gebhart/patrepeval huggingface dataset:
Metabolism of avenanthramide phytoalexins in oats (2004)

Oat leaves produce phytoalexins, avenanthramides, in response to infection by pathogens or treatment with elicitors. The metabolism of avenanthramides was investigated using low molecular weight, partially deacetylated chitin as an elicitor. When oat leaf segments are floated on the elicitor solution, avenanthramides accumulate in the solution. The transfer of elicited oat leaves to solutions containing stable-isotope-labeled avenanthramides resulted in a rapid decrease in the labeled avenanthramides, suggesting the metabolism of avenanthramides. The rate of decrease was enhanced by elicitor treatment, and was dependent on the species of avenanthramides, with avenanthramide B decreasing most rapidly. The rates of biosynthesis and metabolism of avenanthramides A and B were measured using a model of isotope-labeling dynamics. Avenanthramide B was found to be more actively biosynthesized and metabolized than avenanthramide A. Radiolabeled avenanthramide B was incorporated into the cell wall fraction and 99% of incorporated activity was released by alkaline treatment. Gel filtration indicated that high-molecular-weight compounds derived from avenanthramide B were released by alkaline treatment. The decrease in stable-isotope-labeled avenanthramides was suppressed by catalase, salicylhydroxamic acid, and sodium ascorbate, suggesting the involvement of peroxidase in the metabolism. Consistent with this, peroxidase activity that accepts avenanthramide B as a substrate was induced in apoplastic fractions by elicitor treatment. The appearance of multiple basic isoperoxidases was observed by activity staining with 3-amino-9-ethylcarbazole coupled with isoelectric focusing of proteins from elicitor-treated leaves. These findings suggest that accumulated avenanthramides are further metabolized in apoplasts in oat leaves by inducible isoperoxidases.
Experimental demonstration of high spectral efficient 4 × 4 MIMO SCMA-OFDM/OQAM radio over multi-core fiber system (2017)

In this paper, 4 × 4 multiple-input multiple-output (MIMO) radio over 7-core fiber system based on sparse code multiple access (SCMA) and OFDM/OQAM techniques is proposed. No cyclic prefix (CP) is required by properly designing the prototype filters in OFDM/OQAM modulator, and non-orthogonally overlaid codewords by using SCMA is help to serve more users simultaneously under the condition of using equal number of time and frequency resources compared with OFDMA, resulting in the increase of spectral efficiency (SE) and system capacity. In our experiment, 11.04 Gb/s 4 × 4 MIMO SCMA-OFDM/OQAM signal is successfully transmitted over 20 km 7-core fiber and 0.4 m air distance in both uplink and downlink. As a comparison, 6.681 Gb/s traditional MIMO-OFDM signal with the same occupied bandwidth has been evaluated for both uplink and downlink transmission. The experimental results show that SE could be increased by 65.2% with no bit error rate (BER) performance degradation compared with the traditional MIMO-OFDM technique.
Vaccination with a DNA Vaccine Encoding Herpes Simplex Virus Type 1 VP22 Linked to Antigen Generates Long-Term Antigen-Specific CD8-Positive Memory T Cells and Protective Immunity (2004)

Intradermal vaccination with DNA encoding herpes simplex virus type 1 (HSV-1) VP22 linked to antigen leads to spread of antigen within the epithelium and results in enhanced antigen-specific CD8+ T cell immune responses in vaccinated mice. In this study, we characterized the number of antigen-expressing dendritic cells (DCs) in the draining lymph nodes of vaccinated mice and determined whether the linkage of VP22 to antigen would influence the ability of antigen-expressing DCs to activate antigen-specific CD8+ T cells in vivo. Vaccination with DNA encoding HSV-1 VP22 linked to human papillomavirus type 16 E7 antigen generated more antigen-expressing DCs in the draining lymph nodes of vaccinated mice than E7 alone. In addition, the linkage of VP22 to E7 improved the MHC class I presentation of E7 in transfected DCs and led to enhanced activation of E7-specific CD8+ T cells. We also observed that vaccination with DNA encoding VP22 linked to E7 generated more E7-specific CD8+ memory T cells, and enhanced long-term protective antitumor immunity against an E7-expressing tumor in vaccinated mice compared with vaccination with DNA encoding E7 alone. Thus, administration of DNA encoding VP22 linked to antigen represents a plausible approach for the development of protective DNA vaccines.
SB 239063, a p38 MAPK inhibitor, reduces neutrophilia, inflammatory cytokines, MMP-9, and fibrosis in lung (2000)

