gebhart/patrepeval huggingface dataset:
Exaggerated Left Ventricular Dilation and Reduced Collagen Deposition After Myocardial Infarction in Mice Lacking Osteopontin (2001)

Osteopontin (OPN), an extracellular matrix protein, is expressed in the myocardium with hypertrophy and failure. We tested the hypothesis that OPN plays a role in left ventricular (LV) remodeling after myocardial infarction (MI). Accordingly, OPN expression and LV structural and functional remodeling were determined in wild-type (WT) and OPN knockout (KO) mice 4 weeks after MI. Northern analysis showed increased OPN expression in the infarcted region, peaking 3 days after MI and gradually decreasing over the next 28 days. In the remote LV, OPN expression was biphasic, with peaks at 3 and 28 days. In situ hybridization and immunohistochemical analyses showed increased OPN mRNA and protein primarily in the interstitium. Infarct size, heart weight, and survival were similar in KO and WT mice after MI (P=NS), whereas the lung wet weight/dry weight ratio was increased in the KO mice (P<0.005 versus sham-operated mice). Peak LV developed pressure was reduced to a similar degree after MI in the KO and WT mice. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive myocytes was similar in KO and WT mice after MI. In contrast, post-MI LV chamber dilation was approximately twice as great in KO versus WT mice (P<0.001). Myocyte length increased after MI in WT mice (P<0.001) but not in KO mice. Electron microscopy showed increased collagen content in WT mice after MI but not in KO mice after MI. Type I collagen content was increased approximately 3-fold and approximately 7-fold in remote and infarcted regions, respectively, of WT hearts after MI but not in KO hearts (P<0.01 versus WT hearts). Likewise, Northern analyses showed increased collagen I(alpha(1)) mRNA after MI in remote regions of WT hearts but not in KO hearts. Thus, increased OPN expression plays an important role in regulating post-MI LV remodeling, at least in part, by promoting collagen synthesis and accumulation.
GRAMMPS: a generalized mission planner for multiple mobile robots in unstructured environments (2002)

For a system of cooperative mobile robots to be effective in real-world applications it must be able to efficiently execute a wide class of complex tasks in potentially unknown and unstructured environments. Previous research in multi-robot systems has either been limited to relatively structured domains or to small classes of feasible missions. This paper describes a field-capable system called GRAMMPS which addresses this problem by coupling a general-purpose interpreted grammar for task definition with dynamic planning techniques. GRAMMPS supports a general class of local navigation systems and heterogeneous groups of robots, providing optimal execution of missions given current world knowledge. Simulations illustrating the capabilities of this system are provided. Results showing successful runs of this system on two autonomous off-road vehicles are also given.
The Improvement of Irreversible Electroporation Therapy Using Saline-Irrigated Electrodes: A Theoretical Study (2011)

Irreversible electroporation (IRE) is a novel therapy used to ablate tumors with high-field electric pulses applied in short durations. It is important to reduce the generation of heat in IRE to avoid the harmful effects of thermal damage. The objective of this simulation study was to examine the effects of saline irrigation in the reduction of heat upon electrodes used in IRE treatment of hepatocellular carcinoma. We used a two dimensional Finite Element Model of a tumor in a liver with electrodes placed at the center of the tumor. We simulated a typical electroporation protocol with varying thicknesses and conductivities of the saline layer, and we observed the maximum temperature and the distribution of the electric field and temperature in the tissue. Our results showed that the maximum temperature in the tissue decreases with the use of saline, but the surface area of the tumor that could potentially be thermally damaged may increase with the thickness and conductivity of the saline. With the use of saline, one can achieve upwards of a 17% reduction of the maximum temperature at the electrodes. Also, the distribution of temperature and the electric field becomes more homogenous between the electrodes as the conductivity of the saline layer increases for all thicknesses of saline. We conclude that irrigating electrodes with saline may be an effective measure to enhance the efficacy of irreversible electroporation by reducing the maximum temperature at the electrodes and also improving the extent and distribution of the electric field in the tissue. However, the properties of the saline should be adjusted so as to limit the increase of thermal damage propagated in the tissue.
Antidepressant-like activity of (4-phenylpiperazin-1-yl) (quinoxalin-2-yl) methanone (4a), a novel 5-HT 3 receptor antagonist: An investigation in behaviour-based rodent models of depression (2012)

