gebhart/patrepeval huggingface dataset:
Microfluidic platforms for performing surface-based clinical assays (2011)

The need for fast, specific and portable diagnostic systems for clinical assays has, in recent years, led to an explosion of research into microfluidic chip-based immunoassays towards rapid point-of-care analysis. Such devices exploit small dimensions, superior fluidic control and low reagent volumes to allow a number of clinically important procedures to be achieved with improvements on conventional methods, many of which rely on the surface-based binding of antigens to antibodies. Here, we discuss recent developments and innovations in the area of on-chip surface-based immunoassays and provide an outlook on the potential of such platforms for future diagnostics.
Efficient Inner Receiver Design for OFDM-Based WLAN Systems: Algorithm and Architecture (2007)

In this article we propose a complete solution for the so-called inner receiver of an OFDM-WLAN system based on the IEEE 802.11a standard. We concentrate our investigations on three key components forming the inner receiver namely, the synchronizer, the channel estimator and the digital timing loop. The main goal is the joint optimization of the signal processing algorithms along with the implementation friendly VLSI architecture required for these three key components in order to reduce power, area and latency, without compromising the performance excessively. We provide both the mathematical details and extensive computer simulations to validate our design
The Liver X Receptor Agonist GW3965 Improves Recovery from Mild Repetitive Traumatic Brain Injury in Mice Partly through Apolipoprotein E (2013)

Traumatic brain injury (TBI) increases Alzheimer's disease (AD) risk and leads to the deposition of neurofibrillary tangles and amyloid deposits similar to those found in AD. Agonists of Liver X receptors (LXRs), which regulate the expression of many genes involved in lipid homeostasis and inflammation, improve cognition and reduce neuropathology in AD mice. One pathway by which LXR agonists exert their beneficial effects is through ATP-binding cassette transporter A1 (ABCA1)-mediated lipid transport onto apolipoprotein E (apoE). To test the therapeutic utility of this pathway for TBI, we subjected male wild-type (WT) and apoE-/- mice to mild repetitive traumatic brain injury (mrTBI) followed by treatment with vehicle or the LXR agonist GW3965 at 15 mg/kg/day. GW3965 treatment restored impaired novel object recognition memory in WT but not apoE-/- mice. GW3965 did not significantly enhance the spontaneous recovery of motor deficits observed in all groups. Total soluble Aβ(40) and Aβ(42) levels were significantly elevated in WT and apoE-/- mice after injury, a response that was suppressed by GW3965 in both genotypes. WT mice showed mild but significant axonal damage at 2 d post-mrTBI, which was suppressed by GW3965. In contrast, apoE-/- mice showed severe axonal damage from 2 to 14 d after mrTBI that was unresponsive to GW3965. Because our mrTBI model does not produce significant inflammation, the beneficial effects of GW3965 we observed are unlikely to be related to reduced inflammation. Rather, our results suggest that both apoE-dependent and apoE-independent pathways contribute to the ability of GW3965 to promote recovery from mrTBI.
Prebreakdown and breakdown characteristics of micrometric vacuum gaps between broad area electrodes (2002)

The DC prebreakdown and breakdown characteristics of micrometric gaps varying from 25 to 1000 /spl mu/m, between highly polished 2 cm-diameter sphere electrodes, were extensively investigated at /spl sim/10/sup -5/ Torr. The I-V characteristics of the above gaps obey Fowler-Nordheim behaviour confirming that the prebreakdown conduction was dominated by high field electron emission. The breakdown voltage derived from the prebreakdown data took the form of the power relation of gap distance as V/sub h/=Kd/sup /spl alpha//. The breakdown strength of a 50 /spl mu/m gap was as high as 220 V//spl mu/m, which is the highest value reported in literature for broad area electrodes. The breakdown strength decreases as the gap distance increases, with a 1000 /spl mu/m gap breaking down at 44.5 V//spl mu/m. Results of this work are valuable for the design of vacuum gaps in Field Emission Displays.
QCL SPECTROSCOPY AT 9 $\mu$M CALIBRATED WITH A HIGH-POWER THULIUM-BASED FREQUENCY COMB (2012)

Author Institution: IMRA America, Ann Arbor, MI; Campus Point, Dipartimento di Fisica del Politecnico di Milano, Milano, Italy
Stability Analysis in Face Milling Operations, Part 1: Theory of Stability Lobe Prediction (1999)

