gebhart/patrepeval huggingface dataset:
Tuning Nanoparticle Catalysis for the Oxygen Reduction Reaction (2013)

Advances in chemical syntheses have led to the formation of various kinds of nanoparticles (NPs) with more rational control of size, shape, composition, structure and catalysis. This review highlights recent efforts in the development of Pt and non-Pt based NPs into advanced nanocatalysts for efficient oxygen reduction reaction (ORR) under fuel-cell reaction conditions. It first outlines the shape controlled synthesis of Pt NPs and their shape-dependent ORR. Then it summarizes the studies of alloy and core-shell NPs with controlled electronic (alloying) and strain (geometric) effects for tuning ORR catalysis. It further provides a brief overview of ORR catalytic enhancement with Pt-based NPs supported on graphene and coated with an ionic liquid. The review finally introduces some non-Pt NPs as a new generation of catalysts for ORR. The reported new syntheses with NP parameter-tuning capability should pave the way for future development of highly efficient catalysts for applications in fuel cells, metal-air batteries, and even in other important chemical reactions.
A Computer-Controlled Multichannel Stimulation System for Laboratory Use in Functional Neuromuscular Stimulation (1985)

Laboratory instrumentation systems for developing functional neuromuscular stimulation (FNS) orthoses must be flexible in command processing and in multichannel stimulus control and coordination. For research and development of new FNS systems to control the musculoskeletal function of disabled individuals, we have developed a computer-controlled multichannel stimulation system. This system both processes patient generated input commands delivered from a variety of sources, and coordinates the multichannel stimulation to achieve the desired movement. The flexibility provided by this system has proven to be of great value in both upper and lower extremity FNS.
Nickel-Catalyzed Intermolecular Coupling of 1,3-Dienes and Aldehydes via Transmetalation of Nickelacycles with Diisobutylaluminum Acetylacetonate (2002)

Intermolecular coupling reactions of 1,3-dienes and aldehydes via transmetalation of nickelacycle intermediate with (i)Bu(2)Al-acac were investigated. In the reactions, a linear adduct or a branched adduct was produced, depending upon the nature of 1,3-dienes and aldehydes, via two nickelacycles that were relatively stable among the four possible nickelacycles because of the equilibrium with pi-allynickel forms.
Soft Magnetic Properties and Structures of Nanocrystalline Fe-Al-Si-Nb-B Alloy Ribbons (1993)

The soft magnetic properties and structures of nanocrystalline Fe-Al-Si-Nb-B alloy ribbons crystallized from an amorphous state were investigated. The best soft magnetic properties (effective permeability at 100 kHz of 23,000, core loss at 100 kHz, B <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">m</sub> =0.1 T of 9 W/kg, and saturation magnetostriction λ <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">s</sub> of +0.5×10 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">-6</sup> ) were obtained for Fe <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">66</sub> Al <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">8</sub> Si <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">14</sub> Nb <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">3</sub> B <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">9</sub> alloy ribbons. These new alloy ribbons were composed of bcc Fe-based alloy with grain diameters less than 200 Å. It is suggested that the good soft magnetic properties are due to the nanocrystalline microstructure of the Fe-Si-Al alloy.
Identification and sequence analysis of the promoter for the leukocyte integrin beta-subunit (CD18): a retinoic acid-inducible gene (1992)

Leukocyte adhesion receptors (LFA-1; Mac-1; p150,95) are a family of heterodimeric cell-surface adhesion molecules expressed exclusively in granulocytes, lymphocytes, and macrophages. Expression of these proteins is under complex regulatory control, but to date promoters for these genes have not been identified. The CD18 gene codes for the common beta-subunit of the leukocyte adhesion receptors. Transcription of CD18 is highly tissue-specific, hormonally inducible (by retinoic acid [RA]), and coordinately regulated with leukocyte integrin alpha- chains. To identify the CD18 promoter, we screened a human genomic phage library with a human CD18 cDNA probe and obtained a clone that contains an exon coding for the 5′ untranslated region (UTR). Using rapid amplification of cDNA ends (RACE), RNAse protection, S1 nuclease, and primer extension assays, we demonstrated the existence of multiple transcription start sites clustered in a 45-nt region. We investigated the transcription-promoting activity of the genomic sequences 5′ to the CD18 gene by performing transient expression assays with a growth hormone reporter gene in various hematopoietic cell lines. The CD18 promoter was active in Jurkat cells, a lineage that normally expresses CD18 but was considerably less active in K562, an early erythroid line that does not normally express CD18. The genomic sequences upstream of the start site cluster lack CAAT and TATA boxes, but have two Sp1 binding sites and 10 T(G/C)AC(C/A) boxes, which may represent binding sites for RA receptors (RAR). These features distinguish the CD18 promoter from the promoters of other tissue-specific, hormone-inducible genes, and may be representative of leukocyte integrin promoters in general.
Impedance microbiology—a rapid change for microbiologists (1996)