The effects of a second generation p38 mitogen-activated protein kinase (MAPK) inhibitor, SB 239063 [trans-1-(4-hydroxycyclohexyl)-4-(4-fluorophenyl)-5-(2-methoxypyridim idi n-4-yl)imidazole; IC(50) = 44 nM vs. p38 alpha], were assessed in models that represent different pathological aspects of chronic obstructive pulmonary disease (COPD) [airway neutrophilia, enhanced cytokine formation and increased matrix metalloproteinase (MMP)-9 activity] and in a model of lung fibrosis. Airway neutrophil infiltration and interleukin (IL)-6 levels, assessed by bronchoalveolar lavage 48 h after lipopolysaccharide (LPS) inhalation, were inhibited dose dependently by 3-30 mg/kg of SB 239063 given orally twice a day. In addition, SB 239063 (30 mg/kg orally) attenuated IL-6 bronchoalveolar lavage fluid concentrations (>90% inhibition) and MMP-9 activity (64% inhibition) assessed 6 h after LPS exposure. In guinea pig cultured alveolar macrophages, SB 239063 inhibited LPS-induced IL-6 production (IC(50) of 362 nM). In a bleomycin-induced pulmonary fibrosis model in rats, treatment with SB 239063 (2.4 or 4.8 mg/day via osmotic pump) significantly inhibited bleomycin-induced right ventricular hypertrophy (indicative of secondary pulmonary hypertension) and increases in lung hydroxyproline synthesis (indicative of collagen synthesis and fibrosis). Therefore, SB 239063 demonstrates activity against a range of sequelae commonly associated with COPD and fibrosis, supporting the therapeutic potential of p38 MAPK inhibitors such as SB 239063 in chronic airway disease.
Dominance and homozygosity (1997)

Because of the high consanguinity rates in many communities in Israel we had the opportunity to study homozygosity for some dominant disorders. This experience and a review confirmed that in most cases homozygotes of dominant disorders are more severely affected than heterozygotes. In some cases molecular analysis allowed an understanding of the mechanisms involved. While heterozygosity for point mutations or deletions of PAX3 lead to similar manifestations (Waardenburg syndrome), in homozygotes the phenotype is much more severe, probably in direct relation to the loss of function. Charcot-Marie-Tooth 1A is caused by a duplication of PMP22 and further over-expression lead to a more severe disorder. In diseases in which the mutation leads to an abnormal structural protein, the homozygote may be as severely affected as the heterozygote (epidermolysis bullosa simplex) or more severely (achondroplasia, Marfan syndrome). The polyglutamine tract is translated in disorders caused by CAG triplet expansions. In homozygotes for Machado-Joseph disease the onset is earlier and the symptoms are more severe than in heterozygotes, while in Huntington disease homozygotes are affected like heterozygotes.
Gelsolin Binding and Cellular Presentation of Lysophosphatidic Acid (2000)

Lysophosphatidic acid (LPA) in biological fluids binds to serum albumin and other proteins that enhance its effects on cellular functions. The actin-severing protein gelsolin binds LPA with an affinity (K(d) = 6 nm) similar to that of the G protein-coupled LPA receptors encoded by endothelial differentiation genes 2, 4, and 7 (Edg-2, -4, and -7 receptors) and greater than that of serum albumin (K(d) = 360 nm). At concentrations of 10% or less of that in plasma, which are observed in fluids of injured tissues, purified and recombinant gelsolin augment LPA stimulation of nuclear signals and protein synthesis in rat cardiac myocytes (RCMs) that express Edg-2 and -4 receptors. At concentrations of 20% or more of that in plasma, gelsolin suppresses LPA stimulation of RCMs. The lack of effect of gelsolin on RCM responses to monoclonal anti-Edg-4 receptor antibody plus a phorbol ester without LPA attests to its specificity for LPA delivery and the absence of post-receptor effects. Inhibition of gelsolin binding and cellular delivery of LPA by l-alpha-phosphatidylinositol-4,5-bisphosphate (PIP2) and peptides constituting the two PIP2 binding domains of gelsolin suggests competition between LPA and PIP2 for the same sites. Thus, delivery of LPA to RCMs is affinity-coupled to Edg receptors by gelsolin in a PIP2-regulated process.
Neurobiology of neuropathic pain: mode of action of anticonvulsants (2002)

