gebhart/patrepeval huggingface dataset:
Programmed Cell Death and the Control of Cell Survival: Lessons from the Nervous System (1993)

During the development of the vertebrate nervous system, up to 50 percent or more of many types of neurons normally die soon after they form synaptic connections with their target cells. This massive cell death is thought to reflect the failure of these neurons to obtain adequate amounts of specific neurotrophic factors that are produced by the target cells and that are required for the neurons to survive. This neurotrophic strategy for the regulation of neuronal numbers may be only one example of a general mechanism that helps to regulate the numbers of many other vertebrate cell types, which also require signals from other cells to survive. These survival signals seem to act by suppressing an intrinsic cell suicide program, the protein components of which are apparently expressed constitutively in most cell types.
Lewis-acid assisted cross metathesis of acrylonitrile with functionalized olefins catalyzed by phosphine-free ruthenium carbene complex (2005)

The exchange of the PPh3 ligand in the complex [1,3-bis(2,6-dimethylphenyl)4,5-dihydroimidazol-2-ylidene](PPh3)(Cl)2Ru=CHPh (7) for a pyridine ligand at ambient temperature leads to the formation of the stable phosphine-free carbene ruthenium complex [1,3-bis(2,6-dimethylphenyl)4,5-dihydroimidazol-2-ylidene](C5H5N)2(Cl)2 Ru=CHPh (8). The resulted ruthenium complex exhibits highly catalytic activity for the cross metathesis of acrylonitrile with various functionalized olefins under mild conditions, and its activity can be further improved by the addition of a Lewis acid such as Ti(OiPr)4. In the mixture products, the Z-isomer predominates.
Human Cart-1: Structural Organization, Chromosomal Localization, and Functional Analysis of a Cartilage-Specific Homeodomain cDNA (1996)

Homeoproteins control cell fates during development, specifying pattern formation and the ontogeny of specific tissues and organs in embryogenesis. Cart-1 cDNA was recently cloned from a rat chondrosarcoma tumor and it encodes a protein containing a paired-like homeodomain that is selectively expressed in cartilage during early chondrocyte differentiation. Here we report the molecular cloning of the human Cart-1 cDNA from a HeLa cervical carcinoma cDNA library. The human Cart-1 cDNA sequence is 88% identical and the deduced amino acid sequence is 95% identical to the rat sequence, indicating that Cart-1 structure is highly conserved. Northern and reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed Cart-1 mRNA expression in HeLa cervical carcinoma cells and human cervical tissue, but Cart-1 mRNA was not detected in GH3 rat pituitary cells and murine 10T1/2 one-half fibroblast cells. The Cart-1 gene was localized to human chromosome 12 and regionally mapped to the 12q21.3-q22 by PCR analysis of rodent-X-human somatic cell hybrid DNA and the CEPH megabase-insert YAC DNA pools, respectively. The Holt-Oram syndrome, characterized by upper limb and atrial septal dysplasias, also maps to the 12q21.3-q22 region. Cotransfection studies show that Cart-1 inhibits the rat prolactin promoter and that this repression is mediated by footprint II, an AT-rich element that functions as an inhibitory site of prolactin gene expression in nonpituitary cells and which was used to clone Cart-1. Taken together, these data indicate that Cart-1 may also influence cervix development, identify a putative DNA binding site for Cart-1, and, begin to define its functional role as modulator of gene expression.
Progression of Interleukin-2 (IL-2)-Dependent Rat T Cell Lymphoma Lines to IL-2-Independent Growth Following Activation of a Gene (Gfi-1) Encoding a Novel Zinc Finger Protein (1993)