Journal Article Impedance microbiology—a rapid change for microbiologists Get access P. Silley, P. Silley Don Whitley Scientific Limited, Shipley, West Yorkshire Search for other works by this author on: Oxford Academic Google Scholar S. Forsythe S. Forsythe Department of Life Sciences, The Nottingham Trent University, Nottingham, UK Dr S.J. Forsythe, Department of Life Sciences, The Nottingham Trent University, Cliften Lane, Nottingham BG11 8NS, UK. Search for other works by this author on: Oxford Academic Google Scholar Journal of Applied Bacteriology, Volume 80, Issue 3, 1 March 1996, Pages 233–243, https://doi.org/10.1111/j.1365-2672.1996.tb03215.x Published: 01 March 1996 Article history Received: 01 June 1995 Accepted: 08 September 1995 Published: 01 March 1996
Tau Therapeutic Strategies for the Treatment of Alzheimers Disease (2006)

The two classical pathological hallmarks of Alzheimer's disease are deposits of aggregated beta-amyloid (Abeta) peptide and neurofibrillary tangles composed of hyperphosphorylated tau protein. In addition to Abeta pathology, an invariant trait of Alzheimer's disease, disruption of tau processing is a necessary event in the neurotoxic cascade which eventually leads to neuronal death and subsequent dementia. Tau is a neuronal, microtubule-bound protein which becomes hyperphosphorylated as a result of an imbalance of the kinase and phosphatase activities which normally tightly regulate its phosphorylation. In addition to this pathogenic hyperphosphorylation, tau dissociates from microtubules and self-aggregates to form insoluble oligomers which progress to the macroscopic tangles evident in post mortem Alzheimer's disease tissue. Subsequent toxicity may ensue either as a direct toxic effect of free tau oligomers or as a result of altered microtubule-dependent processes. In order to intervene pharmacologically in this disease process, much effort has been expended in order to identify and inhibit the kinases responsible for pathogenic hyperphosphorylation and many candidate kinases have been investigated including glycogen synthase kinase (GSK-3), cyclin-dependant kinase-5 (Cdk-5), MAPK family members (extracellular signal-regulated kinases 1 and 2 [Erk-1 and 2], MEK [MAP kinase kinase], c-Jun NH(2)-terminal kinases (JNKs) and p38), casein kinase, calcium calmodulin-dependant kinase II (CaMK-II), microtubule affinity regulating kinase (MARK), protein kinase A (PKA/cAMP-dependant protein kinase) and others. Focus has also fallen upon the role of the phosphatases responsible for dephosphorylation of tau. This review will describe the tau-related etiology of Alzheimer's disease and other tauopathies as well as the therapeutic strategies to inhibit the hyperphosphorylation of tau.
Glucocorticoids Increase Amyloid-β and Tau Pathology in a Mouse Model of Alzheimer’s Disease (2006)

Various environmental and genetic factors influence the onset and progression of Alzheimer's disease (AD). Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, which controls circulating levels of glucocorticoid hormones, occurs early in AD, resulting in increased cortisol levels. Disturbances of the HPA axis have been associated with memory impairments and may contribute to the cognitive decline that occurs in AD, although it is unknown whether such effects involve modulation of the amyloid beta-peptide (Abeta) and tau. Using in vitro and in vivo experiments, we report that stress-level glucocorticoid administration increases Abeta formation by increasing steady-state levels of amyloid precursor protein (APP) and beta-APP cleaving enzyme. Additionally, glucocorticoids augment tau accumulation, indicating that this hormone also accelerates the development of neurofibrillary tangles. These findings suggest that high levels of glucocorticoids, found in AD, are not merely a consequence of the disease process but rather play a central role in the development and progression of AD.
A stable IgG-like bispecific antibody targeting the epidermal growth factor receptor and the type I insulin-like growth factor receptor demonstrates superior anti-tumor activity (2011)

