gebhart/patrepeval huggingface dataset:
A proactive risk-aware robotic sensor network for Critical Infrastructure Protection (2013)

In this paper, a risk-aware robotic sensor network (RSN) is proposed in the context of Critical Infrastructure Protection. Such a network will be comprised of mobile sensor nodes that perceive various aspects of their environment and topologically reconfigure in order to secure a strategic area of interest. Risk awareness is provided through the application of a recently developed Risk Management Framework to the RSN. The risk level of each node is assessed in terms of their degree of distress, proximity factor, and terrain maneuverability. Risk monitoring alerts are issued whenever any given sensor node's quantitative risk metric exceeds a user-defined threshold value. At this point, a node-in-distress (NID) has been identified as the weak point of the securing structure around which the RSN is deployed. The NID can no longer be used with confidence and the effective perimeter coverage of the RSN has been reduced, thus creating potential security breaches in the area of interest. In response, the remaining nodes will self-organize to maximize the perimeter coverage while minimizing the cost of doing so. A limited set of contingency network topologies is produced via evolutionary multi-objective optimization using the Non-Dominated Sorting Genetic Algorithm (NSGA-II) and then ranked according to a human-guided alternative selection algorithm. The security operator picks the most suitable topology, which is then effectuated upon the environment. Results indicate that NSGA-II is capable of producing feasible network topologies to satisfy maximum perimeter coverage, while reducing the energy required for topology reconfiguration. As far as we are concerned, this is the first time a RSN applied to a CIP scenario is self-organized in response to a risk analysis conducted on every sensor node on the basis of multiple risk features.
[Change of nitric oxide in local muscle of crush injury hind-limbs in rats]. (2006)

The crushing hind-limbs of rats elicited the upregulation of eNOS and iNOS protein expression, the enhancement of NOS activity and the excess production of NO, the latter of which was involved in the mediation of secondary pathological changes in local muscles.
Molecular differences in anticytokine therapies. (2003)

Biologic agents that inhibit proinflammatory cytokines have made a profound impact on the treatment of rheumatoid arthritis (RA). Of the agents that are currently approved by the US Food and Drug Administration (FDA) for this indication, etanercept and infliximab neutralize tumor necrosis factor (TNF), and anakinra inhibits interleukin-1 (IL-1). Adalimumab, which was just recently approved by the FDA, is also a TNF inhibitor. Despite their common ability to inhibit cytokine bioactivity, the molecular structures and mechanisms of action of these biologic agents are significantly different. The TNF-binding moiety of etanercept is derived from soluble TNF receptor subunits. Infliximab is a chimeric (mouse-human) monoclonal antibody to TNF, while adalimumab is a fully human anti-TNF monoclonal antibody. Anakinra has yet another mechanism of action: it is an IL-1 receptor antagonist. The molecular characteristics of these agents may be relevant to clinical efficacy and safety. These agents are still relatively new: to date, the longest reporting time is 5 years, for etanercept. Additional long-term data will be required to determine the relative benefits and drawbacks of different molecular characteristics in these anticytokine agents.
Cancer-Specific Production of N-Acetylaspartate via NAT8L Overexpression in Non–Small Cell Lung Cancer and Its Potential as a Circulating Biomarker (2015)

In order to identify new cancer-associated metabolites that may be useful for early detection of lung cancer, we performed a global metabolite profiling of a non-small cell lung cancer (NSCLC) line and immortalized normal lung epithelial cells from the same patient. Among several metabolites with significant cancer/normal differences, we identified a unique metabolic compound, N-acetylaspartate (NAA), in cancer cells-undetectable in normal lung epithelium. NAA's cancer-specific detection was validated in additional cancer and control lung cells as well as selected NSCLC patient tumors and control tissues. NAA's cancer specificity was further supported in our analysis of NAA synthetase (gene symbol: NAT8L) gene expression levels in The Cancer Genome Atlas: elevated NAT8L expression in approximately 40% of adenocarcinoma and squamous cell carcinoma cases (N = 577), with minimal expression in all nonmalignant lung tissues (N = 74). We then showed that NAT8L is functionally involved in NAA production of NSCLC cells through siRNA-mediated suppression of NAT8L, which caused selective reduction of intracellular and secreted NAA. Our cell culture experiments also indicated that NAA biosynthesis in NSCLC cells depends on glutamine availability. For preliminary evaluation of NAA's clinical potential as a circulating biomarker, we developed a sensitive NAA blood assay and found that NAA blood levels were elevated in 46% of NSCLC patients (N = 13) in comparison with age-matched healthy controls (N = 21) among individuals aged 55 years or younger. Taken together, these results indicate that NAA is produced specifically in NSCLC tumors through NAT8L overexpression, and its extracellular secretion can be detected in blood. Cancer Prev Res; 9(1); 43-52. ©2015 AACR.
Finding the flow in web site search (2002)

