gebhart/patrepeval huggingface dataset:
Quantum light transport in phase-separated Anderson localization fiber (2022)

Abstract Propagation of light by Anderson localization has been demonstrated in micro-nano-structured fibers. In this work, we introduce a phase separated glass Anderson localization optical fiber for quantum applications. By using a spontaneous parametric down-conversion source, multi-photon detection with a single-photon avalanche diode array camera, and signal post-processing techniques, we demonstrate quantum light transport, where spatial correlations between photon pairs are preserved after propagation. In order to better understand and improve light transport, we study light localization, observing a dependence on wavelength. Our results indicate that the proposed phase separated fiber may become an effective platform for quantum imaging and communication.
Draft Genome Sequence of the Toluene-Degrading Pseudomonas stutzeri Strain ST-9 (2015)

Strain ST-9 was isolated from toluene-contaminated soil (Samaria, Israel). The draft genome has an estimated size of 4.8 Mb, exhibits an average G+C content of 60.37%, and is predicted to encode 4,183 proteins, including a gene cluster for aromatic hydrocarbon degradation. It is assigned to genomovar 3 of Pseudomonas stutzeri.
Supplementary Figure 3 from Identification and Characterization of MEL-3, a Novel AR Antagonist That Suppresses Prostate Cancer Cell Growth (2023)

&lt;p&gt;PDF file, 37KB, MEL-3 has no agonistic properties on ClARE.&lt;/p&gt;
Transferrin receptor recycling in rat hepatocytes is regulated by protein phosphatase 2A, possibly through effects on microtubule-dependent transport (1997)

To understand the regulation of receptor-mediated endocytosis in hepatocytes, we have used two specific inhibitors of serine-threonine protein phosphatases (PP), microcystin (MCYST) and okadaic acid (OKA) as probes to alter protein phosphorylation in hepatocytes. We have then examined the impact of these changes on the specific binding and uptake of transferrin (Tf) in hepatocytes. The measurement of PP activity in hepatocyte lysates showed that OKA and MCYST shared a common inhibition of protein phosphatase 2A (PP2A). Our results showed that both OKA (250 nmol/L) and MCYST (500 nmol/L) significantly reduced Tf uptake at steady state (P < or = .05). The measurement of Tf internalization after 15 minutes in protein phosphatase inhibitor-pretreated cells revealed that the initial uptake was also significantly reduced. Binding studies showed that pretreatment with either of the phosphatase inhibitors did not result in significant changes in the K(d) for Tf binding to transferrin receptor (TfR). Additionally, no significant changes in the number of TfR in the plasma membrane were observed in phosphatase inhibitor-pretreated cells. The treatment of hepatocytes with nocodazole (NOC), which results in microtubule disassembly and inhibition of microtubule-based vesicle transport, caused comparable reductions in initial and steady state levels of transferrin accumulation. The changes in transferrin accumulation by both phosphatase inhibitors and nocodazole were accompanied by redistribution of the microtubule-anchored Golgi apparatus and lysosomal network from the perinuclear region to the cell periphery. Our data show that the regulation of Tf uptake by receptor-mediated endocytosis is mediated by PP2A and additionally may occur through regulation of microtubule-based vesicle transport.
Progression of retinopathy is related to glycaemic control even in patients with mild diabetes mellitus (1996)

To study the progression of retinopathy in patients with mild diabetes mellitus, we examined, in a cohort study, 347 patients treated with diet alone at baseline. The patients participated in an ophthalmological screening and control programme, and diet-treated patients who were examined between January 1990 and July 1992 were included in the study and followed until October 1995. Mean follow-up was 3.4 +/- 1.1 years. The alternative classification of the Wisconsin study was used to classify retinopathy, and the mean HbA1c values for the study period, to estimate the level of glycaemic control. At baseline, 314 of the patients (90.5%) had no retinopathy, and 33 (9.5%) had mild non-proliferative diabetic retinopathy. In 296 patients there was no retinopathy progression, in 27 patients there was progression by 1 level in the retinopathy scale, and in 24 patients by 2 levels or more. In 2 patients there was progression to proliferative diabetic retinopathy. The mean HbA1c (%) was 6.5 +/- 1.3. Higher HbA1c correlated to increased progression (r = 0.16; p = 0.005), and in a multivariate analysis, HbA1c remained associated with a progression of retinopathy by 2 levels or more, with a relative risk of 1.4 per percent increase in HbA1c (95% CI 1.1-2.0; p = 0.02). Furthermore, the presence of any retinopathy at baseline was associated with progression with a relative risk of 1.7 (95% confidence interval 1.1-2.8; (p = 0.02). These data indicate that even slightly elevated levels of HbA1c might be associated with a risk of retinopathy progression.
Aβ neurotoxicity depends on interactions between copper ions, prion protein, and N -methyl- d -aspartate receptors (2012)