These preliminary investigations confirm that 4a exhibits antidepressant-like activity in behaviour based rodent models of depression.
Glycosylation of the basic fibroblast growth factor receptor. The contribution of carbohydrate to receptor function. (1988)

We have examined the glycosylation of the basic fibroblast growth factor (bFGF) receptor to determine whether carbohydrates contribute to receptor structure and function. Using a combination of cross-linking and radioreceptor assays, we demonstrated that the two bFGF receptors in baby hamster kidney cells have protein cores of 100 and 125 kDa. They are glycosylated to high mannose forms of 115 and 140 kDa and further processed to their mature forms of 130 and 150 kDa. Because peptide:N-glycosidase F, but not endo-alpha-N-acetylgalactosamidase can reduce the size of the bFGF receptors, the carbohydrate residues of the receptor appear all N-linked. The inability of deglycosylated receptors to bind 125I-bFGF supports the notion that the carbohydrate residues are required for receptor function. Furthermore, the capacity of the wheat germ agglutinin lectin to inhibit 125I-bFGF binding and the biological activity of bFGF suggests that N-acetylglucosamine residues are functionally significant components of the receptor.
Cardiovascular complications of non-steroidal anti-inflammatory drugs. (2005)

Coxibs, such as rofecoxib, celecoxib, and valdecoxib, selectively inhibit cyclooxygenase (COX)-2, the mainly inducible, pro-inflammatory COX isoform. Unlike traditional non-steroidal anti-inflammatory drugs (NSAIDs) most coxibs do not significantly inhibit COX-1 and are therefore less toxic to the gastrointestinal tract. Hence, coxibs widely replaced traditional NSAIDs for treatment of arthritis and other painful inflammatory conditions. In many, but not all, clinical studies, coxibs became associated with higher risks of myocardial infarction (MI) and stroke. Several mechanisms may be involved in the pathogenesis of such complications. First, selective inhibition of COX-1 lowers platelet synthesis of thromboxane (TXA(2)), a thrombogenic and atherogenic eicosanoid. Selective inhibition of COX-2 limits endothelial cell synthesis of prostacyclin (PGI(2)), an arachidonic acid product that opposes the effects of thromboxane. In apoE-/- mice, interruption of TXA(2) signaling by deletion of its receptor (TP) limits atherogenesis, whereas interruption of PGI2 signaling by deletion of its receptor (IP) accelerates atherogenesis. This suggests that selective inhibition of COX-2 can disrupt the physiological balance between thromboxane and prostacyclin and thus increase atherosclerosis, thrombogenesis, and the risk of cardiovascular complications. Second, COX inhibition can raise levels of arachidonic acid, which can inhibit mitochondrial oxidative phosphorylation (OXPHOS) and increase OXPHOS generation of reactive oxygen species. Several NSAIDs, including coxibs and meloxicam, directly uncouple or inhibit OXPHOS. Studies of apoE-/- mice indicate that mitochondrial dysfunction plays an early role in atherogenesis. Third, many NSAIDs exhibit COX-independent properties. For example, in animal models, short-term treatment with celecoxib reduces monocyte chemotaxis by reducing expression of monocyte chemoattractant protein (MCP)-1. However, long-term treatment results in the opposite effect and accelerates atherogenesis. In conclusion, to reduce the risk of cardiovascular complications during long-term coxib therapy, low-dose aspirin supplementation should be considered. An alternative is to use a less COX-2-selective inhibitor such as meloxicam. Genotyping of -765 alleles of the COX-2 gene promoter and examining the polymorphism of other genes involved in eicosanoid metabolism or NSAID degradation may become helpful in predicting patients who are at higher risk of cardiovascular complications during selective COX-2 inhibitor therapy.
[Effect of estradiol on the course of ovalbumin sensitization in guinea pigs]. (1993)