Designing a search system and interface may best be served (and executed) by scrutinizing usability studies.
Subcutaneous Administration of Monoclonal Antibodies in Oncology (2014)

Treatment with monoclonal antibodies (mabs) has become an established component of oncological therapy. The monoclonal antibodies available for this purpose are mainly administered intravenously in individually adapted doses according to body weight over longer treatment times. For other chronic diseases such as, for example, diabetes mellitus, the subcutaneous administration of drugs is an established therapy option. For the subcutaneous administration of larger volumes as needed for mab solutions the extracellular matrix of the subcutaneous tissue represents a problem. The co-formulation with recombinant human hyaluronidase makes the relatively pain-free administration of larger fluid volumes and thus the subcutaneous administration of monoclonal antibodies possible, as illustrated by the development of a subcutaneous formulation of trastuzumab. This constitutes a less invasive, time-optimised and flexible form of administration for patients with HER2-positive breast cancer that, with its fixed dosing possibilities, contributes to therapeutic safety. The example of trastuzumab shows that the subcutaneous administration of monoclonal antibodies can simplify oncological long-term therapy not only for the patients but also for the medical personnel.
New Strategies in Chronic Lymphocytic Leukemia: Shifting Treatment Paradigms (2014)

Over the past two decades, slow but deliberate progress has been made in understanding the genetics of chronic lymphocytic leukemia (CLL) and how the surrounding microenvironment influences leukemia cell survival. The complexity of CLL with respect to different chromosomal aberrations, lack of a common aberrant signaling pathway activation, and associated immune suppression of the disease has been seen a major stumbling block for developing a single targeted therapy similar to imatinib used in chronic myeloid leukemia. The upcoming therapeutic era we are entering with the B-cell receptor (BCR) tyrosine kinase inhibitors ibrutinib and idelalisib appears to be overcoming this obstacle. Indeed, for the large majority of patients, it appears that application of BCR kinase inhibitors can promote durable remissions without the need for chemotherapy. Where other very active targeted agents such as ABT-199, therapeutic antibodies, and chimeric antigen receptor-modified T-cells will be used in CLL also represents a major question that future clinical trials will answer.
Proofs of Networks of Processes (1981)

We present a proof method for networks of processes in which component processes communicate exclusively through messages. We show how to construct proofs of invariant properties which hold at all times during network computation, and terminal properties which hold upon termination of network computation, if network computation terminates. The proof method is based upon specifying a process by a pair of assertions, analogous to pre-and post-conditions in sequential program proving. The correctness of network specification is proven by applying inference rules to the specifications of component processes. Several examples are proved using this technique.
Use of Mathematical Models for Predicting the Metabolic Effect of Large‐Scale Enzyme Activity Alterations (1995)

