gebhart/patrepeval huggingface dataset:
Desorption of an intermediate in the complete oxidation of C2H4 over silver catalyst (1976)

It was found by applying the transient response method that a stable intermediate was formed during the complete oxidation of C2H4 over a silver catalyst which could be desorbed as acetic acid in a stream of pure H2, whereas it was not desorbed in pure He and it was decomposed to CO2 and H2O in a mixture of O2–He.
Electronic Structures and Optical Properties of Open and Capped Carbon Nanotubes (2000)

The electronic structures of a series of carbon nanotubes with different sizes, chiralities, ends, and bond lengths are studied systematically. Their absorption spectra are calculated with the localized density matrix method. The semiempirical model PM3 is employed in the calculation. The nature of optical excitations is investigated by examining their reduced single-electron density matrices. It is found that the optical excitations may be divided into the end modes and the tube modes, which have distinctive energies, features, and structural dependences. The optical gaps of carbon nanotubes scale inversely with tube length. Finite optical gaps have been confirmed and determined for infinitely long carbon nanotubes. The densities of states of carbon nanotubes are calculated at the self-consistent Hartree−Fock level. The calculated absorption spectra and densities of states compare well to the experimental results.
Activation of the TrkB Neurotrophin Receptor Is Induced by Antidepressant Drugs and Is Required for Antidepressant-Induced Behavioral Effects (2003)

Recent studies have indicated that exogenously administered neurotrophins produce antidepressant-like behavioral effects. We have here investigated the role of endogenous brain-derived neurotrophic factor (BDNF) and its receptor trkB in the mechanism of action of antidepressant drugs. We found that trkB.T1-overexpressing transgenic mice, which show reduced trkB activation in brain, as well as heterozygous BDNF null (BDNF(+/)-) mice, were resistant to the effects of antidepressants in the forced swim test, indicating that normal trkB signaling is required for the behavioral effects typically produced by antidepressants. In contrast, neurotrophin-3(+/)- mice showed a normal behavioral response to antidepressants. Furthermore, acute as well as chronic antidepressant treatment induced autophosphorylation and activation of trkB in cerebral cortex, particularly in the prefrontal and anterior cingulate cortex and hippocampus. Tyrosines in the trkB autophosphorylation site were phosphorylated in response to antidepressants, but phosphorylation of the shc binding site was not observed. Nevertheless, phosphorylation of cAMP response element-binding protein was increased by antidepressants in the prefrontal cortex concomitantly with trkB phosphorylation and this response was reduced in trkB.T1-overexpressing mice. Our data suggest that antidepressants acutely increase trkB signaling in a BDNF-dependent manner in cerebral cortex and that this signaling is required for the behavioral effects typical of antidepressant drugs. Neurotrophin signaling increased by antidepressants may induce formation and stabilization of synaptic connectivity, which gradually leads to the clinical antidepressive effects and mood recovery.
Optical levitation particle delivery system for a dual beam fiber optic trap (2000)

We combine a radiation-pressure-based levitation system with a dual fiber, laser trapping system to demonstrate the potential of delivering single particles into the fiber trap. The forces versus position and the trajectory of the particle subjected to the laser beams are examined with an enhanced ray optics model. A sequence of video images taken from the experimental apparatus demonstrates the principle of particle delivery, trapping, and further manipulation.
Altered circadian locomotor activity in APP23 mice: a model for BPSD disturbances (2004)

Over the past decade, clinical Alzheimer's disease research has been challenged with an increased interest in noncognitive symptomatology, commonly referred to as behavioural and psychological signs and symptoms of dementia (BPSD). In accordance, major attention is being paid to behavioural alterations in the phenotyping of transgenic mouse models. Besides an age-dependent decline of cognitive functions, the APP23 model was previously shown to exhibit cage activity disturbances, reminiscent of diurnal rhythm disturbances in Alzheimer patients. To further scrutinize these observations, circadian patterns of horizontal locomotor activity were assessed in 3-, 6- and 12-month-old APP23 mice and wild-type littermates in a test paradigm continuously recording cage activity over a period ranging from 1 to 3 days. At the age of 3 months, APP23 profiles resembled the wild-type pattern to a large extent, although minor differences were already noticeable. Six-month-old APP23 mice displayed an altered activity profile with a first indication of increased activity during the second half of the active phase, reminiscent of sundowning behaviour in Alzheimer patients. This bimodal overnight activity pattern became even more evident at the age of 12 months. The APP23 model was therefore shown to display an age-dependent development of cage activity disturbances and sundowning-like behaviour. A comparison is made with actigraphic recordings of human Alzheimer patients exhibiting sundowning behaviour. This first report of diurnal rhythm disturbances and sundowning-like phenomena in a transgenic mouse model greatly adds to the validity of the APP23 model.
Developmental analysis of murine Promyelocyte Leukemia Zinc Finger (PLZF) gene expression: implications for the neuromeric model of the forebrain organization (1995)