The latent period of ovalbumin (Ova)-induced asthma in Ova-sensitized guinea pigs was shorter in the ovariectomized animals with sc estradiol (E2) 400 or 50 micrograms.d-1 x 14 d and in animals with intact ovary (84 +/- 35, 82 +/- 33, and 100 +/- 32 s, respectively) than in the ovariectomized animals (140 +/- 29 s) (P < 0.05). The histamine (His) content of the lungs and His released from lungs under Ova challenge in vitro increased in the group of ovariectomy with sc E2 50 micrograms.d-1 x 14 d as compared with those without sc E2 (56 +/- 9 and 47 +/- 11 ng/g wet weight vs 44 +/- 10 and 36 +/- 11 ng/g wet weight) (P < 0.05). However, the pD2 values of the contraction of isolated tracheal strips induced by His and those of the relaxation by isoproterenol (Iso) were not affected. These findings suggest that the strengthened effect of E2 on the sensitization may be related to the content and the release of lung His in guinea pigs.
Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid (1993)

An impairment of energy metabolism may underlie slow excitotoxic neuronal death in neurodegenerative diseases. We therefore examined the effects of intrastriatal, subacute systemic, or chronic systemic administration of the mitochondrial toxin 3-nitropropionic acid (3-NP) in rats. Following intrastriatal injection 3-NP produced dose-dependent striatal lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P, calbindin) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of 3-NP produced age-dependent bilateral striatal lesions with a similar neurochemical profile. However, in contrast to the intrastriatal injections, striatal dopaminergic afferent projections were spared. Both freeze-clamp measurements and chemical shift magnetic resonance spectroscopy showed that 3-NP impairs energy metabolism in the striatum in vivo. Microdialysis showed no increase in extracellular glutamate concentrations after systemic administration of 3-NP. The lesions produced by intrastriatal injection or systemic administration of 3-NP were blocked by prior decortication. However, the NMDA antagonist MK-801 did not block the effects of intrastriatal 3-NP, consistent with a non-NMDA excitotoxic mechanism. In contrast to subacute systemic administration of 3-NP, chronic (1 month) administration produced lesions confined to the striatum in which there was relative sparing of NADPH-diaphorase interneurons, consistent with an NMDA excitotoxic process. Chronic administration showed growth-related proliferative changes in dendrites of spiny neurons similar to changes in Huntington's disease (HD). These results are consistent with in vitro studies showing that mild metabolic compromise can selectively activate NMDA receptors while more severe compromise activates both NMDA and non-NMDA receptors. Chronic administration of 3-NP over 1 month produces selective striatal lesions that replicate many of the characteristic histologic and neurochemical features of HD.
Depth Prediction without the Sensors: Leveraging Structure for Unsupervised Learning from Monocular Videos (2019)

Learning to predict scene depth from RGB inputs is a challenging task both for indoor and outdoor robot navigation. In this work we address unsupervised learning of scene depth and robot ego-motion where supervision is provided by monocular videos, as cameras are the cheapest, least restrictive and most ubiquitous sensor for robotics. Previous work in unsupervised image-to-depth learning has established strong baselines in the domain. We propose a novel approach which produces higher quality results, is able to model moving objects and is shown to transfer across data domains, e.g. from outdoors to indoor scenes. The main idea is to introduce geometric structure in the learning process, by modeling the scene and the individual objects; camera ego-motion and object motions are learned from monocular videos as input. Furthermore an online refinement method is introduced to adapt learning on the fly to unknown domains. The proposed approach outperforms all state-of-the-art approaches, including those that handle motion e.g. through learned flow. Our results are comparable in quality to the ones which used stereo as supervision and significantly improve depth prediction on scenes and datasets which contain a lot of object motion. The approach is of practical relevance, as it allows transfer across environments, by transferring models trained on data collected for robot navigation in urban scenes to indoor navigation settings. The code associated with this paper can be found at https://sites.google.com/view/struct2depth.
Specifying peripheral heterochromatin during nuclear lamina reassembly (2014)