The epidermal growth factor receptor (EGFR) and the type I insulin-like growth factor receptor (IGF-1R) are two cell surface receptor tyrosine kinases known to cooperate to promote tumor progression and drug resistance. Combined blockade of EGFR and IGF-1R has shown improved anti-tumor activity in preclinical models. Here, we report the characterization of a stable IgG-like bispecific antibody (BsAb) dual-targeting EGFR and IGF-1R that was developed for cancer therapy. The BsAb molecule (EI-04), constructed with a stability-engineered single chain variable fragment (scFv) against IGF-1R attached to the carboxyl-terminus of an IgG against EGFR, displays favorable biophysical properties for biopharmaceutical development. Biochemically, EI-04 bound to human EGFR and IGF-1R with sub nanomolar affinity, co-engaged the two receptors simultaneously, and blocked the binding of their respective ligands with similar potency compared to the parental monoclonal antibodies (mAbs). In tumor cells, EI-04 effectively inhibited EGFR and IGF-1R phosphorylation, and concurrently blocked downstream AKT and ERK activation, resulting in greater inhibition of tumor cell growth and cell cycle progression than the single mAbs. EI-04, likely due to its tetravalent bispecific format, exhibited high avidity binding to BxPC3 tumor cells co-expressing EGFR and IGF-1R, and consequently improved potency at inhibiting IGF-driven cell growth over the mAb combination. Importantly, EI-04 demonstrated enhanced in vivo anti-tumor efficacy over the parental mAbs in two xenograft models, and even over the mAb combination in the BxPC3 model. Our data support the clinical investigation of EI-04 as a superior cancer therapeutic in treating EGFR and IGF-1R pathway responsive tumors.
Selective Catalysis of the Aerobic Oxidation of Cyclohexane in the Liquid Phase by Carbon Nanotubes (2011)

Putting the N in nanotube: Carbon nanotubes (CNTs) catalyze the aerobic oxidation of cyclohexane into cyclohexanol, cyclohexanone, and adipic acid with excellent activity and controllable selectivity. The catalytic activity is further enhanced by nitrogen dopants in the nanotube (see diagram; AC=activated carbon, MWCNT=multiwalled CNT, N-CNT=nitrogen-doped CNT).
Dural Replacement With Resorbable Collagen (1965)

DEFECTS in the dura mater can result from craniocerebral trauma, neoplastic or inflammatory destruction, surgical removal, and congenital absence. The experimental work of Trotter,<sup>1</sup>Sayad and Harvey,<sup>2</sup>Cone,<sup>3</sup>Penfield,<sup>4</sup>and Keener,<sup>5</sup>indicates that if these dural defects are adjacent to soft tissue, adequate dural regeneration can occur in several weeks. Fibroblasts derived from surrounding mesenchymal tissue move into the defect restoring the continuity of the dura. However, if the defect is adjacent to bone, poor dural regeneration results, since the mesenchymal source for fibroblasts is not readily available. The advantages of closing such a dural defect are multiple. Closure prevents cerebral herniation with subsequent cerebritis, cerebrospinal fluid fistula with ensuing meningitis, and corticomeningeal adhesions with a resultant seizure focus. Materials used for the closure of dural defects have been reviewed by Pudenz,<sup>6</sup>Keener,<sup>7</sup>Teng,<sup>8</sup>and Rosomoff.<sup>9</sup>Replacement materials which have appeared
ELISA-type titertray assay of IgM anti-GM1 autoantibodies (1994)

We report an ELISA-type titertray assay for autoantibodies against the ganglioside GM1. Trays were coated with ganglioside GM1 and reacted with patients' sera; bound IgM was detected with rabbit antibody to human IgM. High-titer serum from a patient was used as calibrator, another patient's serum as the positive control, and the GM1-specific cholera toxin as the control for GM1 coating. Regression curves of serum titers obtained from different patients were linear and parallel. Intra- and interassay CVs were 4.0-7.8% and 5.5-16%, respectively. We detected antibodies at a titer of 1:250 in normal subjects. Analytical specificity of the calibrator serum against GM1 was demonstrated by immune thin-layer chromatography. Anti-GM1 antibodies were increased in patients with chronic inflammatory demyelinating polyradiculoneuropathy (P < 0.002) or multiple sclerosis (P < 0.01). In Guillain-Barré syndrome, preliminary longitudinal studies showed a decrease in anti-GM1 titer that was related to clinical recovery.
The Uncoupling Agent 2,4-Dinitrophenol Improves Mitochondrial Homeostasis following Striatal Quinolinic Acid Injections (2005)

