gebhart/patrepeval huggingface dataset:
1-Methyl-4-phenylpyridinium-induced Apoptosis in Cerebellar Granule Neurons Is Mediated by Transferrin Receptor Iron-dependent Depletion of Tetrahydrobiopterin and Neuronal Nitric-oxide Synthase-derived Superoxide (2004)

In this study, we investigated the molecular mechanisms of toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), an ultimate toxic metabolite of a mitochondrial neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, that causes Parkinson-like symptoms in experimental animals and humans. We used rat cerebellar granule neurons as a model cell system for investigating MPP(+) toxicity. Results show that MPP(+) treatment resulted in the generation of reactive oxygen species from inhibition of complex I of the mitochondrial respiratory chain, and inactivation of aconitase. This, in turn, stimulated transferrin receptor (TfR)-dependent iron signaling via activation of the iron-regulatory protein/iron-responsive element interaction. MPP(+) caused a time-dependent depletion of tetrahydrobiopterin (BH(4)) that was mediated by H(2)O(2) and transferrin iron. Depletion of BH(4) decreased the active, dimeric form of neuronal nitric-oxide synthase (nNOS). MPP(+)-mediated "uncoupling" of nNOS decreased *NO and increased superoxide formation. Pretreatment of cells with sepiapterin to promote BH(4) biosynthesis or cell-permeable iron chelator and TfR antibody to prevent iron-catalyzed BH(4) decomposition inhibited MPP(+) cytotoxicity. Preincubation of cerebellar granule neurons with nNOS inhibitor exacerbated MPP(+)-induced iron uptake, BH(4) depletion, proteasomal inactivation, and apoptosis. We conclude that MPP(+)-dependent aconitase inactivation, Tf-iron uptake, and oxidant generation result in the depletion of intracellular BH(4), leading to the uncoupling of nNOS activity. This further exacerbates reactive oxygen species-mediated oxidative damage and apoptosis. Implications of these results in unraveling the molecular mechanisms of neurodegenerative diseases (Parkinson's and Alzheimer's disease) are discussed.
ChemInform Abstract: An Easy Access to β‐Acyl‐ and β‐Arylpropionaldehydes Through a New Silylated Organotin Homoenolate Equivalent. (1988)

Abstract The propargylic ether (I) is converted into the silyl‐substituted vinylstannane (V) which is coupled with the acid chlorides (VI) or the aryl bromides (IX) to give the vinyl ketones (VII) or the styrenes (X).
Relative Importance Of Plasma Protease Inhibitors In The Inactivation Of Kallikrein In Human Plasma (1981)

Human plasma contains several inhibitors of plasma kallikrein (KAL), including C1-inhibitor (C1INH), α2-macro- globulin (α2M), antithrombin III (ATIII), and α1-antitrypsin (αlAT). Studies in purified systems have allowed us to quantitate the kinetic constants of each isolated inhibitor. We also have demonstrated that high molecular weight kininogen (HMWK) is an important regulator since it decreases the inactivation rate of KAL by all inhibitors except α2M. When purified inhibitors and HMWK are present at plasma concentrations, it can be calculated that C1INH, α2M, ATIII and α1AT account respectively for 49%, 49%, 0.8% and 0.2% of the KAL inhibitory activity. To assess if this prediction derived from purified system adequately describes the inhibition of KAL under more physiological conditions, we incubated KAL with normal human plasma (NHP), C1INH-deficient plasma (C1INH-D), and α2M-deficient plasma (α2M-D). KAL activity_was assessed using H-D-Pro-Phe-Arg- Nan as a substrate. C1INH-D was obtained from a patient with hereditary angioedema. C1INH in C1INH-D was 15% of the normal value as assessed by radial immunodiffusion. α2M-D was obtained by selective and complete inactivation of α2M by methylamine. The pseudo-first-order rate constants for the inactivation of_KAL by NHP, C1INH-D, α2M-D, and plasma deficient in both C1INH and α2M were respectively 8.8, 5.0, 5.5, and 1.8 S-1(×l03). Therefore, C1INH accounted for 63% of the observed inhibition, α2M for 35%, and all the other inhibitors for 2%. When these values were corrected for the concentration of HMWK, C1INH accounted for 47% of the inhibition, α2M for 51%, and all the other inhibitors for <2%. Thus, there is an excellent agreement between the results obtained when KAL is inhibited in purified systems and those obtained when it is inhibited in plasma. Moreover, these results indicate that C1INH and α2M are the only important inhibitors of KAL in NHP.
Lipid fingerprinting of Gram‐positive lactobacilli by intact cells – matrix‐assisted laser desorption/ionization mass spectrometry using a proton sponge based matrix (2011)

