gebhart/patrepeval huggingface dataset:
Regulation of endothelial VCAM-1 expression in murine cardiac grafts. Expression of allograft endothelial VCAM-1 can be manipulated with antagonist of IFN-alpha or IL-4 and is not required for allograft rejection. (1995)

This report provides evidence to support the hypothesis that tumor necrosis factor-alpha (TNF-alpha) and IL-4 promote the expression of new endothelial surface molecules in rejecting murine heterotopic cardiac allografts. The microvascular endothelia of these cardiac allografts all develop strong reactivity with the monoclonal antibodies (mAbs) YN1.1/74 (anti-ICAM-1), M/K-2 (anti-VCAM-1) and MECA-32 (undefined molecule) within 3 to 5 days of graft implantation. Daily treatment of the allograft recipients with pentoxifylline (PTX), soluble TNF receptor (TNFR:Fc), anti-interleukin-4 (IL-4) mAb (11B11), or soluble IL-4 receptor, each abrogate the expression of endothelial VCAM-1 and reduce the endothelial reactivity with the mAbs YN1.1/74 and MECA-32 to levels found in cardiac isografts. This is accompanied by a reduction, but not an elimination, of interstitial leukocytic infiltration. Despite this, cardiac allograft recipients treated with PTX or the mAb 11B11 rejected allografts at the same rate as untreated allograft recipients, ie, within 10 to 12 days after graft implantation. These rejected grafts contained mRNAs for TNF-alpha and IL-4, as well as for all other cytokines that have been associated with rejecting allografts. This suggests that endothelial VCAM-1 expression, which is characteristic of rejection, is not an essential element of the rejection process. Interestingly, the grafts from the PTX-treated recipients continued to display rare, isolated VCAM-1 positive cells in the interstitium, which may be dendritic cells. In general, these studies demonstrate a role for IL-4 and TNF-alpha in the alterations of vascular endothelial phenotype observed in rejecting cardiac allografts. They also demonstrate that endothelial VCAM-1 expression is not essential for the allograft rejection process, and that the role of VCAM-1 in this process may be more subtle than was initially suspected.
Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans (2011)

Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training "specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia [fraction of inspired oxygen (Fi(O(2))) = 21% or 13.5%]. Biopsies were taken from the musculus vastus lateralis, and cycle-ergometric incremental maximum oxygen uptake (VO(2max)) exercise tests were performed under normoxia, before and after the 10-wk training program. The main finding was a significant increase (P < 0.05) of fatty acid oxidation capacity per muscle mass, after endurance and strength training under normoxia [2.6- and 2.4-fold for endurance training normoxia group (ET(N)) and strength training normoxia group (ST(N)); n = 8 and 3] and hypoxia [2.0-fold for the endurance training hypoxia group (ET(H)) and strength training hypoxia group (ST(H)); n = 7 and 7], and higher coupling control of oxidative phosphorylation. The enhanced lipid oxidative phosphorylation (OXPHOS) capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P < 0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in muscle mass-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, and octanoylcarnitine). No significant increase was observed in mitochondrial DNA (mtDNA) content. Physiological OXPHOS capacity increased significantly in ET(N) (P < 0.01), with the same trend in ET(H) and ST(H) (P < 0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active lifestyle induced muscular changes of mitochondrial quality representative of mitochondrial health.
Targeting Cytokines of the Interleukin-12 Family in Autoimmunity (2006)

In the past, autoimmunity was thought to be mediated by antibodies and immune complexes. It has now become clear that many autoimmune diseases, especially tissue specific, are T cell-mediated, or at least T cell-dependent. The pathogenesis of cell-mediated autoimmune diseases, including multiple sclerosis, uveitis, diabetes, arthritis, and others, is now thought to be, in a large measure, driven by interferon-gamma-producing, antigen-specific T cells, which are polarized toward the T helper type 1 (Th1) phenotype. Interleukin (IL)-12 and the more recently discovered IL-23 and IL-27 constitute a unique family of structurally-related, heterodimeric cytokines, which regulate cell-mediated immune responses and Th1-type inflammatory reactions. Thus, these cytokines may have a central role in the development and progression of cell-mediated autoimmune diseases. Therefore, pharmacologically targeting cytokines of the IL-12 family would be useful in the modulation of several autoimmune diseases. This review summarizes the recent findings concerning IL-12 family cytokine-mediated autoreactive inflammatory responses, and also describes some possible therapeutic interventions, including medicinal compounds at mitigating autoimmune inflammation.
Using DSM-5 in Clinical Practice (2015)