Anticonvulsants are widely used for the treatment of neuropathic pain. Here we review the evidence for a number of peripheral and central changes after nerve injury that may provide a basis for the mechanisms of action of anticonvulsant therapies. The roles of sodium channels, calcium channels, and central glutamate mechanisms are emphasized as the main targets for anticonvulsant drugs in neuropathic pain states. The focus of this article is on anticonvulsants; however, opioids and antidepressants can also be effective in increasing inhibitions to control of pain in a manner similar to that of the enhancement of gamma-aminobutyric acid (GABA) function by antiepileptic drugs. A brief account of these approaches to neuropathic pain is also given.
A Comparative Study of Modern Inference Techniques for Discrete Energy Minimization Problems (2013)

Even years ago, Szeliski et al. published an influential study on energy minimization methods for Markov random fields (MRF). This study provided valuable insights in choosing the best optimization technique for certain classes of problems. While these insights remain generally useful today, the phenominal success of random field models means that the kinds of inference problems we solve have changed significantly. Specifically, the models today often include higher order interactions, flexible connectivity structures, large label-spaces of different cardinalities, or learned energy tables. To reflect these changes, we provide a modernized and enlarged study. We present an empirical comparison of 24 state-of-art techniques on a corpus of 2,300 energy minimization instances from 20 diverse computer vision applications. To ensure reproducibility, we evaluate all methods in the OpenGM2 framework and report extensive results regarding runtime and solution quality. Key insights from our study agree with the results of Szeliski et al. for the types of models they studied. However, on new and challenging types of models our findings disagree and suggest that polyhedral methods and integer programming solvers are competitive in terms of runtime and solution quality over a large range of model types.
Rho Family GTPases Regulate p38 Mitogen-activated Protein Kinase through the Downstream Mediator Pak1 (1995)

The stress-activated p38 mitogen-activated protein (MAP) kinase defines a subgroup of the mammalian MAP kinases that appear to play a key role in regulating inflammatory responses. Co-expression of constitutively active forms of Rac and Cdc42 leads to activation of p38 while dominant negative Rac and Cdc42 inhibit the ability of interleukin-1 to increase p38 activity. p21-activated kinase 1 (Pak1) is a potential mediator of Rac/Cdc42 signaling, and we observe that Pak1 stimulates p38 activity. A dominant negative Pak1 suppresses both interleukin-1- and Rac/Cdc42-induced p38 activity. Rac and Cdc42 appear to regulate a protein kinase cascade initiated at the level of Pak and leading to activation of p38 and JNK.
Direct effects of adriamycin on the rat heart sarcolemma. (1984)

Effects of adriamycin on rat heart sarcolemma were investigated by determining several membrane enzyme activities in the absence or presence of different concentrations of the drug. The adenylate cyclase activity was found to be stimulated by 0.001 and 0.01 microM of adriamycin whereas this enzyme activity was inhibited at 100 and 1000 microM concentrations of the drug. Magnesium dependent Na+, K+ ATPase was not effected by adriamycin, however, in presence of 2 mM ouabain, adriamycin (100 microM) had a depressant effect on the Na+, K+ ATPase activity. Ca2+ ATPase activity was found to be stimulated by adriamycin. The drug had no effect on the Mg2+ ATPase and 5'-nucleotidase activities. These data suggest direct as well as specific effects of adriamycin which may be important in drug-induced cardiotoxicity.
Truncated ETV1, Fused to Novel Tissue-Specific Genes, and Full-Length ETV1 in Prostate Cancer (2008)