A method of direct lipid analysis by matrix-assisted laser desorption/ionization (MALDI) mass spectrometry (MS) in intact membranes, without prior extraction/separation steps, is described. Here, we demonstrate the efficacy of a strong base, 1,8-bis(dimethylamino)naphthalene (DMAN; proton sponge), as a novel matrix for MALDI-time-of-flight (TOF) MS analysis of whole cell bacteria. Initially, individual acidic low-molecular-weight analytes such as standard free fatty acids and phospholipids were analyzed using DMAN as matrix. Clear negative-mode MALDI-TOF MS spectra of all analytes show only deprotonated analyte signals at a low picomole limit of detection with the complete absence of matrix-related signals. These results indicate that DMAN represents a suitable matrix for MALDI-TOF MS analysis of mixtures of complex lipids as the intact membranes of microorganisms. DMAN was successfully applied to the analysis of Lactobacillus sanfranciscensis and L. plantarum microorganisms. Different components were sensitively detected in a single spot, including 16:0, 18:2, 18:3, and 21:0 free acids, glycolipids, phosphatidylglycerols (PGs) and cardiolipins. This method might be of general application, offering the advantage of quickly gaining information about lipid components of other gram-positive bacterial membranes.
Annexin 2 Binding to Phosphatidylinositol 4,5-Bisphosphate on Endocytic Vesicles Is Regulated by the Stress Response Pathway (2004)

Annexin 2 is a Ca(2+)-binding protein that has an essential role in actin-dependent macropinosome motility. We show here that macropinosome rocketing can be induced by hyperosmotic shock, either alone or synergistically when combined with phorbol ester or pervanadate. Rocketing was blocked by inhibitors of phosphatidylinositol-3-kinase(s), p38 mitogen-activated protein (MAP) kinase, and calcium, suggesting the involvement of phosphoinositide signaling. Since various phosphoinositides are enriched on inwardly mobile vesicles, we examined whether or not annexin 2 binds to any of this class of phospholipid. In liposome sedimentation assays, we show that recombinant annexin 2 binds to phosphatidylinositol 4,5-bisphosphate (PtdIns-4,5P(2)) but not to other poly- and mono-phosphoinositides. The affinity of annexin 2 for PtdIns-4,5P(2) (K(D) approximately 5 microm) is comparable with those reported for a variety of PtdIns-4,5P(2)-binding proteins and is enhanced in the presence of Ca(2+). Although annexin 1 also bound to PtdIns-4,5P(2), annexin 5 did not, indicating that this is not a generic annexin property. To test whether annexin 2 binds to PtdIns-4,5P(2) in vivo, we microinjected rat basophilic leukemia cells stably expressing annexin 2-green fluorescent protein (GFP) with fluorescently tagged antibodies to PtdIns-4,5P(2). Annexin 2-GFP and anti-PtdIns-4,5P(2) IgG co-localize at sites of pinosome formation, and annexin 2-GFP relocalizes to intracellular membranes in Ptk cells microinjected with Arf6Q67L, which has been shown to stimulate PtdIns-4,5P(2) synthesis on pinosomes through activation of phosphatidylinositol 5 kinase. These results establish a novel phospholipid-binding specificity for annexin 2 consistent with a role in mediating the interaction between the macropinosome surface and the polymerized actin tail.
Retina U-Net: Embarrassingly Simple Exploitation of Segmentation Supervision for Medical Object Detection (2018)

