was registered with ClinicalTrials.gov on August 19, 2019 (Registration No. NCT04061421).
Diphenyleneiodonium induces ROS‐independent p53 expression and apoptosis in human RPE cells (2006)

The diphenyleneiodonium (DPI) is widely used as an inhibitor of flavoenzymes, particularly NADPH oxidase. In this study, we investigated the effect of DPI on the apoptosis of human RPE cells. DPI treatment in ARPE-19 cells evoked a dose- and time-dependent growth inhibition, and also induced DNA fragmentation and protein content of the proapoptotic factor Bax. In addition, DPI significantly induced the expression and phosphorylation of p53, which induces proapoptotic genes in response to DNA damage or irreparable cell cycle arrest. ROS have been implicated as a key factor in the activation of p53 by many chemotherapeutic drugs. Recent data on the regulation of intracellular ROS by DPI are controversial. Therefore, we analyzed whether DPI could contribute to the generation of intracellular ROS. Although there was increase in ROS level from cells treated for 24h with DPI, it was not detectable at early time points, required to induce p53 expression. And DPI-induced p53 expression was not affected by the ROS scavenger NAC. We conclude that DPI induces the expression of p53 by ROS-independent mechanism in ARPE-19 cells, and renders cells sensitive to drug-induced apoptosis by induction of p53 expression.
Systematic Synthesis and Biological Evaluation of α - and β-D-Xylo- and Lyxofuranonucleosides of the Five Naturally Occurring Nucleic Acid Bases (1987)

Abstract The α-and β-D-Xylofuranosyl and -lyxofuranosyl analogues of the five naturally occurring nucleic acid bases have been the subject of a systematic synthesis and examination of some of their biological properties, i.e. antiviral, antimetabolic and cytostatic activities.
Generation and use of long-lasting cell labeling agent for positron emission tomography (PET) imaging (2014)

273 Objectives Cell-based therapies, such as dendritic cell (DC) vaccines, immunotherapy, and stem cell transplants, have become increasingly important in the treatment of cancers. Development of non-invasive monitoring systems to track cells in a patient is critical for better understanding of the biology of these cells and to improve and optimize therapeutic strategies. Therefore, we developed a new cell labeling agent using a PET radiouclide emitter, Zirconium-89 (89Zr). Methods 89Zr-oxine complex was synthesized and used for cell radiolabeling. Radiolabeling of cells with 89Zr-oxine was tested using mouse bone marrow derived DCs, NK cells, and T cells; those cell types often used in cell-mediated therapies. Retention of radiolabel within the cells and survival of the cells after the labeling were examined. The labeled cells were transferred to C57BL/6 mice via a tail vein injection (148-370 kBq/5 million cells per mouse) and serial whole body images were acquired using a microPET imager up to 7 days post-injection. Results Synthesis of 89Zr-oxine complex from 89Zr was accomplished in >97% yield. Sufficient cell labeling with 89Zr-oxine for imaging was achieved within 15 min of incubation at room temperature in PBS. The labeling could be performed in serum free medium, if desired, when radiolabeling some types of cells sensitive to buffer conditions. Importantly, this labeling procedure did not negatively affect cell survival. 89Zr incorporated into the cells was stable and enabled tracking of cells in mice for 7 days using a microPET imager. Compared to conventional 111In-oxine, 89Zr-oxine required only about 1/10 th of the radioactivity to acquire comparable images. Conclusions We have developed a stable cell labeling agent for PET, 89Zr-oxine, that enabled extended tracking of the cells with high sensitivity at a very low radioactive dose. This labeling method can be applied to various cell types used in clinical and basic research.
In vitro binding of an IgE protein to human platelets. (1986)

Bronchoconstriction in extrinsic asthma is initiated by mediators released from IgE-sensitized leukocytes after contact with polyvalent antigen. Because platelets also contain soluble mediators that can cause bronchoconstriction, platelet activation and release of the contents of platelet granules may play a role in IgE-mediated responses under some circumstances. We therefore sought to determine if platelets are capable of binding IgE and if cross-linking this cell-bound IgE initiates secretion of platelet granule contents. Platelets from 10 normal donors were studied by using automated fluorescence analysis and fluorescence microscopy. We detected binding of a purified myeloma IgE protein to 24.1 +/- 9.6% (mean +/- 2 SD) of the gel-filtered platelets from these normal individuals. Although we could detect the binding of IgE and anti-IgE to a minority of cells, every normal individual had a population of platelets that bound IgE. The amount of IgE that bound to normal platelets appeared to be distributed heterogeneously among the IgE-positive platelet population. Platelets from two individuals with type II Glanzmann's thrombasthenia bound normal amounts of heat-aggregated IgG, but less than 3% of the platelets bound detectable IgE. Moreover, a combination of monoclonal antibodies to glycoproteins IIb and IIIa inhibited the binding of the IgE protein to normal platelets but did not affect the binding of aggregated IgG. Thus, the binding of IgE to human platelets appeared to require the presence of the glycoprotein IIb-IIIa complex. Binding of monomeric IgE to platelets, by itself, did not initiate either platelet aggregation or release of 14C-serotonin. However, both aggregation and secretion of serotonin followed the addition of anti-IgE to IgE-sensitized platelets. These studies indicate that human platelets can bind an IgE myeloma protein in vitro and that cross-linking of surface-bound IgE with anti-IgE initiates aggregation and secretion. If platelets have a similar capacity to bind normal IgE in vivo, it is possible that platelets may participate directly in several atopic or inflammatory disorders in man mediated by this class of antibody.
Sorption and transport of linear alkane hydrocarbons in biaxially oriented polyethylene terephthalate (2001)