There are numerous examples showing that the metabolism of cells can be severely impaired if the activity of only one of the participating enzymes undergoes large‐scale alterations, resulting, for example, from spontaneous mutations (inherited or aquired enzymopathies), the administration of toxic drugs or self‐inactivation of enzymes during cell aging. However, a quantitative relationship between the degree of enzyme deficiency and the extent of metabolic dysfunction is very difficult to establish by experimental means. An alternative is to tackle this problem by mathematical modelling. Our approach is based on a comprehensive mathematical model of the energy and redox metabolism for human erythrocytes. We calculate stationary states of the cell metabolism, varying the activity of each of the participating enzymes by several orders of magnitude. The metabolic states are then evaluated in terms of a performance function which relates the metabolic variables to the overall functional fitness of the cell. The performance function for the erythrocyte takes into account the homeostasis of three essential metabolic variables: the energetic state (ATP), the reductive capacity (reduced glutathione), and the osmotic state. Based on the behaviour of the performance function at varying enzyme activities, we estimate those ranges of enzyme activities, in which the metabolic alterations should be either tolerable, associated with non‐chronic or chronic diseases, or letal. For most enzymopathies, the experimental and clinical observations can be satisfactorily rationalized by the computational results. Moreover, a surprisingly high correlation is found between the range of the activity range where disease is predicted by the model and the observed number of diseased probands. Another objective of our study was to contribute to the theory of metabolic control. The well‐elaborated concept of the metabolic control theory is restricted to (infinitely) small activity alterations. In order to quantify the metabolic effect of finite (large‐scale) changes in the activity of an enzyme, we propose, as a control measure, the effective activity E a , defined as the relative activity of an enzyme (with respect to the activity in a reference state) required to bring about a change in the stationary value of a metabolic variable by the (finite) factor α. We demonstrate that none of the existing extrapolation methods using the conventional control coefficient is capable to provide reliable predictions of the effective activities for all enzymes of erythrocyte metabolism.
Industrial Applications Of Excimer Lasers (1986)

Excimer lasers are finding increasing use in both semiconductor and materials processing. In the semiconductor area, this has led to the development of excimer based processes for lithography, film deposition, etching, doping and annealing. In materials processing, the unique capabilities of the excimer laser offers the potential for greatly extending the range of laser based cutting, drilling and marking techniques. This paper is intended to provide an overview of these areas. Attention is given to the means by which the excimer laser addresses the critical needs in each particular case.
Neue Komplexe des Titans mit silylierten Aminoiminophosphoran‐ und Sulfodiimidliganden (1993)

Abstract TiCl 4 bildet mit S(NSiMe 3 ) 2 und Me 2 S(NSiMe 3 ) 2 ein 1 : 1 Addukt ( 1, 2 ), während Ph 2 S(NSiMe 3 ) 2 die disubstituierte Verbindung Ph 2 S(NTiCl 3 ) 2 X4 THF 3 ergibt, die in der Raumgruppe P 1 kristallisiert. Setzt man TiCl 4 mit (Me 3 Si) 2 NPPh 2 NPPh 2 NSiMe 3 um, so wird die imidische Silylgruppe gegen eine TiCl 3 ‐Einheit ausgetauscht. Das Molekül, in dem das Ti‐Atom nur vierfach koordiniert ist, bildet in der Raumgruppe P2 1 /c Einkristalle. In den Komplexen von CpTiCl 3 , Cp*TiCl 3 und Cp*TiF 3 mit Ph 2 P(NSiMe 3 ) 2 H erfolgt ebenfalls keine Chelatisierung wie die Einkristall‐Röntgenstrukturanalyse von Cp*TiCl 2 NPPh 2 NHSiMe 3 6 belegt. Verbindung 6 kristallisiert in der Raumgruppe P 1 .
Scaling properties of a low-actuation pressure microfluidic valve (2003)

Using basic physical arguments, we present a design and method for the fabrication of microfluidic valves using multilayer soft lithography. These on-off valves have extremely low actuation pressures and can be used to fabricate active functions, such as pumps and mixers in integrated microfluidic chips. We characterized the performance of the valves by measuring both the actuation pressure and flow resistance over a wide range of design parameters, and compared them to both finite element simulations and alternative valve geometries.
Mannosylated chitosan nanoparticle–based cytokine gene therapy suppressed cancer growth in BALB/c mice bearing CT-26 carcinoma cells (2006)

Cancer immunotherapy relies on the ability of the immune system to destroy tumor cells selectively and to elicit a long-lasting memory of such activity. Interleukin-12 (IL-12) is an immunomodulatory cytokine produced primarily by antigen-presenting cells, which play an important role in promoting Th1-type immune response and cell-mediated immunity. To augment the antitumor immune action by in vivo IL-12 gene delivery, mannosylated chitosan (MC) was prepared to induce mannose receptor-mediated endocytosis of IL-12 gene directly into dendritic cells which reside within the tumor. Upon characterization, MC was proven to be suitable for IL-12 gene delivery due to good physicochemical properties and low cytotoxicity. In addition, MC exhibited much enhanced IL-12 gene transfer efficiency to dendritic cells rather than chitosan itself in terms of the induction of murine IL-12 p70 and murine IFN-gamma. In animal studies, intratumoral injection of MC/plasmid encoding murine IL-12 complex into BALB/c mice bearing CT-26 carcinoma cells clearly suppressed tumor growth and angiogenesis, and significantly induced cell cycle arrest and apoptosis. Therefore, this study provides a new MC-mediated cytokine gene delivery system for cancer immunotherapy.
Macrophage-derived chemokine production by activated human T cells in vitro and in vivo: preferential association with the production of type 2 cytokines (2000)