During progression of Moloney murine leukemia virus (Mo-MuLV)-induced rat T cell lymphomas, growth selection results in the expansion of cell clones carrying increasing numbers of integrated proviruses. These new provirus insertions reproducibly contribute to enhanced growth, allowing the emergence of cell clones from the initially heterogeneous population of tumor cells. The Mo-MuLV-induced rat T cell lymphoma lines 2780d and 5675d, which are dependent on interleukin-2 (IL-2) for growth in culture (IL-2d), were placed in IL-2-free medium to select for IL-2-independent (IL-2i) mutants. Southern blot analysis of genomic DNA from these mutants, which was hybridized to a Mo-MuLV long terminal repeat probe, revealed that all mutants carried new provirus insertions (from one to four new proviruses per cell line). A locus of integration identified through cloning of the single new provirus detected in one of the IL-2i mutants, 2780i.5, was found to be the target of provirus insertion in 1 additional IL-2i cell line of 24 tested. A full-length cDNA of a gene (growth factor independence-1 [Gfi-1]) activated by promoter insertion in the 2780i.5 cells was cloned and shown to encode a novel zinc finger protein. Gfi-1 is expressed at low levels in IL-2d cell lines cultured in IL-2-containing medium and at high levels in most IL-2i cell lines, including the two harboring a provirus at this locus. Gfi-1 expression in adult animals is restricted to the thymus, spleen, and testis. In mitogen-stimulated splenocytes, Gfi-1 expression begins to rise at 12 h after stimulation and reaches very high levels after 50 h, suggesting that it may be functionally involved in events occurring after the interaction of IL-2 with its receptor, perhaps during the transition from the G1 to the S phase of the cell cycle. In agreement with this, Gfi-1 does not induce the expression of IL-2. Expression of Gfi-1 in 2780d cells following transfer of a Gfi-1/LXSN retrovirus construct contributes to the emergence of the IL-2i phenotype.
Membrane Enzyme Systems Responsible for the Ca2+-Dependent Phosphorylation of Ser27, the Independent Phosphorylation of Tyr10 and Tyr7, and the Dephosphorylation of These Phosphorylated Residues in the -Chain of H/K-ATPase (2000)

H/K-ATPase preparations (the G1 membrane) from pig stomach contain both kinases and phosphatases and show reversible phosphorylation of Tyr(7), Tyr(10), and Ser(27) residues of the alpha-chain of H/K-ATPase. The Tyr-kinase is sensitive to genistein and quercetin and recognized by anti-c-Src antibody. The Ser-kinase is dependent on Ca(2)(+) (K(0.5) = 0.9 microM), sensitive to a PKC inhibitor, and recognized by antibodies against PKCalpha and PKCbetaII. The addition of 3-[(3-cholamidopropyl)dimethylammonio]-1-propane-sulfonic acid (CHAPS) caused a dramatic increase in the phosphorylation of added synthetic copolymer substrates and permitted the phosphorylation of maltose-binding proteins fused with the N-terminal domain of alpha-chains. The phosphotyrosine phosphatase was inhibited by vanadate. The phosphoserine phosphatase was inhibited by okadaic acid and by inhibitor-2. The presence of protein phosphatase-1 was immunologically detected. Column chromatographic separation of CHAPS-solubilized G1 membrane and others indicate the apparent molecular weight of the Src-kinase to be approximately 60 kDa, the PKCalpha and/or PKCbII to be approximately 80 kDa, the Tyr-phosphatase to be 200 kDa, and PP-1 to be approximately 35 kDa. These data show that these membrane-bound enzyme systems are in sufficiently close proximity to be responsible for reversible phosphorylation of Tyr(7), Tyr(10), and Ser(27) of the catalytic subunit of membrane H/K-ATPase in parietal cells, the physiological role of which is unknown.
Sensitivity advantage of swept source and Fourier domain optical coherence tomography (2003)

We present theoretical and experimental results which demonstrate the superior sensitivity of swept source (SS) and Fourier domain (FD) optical coherence tomography (OCT) techniques over the conventional time domain (TD) approach. We show that SS- and FD-OCT have equivalent expressions for system signal-to-noise ratio which result in a typical sensitivity advantage of 20-30dB over TD-OCT. Experimental verification is provided using two novel spectral discrimination (SD) OCT systems: a differential fiber-based 800nm FD-OCT system which employs deep-well photodiode arrays, and a differential 1300nm SS-OCT system based on a swept laser with an 87nm tuning range.
Luminescence in Eu 2+ -doped Ba 2 Si 5 N 8 : fluorescence, thermoluminescence, and upconversion (2000)

Fluorescence emission was investigated in a series of Ba2−xEuxSi5N8 compounds. Two maxima corresponding to the two crystallographic Eu2+ sites are observed. Excitation with intense laser light at 1.047 μm reveals strong fluorescence emission at ∼600 nm due to two-photon-excitation. In Ba1.89Eu0.11Si5N8 the long lasting luminescence was studied. The emission peaking at about 590 nm has been observed in the dark with the naked eye even 15 min after removal of the activating lamp. This effect is due to the recombination of holes and traps consisting of nitrogen vacancies formed by reducing synthesis conditions. The maximum emission was observed at −7°C.
Reduced expression of EphB2 that parallels invasion and metastasis in colorectal tumours (2005)