This paper involves development of an algorithm to predict stability lobes in face milling operation. The modeling is based on frequency domain analysis and is an extension of Budak and Altintas to a three dimensional case. It considers the effects of insert and cutter geometry, cutting conditions, process nonlinearity, entry and exit angles and the fully dimensional structural dynamics of both the machine tool and workpiece, including axial dynamics which are often neglected by many researchers. In addition, the predictive capability of stability lobes by the presented models is compared with those results obtained by time domain simulations.
Neural Scene Decomposition for Multi-Person Motion Capture (2019)

Learning general image representations has proven key to the success of many computer vision tasks. For example, many approaches to image understanding problems rely on deep networks that were initially trained on ImageNet, mostly because the learned features are a valuable starting point to learn from limited labeled data. However, when it comes to 3D motion capture of multiple people, these features are only of limited use. In this paper, we therefore propose an approach to learning features that are useful for this purpose. To this end, we introduce a self-supervised approach to learning what we call a neural scene decomposition (NSD) that can be exploited for 3D pose estimation. NSD comprises three layers of abstraction to represent human subjects: spatial layout in terms of bounding-boxes and relative depth; a 2D shape representation in terms of an instance segmentation mask; and subject-specific appearance and 3D pose information. By exploiting self-supervision coming from multiview data, our NSD model can be trained end-to-end without any 2D or 3D supervision. In contrast to previous approaches, it works for multiple persons and full-frame images. Because it encodes 3D geometry, NSD can then be effectively leveraged to train a 3D pose estimation network from small amounts of annotated data.
Abstract A08: Combination with a novel STING agonist significantly improves efficacy of anti-PD1 therapy in mouse syngeneic tumor models (2018)

Abstract Activated STING (STimulator of INterferon Genes) bound to its natural ligand 2,3-cGAMP (cyclic guanosine-adenosine monophosphate), initiates type I interferon (IFN) and pro-inflammatory cytokine production. IFN upregulation is essential to promote antigen-specific CD8+ T-cell priming and leads to potent anti-tumor activity. To exploit this mechanism we synthesized a new STING agonist, MSA-1, that potently activates both mouse and human STING. Intratumoral (IT) administration of MSA-1 to MC38 syngeneic tumor-bearing mice increased tumor and plasma cytokine levels and was effective at driving complete responses (CRs) in 100% of the animals. Most surviving animals developed tumor-specific adaptive immune memory as demonstrated by robust protection against re-challenge with the same tumor type. Mechanistic studies in immune-deficient mice suggested that the initial antitumor activity is in part due to cytokine-driven cytotoxicity and/or other innate immune mechanisms, which may have contributed to some animals not developing an adaptive immune memory. Importantly, MSA-1 caused long-term tumor regressions or CRs in CT26 and B16-F10 tumor models, both of which are intrinsically resistant to single-agent therapy with a fully murinized anti-mouse PD-1 antibody (muDX400). The antitumor immune response in these models was further enhanced when treating the animals with MSA-1 in combination with muDX400. This combination restored T-cell responses in both blood and tumors of the treated mice and provided long-lived immunologic memory in a majority of the animals. Taken together, these data strongly support the development of STING agonists in combination with Keytruda (humanized anti-PD-1 antibody) for patients with tumors that are partially responsive or nonresponsive to single agent anti-PD-1 therapy. Citation Format: Samanthi A. Perera, Johnny E. Kopinja, Yanhong Ma, Jason Laskey, Kalyan Chakravarthy, Long Cui, Yiping Chen, Jeremy Presland, Sharad Sharma, Shuxia Zhao, Jennifer Piesvaux, Ellen C. Minnihan, Heidi Ferguson, Hyun Chong Woo, Ian Knemeyer, Ilona Kariv, Archie Tse, Saso Cemerski, Jared Cumming, B. Wesley Trotter, Bo-Sheng Pan, George H. Addona, Brian J. Long. Combination with a novel STING agonist significantly improves efficacy of anti-PD1 therapy in mouse syngeneic tumor models [abstract]. In: Proceedings of the AACR Special Conference on Tumor Immunology and Immunotherapy; 2017 Oct 1-4; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2018;6(9 Suppl):Abstract nr A08.
Activin A‐induced apoptosis is suppressed by BCL‐2 (1995)