A conserved organizational feature of eukaryotic nuclei is the peripheral heterochromatin compartment, which provides a protected area for epigenetically silent genes and gene-poor DNA. In metazoan cells this compartment is associated with the nuclear lamina, the protein meshwork at the inner edge of the nucleus. Heterochromatin-nuclear lamina interactions promote epigenetic gene silencing, which may drive many normal and diseased biological processes. We recently obtained evidence that a previously unstudied human protein, PRR14, participates in the tethering of heterochromatin to the inner nuclear periphery. PRR14 associates with the nuclear lamina and attaches to heterochromatin through its binding partner, heterochromatin protein 1 (HP1). After disassembly early in mitosis, PRR14 reassembles in two steps, first binding to anaphase chromosomes through HP1, followed by association with the nuclear lamina in telophase. PRR14 may thereby play a role in specifying HP1-bound heterochromatin for reattachment to the nuclear lamina at mitotic exit. Here we review the relevant literature, summarize our initial work, and provide additional comments and findings.
Estrogen receptors: selective ligands, partners, and distinctive pharmacology. (2000)

The action of nuclear hormone receptors is tripartite, involving the receptor, its ligands, and its co-regulator proteins. The estrogen receptor (ER), a member of this superfamily, is a hormone-regulated transcription factor that mediates the effects of estrogens and anti-estrogens (e.g., tamoxifen) in breast cancer and other estrogen target cells. This chapter presents our recent work on several aspects of estrogen action and the function of the ER: 1) elucidation of ER structure-function relationships and development of ligands that are selective for one of the two ER subtypes, ERalpha or ERbeta; 2) identification of ER-selective co-regulators that potentiate the inhibitory effectiveness of anti-estrogens and dominant-negative ERs and modulate the activity of estrogens; 3) characterization of genes that are regulated by the anti-estrogen-ER versus the estrogen-ER complex; and 4) elucidation of the intriguing pharmacology of these ER complexes at different gene regulatory sites. These findings indicate that different residues of the ER hormone-binding domain are involved in the recognition of structurally distinct estrogens and anti-estrogens and highlight the exquisite precision of the regulation of ER activities by ligands, with small changes in ligand structure resulting in major changes in receptor character. Studies also explore the biology and distinct pharmacology mediated by ERalpha and ERbeta complexed with different ligands through different target genes. The upregulation of the anti-oxidant detoxifying phase II enzyme, quinone reductase, by the anti-estrogen-occupied ER, mediated via the electrophile response element in the QR gene, may contribute to the beneficial antioxidant effects of anti-estrogens in breast cancer and illustrates the activation of some genes by ER via non-estrogen response element sequences. The intriguing biology of estrogen in its diverse target cells is thus determined by the structure of the ligand, the ER subtype involved, the nature of the hormone-responsive gene promoter, and the character and balance of co-activators and co-repressors that modulate the cellular response to the ER-ligand complex. The continuing development of novel ligands and the study of how they function as selective agonists or antagonists through ERalpha or ERbeta should allow optimized tissue selectivity of these agents for hormone replacement therapy and treatment and prevention of breast cancer.
A Survey of Augmented Reality (1997)

This paper surveys the field of augmented reality (AR), in which 3D virtual objects are integrated into a 3D real environment in real time. It describes the medical, manufacturing, visualization, path planning, entertainment, and military applications that have been explored. This paper describes the characteristics of augmented reality systems, including a detailed discussion of the tradeoffs between optical and video blending approaches. Registration and sensing errors are two of the biggest problems in building effective augmented reality systems, so this paper summarizes current efforts to overcome these problems. Future directions and areas requiring further research are discussed. This survey provides a starting point for anyone interested in researching or using augmented reality.
Inhibition of Tumor Growth by NK1.1+ Cells and CD8+ T Cells Activated by IL-15 through Receptor β/Common γ Signaling in trans (2008)