EphB2, a receptor tyrosine kinase regulated by the beta-catenin/Tcf4 complex, is expressed in the proliferative compartment of mouse intestine and regulates bidirectional migration of intestinal precursor cells in the crypt-villus axis through repulsive interaction with Ephrin-B ligands. Recently, it has been shown that reduction of EphB activity accelerates colon tumour progression in the Apc(Min/+) mice. In this study, we examined the expression of EphB2 in normal colon, adenomas, primary colorectal cancers (CRCs), lymph node metastases and liver metastases using immunohistochemistry on tissue microarrays. In addition, EphB2 was overexpressed in SW480 colon cancer cells to study its effect in vitro. We found that EphB2 was expressed in 100% of normal colon crypt base cells, 78% of adenomas, 55.4% of primary CRCs, 37.8% of lymph node metastases and 32.9% of liver metastases (all differences were statistically significant at P < 0.001 compared with primary CRCs). Patients with CRCs that lose EphB2 expression had more advanced tumour stage (P = 0.005), poor differentiation (P < 0.001), poor overall survival (P = 0.005) and disease-free survival (P = 0.001), with the latter being independent of tumour stage. In vitro studies showed that overexpression of EphB2 inhibited colon cancer cell growth in colony formation assay and activation of EphB2 receptor inhibited colon cancer cell adhesion and migration. Our data demonstrated a progressive loss of EphB2 expression in each critical step of colon carcinogenesis, including the onset of invasion, dedifferentiation and metastasis which are paralleled by adverse patient outcome. EphB2 may achieve its tumour suppressor function through regulation of cell survival, adhesion and migration.
Reduction or prevention of aspirin‐induced occult gastrointestinal blood loss in man (1969)

The purpose of this study was to determine if the occult gastrointestinal blood loss produced by aspirin administered in the form of conventional tablets may be reduced or prevented by using aspirin in solutions. Fifty‐seven healthy subiects received 2.6 or 3.9 Gm. of aspirin daily for 8 day periods. Blood loss in the feces was determined by the Cr 51 method. The average daily blood loss was 0.5 ml. during drug‐free control periods and 3 ml. above control values when aspirin tablets were taken. After calcium‐aspirin solution with low buffer capacity and a calcium‐sodium‐aspirin solution with medium buffer capacity, average daily blood loss was 48 and 32 per cent of that produced by aspirin tablets. Highly buffered sodium‐aspirin solutions, with or without acetaminophen and caffeine, caused no bleeding. Thus, aspirininduced occult gastrointestinal blood loss may be reduced significantly or prevented by administering the drug in a solution of sufficient buffer capacity to reduce appreciably the acidity of gastric fluids. Since aspirin in solution not only causes little or no bleeding but also is more rapidly absorbed and yields higher drug concentrations in the plasma than do tablets, it is concluded that aspirin‐induced gastrointestinal bleeding is a local rather than a systemic effect under the experimental conditions.
Towards passive brain–computer interfaces: applying brain–computer interface technology to human–machine systems in general (2011)

Cognitive monitoring is an approach utilizing realtime brain signal decoding (RBSD) for gaining information on the ongoing cognitive user state. In recent decades this approach has brought valuable insight into the cognition of an interacting human. Automated RBSD can be used to set up a brain-computer interface (BCI) providing a novel input modality for technical systems solely based on brain activity. In BCIs the user usually sends voluntary and directed commands to control the connected computer system or to communicate through it. In this paper we propose an extension of this approach by fusing BCI technology with cognitive monitoring, providing valuable information about the users' intentions, situational interpretations and emotional states to the technical system. We call this approach passive BCI. In the following we give an overview of studies which utilize passive BCI, as well as other novel types of applications resulting from BCI technology. We especially focus on applications for healthy users, and the specific requirements and demands of this user group. Since the presented approach of combining cognitive monitoring with BCI technology is very similar to the concept of BCIs itself we propose a unifying categorization of BCI-based applications, including the novel approach of passive BCI.
Opiate-Induced Persistent Pronociceptive Trigeminal Neural Adaptations: Potential Relevance to Opiate-Induced Medication Overuse Headache (2009)