Activin A, a member of TGFβ superfamily has various activities including induction of apoptosis in mammalian cells. However, it remains unknown how activin A induces cell death. To clarify this, we investigated the expression of BCL‐2 and BAX, and the effect of BCL‐2 overexpression on activin A‐induced apoptosis in B cell hybridoma cell lines. The activin A‐sensitive cell lines expressed BAX but not BCL‐2 and that activin A did not increase BAX levels. Overexpression of human BCL‐2 suppressed activin A‐induced apoptosis in these cells. Thus, activin A has been shown to induce apoptosis by a BCL‐2‐inhibitable mechanism without activating BAX.
Approximate reachability don't cares for CTL model checking (1998)

RDCs (Reachability Don't Cares) can have a dramatic impact on the cost of CTL model checking (J. Yuan et al., 1997). Unfortunately, RDCs, being a global property, are often much more difficult to compute than the satisfying set of typical CTL formulas. We address this problem through the use of Approximate Reachability Don't Cares (ARDCs), computed with the algorithms developed for the VERITAS sequential synthesis package (H. ho et al., 1990; 1996). Approximate reachable states represent an upper bound on the set of true reachable states, and thus a lower bound on the set of unreachable (Don't Care) states. ARDCs can be 10X to 100X (or much more for very large circuits) cheaper to compute than RDCs, and in some cases have the same dramatic effect on CTL model checking as the real RDCs. We also discuss the application of ARDCs to the problem of exact computation of the RDCs themselves. Experiments on industrial benchmarks show that order of magnitude speedups are possible, and occur frequently. The experimental results presented strongly support our claim that ARDCs play a safe and important way out of a serious dilemma: RDCs are necessary for tractable model checking of many large circuits, but the computation of the RDCs themselves is often intractable. We include, and theoretically justify, significant extensions of the VERITAS algorithms, and show that they can be up to an order of magnitude faster, while computing a virtually identical upper bound.
Design of an Electric Machine for a 48-V Mild Hybrid Vehicle (2018)

Through a systematic optimization study using high-fidelity finite-element (FE) models, torque capability of three common synchronous machine technologies, namely a permanent magnet (PM) synchronous machine (PMSM) with V-shaped rare-earth (RE) rotor magnets, a PMSM with deep V-shaped ferrite rotor magnets, and a synchronous reluctance machine (SynRM) with four layers of conforming flux barriers are compared for an application in a 48-V mild hybrid electric car. The optimization of the deep V-shaped ferrite PMSM automatically resulted in a spoke-type PM layout for maximum torque production. Yet, an optimized SynRM with conforming flux barriers was achieved that could produce a higher torque than ferrite PMSM. One machine technology is selected and is subsequently subjected to a large-scale FE model-based drive-cycle design optimization. Various pole-slot combinations are methodically compared in terms of drive-cycle losses, active material cost, torque ripple, and PM demagnetization level. More than 20,000 designs were analyzed over ten energy-centric torque-speed points to identify an optimal design solution. The results of multi-physics analysis incorporating electromagnetics, computational fluid dynamics (CFD), and structural analyses are provided, including a study on two different water jacket concepts. A final design is prototyped and initial experimental results are provided.
Toxic effects of antileishmanial reverse-phase evaporation liposomes containing dicetyl phosphate in monkeys (1995)

Liposomes containing or lacking encapsulated pen-tavalent antimony (Sb), a widely used antileishmanial agent, were administered to cynomolgous monkeys to investigate possible toxicity. The liposomes consisted of either reverse-phase evaporation vesicles (REV) composed of dipalmitoyl phosphatidylcholine, choles- terol (CHOL), and dicetyl phosphate (DCP) or mul- tilamellar vesicles (MLV) composed of dimyristoyl phosphatidylcholine and dimyristoyl phosphatidylglycerol, with or without CHOL. Toxicity was observed in monkeys receiving REV containing or lacking Sb as evidenced by thrombocytopenia, splenomegaly, and hemorrhage. The severity of the symptoms was potentiated by two factors, the presence of Sb in REV and the frequency of REV administration. In contrast, no significant adverse reactions were observed in animals treated with MLV containing or lacking Sb. Since the main difference between REV and MLV was the presence of DCP in REV, this observation suggested that toxicity was due, at least partly, to DCP. An alternative theoretical mechanism for the toxic reaction was also investigated, namely, thrombocytopenia caused by complement activation induced by naturally occurring autoantibodies to liposomal components. All monkeys in the present study had high levels of autoantibodies to lipids that were detected by complement-dependent lysis of test liposomes. The levels of these antibodies decreased after injection of MLV or REV, indicating that both REV and MLV reacted with preexisting autoantibodies to lipids in monkey serum that were able to cause complement activation. Al- though complement-activating autoantibodies to lipids were present with both REV and MLV, in view of the observation that toxicity occurred exclusively with REV, our results suggest that REV induced the toxicity.
Joint Communication and Computation in Hybrid Cloud/Mobile Edge Computing Networks (2022)