In this study, we describe the properties of novel ETV1 fusion genes, encoding N-truncated ETV1 (dETV1), and of full-length ETV1, overexpressed in clinical prostate cancer. We detected overexpression of novel ETV1 fusion genes or of full-length ETV1 in 10% of prostate cancers. Novel ETV1 fusion partners included FOXP1, an EST (EST14), and an endogenous retroviral repeat sequence (HERVK17). Like TMPRSS2, EST14 and HERVK17 were prostate-specific and androgen-regulated expressed. This unique expression pattern of most ETV1 fusion partners seems an important determinant in prostate cancer development. In transient reporter assays, full-length ETV1 was a strong transactivator, whereas dETV1 was not. However, several of the biological properties of dETV1 and full-length ETV1 were identical. On stable overexpression, both induced migration and invasion of immortalized nontumorigenic PNT2C2 prostate epithelial cells. In contrast to dETV1, full-length ETV1 also induced anchorage-independent growth of these cells. PNT2C2 cells stably transfected with dETV1 or full-length ETV1 expression constructs showed small differences in induced expression of target genes. Many genes involved in tumor invasion/metastasis, including uPA/uPAR and MMPs, were up-regulated in both cell types. Integrin beta3 (ITGB3) was clearly up-regulated by full-length ETV1 but much less by dETV1. Based on the present data and on previous findings, a novel concept of the role of dETV1 and of full-length ETV1 overexpression in prostate cancer is proposed.
Sequence to Sequence Transduction with Hard Monotonic Attention (2017)

We present a supervised sequence to sequence transduction model with a hard attention mechanism which combines the more traditional statistical alignment methods with the power of recurrent neural networks. We evaluate the model on the task of morphological inflection generation and show that it provides state of the art results in various setups compared to the previous neural and non-neural approaches. Eventually we present an analysis of the learned representations for both hard and soft attention models, shedding light on the features such models extract in order to solve the task.
Infantile NTRK -associated Mesenchymal Tumors (2017)

Pediatric fibroblastic/myofibroblastic lesions are a relatively common group of tumors with varying morphologies, for which the molecular mechanisms are becoming increasingly well characterized. Congenital infantile fibrosarcoma (CIFS), perhaps the most well studied of these lesions is characterized by a recurrent ETV6-NTRK3 gene fusion. However, a notable subset of locally aggressive congenital/infantile soft tissue lesions with similar morphologic features to CIFS, have not to-date, shown evidence of any canonical molecular aberration. We describe 6 patients with mesenchymal tumors composed of infiltrative fibroblastic/myofibroblastic tumor cells and showing a morphologic spectrum of features much analogous to that previously described in CIFS but without ETV6 fusion transcripts. These tumors lacked a uniform immunoprofile, but showed variable expression of CD34, S100, smooth muscle actin, and CD30. All patients first developed a mass in infancy (≤2 months of age). Using next-generation DNA sequencing, TMP3-NTRK1 fusions were identified in 4 cases, an LMNA-NTRK1 fusion in one case, and a variant EML4-NTRK3 fusion in one case. Similar to infantile fibrosarcoma, these tumors were locally aggressive (with local recurrences if incompletely excised) and rarely metastasized (lung metastases in one patient). Proper identification of these tumors including investigation for NTRK family gene rearrangements is essential for diagnostic accuracy, as well as for clinical management decisions. Given the morbidity associated with radical resection of large soft tissue tumors, children with unresectable, recurrent, and/or metastatic disease may benefit from treatment with NTRK targeted therapies.
Efficacy of chlorothalonil against 15 wood decay fungi. (1992)

A comparison of the wood preservative efficacies of chlorothalonil, pentachlorophenol and chromated copper arsenate (CCA) was made using standard laboratory soil block methodologies. Fifteen fungal strains recommended by American Wood Preservers' Association Standard E 10-91 were tested. As has been previously reported in laboratory tests, CCA did not perform well, having relatively high toxicity thresholds against the test fungi. Chlorothalonil and pentachlorophenol were more efficacious, and showed comparable preservative activity.
Autoantibodies, lupus and the science of sabotage (2004)