Abstract The popularity of the DSM system led to it being used in ways for which it was never intended. DSM-5 can be misused as a guide to treatment, which it is not. Moreover, rapid symptom checks based on its criteria do not provide an adequate framework for either diagnosis or understanding patients. DSM-5 should be consulted before writing anything down on a patient chart. When completing a formal report, one should confirm that one’s conclusions correspond to the criteria in the manual. The best way to use DSM-5 is to confirm diagnoses that have been made clinically. The manual has to be a check, not a checklist.
Enhanced power solitons in optical fibres withperiodic dispersion management (1996)

The authors examine the formation of stable soliton-like pulses in optical fibres with a periodic dispersion map. It is found that increased energy is required to launch a pulse of given width compared to the equivalent uniform fibre with equal path-average dispersion. The stable pulse shapes in dispersion managed systems are significantly different to the hyperbolic secant solitons found in uniform fibres.
Hybrid Control for Robot Navigation - A Hierarchical Q-Learning Algorithm (2008)

Autonomous mobile robots have been widely studied and applied not only as a test bed to academically demonstrate the achievement of artificial intelligence but also as an essential component of industrial and home automation. Mobile robots have many potential applications in routine or dangerous tasks such as delivery of supplies in hospitals, cleaning of offices, and operations in a nuclear plant. One of the fundamental and critical research areas in mobile robotics is navigation, which generally includes local navigation and global navigation. Local navigation, often called reactive control, learns or plans the local paths using the current sensory inputs without prior complete knowledge of the environment. Global navigation, often called deliberate control, learns or plans the global paths based on a relatively abstract and complete knowledge about the environment. In this article, hybrid control architecture is conceived via combining reactive and deliberate control using a hierarchical Q-learning (HQL) algorithm.
The Ecology of an Order-Driven Market (1998)

An order-driven market, which has no market makers, separates into limit-order and market-order traders, who balance supply and demand for immediacy. Empirical evidence confirms that a bid–ask spread is a natural property of an order-driven market. Mean reversion in price following liquidity trades compensates the marginal investor for placing a limit order. Complex market ecology suggests that regulators should permit markets to evolve naturally.
Sensor-Based Chatter Detection and Avoidance by Spindle Speed Selection (1992)

This paper presents the results of a series of experimental studies of a control system which, based on information from available sensors (in this case a microphone was primarily used), automatically adjusts the spindle speed and the feed rate so as to achieve stable milling. It is seen that by iteratively adjusting the spindle speed so that the frequency with which the teeth pass is equal to the dominant frequency in the spectrum of the sensor output, the system will very quickly be driven into a stable region, if such a stable region exists. Experimental results which confirm the applicability of this control scheme to a variety of milling operations are presented. They include slotting and partial immersion cuts in cast iron and aluminum. Since this strategy is based on information supplied by the sensors, it is capable of adapting to tool changes, thin webs, corners, etc… which cause changes in the dynamics of the machine-tool-workpiece system and therefore may cause chatter to arise during the course of a milling operation. This strategy does not require an a priori knowledge of the dynamics of the machine-tool-workpiece system as do most of the off-line methods.
Identification and Fracture Outcomes of Undiagnosed Low Bone Mineral Density in Postmenopausal Women: Results From the National Osteoporosis Risk Assessment (2002)

Siris, Ethel S.; Miller, Paul D.; Barrett-Connor, Elizabeth; Faulkner, Kenneth G.; Wehren, Lois E.; Abbott, Thomas A.; Berger, Marc L.; Santora, Arthur C.; Sherwood, Louis M.
Sensitivities of Human Monocytes and Epithelial Cells to Pneumolysin Are Different (2002)

The Streptococcus pneumoniae pore-forming toxin, pneumolysin, is an important virulence factor in pneumococcal pneumonia. The effect of pneumolysin on human lung epithelial and monocyte cell viability was compared. Pneumolysin caused a dose-dependent loss of viability of human lung epithelial (A549 and L132) and monocyte (U937 and THP-1) cell lines. Analysis of the dose-response curves revealed similar log 50% inhibitory concentration (pIC(50)) values for A549, L132, and THP-1 of 0.12+/- 0.1, 0.02+/- 0.04, and 0.12+/- 0.13 hemolytic units (HU), respectively, but U937 cells showed a significantly greater pIC(50) of 0.42+/- 0.12 HU. Differentiation of A549 and L132 with phorbol ester or THP-1 with gamma interferon had no effect on their sensitivity to pneumolysin. However, a significant decrease in the potency of pneumolysin against U937 cells followed gamma interferon treatment. The Hill slopes of the inhibition curves were greater than unity, indicating that pneumolysin may act with positive cooperativity. Analysis of pneumolysin-treated THP-1 cells by electron microscopy revealed membrane lesions of between 100 and 200 nm in diameter.
The disease progression explorer (1999)