It is now generally accepted that excitotoxic cell death involves bioenergetic failure resulting from the cycling of Ca2+ and the generation of reactive oxygen species (ROS) by mitochondria. Both Ca2+ cycling and ROS formation by mitochondria are dependent on the mitochondrial membrane potential (Deltapsi(m)) that results from the proton gradient that is generated across the inner membrane. Mitochondrial uncoupling refers to a condition in which protons cross the inner membrane back into the matrix while bypassing the ATP synthase. As a consequence of this "short-circuit," there is a reduction in Deltapsi(m). We have previously demonstrated that animals treated with the classic uncoupling agent 2,4-dinitrophenol (DNP) show significant protection against brain damage following striatal injections of the NMDA agonist quinolinic acid (QA). In an effort to elucidate the mechanism of neuroprotection, we have assessed the effects of DNP on several parameters of mitochondrial function caused by QA. The results presented herein demonstrate that treatment with DNP attenuates QA-induced increases in mitochondrial Ca2+ levels and ROS formation and also improves mitochondrial respiration. Our findings indicate that DNP may confer protection against acute brain injury involving excitotoxic pathways by mechanisms that maintain mitochondrial function.
Self‐Healing Stretchable Wires for Reconfigurable Circuit Wiring and 3D Microfluidics (2013)

This article describes the fabrication of self-healing stretchable wires formed by embedding liquid metal wires in microchannels composed of self-healing polymer. These stretchable wires can be completely severed with scissors and rapidly self-heal both mechanically and electrically at ambient conditions. By cutting the channels strategically, the pieces can be re-assembled in a different order to form complex microfluidic networks in 2D or 3D space.
Microscopy and Microanalysis (2016)

Chloroplasts are the powerhouse organelles that host photosynthesis and other processes essential for plant life.When cells divide, chloroplasts also have to divide so that the correct number of chloroplasts per cell is maintained.This division is initiated by assembling a specific protein (called FtsZ) into filamentous and then ring-like structures (Z-rings) at the middle of the chloroplast.The Z-ring then recruits additional components that cause the ring and the chloroplast to constrict, leading ultimately to the formation of two daughter chloroplasts.The Z-ring is thus a dynamic structure, the functioning of which depends on the concerted action of a range of proteins that interact with the Z-ring by binding to it and then leaving the ring again.The same is true for the basic building block of the ring, FtsZ.This coming and going of FtsZ is called FtsZ turnover.Here we describe an analysis of FtsZ turnover and how it depends on the presence of a protein that negatively affects Z-ring formation, ARC3.The question was: does ARC3 inhibit FtsZ assembly, or does it cause disassembly of existing FtsZ filaments?We found that in the presence of ARC3, GFP-labled FtsZ turnover was 3-fold faster than when ARC3 was absent, indicating that ARC3 promotes disassembly of existing FtsZ rings and filaments.
Alendronate decreases orthotopic PC-3 prostate tumor growth and metastasis to prostate-draining lymph nodes in nude mice (2008)

Our results demonstrate that alendronate treatment opposes growth of orthotopic PC-3 tumors and decreases tumor metastasis to prostate-draining lymph nodes. This effect could be at least partly explained by decreased angiogenesis and increased apoptosis. The results suggest that bisphosphonates have anti-tumoral and anti-invasive effects on primary prostate cancer.
Factored language models and generalized parallel backoff (2003)

We introduce factored language models (FLMs) and generalized parallel backoff (GPB). An FLM represents words as bundles of features (e.g., morphological classes, stems, data-driven clusters, etc.), and induces a probability model covering sequences of bundles rather than just words. GPB extends standard backoff to general conditional probability tables where variables might be heterogeneous types, where no obvious natural (temporal) backoff order exists, and where multiple dynamic backoff strategies are allowed. These methodologies were implemented during the JHU 2002 workshop as extensions to the SRI language modeling toolkit. This paper provides initial perplexity results on both CallHome Arabic and on Penn Treebank Wall Street Journal articles. Significantly, FLMs with GPB can produce bigrams with significantly lower perplexity, sometimes lower than highly-optimized baseline trigrams. In a multi-pass speech recognition context, where bigrams are used to create first-pass bigram lattices or N-best lists, these results are highly relevant.
Swish: a Self-Gated Activation Function (2017)