Promyelocyte Leukemia Zinc Finger (PLZF) is a Kruppel-like zinc finger gene previously identified in a unique case of acute promyelocytic leukemia (APL) as the counterpart of a reciprocal chromosomal translocation involving the retinoic acid receptor alpha gene (RAR alpha). PLZF is highly conserved throughout evolution from yeast to mammals. To elucidate its role, we isolated the murine PLZF gene and studied its expression during embryogenesis. PLZF is expressed in an extremely dynamic pattern with transcripts appearing at E 7.5 in the anterior neuroepithelium and quickly spreading to the entire neuroectoderm until E 10. At E 8.5, PLZF is transcribed in most of the endoderm. During mid to late gestation PLZF is expressed in restricted domains of the developing CNS as well as in specific organs and body structures. We have focused our attention on the developing forebrain where PLZF is transcribed in a transverse, segment-like domain corresponding to the anterior pretectum, in the alarmost part of the dorsal thalamus, in the epithalamus, and in the hypothalamus along a defined longitudinal subdomain. Furthermore, PLZF is expressed in several segmentary boundaries, among them, the zona limitans intrathalamica. Combined analysis with other regionally restricted genes, such as Orthopedia and Dlx1, indicates that in the hypothalamus the PLZF domain is contained within that of Orthopedia and both are complementary to that of Dlx1. Our data suggest a role for PLZF in the establishment and maintenance of transverse identities, longitudinal subdomains, and interneuromeric boundaries, providing additional evidences in favor of the neuromeric organization of the forebrain.
Interrelationships in energy planning : the case of the tobacco-curing industry in Thailand (1981)

The rapid rise in energy costs, especially oil prices, has created major dislocations in the economies of most oil-importing countries. The exploitation of domestic energy resources is one means of mitigating these effects but factors other than energy costs must also be considered. A study of the energy consumption patterns of the tobacco-curing industry in Thailand shows the importance of such factors as the reliability of supply, quality control, convenience in use, associated labor and capital costs, and the quality of output. In the Thai case, low-speed diesel fuel is clearly preferred to lignite as a heating fuel, in spite of its far greater cost. Governmental development policies should be directed at upgrading the quality and usability of domestic fuel and could reverse this trend.
The many questions on the use of biomarkers for neurodegenerative diseases in clinical practice (2014)

OPINION article Front. Aging Neurosci., 18 March 2014Sec. Neurocognitive Aging and Behavior Volume 6 - 2014 | https://doi.org/10.3389/fnagi.2014.00045
Neutrophil-independent mechanisms of caspase-1– and IL-18–mediated ischemic acute tubular necrosis in mice (2002)

Having recently described the injurious role of caspase-1–mediated production of the proinflammatory cytokine IL-18 in ischemic acute renal failure (ARF), we report here on the effect of the newly developed caspase inhibitor Quinoline-Val-Asp(Ome)-CH2-OPH (OPH-001) on caspase-1, IL-18, neutrophil infiltration, and renal function in ischemic ARF. C57BL/6 mice with ischemic ARF treated with OPH-001 had a marked (100%) reduction in blood urea nitrogen (BUN) and serum creatinine and a highly significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle-treated mice. OPH-001 significantly reduced the increase in caspase-1 activity and IL-18 and prevented neutrophil infiltration in the kidney during ischemic ARF. To evaluate whether this lack of neutrophil infiltration was contributing to the protection against ischemic ARF, a model of neutrophil depletion was developed. Neutrophil-depleted mice had a small (18%) reduction in serum creatinine during ischemic ARF but no reduction in ATN score despite a lack of neutrophil infiltration in the kidney. Remarkably, caspase-1 activity and IL-18 were significantly increased in the kidney in neutrophil-depleted mice with ARF. In addition, IL-18 antiserum–treated neutrophil-depleted mice with ischemic ARF had a significant (75%) reduction in serum creatinine and a significant reduction in ATN score compared with vehicle-treated neutrophil-depleted mice. These results suggest a novel neutrophil-independent mechanism of IL-18–mediated ischemic ARF.
A new, field-proven, cost-effective solution for MEG regeneration unit issues in offshore Australia gas production (2011)