Anti-double-stranded DNA antibodies (anti-dsDNA) and antiphospholipid antibodies (APL) are important in the pathogenesis of systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS) respectively. Not all anti-dsDNA or APL antibodies can cause clinical effects. Those that are particularly likely to cause tissue damage tend to be of IgG isotype and to possess particular binding properties. Rigorous statistical analysis of published sequences of human monoclonal anti-DNA and APL antibodies showed that IgG antibodies with binding properties characteristic of pathogenicity tend to have multiple somatic mutations in their variable regions. The distribution of these mutations suggests that they have been selected by antigen. This leads to accumulation of certain residues at the antigen-binding sites of these antibodies. Arginine residues are especially important. A computer-generated model of the pathogenic human monoclonal anti-DNA antibody B3 predicted that arginines in the heavy and light chain complementarity-determining regions (CDRs) would interact with dsDNA. We expressed cloned sequences encoding the B3 heavy and light chains in vitro to produce whole IgG. The cloned sequences of the heavy and light chains were manipulated to express a range of variant IgG antibodies. Binding assays on the expressed antibodies showed that altering specific arginine residues reduced binding to dsDNA in a way consistent with computer generated structural models. Changing the pattern of somatic mutations in the light chain altered binding to both dsDNA and histones, but in different ways. A single arginine-to-serine mutation in light-chain CDR1 of B3 reduced binding to both those antigens and may also have reduced the pathogenicity of the expressed antibodies in severe combined immunodeficiency (SCID) mice. Monoclonal human APL were expressed using the same system. Nineteen different heavy-light combinations were expressed. The ability to bind cardiolipin correlated well with the presence of exposed arginine residues in the heavy- and light-chain CDRs. The heavy chain of the pathogenic APL antibody IS4 contains four exposed arginines in CDR3. The results of mutagenesis studies suggested that two of these promote binding to cardiolipin whereas the other two have no such effect.
Transforming Growth Factors β1, β2, and β3 and Their Receptors Are Differentially Regulated during Normal and Impaired Wound Healing (1996)

A series of studies has shown that application of transforming growth factor beta (TGF-beta) to a wound has a beneficial effect, especially in animals with wound healing disorders. In this study we have investigated the regulation of TGF-beta1, beta2, and beta3 and their receptors during the repair process. We found a large induction of all three TGF-beta isoforms and also of TGF-beta types I and II receptors, although the time course of induction and the absolute expression levels were different for these genes. Furthermore, each TGF-beta isoform had distinct sites of expression in the wound. Systemic treatment with glucocorticoids significantly altered the expression levels of TGF-betas and TGF-beta receptors. Whereas expression of TGF-beta1, TGF-beta2, and TGF-beta type II receptor was suppressed by glucocorticoids in normal and wounded skin, expression of TGF-beta3 and TGF-beta receptor type I mRNA was stimulated. These findings provide an explanation for the beneficial effect of exogenous TGF-beta in the treatment of impaired wound healing in glucocorticoid-treated animals. Furthermore, they suggest that a disturbed balance between the levels of the three TGF- beta isoforms and their receptors might underlie the wound healing defect seen in glucocorticoid-treated animals.
The physical chemistry of lipids : from alkanes to phospholipids (1986)

Lipids are one of the three major classes of biologically essential organic molecules. They are found in all living organisms and play a critical role in maintaining the integrity of all living things, plant and animal, because they form the barrier separating the living cell from the outside world. They are a major source of cellular energy and function in living organisms in many specific ways: as antigens, receptors, sensors, electrical insulators and biological detergents. Lipids are stored in the cells of plants and animals to be used as building blocks for membranes during growth and repair. The white matter of the brain, spinal cord, and nerves contain lipids. Lipids play a role in many diseases such as atherosclerosis, obesity, familial lipidoses and others. The food industry uses lipids not only for their nutritional value but also as emulsifiers, stabilizers, and moisturizers, which are important in processed food technology. Lipids also play an important role in industry . Lipids are used as lubricants and constituents in cosmetics and many pharmaceutical preparations. This book is oriented toward understanding the structure, function, and behavior of lipids in biological systems. The focus is on the summarizing of the physical and chemical data for a wide variety of lipids, concentrating in particular on the changes in state and structure that occur with changes in temperature and during lipid-water and lipid-lipid interactions. A thorough understanding of the states and structures of all lipid classes provides a firm basis for understanding the more complex interactions of lipids with proteins, nucleic acids, and complex carbohydrates. In general, the chapterswould be similar to those of individual lipid classes in the previous book, i.e. introduction with relevance to biology, crystalline structure(s), changes in crystalline packing due to chemical substitution, phase behavior (including structural changes, thermodynamics and kinetics), interaction with other lipids, interaction in aqueous systems, interfacial behavior, interaction between other classes of lipids with water with particular relevance to biological systems. There will be an additional five chapters. Existing chapters would be revised and update with more recent data and general conclusions concerning all the data.