N-methyl-d-aspartate receptors (NMDARs) mediate critical CNS functions, whereas excessive activity contributes to neuronal damage. At physiological glycine concentrations, NMDAR currents recorded from cultured rodent hippocampal neurons exhibited strong desensitization in the continued presence of NMDA, thus protecting neurons from calcium overload. Reducing copper availability by specific chelators (bathocuproine disulfonate, cuprizone) induced nondesensitizing NMDAR currents even at physiologically low glycine concentrations. This effect was mimicked by, and was not additive with, genetic ablation of cellular prion protein (PrP(C)), a key copper-binding protein in the CNS. Acute ablation of PrP(C) by enzymatically cleaving its cell-surface GPI anchor yielded similar effects. Biochemical studies and electrophysiological measurements revealed that PrP(C) interacts with the NMDAR complex in a copper-dependent manner to allosterically reduce glycine affinity for the receptor. Synthetic human Aβ(1-42) (10 nM-5 μM) produced an identical effect that could be mitigated by addition of excess copper ions or NMDAR blockers. Taken together, Aβ(1-42), copper chelators, or PrP(C) inactivation all enhance the activity of glycine at the NMDAR, giving rise to pathologically large nondesensitizing steady-state NMDAR currents and neurotoxicity. We propose a physiological role for PrP(C), one that limits excessive NMDAR activity that might otherwise promote neuronal damage. In addition, we provide a unifying molecular mechanism whereby toxic species of Aβ(1-42) might mediate neuronal and synaptic injury, at least in part, by disrupting the normal copper-mediated, PrP(C)-dependent inhibition of excessive activity of this highly calcium-permeable glutamate receptor.
Electric-Field Enhancement of a Gate-All-Around Nanowire Thin-Film Transistor Memory (2010)

A high-performance gate-all-around (GAA) poly-Si nanowire (NW) SONOS-type memory thin-film transistor (TFT) is presented. The presence of the corners of the GAA structure resulted in the program speed and memory window of this device being superior to those of a planar poly-Si TFT device. When erasing, planar devices exhibit a threshold-voltage shift resulting from gate injection; the GAA device was immune to this behavior. The presence of a nonuniform electric field in the channel region during programming and erasing was confirmed through simulation. The device also exhibited superior endurance and data-retention behavior.
SIR estimation on common pilot channel with the knowledge of data to pilot power ratio for closed loop power control in WCDMA FDD downlink (2005)

For the closed loop power control (CLPC) of WCDMA FDD downlink, the signal to interference ratio (SIR) is typically estimated by using the dedicated pilot symbols in the dedicated physical control channel (DPCCH). In this paper it is shown that by estimating the SIR on the common pilot channel (CPICH) along with the knowledge of DPCH to CPICH power ratio, the CLPC performs much better as compared to the case when the SIR is estimated on the DPCCH pilot symbols only. It is proposed that additional slot formats be introduced in the 3GPP forward link slot formats with a reduced number of DPCCH pilot symbols and a corresponding increase in the data symbols. These slot formats could be utilized when the CPICH is available and will also result in an increase in the data throughput.
<p>Emergence of Hypervirulent Ceftazidime/Avibactam-Resistant <em>Klebsiella pneumoniae</em> Isolates in a Chinese Tertiary Hospital</p> (2020)

The newly emerged hypervirulent CAZ/AVI-resistant KP strain might cause a serious threat to public health, suggesting an urgent need for enhanced clinical awareness and epidemiologic surveillance.
Supplementary Tables 1-2 and Figures 1-10 from Inhibition of Tryptophan-Dioxygenase Activity Increases the Antitumor Efficacy of Immune Checkpoint Inhibitors (2023)

&lt;p&gt;Supplementary tables and figures&lt;/p&gt;
Optimizing Startshot lightsail design: a generative network-based approach (2021)