Several gas fields are being developed off the coast of Western Australia. The risk for hydrate blockages in these fields is high and presents several challenges for hydrate inhibition, including high subcoolings, low water salinities, and high system temperatures. The current strategy is to use mono-ethylene glycol (MEG) for hydrate inhibition, which includes MEG regeneration units (MRUs) in the design of the facilities. The installation and maintenance of MRUs capable of handling the large required volumes of MEG is costly and other issues such as scale, foaming, and accumulation are a concern when using an MRU. Therefore, the use of a low dosage hydrate inhibitor (LDHI) is being considered for some developments. Kinetic hydrate inhibitors (KHIs) are typically considered for gas fields, not anti-agglomerate low dosage hydrate inhibitors (AA-LDHIs). KHIs, however, are not effective at high subcoolings and can become unstable when subjected to the high temperatures of the MRUs. Instead, a new generation of AA-LDHI chemistry can be considered for Australian gas fields. Field data will be presented supporting the new AA-LDHI’s effectiveness in inhibiting hydrate blockages in a gas/condensate field, eliminating the need for MEG and the MRU. The new AA-LDHI chemistry is being evaluated for several Australia projects, and data supporting the chemistry’s stability at temperatures greater than 150°C and its effectiveness with low-water salinities will also be presented. The new AA-LDHI chemistry could eliminate the need for MEG or greatly reduce the volume of MEG required for inhibition, which would reduce CAPEX and OPEX.
Thermal-Frequency-Drift Compensation (1942)

The conditions necessary for minimizing frequency drift with variation of ambient temperature are examined for various types of circuits. In fixed-tuned circuits the drift can be eliminated by a comparatively simple adjustment of the temperature coefficient of capacitance. In variable-tuned circuits, expressions for coefficient adjustment resulting in minimum integrated drift are given, together with simpler expressions resulting in an approximate minimum. It is shown to be practicable in some instances to design circuits in which the drift is better than ten parts per million per degree centigrade, over normally used frequency ranges, by complementary adjustment of the temperature coefficients of inductance and capacitance. Frequency drift in superheterodyne receiver circuits is discussed, and it is found that the local-oscillator circuit is peculiarly adaptable to drift correction by reason of the complex nature of its capacitance network. Such padded circuits can be very effectively corrected by simple adjustment of the various capacitive coefficients, the drift factor being tracked in a manner analogous to the frequency tracking. The padding of variable-capacitance-tuned circuits for the express purpose of drift correction presents the simplest means of minimizing thermal drift in such circuits. The necessary expressions are given, together with the results of some experimental work.
The design of fault-tolerant linear digital state variable systems: theory and techniques (1993)

A theory for error detection in linear digital state variable systems is described. With the aid of a tool called the gain matrix, it is shown that the effect of error propagation along different paths of the circuit can be analyzed. For circuits with operator fanout, it is shown that despite the fact that single faulty operators cause multiple state variables to be erroneous, no more additional check variables are required than for circuits without operator fanout. It is further shown that hardware optimization can be performed by sharing hardware functions between the original state variable system and its error detection circuitry. The analysis is performed for both single and multiple faulty operators. A scheme for error correction that performs error correction in real time is proposed. Experimental results that illustrate the practical viability of the proposed scheme are discussed.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
Bile Acids Induce the Expression of the Human Peroxisome Proliferator-Activated Receptor α Gene via Activation of the Farnesoid X Receptor (2003)