Macrophage-derived chemokine (MDC), a potent chemoattractant for chronically activated Th2 lymphocytes, is constitutively expressed by dendritic cells, B cells, macrophages, and thymic medullary epithelial cells, whereas monocytes, NK cells, and T lymphocytes produce MDC only upon appropriate stimulation. In this study, we show in vitro MDC production also by activated T cells, which preferentially associate with the production of Th2 cytokines, IL-4, IL-5, and IL-6, and inversely correlate with the production of the Th1 cytokine, IFN-γ. Moreover, high levels of MDC were detected in the sera of the great majority of subjects suffering from mycosis fungoides / Sézary syndrome or atopic dermatitis, which are considered as disorders characterized by the predominant expansion and activation of Th2 cells, respectively. By contrast, serum MDC levels in subjects with multiple sclerosis or Crohn's disease, which are characterized by a Th1 predominance, did not differ significantly from those of healthy controls. Finally, MDC expression was detected in the skin biopsy specimens of subjects with atopic dermatitis, where it was expressed by both dendritic cells and T lymphocytes. Taken together, these findings suggest that MDC production by activated T cells may occur both in vitro and in vivo, particularly in association with Th2 cytokines, thus providing an important amplification circuit for Th2-mediated responses.
Modulation of Vigilance in the Primary Hypersomnias by Endogenous Enhancement of GABA A Receptors (2012)

The biology underlying excessive daytime sleepiness (hypersomnolence) is incompletely understood. After excluding known causes of sleepiness in 32 hypersomnolent patients, we showed that, in the presence of 10 μM γ-aminobutyric acid (GABA), cerebrospinal fluid (CSF) from these subjects stimulated GABA(A) receptor function in vitro by 84.0 ± 40.7% (SD) relative to the 35.8 ± 7.5% (SD) stimulation obtained with CSF from control subjects (Student's t test, t = 6.47, P < 0.0001); CSF alone had no effect on GABA(A) signaling. The bioactive CSF component had a mass of 500 to 3000 daltons and was neutralized by trypsin. Enhancement was greater for α2 subunit- versus α1 subunit-containing GABA(A) receptors and negligible for α4 subunit-containing ones. CSF samples from hypersomnolent patients also modestly enhanced benzodiazepine (BZD)-insensitive GABA(A) receptors and did not competitively displace BZDs from human brain tissue. Flumazenil--a drug that is generally believed to antagonize the sedative-hypnotic actions of BZDs only at the classical BZD-binding domain in GABA(A) receptors and to lack intrinsic activity--nevertheless reversed enhancement of GABA(A) signaling by hypersomnolent CSF in vitro. Furthermore, flumazenil normalized vigilance in seven hypersomnolent patients. We conclude that a naturally occurring substance in CSF augments inhibitory GABA signaling, thus revealing a new pathophysiology associated with excessive daytime sleepiness.
Macro-bending loss properties of photonic crystalfibre (2001)

Photonic crystal fibres are examined with respect to bending loss. An equivalent step-index fibre is modelled using an effective-index approach for the microstructured cladding. Measurements have been performed in a broad spectral range, and the results agree well with the calculated losses.
Cancer-Specific Functions of SIRT1 Enable Human Epithelial Cancer Cell Growth and Survival (2005)