The Starshot lightsail project aims to build an ultralight spacecraft ("nanocraft") that can reach Proxima Centauri b in approximately 20 years, requiring propulsion with a relativistic velocity of ~60 000 km/s. The spacecraft's acceleration approach currently under investigation is based on applying the radiation pressure from a high-power laser array located on Earth to the spacecraft lightsail. However, the practical realization of such a spacecraft imposes extreme requirements to the lightsail's optical, mechanical, thermal properties. Within this work, we apply adjoint topology optimization and variational autoencoder-assisted inverse design algorithm to develop and optimize a silicon-based lightsail design. We demonstrate that the developed framework can provide optimized optical and opto-kinematic properties of the lightsail. Furthermore, the framework opens up the pathways to realizing a multi-objective optimization of the entire lightsail propulsion system, leveraging the previously demonstrated concept of physics-driven compressed space engineering
Geometry-preserving Encryption for 3D Meshes (2013)

This paper introduces a geometry-preserving protection paradigm that heavily distorts 3D objects while preserving some intrinsic geometrical property (e.g. the bounding box or the convex hull), thereby avoiding a global corruption of the whole 3D scene. Backward compatibility is guaranteed de facto : legacy non-compliant rendering engines can display 3D scenes containing protected objects, but only compliant renderers with the necessary credentials can display deprotected objects. We propose a couple of permutation-based encryption algorithms embracing this geometry-preserving strategy and then detail some challenges related to them. For instance, we discuss the sideeffects of such protection mechanisms on other baseline 3D primitives, e.g. the rendering time, as well as the difficulty of assessing the security of such algorithms.
Fast Graph Refinement and Implicit Neural Representation for Tissue Tracking (2022)

Tracking of tissue in the surgical environment is often done via locating frame-to-frame keypoint correspondences, and then using these correspondences to warp a prior underlying model such as a spline, mesh, or embedded deformation. We introduce a novel learned model which takes keypoint correspondences as input and enables a prior-free estimation of deformation at any location. For fast point tracking, our model allows for sparse queries, unlike dense grid based CNNs, which run on full images. Our model begins with a novel graph-based point refinement scheme which refines matched keypoints, updating their features and movement instead of discarding possible outliers. Then, we use these refined matches to learn a novel neural implicit representation for estimating movement of any location given its k-nearest neighbor (k-NN) keypoints. We name our implicit deformation model KINFlow (k-NN implicit neural flow). We demonstrate the performance of KINFlow photometrically on three different datasets. KINFlow is the first model to use a graph network to estimate flow of arbitrary query points, and can estimate movement of 1024 points in under 3 ms.
A local group differences test for subject-level multivariate density neuroimaging outcomes (2019)

A great deal of neuroimaging research focuses on voxel-wise analysis or segmentation of damaged tissue, yet many diseases are characterized by diffuse or non-regional neuropathology. In simple cases, these processes can be quantified using summary statistics of voxel intensities. However, the manifestation of a disease process in imaging data is often unknown, or appears as a complex and nonlinear relationship between the voxel intensities on various modalities. When the relevant pattern is unknown, summary statistics are often unable to capture differences between disease groups, and their use may encourage post hoc searches for the optimal summary measure. In this study, we introduce the multi-modal density testing (MMDT) framework for the naive discovery of group differences in voxel intensity profiles. MMDT operationalizes multi-modal magnetic resonance imaging (MRI) data as multivariate subject-level densities of voxel intensities and utilizes kernel density estimation to develop a local two-sample test for individual points within the density space. Through simulations, we show that this method controls type I error and recovers relevant differences when applied to a specified point. Additionally, we demonstrate the ability to maintain power while controlling the family-wise error rate and false discovery rate when applying the test over a grid of points within the density space. Finally, we apply this method to a study of subjects with either multiple sclerosis (MS) or conditions that tend to mimic MS on MRI, and find significant differences between the two groups in their voxel intensity profiles within the thalamus.
Peptide‐Directed DNA‐Templated Protein Labelling for The Assembly of a Pseudo‐IgM (2019)

Abstract The development of methods for conjugation of DNA to proteins is of high relevance for the integration of protein function and DNA structures. Here, we demonstrate that protein‐binding peptides can direct a DNA‐templated reaction, selectively furnishing DNA–protein conjugates with one DNA label. Quantitative conversion of oligonucleotides is achieved at low stoichiometries and the reaction can be performed in complex biological matrixes, such as cell lysates. Further, we have used a star‐like pentameric DNA nanostructure to assemble five DNA–Rituximab conjugates, made by our reported method, into a pseudo‐IgM antibody structure that was subsequently characterized by negative‐stain transmission electron microscopy (nsTEM) analysis.
Data from Zinc Metallochaperones Reactivate Mutant p53 Using an ON/OFF Switch Mechanism: A New Paradigm in Cancer Therapeutics (2023)

