gebhart/patrepeval huggingface dataset:
DAIR: A Framework for Managing Enterprise Wireless Networks Using Desktop Infrastructure (2005)

We present a framework for managing and troubleshooting enterprise wireless networks using desktop infrastructure. The framework is called DAIR, which for Dense Array of Inexpensive Radios. Prior proposals in this area either rely solely upon access points (APs) and mobile clients to monitor the wireless network, or augment them with dedicated sensor nodes. We believe that these approaches can be improved upon. One cannot cover the entire spectrum in a comprehensive manner using only APs and mobile clients. An ordinary, single-radio AP can not monitor multiple channels effectively, without adversely impacting the associated clients. Due to power constraints, mobile devices can not continuously monitor the wireless networks. Deploying dedicated sensor nodes is an expensive proposition. Our solution is based on two simple observations. First, in most enterprise environments, one finds plenty of desktop machines with good wired connectivity, and spare CPU and disk resources. Second, inexpensive USB-based wireless adapters are commonly available. By attaching these adapters to desktop machines, and dedicating the adapters to the task of monitoring the wireless network, we create a low cost management infrastructure. In this paper, we show how the DAIR framework is wellsuited for solving many wireless management problems including detection of unauthorized access points, handling malfunctioning APs, and performance monitoring. In each case, we show how the DAIR framework takes advantage of the key attributes of the desktop infrastructure: dense deployment, stationarity, wired connectivity, and spare CPU and disk resources.
Optimized lipopolyplex formulations for gene transfer to human colon carcinoma cells under in vitro conditions (2005)

Lipopolyplex formulations of PEI25br in combination with multivalent CLs (DOCSPER, DOSPER) are promising tools for in vitro and potentially also in vivo gene transfer to colorectal cancer cells.
Lipoprotein (a) is a substrate for factor XIIIa and tissue transglutaminase. (1991)

The mechanisms which mediate deposition of lipoprotein (a) (Lp(a)), an atherogenic lipoprotein particle, onto the vessel wall and cell surfaces are unknown. An irreversible deposition of Lp(a) may require the presence of enzymes that catalyze its binding to surface-oriented structures. Transglutaminases catalyze cross-linking of proteins as well as incorporation of primary amines into protein substrates. We studied whether tissue transglutaminase and/or activated Factor XIII (plasma derived or recombinant FXIIIa) incorporate primary amines into Lp(a). In the presence of Ca2+, Factor XIIIa and tissue transglutaminase catalyze incorporation of monodansylcadaverine or [14C]putrescine into purified Lp(a) in a specific and time-dependent manner. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated that monodansylcadaverine became incorporated into the apo(a) portion of Lp(a). Lp(a) purified from five different donors showing different apo(a) phenotypes were substrates for tissue transglutaminases (TG). Western blot analysis confirmed that apo(a) was the major monodansylcadaverine carrying protein moiety of Lp(a). Tissue TG also extensively cross-linked the apo(a) portion of the Lp(a) particle. Characterization of the specificity of tissue TG showed that fibronectin, alpha 2-plasmin inhibitor, and apo(a) could be readily labeled with monodansylcadaverine by tissue TG, but other proteins including low density lipoprotein, IgG, alpha 1-proteinase inhibitor, and albumin showed poor or no reactivity. Direct comparison of Lp(a) with low density lipoprotein showed that apoB 100 was a poor substrate for transglutaminases. Recombinant apolipoprotein (a) proved to be an excellent substrate for TGs in that 1 mol of recombinant apolipoprotein (a) incorporated as much as 15 mol of [14C]putrescine, which corresponded to five times the amount of amine incorporated into Lp(a). The susceptibility of Lp(a) to transglutaminases suggests a mechanism whereby the interaction of Lp(a) with surface receptors and other surface oriented structures could be enzymatically altered.
Books on September 11, 2001 (2017)

PV VI #2-3
Value Aggregation for Collaborative Design Decision-Making (2006)