Peroxisome proliferator-activated receptor alpha (PPARalpha) is a nuclear receptor that controls lipid and glucose metabolism and exerts antiinflammatory activities. PPARalpha is also reported to influence bile acid formation and bile composition. Farnesoid X receptor (FXR) is a bile acid-activated nuclear receptor that mediates the effects of bile acids on gene expression and plays a major role in bile acid and possibly also in lipid metabolism. Thus, both PPARalpha and FXR appear to act on common metabolic pathways. To determine the existence of a molecular cross-talk between these two nuclear receptors, the regulation of PPARalpha expression by bile acids was investigated. Incubation of human hepatoma HepG2 cells with the natural FXR ligand chenodeoxycholic acid (CDCA) as well as with the nonsteroidal FXR agonist GW4064 resulted in a significant induction of PPARalpha mRNA levels. In addition, hPPARalpha gene expression was up-regulated by taurocholic acid in human primary hepatocytes. Cotransfection of FXR/retinoid X receptor in the presence of CDCA led to up to a 3-fold induction of human PPARalpha promoter activity in HepG2 cells. Mutation analysis identified a FXR response element in the human PPARalpha promoter (alpha-FXR response element (alphaFXRE)] that mediates bile acid regulation of this promoter. FXR bound the alphaFXRE site as demonstrated by gel shift analysis, and CDCA specifically increased the activity of a heterologous promoter driven by four copies of the alphaFXRE. In contrast, neither the murine PPARalpha promoter, in which the alphaFXRE is not conserved, nor a mouse alphaFXRE-driven heterologous reporter, were responsive to CDCA treatment. Moreover, PPARalpha expression was not regulated in taurocholic acid-fed mice. Finally, induction of hPPARalpha mRNA levels by CDCA resulted in an enhanced induction of the expression of the PPARalpha target gene carnitine palmitoyltransferase I by PPARalpha ligands. In concert, these results demonstrate that bile acids stimulate PPARalpha expression in a species-specific manner via a FXRE located within the human PPARalpha promoter. These results provide molecular evidence for a cross-talk between the FXR and PPARalpha pathways in humans.
THE INFLATIONARY FORCE PRODUCED BY PULMONARY VASCULAR DISTENTION IN EXCISED LUNGS. THE POSSIBLE RELATION OF THIS FORCE TO THAT NEEDED TO INFLATE THE LUNGS AT BIRTH (1959)

Among the forces that may contribute to the first inflation of the lungs after birth, those de- veloped through changes in the pulmonary circu- latory system have been assigned primary impor- tance by Jaykka (1), Bonham Carter (2) and Adams, Karlberg and Lind (3). Possibly the ear- liest basis for this view was provided during the last century by von Basch (4) who showed in ani- mals and also in experimental models that pulmo- nary vascular congestion, presumably at the capil- lary level, tends to increase the volume of gas in the lungs. Recently, it was demonstrated in ex- cised cats' lungs that the expansile force resulting from vascular congestion is greatest when the lungs are collapsed (5). Together, these findings might be taken as evidence underscoring the role of vas- cular distention in expanding the lungs at birth. Before this view is accepted, however, two facts must be established. One is that the increase in pulmonary blood flow precedes the first breath. This is contrary to the findings of Dawes in fetal lambs that pulmonary blood flow is increased only after inflation has occurred (6). The other is that the force developed through vascular filling or con- gestion is sufficiently large to cause air to enter the lung. The object of this study was to test this sec- ond possibility. Experiments were carried out to compare the distending forces produced by a wide range of pulmonary vascular pressures with the force required to inflate the lungs. Measure- ments were made on excised lungs of adult cats and dogs that were freed of gas to simulate their condition at birth, and on lungs of puppies and newborn infants that had not breathed.
Exploiting reality with multicast groups (1995)

This article describes our investigation into developing large distributed simulations. The architecture we describe logically partitions virtual environments by associating spatial, temporal, and functional classes with network multicast groups. We exploit the actual characteristics of the real-world large scale environments being simulated by focusing or restricting an entity's processing and network resources to its area of interest via a local area-of-interest manager. For example, a simulated infantryman in a virtual environment doesn't need to know the condition of a simulated truck 20 virtual kilometres away.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
Primary Severe Acute Respiratory Syndrome Coronavirus Infection Limits Replication but Not Lung Inflammation upon Homologous Rechallenge (2012)