Facing a vast amount of connections, huge performance demands, and the need for reliable connectivity, the sixth generation of communication networks (6G) is envisioned to implement disruptive technologies that jointly spur connectivity, performance, and reliability. In this context, this paper proposes, and evaluates the benefit of, a hybrid central cloud (CC) computing and mobile edge computing (MEC) platform, especially introduced to balance the network resources required for joint computation and communication. Consider a hybrid cloud and MEC system, where several power-hungry multi-antenna unmanned aerial vehicles (UAVs) are deployed at the cell-edge to boost the CC connectivity and relieve part of its computation burden. While the multi-antenna base stations are connected to the cloud via capacity-limited fronthaul links, the UAVs serve the cell-edge users with limited power and computational capabilities. The paper then considers the problem of maximizing the weighted network sum-rate subject to per-user delay, computational capacity, and power constraints, so as to determine the beamforming vectors and computation allocations. Such intricate non-convex optimization problem is tackled using an iterative algorithm that relies on $\ell_0$-norm relaxation, successive convex approximation, and fractional programming, and has the compelling ability to be implemented in a distributed fashion across the multiple UAVs and the CC. The paper results illustrate the numerical prospects of the proposed algorithm for enabling joint communication and computation, and highlight the appreciable improvements of data processing delays and throughputs as compared to conventional system strategies.
Response of human hematopoietic stem and progenitor cells to energetic carbon ions (2009)

RBE values of carbon ions are low, as expected for radiosensitive cells. The observed frequencies of apoptotic cells and chromosome aberrations in HSPC are similar to those reported for human peripheral blood lymphocytes suggesting that at least with respect to apoptosis and chromosomal aberrations mature lymphocytes reflect the respective radiation responses of their proliferating progenitors.
Memoryless polynomial adaptive predistortion [TV transmitters] (2002)

In this paper we investigate algorithms to adaptively adjust the coefficients of memoryless polynomial structures used to precompensate for the nonlinear amplitude and phase distortion of the high-power amplifier in a terrestrial digital television transmitter. The results of the investigation are twofold. First the phase error is a non-Euclidean measure of the absolute symbol error. For small inputs, noise causing a small Euclidean change can create a large phase error. We compensate for this heuristically by not updating the predistorter coefficients for small inputs. This thresholding is shown to decrease the residual error of the phase predistorter. Second, the pre-compensation nature of the amplitude correction requires a modification to the traditional LMS algorithm. This modification will be seen to produce a smaller residual error than traditional LMS. We demonstrate the superior performance of our algorithms via simulations based on the measured characteristics of production high-power amplifiers.
Genotoxicity and mutagenicity of nickel(II) and iron(III) and interactions between these microelements (2018)

Abstract. Background: Nickel and iron are essential and necessary elements required for correct functioning of the human body when found in trace amounts, but their excess can be toxic for cells. They are widely used in numerous industrial applications as components in orthopedic implants and in dietary supplementation. The aim of this study was to examine the effect of nickel(II) and iron(III) and their combinations on genotoxicity and mutagenicity in BALB/3T3 and HepG2 cells. Materials and methods: Genotoxicity of nickel and iron and their mixture was assessed by analyzing induction of ­micronucleus formation and DNA damage by comet assay in BALB/3T3 and HepG2 cells. Mutagenicity of iron(III) and nickel(II) and their mixtures was assessed by Ames assay. Results: A statistically significant increase of DNA damage through use of both microelements in both cell lines was observed. The micronucleus assay performed with the use of all concentrations showed a statistically significant induction of chromosomal aberrations in both tested microelements in both cell lines. The results obtained from both cell lines in both tests show that BALB/3T3 cells are more sensitive when compared to the HepG2 cells after incubation with both microelements. Additions of iron(III) at 200 µM plus nickel(II) at 1,000 µM showed antagonistic effects in a decrease of genotoxicity as assessed by comet and micronuclei assays in both cell lines. In the case of nickel(II) at 200 µM plus iron(III) at 1,000 µM, a synergistic effect was observed. The results of Ames assay show that both tested microelements caused an increased number of reverse mutations. Conclusion: Nickel(II) and iron(III) are genotoxic. Nickel chloride evokes frameshift mutation more often than base-pair substitution mutation. However, in the case of iron chloride, the frequency in frameshift and base-pair substitution mutation was similar. Iron(III) at concentrations of 200 µM plays a protective role against nickel(II) genotoxicity and mutagenicity.
Scalable TaN metal source/drain & gate InGaAs/Ge n/pMOSFETs (2011)