In recent years, engineering collaboration and teamwork has been a hot topic within the research community of engineering design. With the increasing complexity of design problems and shorter design lead time, companies are pressed to conduct product development projects with a team of experts from various technical domains who are oftentimes from different geographical locations.
CDMA RF System Engineering (1998)

From the Publisher:
Understand the essentials of CDMA wireless technology and develop the knowledge you need to design and operate either co-located AMPS and CDMA or dedicated CDMA systems with this unique reference. Drawing upon his recent experience in building the first major CDMA network in North America, the author helps you acquire the knowledge you need to engineer and implement an IS-95 based CDMA system.

Examining both the theoretical and practical side of CDMA engineering, this comprehensive guide is an excellent resource for practicing RF and system engineers who will find the modular-oriented chapters on spread-spectrum multiple access technique, design and performance engineering, CDMA traffic engineering, and regulatory implications especially useful. Engineering managers and directors seeking proficiency in CDMA technology will appreciate the author's ability to supply a big picture perspective where only the most important and relevant information to designing and optimizing a CDMA system is presented. A systemic approach makes this an ideal book for use in technical training and academic classes.
Analysis of cover of the femoral head in normal and dysplastic hips (2008)

We present a new CT-based method which measures cover of the femoral head in both normal and dysplastic hips and allows assessment of acetabular inclination and anteversion. A clear topographical image of the head with its covered area is generated. We studied 36 normal and 39 dysplastic hips. In the normal hips the mean cover was 73% (66% to 81%), whereas in the dysplastic group it was 51% (38% to 64%). The significant advantage of this technique is that it allows the measurements to be standardised with reference to a specific anatomical plane. When this is applied to assessing cover in surgery for dysplasia of the hip it gives a clearer understanding of where the corrected hip stands in relation to normal and allows accurate assessment of inclination and anteversion.
Toxicological and Pharmacological Effects of D‐Arginine (2005)

D-Arginine is extensively used in studies on L-arginine/nitric oxide pathway as an inactive form of L-arginine, even in man. In addition, it has previously been reported that this D-amino acid appears to have pharmacological activity. The present work aimed at evaluating the toxicity and pharmacology of D-arginine administered by the intraperitoneally route in albino male mice. Toxicity of D-arginine, alone as well as in the presence of propranolol and betamethasone was evaluated. D-Arginine in mice showed a light toxicity order (DL50: 2800 mg/kg). Previous injection of the beta-adrenoceptor blocker, propranolol (2 mg/kg, intraperitoneally), or betamethasone (0.5 mg/kg, intraperitoneally) produced a decrease in the toxicity of D-arginine (LD50: 3600 mg/kg, 3300 mg/kg, respectively). Also, a neuropharmacological screening of D-arginine using behavioural, neurological, autonomic, barbiturate-induced sleep time and pentylenetetrazole-induced convulsions tests were performed. D-Arginine 700 mg/kg displayed central stimulant properties, whereas a depressant profile was observed at a dose of 1400 mg/kg. In addition, D-arginine 1400 mg/kg produced a potentiation of pentobarbital sleeping time and a marked anticonvulsivant action against pentylenetetrazole.
CCR5 Antagonist Blocks Metastasis of Basal Breast Cancer Cells (2012)

The roles of the chemokine CCL5 and its receptor CCR5 in breast cancer progression remain unclear. Here, we conducted microarray analysis on 2,254 human breast cancer specimens and found increased expression of CCL5 and its receptor CCR5, but not CCR3, in the basal and HER-2 genetic subtypes. The subpopulation of human breast cancer cell lines found to express CCR5 displayed a functional response to CCL5. In addition, oncogene transformation induced CCR5 expression, and the subpopulation of cells that expressed functional CCR5 also displayed increased invasiveness. The CCR5 antagonists maraviroc or vicriviroc, developed to block CCR5 HIV coreceptor function, reduced in vitro invasion of basal breast cancer cells without affecting cell proliferation or viability, and maraviroc decreased pulmonary metastasis in a preclinical mouse model of breast cancer. Taken together, our findings provide evidence for the key role of CCL5/CCR5 in the invasiveness of basal breast cancer cells and suggest that CCR5 antagonists may be used as an adjuvant therapy to reduce the risk of metastasis in patients with the basal breast cancer subtype.
Glutamate Receptor Antagonists (2004)