Managing and treating chronic, multifactorial diseases, such as atherosclerosis, osteoporosis, asthma, and periodontal disease, requires understanding the role of each risk factor in the disease and the interrelationships between risk factors. The discovery of a new risk factor often generates a new way of looking at the disease process and how to anticipate its expected progression. The Disease Progression Explorer concept was designed to support the transfer of information about a new risk factor for a disease from the research lab to clinical practice. Through the use of the Disease Progression Explorer, this transfer is supported by a graphical system that shows directly how risk factors, alone and in combination, influence the expected course of the disease and shows how disease management strategies and therapies can affect the patient's anticipated outcome. This paper describes a Disease Progression Explorer for periodontal disease called the Perio-DPE.
The Importance of Chemistry in the Development of High‐Performance Ceramics (1987)

Abstract Due to their mechanical, thermal and chemical stability, high‐performance ceramics have a range of properties which makes it possible in many fields to go beyond the limits of use of the various classes of materials nowadays available. In spite of this favorable starting situation, the worldwide endeavors to introduce this new group of materials have suffered some setbacks in both conventional applications and in new technologies. The ultimate reason is that these materials are very brittle. After the introduction of fracture mechanics, designers in many fields have learned how to handle brittle materials and how to exploit the potential of their properties in components subject to extreme loadings. Materials scientists have also been very successful in developing ceramics with high strength and fracture toughness characteristics. Nevertheless, the field of use has hitherto been restricted, since, in many cases, the reliability of the components is inadequate. Small and very small defects, such as micropores and cracks, as well as any other chemical and physical inhomogeneity in the structure can cause catastrophic failure of the components due to the high brittleness. Since, on the one hand, these defects are as a rule caused by inadequate control of the process sequences and, on the other, the production processes comprise a large number of chemical process steps, it is to be hoped that consistent application of the way of thinking and procedures of a chemist will make an important contribution in overcoming these difficulties.
Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. (2005)

Protein kinase B, also known as Akt, is a serine/threonine kinase and plays a critical role in the modulation of cell development, growth, and survival. Interestingly, Akt is ubiquitously expressed throughout the body, but its expression in the nervous system is substantially up-regulated during cellular stress, suggesting a more expansive role for Akt in the nervous system that may involve cellular protection. In this regard, a body of recent work has identified a robust capacity for Akt and its downstream substrates to foster both neuronal and vascular survival during apoptotic injury. Cell survival by Akt is driven by the modulation of both intrinsic cellular pathways that oversee genomic DNA integrity and extrinsic mechanisms that control inflammatory microglial activation. A series of distinct pathways are regulated by Akt that include the Forkhead family of transcription factors, GSK-3 beta, beta-catenin, c-Jun, CREB, Bad, IKK, and p53. Culminating below these substrates of Akt are the control of caspase mediated pathways that promote genomic integrity as well as prevent inflammatory cell demise. With further levels of progress in defining the cellular role of Akt, the attractiveness of Akt as a vital and broad cytoprotectant for both neuronal and vascular cell populations should continue to escalate.
A novel MUX-FF circuit for low power and high speed serial link interfaces (2010)

In this paper, a novel multiplexer-flip-flop (MUX-FF) topology using the current mode logic (CML) is presented. A CML multiplexer-latch (MUX-latch) is proposed by combining a multiplexer and the loopback storage part of a latch into a single module so that the buffer part of a latch can be removed. A MUX-FF is implemented by cascading two stages of MUX-latches. The output of a MUX-FF is edge-triggered, so it is insensitive to input noise. All the paths from inputs to the output are symmetric. Power and area can be reduced due to the removal of DFFs. Simulation results show that a MUX-FF can achieve a similar frequency as a conventional tree-type MUX by saving 56% of area and 72% of power consumption.
Structure-activity Relationship for FR901464: A Versatile Method for the Conversion and Preparation of Biologically Active Biotinylated Probes (2004)

The structure-activity relationship for FR901464, a potent cell-cycle inhibitor, was examined by synthesizing its analogs. A versatile method for converting FR901464 was devised. This method made it possible to synthesize biologically active FR901464-biotin conjugates which could be used to isolate the binding proteins.
Mixed-Criticality on the AFDX Network: Challenges and Potential Solutions (2018)

In this paper, we first assess the most relevant existing solutions enabling mixed-criticality on the AFDX and select the most adequate one. Afterwards, the specification of an extended AFDX, based on the Burst-Limiting Shaper (BLS), is detailed to fulfill the main avionics requirements and challenges. Finally, the preliminary evaluation of such a proposal is conducted through simulations. Results show its ability to guarantee the highest criticality traffic constraints, while limiting its impact on the current AFDX traffic.
Efficient mutagenesis of the rhodopsin gene in rod photoreceptor neurons in mice (2011)