SIRT1 is a conserved NAD-dependent deacetylase that regulates life span in accord with nutritional provision. In mammalian cells, SIRT1 also down-regulates stress-induced p53 and FoxO pathways for apoptosis, thus favoring survival under stress. The functioning of SIRT1 under normal, nonstressed conditions of cell growth is unknown. Here we have asked if SIRT1 has the capacity to influence cell viability in the absence of applied stress. For this purpose we used synthetic small interfering RNA to silence SIRT1 gene expression by RNA interference (RNAi). We show that the process of RNAi, by itself, does not affect cell growth and is not sufficient to activate a cellular stress response (indicated by lack of activation of endogenous p53). We also show that, in the absence of applied stress, SIRT1 silencing induces growth arrest and/or apoptosis in human epithelial cancer cells. In contrast, normal human epithelial cells and normal human diploid fibroblasts seem to be refractory to SIRT1 silencing. Combined gene knockout with RNAi cosilencing experiments indicate that SIRT1 and Bcl-2 may suppress separable apoptotic pathways in the same cell lineage and that the SIRT1-regulated pathway is independent of p53, Bax, and caspase-2. Alternatively, SIRT1 may suppress apoptosis downstream from these apoptotic factors. In either case, we show that FoxO4 (but not FoxO3) is required as proapoptotic mediator. We further identify caspase-3 and caspase-7 as downstream executioners of SIRT1/FoxO4-regulated apoptosis. Our work identifies SIRT1 as a novel target for selective killing of cancer versus noncancer epithelial cells.
Integrin signalling: The tug-of-war in heart hypertrophy (2006)

The mechanical stress imposed by hemodynamic overload on heart walls is a primary event in triggering the cardiac hypertrophic response. Integrins, a class of membrane receptors, are major players in transmitting the mechanical force across the plasma membrane and sensing the mechanical load in cardiomyocytes. In fact, integrins, together with a number of associated cytoskeletal proteins, connect the sarcomeric contractile apparatus to the extracellular matrix across the plasma membrane and trigger intracellular signaling pathways activating the cardiomyocyte hypertrophy program. In this review, we will discuss the role of the muscle-specific integrin isoform beta1D and of associated proteins such as FAK, melusin, vinculin, zyxin, VASP, and migfilin that are the most upstream elements ("initiators") activated by mechanical strain. These molecules trigger a coordinated downstream signaling cascade involving proteins such as AKT, RAS, and MAPKs that execute the biochemical program leading to cardiomyocyte hypertrophy. Better understanding of the functional role of the initiator elements is of key importance to developing novel strategies to control cardiac hypertrophy and prevent heart failure.
A macrolide 3-O-acyltransferase gene from the midecamycin-producing species Streptomyces mycarofaciens (1992)

The Streptomyces mycarofaciens mdmB gene encodes a 3-O-acyltransferase that catalyzes the addition of acetyl and propionyl groups to position 3 of the lactone ring in 16-member macrolide antibiotics like midecamycin and spiramycin. A putative O-methyltransferase gene (mdmC) is immediately downstream of mdmB, and both of these genes are closely linked to the mdmA midecamycin resistance gene.
Wound infiltration with magnesium sulphate and ropivacaine mixture reduces postoperative tramadol requirements after radical prostatectomy (2009)

Co-administration of MgSO(4) with ropivacaine for postoperative infiltration analgesia after radical retropubic prostatectomy produces a significant reduction in tramadol requirements.
Flow Fields: Dense Correspondence Fields for Highly Accurate Large Displacement Optical Flow Estimation (2015)

Modern large displacement optical flow algorithms usually use an initialization by either sparse descriptor matching techniques or dense approximate nearest neighbor fields. While the latter have the advantage of being dense, they have the major disadvantage of being very outlier-prone as they are not designed to find the optical flow, but the visually most similar correspondence. In this article we present a dense correspondence field approach that is much less outlier-prone and thus much better suited for optical flow estimation than approximate nearest neighbor fields. Our approach does not require explicit regularization, smoothing (like median filtering) or a new data term. Instead we solely rely on patch matching techniques and a novel multi-scale matching strategy. We also present enhancements for outlier filtering. We show that our approach is better suited for large displacement optical flow estimation than modern descriptor matching techniques. We do so by initializing EpicFlow with our approach instead of their originally used state-of-the-art descriptor matching technique. We significantly outperform the original EpicFlow on MPI-Sintel, KITTI 2012, KITTI 2015 and Middlebury. In this extended article of our former conference publication we further improve our approach in matching accuracy as well as runtime and present more experiments and insights.