GLUR5 Antagonists as Novel Migraine Therapies BACKGROUND: L‐glutamate activates neurons in the trigeminal nucleus caudalis (TNC). Furthermore, non‐NMDA ionotropic glutamate receptors such as GluR5 are expressed in rat trigeminal ganglion (TG), and GluR5 receptors play an important role in central sensitization (CS). CS is implicated in, and the trigeminal system is at the core of, migraine. Therefore, we hypothesized that GluR5 receptor antagonists would be effective in preclinical models of migraine. OBJECTIVES: 1) To test the potency and efficacy of GluR5 antagonists with varying degrees of affinity and selectivity for the GluR5/kainate receptor in the dural plasma protein extravasation (PPE) and the c‐fos models of migraine. 2) To test these GluR5 receptor antagonists for their ability to contract the rabbit saphenous vein (RSV) in vitro. METHODS: GluR5 antagonists were synthesized in the Lilly Research Laboratories. Ligand binding studies using recombinant human non‐NMDA receptors expressed in HEK293 cell membranes were used to determine compound affinity. We evaluated parenterally administered compounds in the PPE and the c‐fos models induced by electrical stimulation of male rats TG. Fos protein in the TNC was measured in the c‐fos experiment. Ring preparations of RSV were suspended in tissue baths and isometric contractions were recorded following incremental increases in the concentration of the test compound. Sumatriptan was used as a positive control for the RSV studies. RESULTS: LY293558, LY382884 and LY435735 dose‐dependently blocked protein extravasation in the PPE model. The rank order of potency correlated with affinity for GluR5. In contrast, LY300168, a potent and selective AMPA antagonist, did not block protein extravasation, even at relatively high doses. LY293558 and LY435735 also blocked c‐fos expression in the TNC. LY293558 and LY382884 did not contract the tissue in the RSV assay at concentrations up to 100 mM. CONCLUSIONS: The inhibitory effects of GluR5 antagonists in the PPE and c‐fos preclinical models of migraine suggest a novel role for GluR5 antagonism in migraine therapy. The lack of efficacy of the selective AMPA antagonist LY300168 in PPE does not support a role for this mechanism in migraine. The lack of activity of these compounds in the RSV provides a therapeutic advantage of GluR5 antagonists over current vasoactive migraine therapies. These pharmacological properties of GluR5 antagonists suggest that they could be used in the treatment of acute migraine without a cardiovascular liability.
Cardiomyocyte ATP release through pannexin 1 aids in early fibroblast activation (2012)

Fibrosis following myocardial infarction is associated with increases in arrhythmias and sudden cardiac death. Initial steps in the development of fibrosis are not clear; however, it is likely that cardiac fibroblasts play an important role. In immune cells, ATP release from pannexin 1 (Panx1) channels acts as a paracrine signal initiating activation of innate immunity. ATP has been shown in noncardiac systems to initiate fibroblast activation. Therefore, we propose that ATP release through Panx1 channels and subsequent fibroblast activation in the heart drives the development of fibrosis in the heart following myocardial infarction. We identified for the first time that Panx1 is localized within sarcolemmal membranes of canine cardiac myocytes where it directly interacts with the postsynaptic density 95/Drosophila disk large/zonula occludens-1-containing scaffolding protein synapse-associated protein 97 via its carboxyl terminal domain (amino acids 300-357). Induced ischemia rapidly increased glycosylation of Panx1, resulting in increased trafficking to the plasma membrane as well as increased interaction with synapse-associated protein 97. Cellular stress enhanced ATP release from myocyte Panx1 channels, which, in turn, causes fibroblast transformation to the activated myofibroblast phenotype via activation of the MAPK and p53 pathways, both of which are involved in the development of cardiac fibrosis. ATP release through Panx1 channels in cardiac myocytes during ischemia may be an early paracrine event leading to profibrotic responses to ischemic cardiac injury.
A Real Coded Genetic Algorithm with an Explorer and an Exploiter Populations. (1997)