The choice of activation functions in deep networks has a significant effect on the training dynamics and task performance. Currently, the most successful and widely-used activation function is the Rectified Linear Unit (ReLU). Although various alternatives to ReLU have been proposed, none have managed to replace it due to inconsistent gains. In this work, we propose a new activation function, named Swish, which is simply $f(x) = x \cdot \text{sigmoid}(x)$. Our experiments show that Swish tends to work better than ReLU on deeper models across a number of challenging datasets. For example, simply replacing ReLUs with Swish units improves top-1 classification accuracy on ImageNet by 0.9% for Mobile NASNet-A and 0.6% for Inception-ResNet-v2. The simplicity of Swish and its similarity to ReLU make it easy for practitioners to replace ReLUs with Swish units in any neural network.
Selection of novel analogs of thalidomide with enhanced tumor necrosis factor alpha inhibitory activity. (1996)

Analogs of thalidomide designed to better inhibit TNF alpha production in vitro have correspondingly greater efficacy in vivo. These finding may have therapeutic implication for the treatment of human diseases characterized by acute and extensive TNF alpha production such as tuberculous meningitis or toxic shock.
Genetic interactions between <i>Hoxa1</i> and <i>Hoxb1</i> reveal new roles in regulation of early hindbrain patterning (1998)

In the developing vertebrate hindbrain Hoxa1 and Hoxb1 play important roles in patterning segmental units (rhombomeres). In this study, genetic analysis of double mutants demonstrates that both Hoxa1 and Hoxb1 participate in the establishment and maintenance of Hoxb1 expression in rhombomere 4 through auto- and para-regulatory interactions. The generation of a targeted mutation in a Hoxb1 3' retinoic acid response element (RARE) shows that it is required for establishing early high levels of Hoxb1 expression in neural ectoderm. Double mutant analysis with this Hoxb1(3'RARE) allele and other targeted loss-of-function alleles from both Hoxa1 and Hoxb1 reveals synergy between these genes. In the absence of both genes, a territory appears in the region of r4, but the earliest r4 marker, the Eph tyrosine kinase receptor EphA2, fails to be activated. This suggests a failure to initiate rather than maintain the specification of r4 identity and defines new roles for both Hoxb1 and Hoxa1 in early patterning events in r4. Our genetic analysis shows that individual members of the vertebrate labial-related genes have multiple roles in different steps governing segmental processes in the developing hindbrain.
FoxO Are Critical Mediators of Hematopoietic Stem Cell Resistance to Physiologic Oxidative Stress. (2006)

Abstract Hematopoietic development and long-term homeostasis are tightly regulated by a dynamic balance of stem cell self-renewal and differentiation. To understand the role of the FoxO family of transcription factors in these processes, we studied the impact of somatic deletion of all FoxO genes in the adult hematopoietic system of mice engineered with the interferon-inducible Mx-Cre transgene and various conditional FoxO alleles: FoxO1L/L; FoxO3 L/L; and/or FoxO4 L/L. Cre-mediated excision of FoxO1, FoxO3 and FoxO4 (FoxO1/O3/O4L/L), resulted in myeloid lineage expansion, lymphoid developmental abnormalities and a marked decrease of the lineage-negative, Sca-1+, c-Kit+ (LSK) compartment, containing the hematopoietic stem cell (HSC) population, but normal numbers of myeloid progenitors. Furthermore, FoxO1/O3/O4L/L null bone marrow cells were defective in competitive and noncompetitive repopulation assays. This FoxO deficient defect correlated with enhanced cell cycling and increased apoptosis of HSC cells. Notably, there was an HSC-restricted elevation in the level of reactive oxygen species (ROS) that was not observed in committed progenitors, and was associated with decreased catalase and MnSOD expression. Furthermore, in vivo treatment with the anti-oxidative agent N-acetyl-cysteine (NAC) resulted in complete reversion of the FoxO deficient HSC phenotype. Taken together, these results demonstrate that, in the HSC compartment, FoxO proteins are mediators of quiescence and enhanced survival and play essential regulatory roles in the response to physiologic oxidative stress, a function that may contribute to the long-term regenerative potential of the hematopoietic stem cell compartment.