We propose a scalable CMOS fabrication process for high mobility InGaAs/Ge dual channels using a common TaN metal source/drain and gate (Metal-SD&G) under consideration of material band lineup. By combining common TaN Metal-SD with compatible TaN/Al 2 O 3 gate stacks, we have successfully demonstrated operation of both InGaAs nMOS and Ge pMOS devices fabricated at the same time. Excellent InGaAs/Ge n/pMOSFET performances, such as the SS of 70mV/dec and 100mV/dec for InGaAs nMOS and Ge pMOS, respectively, have been achieved. We have also verified the scalability of TaN Metal-SD&G InGaAs nMOSFETs down to 50nm with high immunity to SCEs.
AMP-activated protein kinase promotes human prostate cancer cell growth and survival (2009)

The molecular mechanisms underlying the development and progression of prostate cancer are poorly understood. AMP-activated protein kinase (AMPK) is a serine-threonine kinase that is activated in response to the hypoxic conditions found in human prostate cancers. In response to energy depletion, AMPK activation promotes metabolic changes to maintain cell proliferation and survival. Here, we report prevalent activation of AMPK in human prostate cancers and provide evidence that inhibition or depletion of AMPK leads to decreased cell proliferation and increased cell death. AMPK was highly activated in 40% of human prostate cancer specimens examined. Endogenous AMPK was active in both the androgen-sensitive LNCaP cells and the androgen-independent CWR22Rv1 human prostate cancer cells. Depletion of AMPK catalytic subunits by small interfering RNA or inhibition of AMPK activity with a small-molecule AMPK inhibitor (compound C) suppresses human prostate cancer cell proliferation. Apoptotic cell death was induced in LNCaP and CWR22Rv1 cells at compound C concentrations that inhibited AMPK activity. The evidence provided here is the first report that the activated AMPK pathway is involved in the growth and survival of human prostate cancer and offers novel potential targets for chemoprevention of human prostate cancer.
Transcriptional suppression of the miR-15/16 family by c-Myc in malignant pleural mesothelioma (2019)

MicroRNA downregulation is frequent in malignant pleural mesothelioma (MPM), but the mechanisms responsible for loss of miR-15/16 and miR-193a are yet to be elucidated and were investigated in this study. Copy Number Variation (CNV) of microRNA-coding genes was analyzed in MPM cells by digital droplet PCR (ddPCR) and revealed heterozygous loss of miR-193a and miR-15a/16-1, but no change in miR-15b/16-2. Epigenetic control of microRNA expression was inferred following decitabine and Trichostatin A (TSA) treatment which did not substantially affect microRNA expression. Knockdown of c-Myc expression led to upregulation of <i>SMC4</i>, miR-15b and 16, and to a lesser extent <i>DLEU2</i> and miR-15a, whereas c-Myc overexpression repressed microRNA expression. Chromatin immunoprecipitation (ChIP) assays confirmed the interaction of c-Myc with the <i>DLEU2</i> and <i>SMC4</i> promoters. Tumor microRNA expression was determined in samples from MPM patients, with samples of pleura from cardiac surgery patients used as controls. In tumor samples, a strong correlation was observed between the expression of miR-15b and 16 (R<sup>2</sup>=0.793), but not miR-15a and 16. Our data suggest that in MPM, the downregulation of miR-15/16 is due to transcriptional repression by c-Myc, primarily via control of the miR-15b/16-2 locus, while miR-193a-3p loss is due to genomic deletion.