We introduce the concept of a bi-population scheme for real-coded GAs (bGAs) consisting of an explorer sub-GA and an exploiter sub-GA. The explorer sub-GA mainly performs global exploration of the search space, and incorporates a restart mechanism to help avoid being trapped at local optima. The exploiter sub-GA performs exploitation of fit local areas of the search space around the neighborhood of the best-so-far solution. Two types of bGA are presented, aimed at addressing different classes of problems. We also explore a method for adaptive load balancing between the two sub-GAs within a bGA, which uses knowledge of the number of restarts occurring in the explorer sub-GA. The proposed technique exhibits performance significantly superior to standard GAs on two complex highly multimodal problems.
Mask Scoring R-CNN (2019)

Letting a deep network be aware of the quality of its own predictions is an interesting yet important problem. In the task of instance segmentation, the confidence of instance classification is used as mask quality score in most instance segmentation frameworks. However, the mask quality, quantified as the IoU between the instance mask and its ground truth, is usually not well correlated with classification score. In this paper, we study this problem and propose Mask Scoring R-CNN which contains a network block to learn the quality of the predicted instance masks. The proposed network block takes the instance feature and the corresponding predicted mask together to regress the mask IoU. The mask scoring strategy calibrates the misalignment between mask quality and mask score, and improves instance segmentation performance by prioritizing more accurate mask predictions during COCO AP evaluation. By extensive evaluations on the COCO dataset, Mask Scoring R-CNN brings consistent and noticeable gain with different models and outperforms the state-of-the-art Mask R-CNN. We hope our simple and effective approach will provide a new direction for improving instance segmentation. The source code of our method is available at \url{https://github.com/zjhuang22/maskscoring_rcnn}.
High-Performance Oxide Thin Film Transistors Passivated by Various Gas Plasmas (2008)

Abstract not Available.
Estrogens suppress RANK ligand-induced osteoclast differentiation via a stromal cell independent mechanism involving c-Jun repression (2000)

Loss of ovarian function following menopause results in a substantial increase in bone turnover and a critical imbalance between bone formation and resorption. This imbalance leads to a progressive loss of trabecular bone mass and eventually osteoporosis, in part the result of increased osteoclastogenesis. Enhanced formation of functional osteoclasts appears to be the result of increased elaboration by support cells of osteoclastogenic cytokines such as IL-1, tumor necrosis factor, and IL-6, all of which are negatively regulated by estrogens. We show here that estrogen can suppress receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF)-induced differentiation of myelomonocytic precursors into multinucleated tartrate-resistant acid phosphatase-positive osteoclasts through an estrogen receptor-dependent mechanism that does not require mediation by stromal cells. This suppression is dose-dependent, isomer-specific, and reversed by ICI 182780. Furthermore, the bone-sparing analogues tamoxifen and raloxifene mimic estrogen's effects. Estrogen blocks RANKL/M-CSF-induced activator protein-1-dependent transcription, likely through direct regulation of c-Jun activity. This effect is the result of a classical nuclear activity by estrogen receptor to regulate both c-Jun expression and its phosphorylation by c-Jun N-terminal kinase. Our results suggest that estrogen modulates osteoclast formation both by down-regulating the expression of osteoclastogenic cytokines from supportive cells and by directly suppressing RANKL-induced osteoclast differentiation.
Characterization of SRp46, a Novel Human SR Splicing Factor Encoded by a PR264/SC35 Retropseudogene (1998)