Our knowledge regarding immune-protective and immunopathogenic events in severe acute respiratory syndrome coronavirus (SARS-CoV) infection is limited, and little is known about the dynamics of the immune response at the primary site of disease. Here, an African green monkey (AGM) model was used to elucidate immune mechanisms that facilitate viral clearance but may also contribute to persistent lung inflammation following SARS-CoV infection. During primary infection, SARS-CoV replicated in the AGM lung for up to 10 days. Interestingly, lung inflammation was more prevalent following viral clearance, as leukocyte numbers peaked at 14 days postinfection (dpi) and remained elevated at 28 dpi compared to those of mock-infected controls. Lung macrophages but not dendritic cells were rapidly activated, and both cell types had high activation marker expression at late infection time points. Lung proinflammatory cytokines were induced at 1 to 14 dpi, but most returned to baseline by 28 dpi except interleukin 12 (IL-12) and gamma interferon. In SARS-CoV homologous rechallenge studies, 11 of the 12 animals were free of replicating virus at day 5 after rechallenge. However, incidence and severity of lung inflammation was not reduced despite the limited viral replication upon rechallenge. Evaluating the role of antibodies in immune protection or potentiation revealed a progressive increase in anti-SARS-CoV antibodies in lung and serum that did not correlate temporally or spatially with enhanced viral replication. This study represents one of the first comprehensive analyses of lung immunity, including changes in leukocyte populations, lung-specific cytokines, and antibody responses following SARS-CoV rechallenge in AGMs.
The middlebox manifesto (2011)

Most network deployments respond to changing application, workload, and policy requirements via the deployment of specialized network appliances or "middleboxes". Despite the critical role that middleboxes play in introducing new network functionality, they have been surprisingly ignored in recent efforts for designing networks that are amenable to innovation. We make the case that enabling innovation in middleboxes is at least as important, if not more important, as that for traditional switches and routers. To this end, our vision is a world with software-centric middlebox implementations running on general-purpose hardware platforms that are managed via open and extensible management APIs. While these principles have been applied in other contexts, they introduce unique opportunities and challenges in the context of middleboxes that we highlight in this paper.
Update on the association between dry eye disease and meibomian gland dysfunction (2019)

Dry eye disease is one of the most common ophthalmic complaints; it results from the activity of various pathways and is considered a multifactorial disease. An important factor that contributes to the onset of dry eye disease is meibomian gland dysfunction. Meibomian gland dysfunction causes a disruption in the tear film lipid layer which affects the rate of tear evaporation. This evaporation leads to tear hyperosmolarity, eventually triggering the onset of dry eye disease. Dry eye disease and meibomian gland dysfunction are strongly associated with each other, such that many of their risk factors, signs, and symptoms overlap. This review aimed to provide an update on the association between dry eye disease and meibomian gland dysfunction. A stepwise approach for diagnosis and management is summarised.
Einleitung (2009)

Das Thema Fahrerassistenzsysteme ist bei Automobilherstellern, Zulieferern und in der universitären Forschung seit geraumer Zeit aktuell und hat in den vergangenen Jahren auch das Interesse der Öffentlichkeit geweckt. Die Zahl der am Markt verfügbaren Systeme und ihr Funktionsumfang zur Unterstützung des Fahrers bei der Ausführung der Fahraufgabe nehmen stetig zu. Bedingt durch die jüngsten Entwicklungen wird der Begriff Fahrerassistenzsysteme (in unserer abgekürzten Welt kurz mit FAS bezeichnet) heute zumeist mit Systemen der Aktiven Sicherheit, d. h. Systemen, die das Eintreten eines Unfalls verhindern, in Verbindung gebracht. Tatsächlich kann dieser Begriff jedoch sehr viel breiter gefasst werden, denn schon mit der Erfindung des elektrischen Starters, der die manuelle Kurbel ablöste, war ein erstes Fahrerassistenzsystem geboren, das das Fahren erleichterte. Auch Dinge wie die automatische Blinkerhebelrückstellung oder das synchronisierte Handschaltgetriebe werden heute als Selbstverständlichkeiten angesehen, sind im eigentlichen Sinne jedoch als Fahrerassistenzsysteme zu verstehen.