Abstract Equilibrium sorption and uptake kinetics of n ‐butane and n ‐pentane in uniform, biaxially oriented, semicrystalline polyethylene terephthalate films were examined at 35 °C and for pressures ranging from 0 to approximately 76 cmHg. Sorption isotherms were well described by the dual‐mode sorption model. Sorption kinetics were described either by Fickian diffusion or a two‐stage model incorporating Fickian diffusion at short times and protracted polymer structural relaxation at long times. Diffusion coefficients increased with increasing penetrant concentration. n ‐Butane solubility was lower than that of n ‐pentane, consistent with the more condensable nature of n ‐pentane. However, n ‐butane diffusion coefficients were higher than those of n ‐pentane. Infinite‐dilution, estimated amorphous phase diffusion and solubility coefficients were well correlated with penetrant critical volume and critical temperature, respectively. © 2001 John Wiley &amp; Sons, Inc. J Polym Sci B: Polym Phys 39: 1160–1172, 2001
RNA Ligases (1991)

T4 RNA ligase, the product of the phage gene 63, is purified from phage-infected cells. It catalyzes the ATP-dependent covalent joining of single-stranded 5'-phosphoryl termini of DNA or RNA to single-stranded 3'-hydroxyl termini of DNA or RNA. This unit describes specific reaction conditions as well as applications such as radioactive labeling of 3' termini of RNA, circularizing deoxy- and ribo-oligonucleotides, ligating oligomers for oligonucleotide synthesis, and stimulating the blunt-end ligation activity of T4 DNA ligase.
Five‐year risk of incident disease following a diagnosis of chronic rhinosinusitis (2015)

The risk of other diseases associated with CRS adds to the burden of an already highly burdensome condition, and suggests either that CRS promotes onset of other diseases or is an indicator of systemic disease processes. Different patterns of association with diseases by CRS phenotype may be due to CRSwNP sample size limitations or reflect a different pattern of disease onset by phenotype. These findings have implications for screening guidelines and care of CRS patients.
A Simple Scheme for Jitter Reduction in Phase-Differential Carrier Frequency Recovery Loop (2006)

A very simple and efficient scheme for jitter reduction is proposed for a carrier frequency recovery loop using phase differential frequency estimation, which estimates the current frequency offset based on the difference of the average phases of two successive intervals. Analytical and numerical results presented in this paper show that by simply overlapping the observation intervals by half for frequency offset estimations, both the steady-state and transient performances can be improved. The proposed scheme does not require any additional hardware circuitry, but results in improved performance even with reduced complexity.
Aqueous-Phase Oxidation of Epitaxial Graphene on the Silicon Face of SiC(0001) (2013)

To explore the chemical and electronic states of oxidized epitaxial graphene (EG) grown on the Si face of SiC(0001), we employ the Hummers oxidizing agents (H2SO4 + NaNO3 + KMnO4) under different reaction conditions that oxidize the graphene layer. The resulting material is characterized with scanning tunneling microscopy (STM), scanning tunneling spectroscopy (STS), Raman spectroscopy, and X-ray photoelectron spectroscopy (XPS). A mild "drop-cast" procedure at 60 °C is found to be equally effective at oxidizing EG as the conventional Hummers procedure. This aqueous-phase oxidation reaction appears to proceed in an autocatalytic manner as indicated by the concurrent observation of patches of oxidized and clean graphene areas in atomically resolved STM images on partially oxidized EG. STS further reveals substantial changes in electronic structure for oxidized EG including the opening of a local band gap of ∼0.4 eV. The oxidation is confined to the graphene layers as verified by XPS characterization of the underlying SiC substrate. In contrast to EG oxidized in ultrahigh vacuum that contains only epoxy groups and can be fully reverted back to pristine EG following annealing at 260 °C, aqueous-phase oxidized EG possesses carbonyl and hydroxyl groups in addition to the dominant epoxy groups and thus remains partially oxidized even following annealing at 1000 °C.
DIFFERENT SPECIFICITIES OF CLONED T CELLS ASSESSED BY IN VITRO PROLIFERATION ASSAYS AND BY THE ABILITY TO MEDIATE SKIN GRAFT REJECTION IN VIVO (1987)

The experiments presented here have compared the specificities of T cell clones as determined by in vitro proliferative responses and their specificities as reflected by their ability to mediate skin graft rejection in vivo. Two proliferative T cell clones with distinct in vitro specificities were evaluated for their ability to mediate rejection of skin grafts from C57BL/10 Scn nu/nu mice. Clone 14.11 (L3T4+, Lyt2-) was specifically stimulated to proliferate in vitro by I-Ad determinants, while clone 3.3.10 (also L3T4+, Lyt2-) recognized M1sa products in the context of MHC-encoded cell surface determinants. The results demonstrate that both clone 14.11 and clone 3.3.10 T cells are capable of mediating rejection of DBA/2 (H-2d, M1sa) skin grafts from B10 nu/nu mice. Surprisingly, neither clone 3.3.10 T cells nor clone 14.11 T cells were found to be effective at rejecting skin grafts from the D1.C congenic donor strain of mice (also H-2d, M1sa) from B10 nu/nu mice. Further, clone 14.11 T cells were also found to be ineffective at rejecting B10.D2 (H-2d, M1sb) skin grafts from B10 nu/nu mice. These data indicate the existence of a striking dichotomy between the specificity of alloreactive T cell clones as determined by in vitro proliferation studies and their functional capabilities in vivo.