Dominant mutations in the rhodopsin gene, which is expressed in rod photoreceptor cells, are a major cause of the hereditary-blinding disease, autosomal dominant retinitis pigmentosa. Therapeutic strategies designed to edit such mutations will likely depend on the introduction of double-strand breaks and their subsequent repair by homologous recombination or non-homologous end joining. At present, the break repair capabilities of mature neurons, in general, and rod cells, in particular, are undefined. To detect break repair, we generated mice that carry a modified human rhodopsin-GFP fusion gene at the normal mouse rhodopsin locus. The rhodopsin-GFP gene carries tandem copies of exon 2, with an ISceI recognition site situated between them. An ISceI-induced break can be repaired either by non-homologous end joining or by recombination between the duplicated segments, generating a functional rhodopsin-GFP gene. We introduced breaks using recombinant adeno-associated virus to transduce the gene encoding ISceI nuclease. We found that virtually 100% of transduced rod cells were mutated at the ISceI site, with ∼85% of the genomes altered by end joining and ∼15% by the single-strand annealing pathway of homologous recombination. These studies establish that the genomes of terminally differentiated rod cells can be efficiently edited in living organisms.
The design and analysis of graphical passwords (1999)

In this paper we propose and evaluate new graphical password schemes that exploit features of graphical input displays to achieve better security than text-based passwords. Graphical input devices enable the user to decouple the position of inputs from the temporal order in which those inputs occur, and we show that this decoupling can be used to generate password schemes with substantially larger #memorable# password spaces. In order to evaluate the security of one of our schemes, we devise a novel way to capture a subset of the #memorable&quot; passwords that, we believe, is itself a contribution. In this work we are primarily motivated by devices such as personal digital assistants #PDAs# that o#er graphical input capabilities via a stylus, and we describe our prototype implementation of one of our password schemes on suchaPDA, namely the Palm Pilot TM . 1 Introduction For the vast majority of computer systems, passwords are the method of choice for authenticating users. It ...
Tracing Leptin's Partners in Regulating Body Weight (2000)

OBESITY RESEARCHAlthough the hormone leptin hasn't turned out to be a magic bullet for obesity, its discovery has stimulated basic lab research which has been sketching out a much clearer picture of just how the body controls its weight. Researchers have identified a wealth of molecules involved in weight regulation, some of which cooperate with leptin to suppress appetite, while others blunt the hormone's fat-busting effects. Combining all these new molecular actors together in one leptin-conducted performance will be a daunting task, but they are already providing new targets for antiobesity drugs.
The Human Polymeric Immunoglobulin Receptor Facilitates Invasion of Epithelial Cells by<i>Streptococcus pneumoniae</i>in a Strain-Specific and Cell Type-Specific Manner (2002)

Streptococcus pneumoniae is a gram-positive bacterial pathogen that causes invasive life-threatening disease worldwide. This organism also commonly colonizes the upper respiratory epithelium in an asymptomatic fashion. To invade, this pathogen must traverse the respiratory epithelial barrier, allowing it to cause disease locally or disseminate hematogenously throughout the body. Previous work has demonstrated that S. pneumoniae choline-binding protein A, a pneumococcal surface protein, interacts specifically with the human polymeric immunoglobulin receptor, which is expressed by cells in the respiratory epithelium. Choline-binding protein A is required for efficient colonization of the nasopharynx in vivo. Additionally, a recent study showed that the R6x laboratory strain of S. pneumoniae invades a human pharyngeal cell line in a human polymeric immunoglobulin receptor-dependent manner. These findings raised the possibility that the interaction between choline-binding protein A and human polymeric immunoglobulin receptor may be a key determinant of S. pneumoniae pathogenesis. However, the strain used in prior invasion studies, R6x, is an unencapsulated, nonpathogenic strain. In the present study we determined the relative ability of strain R6x or pathogenic strains to invade a variety of human polymeric immunoglobulin receptor-expressing epithelial cell lines. The results of this work suggest that human polymeric immunoglobulin receptor-dependent enhanced invasion of epithelial cells by S. pneumoniae is a limited phenomenon that occurs in a strain-specific and cell type-specific manner.
Steroid Treatment in Acute Ischaemic Stroke (1988)

The files of 556 patients with a history of ischaemic stroke were reviewed. The disability and mortality rates were compared between 277 patients with a steroid treatment in the acute stage and 279 without. Comparison of the whole group showed that the steroid-treated patients had less improvement of their disability and a higher mortality rate than the non-steroid group. However, in the former more patients with a severe stroke were present. Statistical analysis of a subset of 208 patients with completed stroke in the middle cerebral artery territory showed no marked difference in the outcome and the adverse reactions between the steroid- and non-steroid-treated patients.