The task of localizing and categorizing objects in medical images often remains formulated as a semantic segmentation problem. This approach, however, only indirectly solves the coarse localization task by predicting pixel-level scores, requiring ad-hoc heuristics when mapping back to object-level scores. State-of-the-art object detectors on the other hand, allow for individual object scoring in an end-to-end fashion, while ironically trading in the ability to exploit the full pixel-wise supervision signal. This can be particularly disadvantageous in the setting of medical image analysis, where data sets are notoriously small. In this paper, we propose Retina U-Net, a simple architecture, which naturally fuses the Retina Net one-stage detector with the U-Net architecture widely used for semantic segmentation in medical images. The proposed architecture recaptures discarded supervision signals by complementing object detection with an auxiliary task in the form of semantic segmentation without introducing the additional complexity of previously proposed two-stage detectors. We evaluate the importance of full segmentation supervision on two medical data sets, provide an in-depth analysis on a series of toy experiments and show how the corresponding performance gain grows in the limit of small data sets. Retina U-Net yields strong detection performance only reached by its more complex two-staged counterparts. Our framework including all methods implemented for operation on 2D and 3D images is available at github.com/pfjaeger/medicaldetectiontoolkit.
Interactions between mesenchymal stem cells and T cells on a single cell level a nanowell array (2012)

Mesenchymal stem cells (MSCs) have been thought to be a potential mode of therapy for immuno-related pathologies, particularly autoimmune diseases. Specifically, the ability to impart immunomodulatory effects on target inflammatory sites makes the use of MSCs particularly attractive for patients affected by taking immunosuppressive medicine, which works to downregulate the immune system on a systemic level. Despite its promises, the interaction between MSCs and T-cells, a key player in the pathophysiology of autoimmune diseases, is not yet well understood, thereby preventing further progress in the clinic. A major obstacle is the highly heterogeneous nature of MSCs in-vitro. Bulk assays commonly carried out discount the inherent heterogeneity, and thus do not provide information with regards to single-cell contributions that may play a critical role in the overall bulk response. To address these issues, we propose to study the single-cell interaction between MSCs and CD4 T cells in a nanowell array. Using the nanowell assay, we demonstrate that individual MSCs appear capable of dynamically modulating the T cell proliferation rate in response to persistent cell-cell interactions in a microenviroment. Based on these results, we anticipate the use of our nanowell assay in the classification of subpopulations within MSCs, ultimately leading to specific therapeutic interventions.
Zur Neufassung der Verbandsklagebefugnis nach § 13 Abs. 2 Nr. 2 UWG (1996)

Article Zur Neufassung der Verbandsklagebefugnis nach § 13 Abs. 2 Nr. 2 UWG was published on January 1, 1996 in the journal Deutsche Zeitschrift für Wirtschafts- und Insolvenzrecht (volume 6, issue 12).
ErrorTracer: design error diagnosis based on fault simulation techniques (1999)

This paper addresses the problem of locating error sources in an erroneous combinational or sequential circuit. We use a fault simulation-based technique to approximate each internal signal's correcting power. The correcting power of a particular signal is measured in terms of the signal's correctable set, namely, the maximum set of erroneous input vectors or sequences that can be corrected by resynthesizing the signal. Only the signals that can correct every given erroneous input vector or sequence are considered as a potential error source. Our algorithm offers three major advantages over existing methods. First, unlike symbolic approaches, it is applicable for large circuits. Second, it delivers more accurate results than other simulation-based approaches because it is based on a more stringent condition for identifying potential error sources. Third, it can be generalized to identify multiple errors theoretically. Experimental results on diagnosing combinational and sequential circuits with one and two random errors are presented to show the effectiveness and efficiency of this new approach.
Design of a financial portal (2001)

article Share on Design of a financial portal Authors: Kemal Saatcioglu Koc Univ., Istanbul, Turkey Koc Univ., Istanbul, TurkeyView Profile , Jan Stallaert Univ. of Southern California, Los Angeles Univ. of Southern California, Los AngelesView Profile , Andrew B. Whinston Univ. of Texas at Austin, Austin Univ. of Texas at Austin, AustinView Profile Authors Info & Claims Communications of the ACMVolume 44Issue 6June 2001 pp 33–38https://doi.org/10.1145/376134.376151Published:01 June 2001Publication History 12citation1,301DownloadsMetricsTotal Citations12Total Downloads1,301Last 12 Months22Last 6 weeks1 Get Citation AlertsNew Citation Alert added!This alert has been successfully added and will be sent to:You will be notified whenever a record that you have chosen has been cited.To manage your alert preferences, click on the button below.Manage my Alerts New Citation Alert!Please log in to your account Save to BinderSave to BinderCreate a New BinderNameCancelCreateExport CitationPublisher SiteGet Access
Construction of mathematic model for automatic summarization (2005)