IL-15 is an important cytokine involved in the survival and function of CD8(+) T cells and NK cells. IL-15 can be presented by IL-15Ralpha (IL-15RA) to bind with the shared IL-2/IL-15Rbeta and common gamma-chains, which activate signaling pathways on NK cells and CD8(+) T cells. In the present study, we characterized the function of trans-presented IL-15 on NK cells and CD8(+) T cells using TC-1 tumor cells transduced with a retrovirus encoding IL-15 linked to IL-15RA (IL-15/IL-15RA). We demonstrated that the expression of IL-15/IL-15RA on TC-1 cells led to increased percentages of tumor-infiltrating NK cells, NKT cells, and CD8(+) T cells, resulting in the inhibition of tumor growth in challenged mice. Additionally, in vivo Ab depletion experiments demonstrated that NK1.1(+) cells and CD8(+) T cells were important in this inhibition of tumor growth. Furthermore, this accumulation of immune cells and inhibition of tumor growth was abolished by a single amino acid mutation in the common gamma-chain binding site on IL-15. We also observed that IL-15/IL-15RA-transduced TC-1 cells led to the activation of STAT5 in NK and CD8(+) T cells in trans, which was abolished in the mutated IL-15/IL-15RA-transduced TC-1 cells. Taken together, our data suggest that common gamma-chain binding-dependent activation of the shared IL-15/IL-2Rbeta/common gamma signaling pathway may play an important role in the activation of NK cells and CD8(+) T cells, resulting in IL-15/IL-15RA trans-presentation-mediated inhibition of tumor growth.
Magnetic Maneuvering of Endoscopic Capsules by Means of a Robotic Navigation System (2009)

The use of video capsules for noninvasive explorations of the digestive tube is progressively increasing today. At present, the motion of these wireless endoscopic devices cannot be controlled and they proceed by means of visceral peristalsis and gravity. Aimed at enabling a motion control, the technique described here uses an external magnetic field applied to the video capsule, previously coated with a magnetic shell. As a source of controlled magnetic field, a robotic magnetic navigation system, recently introduced in the clinical practice to magnetically steer cardiovascular interventional devices, was suggested in a previous study to be deserving of investigation. The attractive potentialities of this system, along with its current limitations, in order to maneuver endoscopic capsules were studied in this work for the first time, both from a theoretical and an experimental point of view. The actual capabilities were experimentally assessed with preliminary motion control tests on a conventional video capsule inside a human-sized plastic phantom. Results demonstrated the possibility of achieving controlled magnetic maneuvers within the considered environment.
Expression of the iap gene coding for protein p60 of Listeria monocytogenes is controlled on the posttranscriptional level (1991)

Expression of the iap gene of Listeria monocytogenes encoding a major extracellular protein (p60) was analyzed. Different start sites for transcription of the iap gene were identified by primer extension analysis in L. monocytogenes and in a recombinant Escherichia coli clone. The mutant RIII of L. monocytogenes represents a member of the frequently occurring L. monocytogenes R mutants, which form cell chains and produce greatly reduced amounts of p60. However, the concentrations of iap-specific mRNA were similar in mutant RIII and the wild-type strain. The introduction of additional copies of the iap gene from wild-type L. monocytogenes led to an equal increase of iap mRNA in both strains, but overexpression of protein p60 was only observed in the wild-type strain. The nucleotide sequences of both iap genes and their 5' noncoding regions were identical in all parts that are essential for efficient transcription of the iap gene, translation of the iap-specific mRNA, and transport of the p60 protein. These data suggest that the expression of the iap gene in L. monocytogenes is controlled on the posttranscriptional level by a specific factor that is defective in mutant RIII.