The highly conserved SR family contains a growing number of phosphoproteins acting as both essential and alternative splicing factors. In this study, we have cloned human genomic and cDNA sequences encoding a novel SR protein designated SRp46. Nucleotide sequence analyses have revealed that the SRp46 gene corresponds to an expressed PR264/SC35 retropseudogene. As a result of mutations and amplifications, the SRp46 protein significantly differs from the PR264/SC35 factor, mainly at the level of its RS domain. Northern and Western blot analyses have established that SRp46 sequences are expressed at different levels in several human cell lines and normal tissues, as well as in simian cells. In contrast, sequences homologous to SRp46 are not present in mice. In vitro splicing studies indicate that the human SRp46 recombinant protein functions as an essential splicing factor in complementing a HeLa cell S100 extract deficient in SR proteins. In addition, complementation analyses performed with beta-globin or adenovirus E1A transcripts and different splicing-deficient extracts have revealed that SRp46 does not display the same activity as PR264/SC35. These results demonstrate, for the first time, that an SR splicing factor, which represents a novel member of the SR family, is encoded by a functional retropseudogene.
Coupling of a New, Active Morphine Derivative to Sepharose for Affinity Chromatography (1972)

A new, pharmacologically active morphine derivative, 6-succinylmorphine, was synthesized. The properties of this compound and evidence for its structure are presented. Succinylmorphine was covalently coupled to ethylamino-Sepharose. Morphine-Sepharose containing up to 40 mug of morphine did not block the electrically stimulated contraction of isolated guinea pig ileum, but after alkaline hydrolysis of beads containing 2 mug of morphine the supernatant completely blocked contraction. This block was reversed by the specific morphine antagonist naloxone. Antibodies to morphine were removed from serum by morphine-Sepharose, but not by ethylamino-Sepharose, providing evidence of the efficacy of the beads for affinity chromatography.
Identification through bioinformatics of cDNAs encoding human thymic shared Ag-1/stem cell Ag-2. A new member of the human Ly-6 family (1996)

The Ly-6 family of cell surface molecules includes many members that have been characterized in the mouse. Until recently, very few Ly-6 family members had been described in the human. A significant development with important implications for novel gene discovery has been the growth of the public Expressed Sequence Tag (EST) database. Here we report that, through the application of bioinformatics analysis to the dbEST database, we obtained the sequence of human TSA-1/SCA-2, a new member of the human Ly-6 family. In addition, we identified full-length clones encoding this molecule as well as expression data in various tissues. Sequencing of the clones identified this way confirmed the sequence predicted through bioinformatics. This study constitutes an example of the application of bioinformatics to the analysis of the recently expanded databases for the identification of genes of potential importance in the immune system.
Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3 (2011)

SHANK3 is a synaptic scaffolding protein enriched in the postsynaptic density (PSD) of excitatory synapses. Small microdeletions and point mutations in SHANK3 have been identified in a small subgroup of individuals with autism spectrum disorder (ASD) and intellectual disability. SHANK3 also plays a key role in the chromosome 22q13.3 microdeletion syndrome (Phelan-McDermid syndrome), which includes ASD and cognitive dysfunction as major clinical features. To evaluate the role of Shank3 in vivo, we disrupted major isoforms of the gene in mice by deleting exons 4-9. Isoform-specific Shank3(e4-9) homozygous mutant mice display abnormal social behaviors, communication patterns, repetitive behaviors and learning and memory. Shank3(e4-9) male mice display more severe impairments than females in motor coordination. Shank3(e4-9) mice have reduced levels of Homer1b/c, GKAP and GluA1 at the PSD, and show attenuated activity-dependent redistribution of GluA1-containing AMPA receptors. Subtle morphological alterations in dendritic spines are also observed. Although synaptic transmission is normal in CA1 hippocampus, long-term potentiation is deficient in Shank3(e4-9) mice. We conclude that loss of major Shank3 species produces biochemical, cellular and morphological changes, leading to behavioral abnormalities in mice that bear similarities to human ASD patients with SHANK3 mutations.