Automatic summarization is need of the era. Mathematical method can help logic analysis. However, there is no any previous study about mathematic description of automatic summarization. A mathematic model of automatic summarization is established and discussed in the paper. The model makes use of meta-knowledge to describe the composition of summary and help to calculate the semantic distance between summary and source document. It is proposed that how to get meta-knowledge aggregate and their weight are the key problems in the model. There is also a discussion of how to select output summary in the paper. The mathematic description of automatic summarization is useful for the application of automatic summarization and automatic assessment for summaries. An experiment and results are described in the paper to explain the application of mathematic model in details.
Defining a novel domain of staphylococcal toxic shock syndrome toxin-1 critical for major histocompatibility complex class II binding, superantigenic activity, and lethality (2000)

Staphylococcal toxic shock syndrome toxin-1 (TSST-1) is implicated in the pathogenesis of superantigen-mediated shock. We previously identified TSST-1 residues G31/S32 to be important for major histocompatibility complex (MHC) class II binding, as well as superantigenic and lethal activities. However, the site-directed TSST-1 mutant toxin, G31R, could still induce mitogenesis and low-level TNF alpha secretion, suggesting that additional MHC class II binding sites other than G31/S32 may exist. In the current study, a TSST-1-neutralizing monoclonal antibody, MAb5, was found to inhibit TSST-1 binding to human peripheral blood mononuclear cells, neutralize TSST-1-induced mitogenesis and cytokine secretion, and protect against TSST-1-induced lethality in vivo. Epitope mapping revealed that MAb5 bound to TSST-1 residues 51-56 (T(51-56); 51YYSPAF56). Peptide T(51-56) was synthesized and found to also inhibit TSST-1 binding to human monocytes as well as TSST-1-induced mitogenesis, cytokine secretion, and lethality in vivo. This T(51-56) epitope, located within the beta 3/beta 4 loop, and the previously identified G31/S32 epitope, within the beta 1/beta 2 loop of TSST-1, are separated within the primary sequence, but spatially juxtaposed to each other. Collectively, these findings suggest that a discontinuous epitope comprising of regions within both the beta 1/beta 2 and beta 3/beta 4 loops, are critical for MHC class II binding, and the consequent superantigenic and lethal activities of TSST-1.
Tachycardia and myocardial ischaemia following subconjunctival injection of mydricaine (number 02) for vitrectomy procedure (2005)

Mydricaine is a mydriatic agent used routinely at the Royal Adelaide Hospital in subconjunctival injections that are given prior to all vitreoretinal surgery. The drug is manufactured by the hospital pharmacy and each vial of 0.4 mL mydricaine number 02 consists of a mixture of 1.3 mg atropine sulphate, 0.12 mg adrenaline and 8.4 mg procaine hydrochloride. Mydricaine is routinely used by many vitreoretinal units, even though the drug is not listed in the British National Formulary (BNF) or Monthly Index of Medical Specialities (MIMS). Therefore, published case reports provide the main forum for reporting side-effects. The case presented is of a patient with no previous ischaemic heart disease who developed transient myocardial ischaemia with tachycardia following the administration of subconjunctival mydricaine number 02. To the authors' knowledge this is the first case report documenting myocardial ischaemia in a patient with no previous ischaemic heart disease following mydricaine administration.
Calcium Channel Blockers in Psychiatric Disorders: A Review of the Literature (1999)

CCBs do not at present have an established place in psychiatric treatment. Nonetheless, clinicians faced with a manic patient not responsive to other antimanic drugs, either alone or in combination, might consider adding verapamil as an adjunct. A study bearing on this specific issue is needed to determine whether or not such off-label use would really be justified.
Rhodium-Catalyzed Cycloadditions between 3-Diazoindolin-2-imines and 1,3-Dienes (2017)

Azepino[2,3-b]indoles were regioselectively prepared through rhodium-catalyzed formal aza-[4 + 3] cycloaddition between 3-diazoindolin-2-imines and 1,3-dienes in moderate to good yields. Using 2-[(trimethylsilyl)oxy]-1,3-butadiene as the diene component, azepino[2,3-b]indol-4(1H)-ones were constructed. Furthermore, the reactions of cyclic dienes, such as 1,3-cyclohexadiene and 1,3-cyclopentadiene, furnished the corresponding [3 + 2] cycloaddition products.
Horse Liver Alcohol Dehydrogenase can Accept NADP<sup>+</sup> as Coenzyme in High Concentrations of Acetonitrile (1995)