&lt;div&gt;Abstract&lt;p&gt;&lt;b&gt;Purpose:&lt;/b&gt; Zinc metallochaperones (ZMC) are a new class of anticancer drugs that reactivate zinc-deficient mutant p53 by raising and buffering intracellular zinc levels sufficiently to restore zinc binding. &lt;i&gt;In vitro&lt;/i&gt; pharmacodynamics of ZMCs indicate that p53-mutant activity is ON by 4–6 hours and is OFF by 24. We sought to understand the mechanism of this regulation and to translate these findings preclinically. We further sought to innovate the formulation of ZMCs to improve efficacy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Experimental Design:&lt;/b&gt; We performed &lt;i&gt;in vitro&lt;/i&gt; mechanistic studies to determine the role of cellular zinc homeostatic mechanisms in the transient pharmacodynamics of ZMCs. We conducted preclinical pharmacokinetic, pharmacodynamic, and efficacy studies using a genetically engineered murine pancreatic cancer model (KPC) to translate these mechanistic findings and investigate a novel ZMC formulation.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; &lt;i&gt;In vitro&lt;/i&gt;, cellular zinc homeostatic mechanisms that restore zinc to its physiologic levels function as the OFF switch in ZMC pharmacodynamics. &lt;i&gt;In vivo&lt;/i&gt; pharmacokinetic studies indicate that ZMCs have a short half-life (&lt; 30 minutes), which is sufficient to significantly improve survival in mice expressing a zinc-deficient allele (p53&lt;sup&gt;R172H&lt;/sup&gt;) while having no effect in mice expressing a non–zinc-deficient allele (p53&lt;sup&gt;R270H&lt;/sup&gt;). We synthesized a novel formulation of the drug in complex with zinc and demonstrate this significantly improves survival over ZMC1.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Conclusions:&lt;/b&gt; Cellular zinc homeostatic mechanisms function as an OFF switch in ZMC pharmacodynamics, indicating that a brief period of p53-mutant reactivation is sufficient for on-target efficacy. ZMCs synthesized in complex with zinc are an improved formulation. &lt;i&gt;Clin Cancer Res; 24(18); 4505–17. ©2018 AACR&lt;/i&gt;.&lt;/p&gt;&lt;/div&gt;
A role for transient receptor potential vanilloid 4 in tonicity‐induced neurogenic inflammation (2010)

Activation of TRPV4 stimulates neuropeptide release from afferent nerves and induces neurogenic inflammation. This mechanism may mediate the generation and maintenance of inflammation after injury and during diseases, in which there are changes in extracellular osmolarity. Antagonism of TRPV4 may offer a therapeutic approach for inflammatory hyperalgesia and chronic inflammation.
Amino acid sequence at the allosteric site of sheep heart phosphofructokinase. (1980)

Covalent modification of sheep heart phosphofructokinase with the affinity labeling reagent p-fluorosulfonyl[14C]benzoyl-5'-adenosine caused a loss of allosteric properties. This modification appears to occur at the binding site that is specific for the allosteric activators AMP, cAMP, and ADP (Mansour, T.E., and Colman, R.F. (1978) Biochem. Biophys. Res. Commun. 81, 1370-1376). In the current study, the site of modification has been demonstrated to be a lysine residue. A nonapeptide containing a covalently bound [14C]carboxybenzenesulfonyl group attached to alysine residue has been isolated following tryptic digestion. The amino acid sequence of the peptide is Asn-Phe-Ala-Thr-Lys-Met-Gly-Ala-Lys. The fifth residue in this sequence, lysine, contained the covalently bonded reagent.
Abstract 9453: Dual Probe Hybrid Molecular PET/MR Imaging of Post-infarct Myocardial Inflammation and Healing (2012)