Medication overuse headache (MOH) is a challenging, debilitating disorder that develops from the frequent use of medications taken for the treatment of migraine headache pain. MOH affects an estimated 3-5% of the general population. The mechanisms underlying the development of MOH remain unknown. Opiates are one of the major classes of medications used for the treatment of migraine at least in some countries, including the USA. Although the effects of repeated opiate use for headache are unknown, it is possible that opiate use may contribute to increased frequency and occurrence of such headaches. Recent preclinical studies exploring the neuroadaptive changes following sustained exposure to morphine may give some insights into possible causes of MOH. Peripherally, these changes include increased expression of calcitonin gene-related peptide (CGRP) in trigeminal primary afferent neurons. Centrally, they include increased excitatory neurotransmission at the level of the dorsal horn and nucleus caudalis. Critically, these neuroadaptive changes persist for long periods of time and the evoked release of CGRP is enhanced following morphine pretreatment. Stimuli known to elicit migraine, such as nitric oxide donors or stress, produce hyperalgesia in morphine- but not in saline-pretreated rats even long after the discontinuation of the opiate. CGRP plays a prominent role in initiating vasodilation of the intracranial blood vessels and subsequent headache. Furthermore, studies have demonstrated increased excitability of the nociceptive pathway in migraine sufferers, and CGRP receptor antagonists have been shown to be efficacious in migraine pain. Thus, such persistent neuroadaptive changes may be relevant to the processes that promote MOH.
Mutational specificity of depurination. (1984)

The mutagenic consequences of damage to DNA produced by low pH and high temperature have been determined in a forward mutational system capable of detecting all classes of mutagenic events. When damaged single-stranded DNA from bacteriophage M13mp2 is used to transfect competent Escherichia coli cells, a 15-fold increase in mutation frequency, measured as loss of alpha-complementation by the lac DNA in the phage, is observed compared with an untreated DNA control transfection. The enhanced mutagenicity is largely dependent on induction of the error-prone SOS response and is proportional to the number of lethal hits introduced into the DNA. The effect is abolished by treatment of the damaged DNA before transfection with either apurinic/apyrimidinic endonuclease or alkali. Based on these observations and the rate constants for formation of the known heat/acid-produced lesions in DNA, it is concluded that the majority of the induced mutagenesis results from apurinic sites. DNA sequence analysis of 87 spontaneous and 124 induced mutants indicates that the major effect is on single base-substitution mutagenesis with a small increase in (deletion) frame-shift frequency. Approximately 80% of the base-substitution mutations occur at purine positions in the viral strand, consistent with depurination as the predominant premutagenic lesion. The preference of guanine over adenine sites mutated is consistent with the preference for depurination of guanine over adenine. Transversions are observed for 57 of 79 (72%) induced base substitutions, with a strong preference for insertion of adenine residues opposite the putative apurinic site. These data in a forward mutational system provide insight into the mechanisms used by a cell to replicate DNA containing noncoding lesions.
Characteristics of Band-to-Band Tunneling Hot Hole Injection for Erasing Operation in Charge-Trapping Memory (2006)

In this paper, we present a combined charge-pumping measurement method for charge distribution profiling in charge-trapping memory. Electron and hole distributions after channel hot electron (CHE) or channel-initialed secondary electron (CHISEL) programming and band-to-band tunneling hot hole (BBHH) erasing are accurately determined. It is shown that BBHH-induced hot holes distribute in a narrow region near the drain junction, and cannot neutralize all the electrons particularly in CHISEL-programmed devices. The influence of the BBHH erasing condition on the width of hole distribution is demonstrated, and the effects on the characteristics of erasing speed and P/E cycling endurance are investigated and analyzed. It is shown that in the CHE-programmed devices, the erasing speed can be enhanced and endurance characteristics can be improved if a high drain voltage is used during erasing operation.
Feature Mapping for Learning Fast and Accurate 3D Pose Inference from Synthetic Images (2018)

International audience
MK: a pluripotential embryonic stem-cell-derived neuroregulatory factor (1992)