The coenzyme specificity of horse liver alcohol dehydrogenase assayed in mixtures of acetonitrile and buffer, 0.01 M Tris/HCl pH 7.4, was investigated. The enzyme could accept NADP + as coenzyme if it was first bioimprinted with NADP + , i.e. precipitated from an aqueous buffer with 1‐propanol in the presence of NADP + , dried, and then assayed in a system with less than 10% buffer. When assayed in a system with 25% buffer, no activity with NADP + as coenzyme was observed. The activity was measured with a coenzyme regeneration assay with cinnamoyl alcohol and octylaldehyde as substrates. Other methods to prepare a binary complex of horse liver alcohol dehydrogenase and NADP + , i.e. if the enzyme was immobilized on silica and NADP + added afterwards or if it was deposited on Celite together with NADP + , failed to show any bio‐imprinting effect. The activity of horse liver alcohol dehydrogenase bio‐imprinted with NADP + and assayed in acetonitrile/buffer mixtures with less than 10% buffer showed the same or higher activity than an enzyme preparation prepared by bio‐imprinting with NAD + . The hypothesis is that the conformation of the active site of horse liver alcohol dehydrogenase is modified to one that is complementary to the ligand present during precipitation and drying. This is possible because of the restricted motility of the enzyme conformation in high concentrations of organic solvent. In the presence of more than 10% buffer the mobility increases in such a way that the imposed conformation with activity towards NADP + disappears.
Covalent Grafting to μ-Hydroxy-Capped Surfaces? A Kaolinite Case Study (2011)

All μ-hydroxyl groups are frequently encountered capping groups found on the external surfaces of various minerals that are often used as fillers in composite materials. Covalent grafting to this functional group would therefore offer a versatile and attractive route to surface modification. The octahedral layer of kaolinite is composed of μ-bridged aluminol groups. In particular, intercalation compounds of kaolinite, where all basal planes are exposed and may be modified, are ideally suited to study the feasibility of such covalent graftings. The huge (internal) specific surface area greatly improves the sensitivity of the analytics and renders kaolinite an ideal model compound. Herein we analyze the mode of bonding of ethylene glycol (EG), intercalated into kaolinite (EG kaolinite), by solid-state NMR techniques. 27Al MQMAS allows for distinction between intercalated and grafted EG molecules because the chemical surroundings of octahedrally coordinated aluminum nuclei in the layer are significantly changed by the formation of a covalent bond. Moreover, the temperature-dependent dynamics of the EG molecules in the interlamellar space are examined by wide-line solid-state 1H NMR measurements. The EG molecules perform a circular motion around the covalently bonded hydroxyl group in the interlamellar space. Analysis of the 13C–27Al REAPDOR measurement in conjunction with the EG dynamics allows for determination of the 13C···27Al distance between octahedral aluminum and the bonded carbon atom of EG. This distance is 3.1 Å. A thorough description of the bonding mode of the EG molecules is provided and proves beyond any doubt the covalent grafting. This suggests that the reactivity of μ-hydroxyl groups, in general, is sufficient to realize a covalent surface modification of a wide range of minerals.
The adult spine : principles and practice (1991)

Introduction: the history of spinal disorders, Leon L. Wiltse the future of spinal treatment, John W. Frymoyer et al. Part 1 Epidemiology, disability and societal impact. Part 2 General issues of spinal disorders: general operative considerations diagnostic studies general and degenerative conditions metabolic disease inflammatory disorders spinal injury spinal neoplasms and vascular malformations. Part 3 Cervical spine: traumatic disorders of the cervical spine degenerative conditions of the cervical spine. Part 4 Thoracic and thoracolumbar spine: trauma of the thoracolumbar spine adult spine deformities. Part 5 Lumbar spine and sacrum: low back disorders physical therapy and education congenital abnormalities degenerative conditions and disc herniation - diagnosis and treatment stenosis/neurogenic claudication segmental instability. Part 6 Sacrum and coccyx.