Background: Myocardial infarction elicits a strong inflammatory response, with profound recruitment of innate immune cells. The magnitude of inflammation influences infarct size and severity of post-MI ventricular dysfunction. Inflammatory monocytes and macrophages produce substantial amounts of myeloperoxidase (MPO), which leads to oxidative stress. In addition, plasma transglutaminase factor XIII (FXIII) plays a key role in wound healing, via its contribution to extracellular matrix organization. Thus, we hypothesize that targeted molecular imaging of FXIII and MPO activity using a hybrid PET/ MRI approach will enable simultaneous in vivo assessment of infarct healing and post-infarct inflammation. Methods and Results: To assess in vivo FXIII activity, we developed a fluorine-18 labeled affinity peptide (18F-FXIII), with a blood half-life of 13.3 min, using a facile ‘click-chemistry’ approach. FXIII recognizes the PET probe as a substrate and cross-links it to extracellular matrix proteins, leading to local entrapment within the healing infarct. 18F-FXIII and gadolinium-based activatable sensor of MPO activity (MPO-Gd) were injected in C57BL/6 mice on day 4 after permanent coronary ligation. PET/MR imaging was performed and fusion was facilitated using external fiducial markers. 18F-FXIII uptake in the heart was significantly higher in animals with MI as compared to controls, as measured by scintillation counting (percent injected dose per gram tissue 0.29±0.01 vs 0.17± 0.03, p&lt;0.03). On autoradiography, 18F-FXIII uptake correlated well with infarct area on TTC staining. PET/MR imaging allowed for simultaneous in vivo assessment of MPO and FXIII activity (Figure). Conclusion: Dual probe hybrid PET/MR imaging with 18F-FXIII and MPO-Gd allows non-invasive assessment of post-infarct myocardial inflammation and infarct healing.
Confined Pt11+ Water Clusters in a MOF Catalyze the Low‐Temperature Water–Gas Shift Reaction with both CO2 Oxygen Atoms Coming from Water (2018)

The synthesis and reactivity of single metal atoms in a low-valence state bound to just water, rather than to organic ligands or surfaces, is a major experimental challenge. Herein, we show a gram-scale wet synthesis of Pt<sub>1</sub> <sup>1+</sup> stabilized in a confined space by a crystallographically well-defined first water sphere, and with a second coordination sphere linked to a metal-organic framework (MOF) through electrostatic and H-bonding interactions. The role of the water cluster is not only isolating and stabilizing the Pt atoms, but also regulating the charge of the metal and the adsorption of reactants. This is shown for the low-temperature water-gas shift reaction (WGSR: CO + H<sub>2</sub> O → CO<sub>2</sub> + H<sub>2</sub> ), where both metal coordinated and H-bonded water molecules trigger a double water attack mechanism to CO and give CO<sub>2</sub> with both oxygen atoms coming from water. The stabilized Pt<sup>1+</sup> single sites allow performing the WGSR at temperatures as low as 50 °C.
Protein Phosphatase-2Cα as a Positive Regulator of Insulin Sensitivity through Direct Activation of Phosphatidylinositol 3-Kinase in 3T3-L1 Adipocytes (2004)

During differentiation, expression of protein phosphatase-2Calpha (PP2Calpha) is increased in 3T3-L1 adipocytes. To elucidate the role of PP2Calpha in insulin signaling, we overexpressed wild-type (WT) PP2Calpha by adenovirus-mediated gene transfer in 3T3-L1 adipocytes. Overexpression of PP2Calpha-WT enhanced the insulin sensitivity of glucose uptake without any changes in the early steps of insulin signaling. Infection with adenovirus 5 expressing PP2Calpha-WT increased phosphatidylinositol 3-kinase (PI3K) activities in the immunoprecipitate using antibody against the p85 or p110 subunit under both basal and insulin-stimulated conditions, followed by activation of downstream steps in the PI3K pathway, such as phosphorylation of Akt, glycogen synthase kinase-3, and atypical protein kinase C. In contrast, overexpression of the phosphatase-defective mutant PP2Calpha(R174G) did not produce such effects. Furthermore, overexpression of PP2Calpha-WT (but not PP2Calpha(R174G)) decreased the (32)P-labeled phosphorylation state as well as the gel mobility shift of the p85 subunit, suggesting that dephosphorylation of the p85 subunit by PP2Calpha activation might stimulate PI3K catalytic activity. Moreover, knockdown of PP2Calpha by transfection of small interfering RNA led to a significant decrease in Akt phosphorylation. In addition, microinjection of anti-PP2Calpha antibody or PP2Calpha small interfering RNA led to decreased insulin-stimulated GLUT4 translocation. In conclusion, PP2Calpha is a new positive regulator of insulin sensitivity that acts through a direct activation of PI3K in 3T3-L1 adipocytes.