MK is a gene encoding a secreted heparin-binding polypeptide originally isolated by differential screening for genes induced by retinoic acid (RA) in HM-1 embryonal carcinoma cells. Here we report that MK is expressed at high levels in both embryonal carcinoma and pluripotential embryonic stem cells and their differentiated derivatives. MK expression in these cell types is unaffected by the presence or absence of RA. Recombinant MK protein (rMK) was produced by transient expression in COS cells and purified by heparin affinity chromatography. rMK is a weak mitogen for 10T1/2 fibroblast cells but inactive as a mitogen for Swiss 3T3 fibroblasts. rMK is a potent mitogen for neurectodermal precursor cell types generated by treatment of 1009 EC cells with RA but has no mitogenic or neurotrophic effects on more mature 1009-derived neuronal cell types. rMK is active as an in vitro neurotrophic factor for E12 chick sympathetic neurons and its activity is markedly potentiated by binding the factor to tissue-culture plastic in the presence of heparin. Stable 10T1/2 cells lines have been established which express MK. These cells do not exhibit any overt evidence of cell transformation but extracellular matrix preparations derived from these cells are a potent source of MK biological activity. It is concluded that MK is a multifunctional neuroregulatory molecule whose biological activity depends upon association with components of the extracellular matrix.
Isoform-specific effect of apolipoprotein E on cell survival and beta-amyloid-induced toxicity in rat hippocampal pyramidal neuronal cultures. (1998)

Although the genetic link between the epsilon4 allele of apolipoprotein E (apoE) and Alzheimer's disease is well established, the isoform-specific activity of apoE underlying this correlation remains unclear. To determine whether apoE influences the neurotoxic actions of beta-amyloid (Abeta), we examined the effect of native preparations of apoE3 and E4 on Abeta-induced toxicity in primary cultures of rat hippocampal pyramidal neurons. The source of apoE was conditioned medium from HEK-293 cells stably transfected with human apoE3 or E4 cDNA. ApoE4 (10 microg/ml) alone was toxic to the cultures, whereas apoE3 had no effect. ApoE3 treatment prevented the toxicity induced by 10 microM Abeta(1-40) or Abeta(25-35). The apoE3 protective effect appears to be specific to Abeta-induced toxicity, because apoE3 did not protect against the cytotoxicity produced by NMDA or staurosporine, nor did apoE3 affect the increase in intracellular calcium induced by either NMDA or KCl. ApoE3 had no effect on the toxicity produced by Abeta in the presence of receptor-associated protein, an inhibitor of apoE receptors, particularly the LDL-receptor-related protein. Interaction with apoE receptors may not mediate the toxic actions of apoE4, because receptor-associated protein did not affect apoE4-induced neurotoxicity. Consistent with our previous biochemical experiments, analysis of the culture medium revealed that SDS-stable apoE3:Abeta complex is present in greater abundance than apoE4:Abeta complex. Thus, the protection from Abeta-induced neurotoxicity afforded by apoE3 treatment may result from clearance of the peptide by apoE3:Abeta complex formation and uptake by apoE receptors.
Mutations in a novel gene, VMD2, encoding a protein of unknown properties cause juvenile-onset vitelliform macular dystrophy (Best's disease) (1998)

Vitelliform macular dystrophy (Best's disease) is an autosomal dominant, early-onset form of macular degeneration in which the primary defect is thought to occur at the level of the retinal pigment epithelium. Genetic linkage has mapped the disease locus to chromosome 11q12-q13.1 within a 980 kb interval flanked by markers at loci D11S4076 and uteroglobin. To identify the disease gene, we systematically characterized genes from within the critical region and analysed the coding regions for mutations in 12 patients from large multigeneration Best's disease families. Following this approach, we identified a novel gene of unknown function carrying heterozygous mutations in all 12 probands. Of these, 10 result in distinct missense mutations of amino acids that are highly conserved throughout evolution, spanning a phylogenetic distance from Caenorhabditis elegans to human, and include V9M, A10T, W24C, R25Q, R218Q, Y227N, Y227C, V235M, P297A and F305S. One deletion mutation, DeltaI295, was found in two families and segregates with the disease in both cases. Northern blot analysis reveals tissue-specific expression for this gene, exclusively in the retinal pigment epithelium. In conclusion, our data provide strong evidence that mutations in the gene that we have identified cause Best's disease.