gebhart/patrepeval huggingface dataset:
Identification and activity of a phytotoxin produced by<i>Calonectria ilicicola</i>, the causal agent of soybean red crown rot (2011)

Abstract A phytotoxin isolated from Calonectria ilicicola, the causal agent of soybean red crown rot, was identified as PF1070A, a cyclic peptide consisting of four amino acids. This compound is known as an antitumour antibiotic and to induce synthesis of metallothionein in mouse Ltk- cells. We tested PF1070A against three soybean cultivars that differ in susceptibility to C. ilicicola; however, there was no significant difference among their responses to the toxin. We determined the amount of PF1070A produced by 17 isolates of C. ilicicola, and found that there was a strong positive correlation between virulence and PF1070A production. Together, these results suggest that the phytotoxin PF1070A has a role in the virulence of C. ilicicola.
High-speed architectures for Reed-Solomon decoders (2001)

New high-speed VLSI architectures for decoding Reed-Solomon codes with the Berlekamp-Massey algorithm are presented in this paper. The speed bottleneck in the Berlekamp-Massey algorithm is in the iterative computation of discrepancies followed by the updating of the error-locator polynomial. This bottleneck is eliminated via a series of algorithmic transformations that result in a fully systolic architecture in which a single array of processors computes both the error-locator and the error-evaluator polynomials. In contrast to conventional Berlekamp-Massey architectures in which the critical path passes through two multipliers and 1+[log/sub 2/,(t+1)] adders, the critical path in the proposed architecture passes through only one multiplier and one adder, which is comparable to the critical path in architectures based on the extended Euclidean algorithm. More interestingly, the proposed architecture requires approximately 25% fewer multipliers and a simpler control structure than the architectures based on the popular extended Euclidean algorithm. For block-interleaved Reed-Solomon codes, embedding the interleaver memory into the decoder results in a further reduction of the critical path delay to just one XOR gate and one multiplexer, leading to speed-ups of as much as an order of magnitude over conventional architectures.
Extracellular matrix regulates endothelial functions through interaction of VEGFR‐3 and integrin α<sub>5</sub>β<sub>1</sub> (2004)

Endothelium extracellular matrix (ECM) interactions can provide distinct spatial and molecular signals which control cellular proliferation, migration, and differentiation. Here, we investigated the role of fibronectin (FN), a major ECM protein, on the functions of lymphatic endothelial cells (LEC). We observed that FN, the ligand for integrin alpha5beta1, selectively promoted the growth of LEC as compared with vitronectin (VN) in the presence of the ligand for vascular endothelial growth factor receptor 3 [VEGFR-3 (VEGF-C156S)]. Upon investigating the mechanisms whereby ECM components regulate VEGFR-3 signaling, we found that FN transactivated VEGFR-3 and significantly enhanced the phosphorylation of VEGFR-3 induced by VEGF-C156S as compared to VN. An enhanced association of the integrin subunit alpha5 or beta1 with VEGFR-3, after stimulation with VEGF-C156S, was observed by co-immunoprecipitation. While blockade of integrin alpha5beta1 inhibited the VEGF-C156S-induced phosphorylation of VEGFR-3, no similar effect was obtained by blocking integrin alphavbeta3. FN also protected the endothelial cells from serum deprivation-induced apoptosis. Moreover, while the specific PI3 kinase inhibitor, LY294002, abolished this FN-mediated cell survival, the MAPK kinase inhibitor, PD98059, had no significant effect. Furthermore, a dominant-negative mutant of VEGFR-3 (G857R) reduced VEGF-C156S or FN-mediated cell survival, as well as the activities of PI3 kinase/Akt. Our results indicate that integrin alpha5beta1 participates in the activation of both VEGFR-3 and its downstream PI3 kinase/Akt signaling pathway, which is essential for FN-mediated lymphatic endothelial cell survival and proliferation.
In vitro effects of recombinant interleukin 7 on growth and differentiation of bone marrow pro-B- and pro-T-lymphocyte clones and fetal thymocyte clones. (1989)

We have studied the effects of recombinant (r) interleukin 7 (IL-7) on growth and differentiation of marrow pro-B-lymphocyte clones (CB/Bm7, LyD9, LyB9), marrow pro-T-lymphocyte clones (C4-77/3, C4-86/18, C4-95/16), and fetal thymocyte clones (FTH5, FTA2, FTD5) in the presence or absence of the bone marrow stroma clone RP.0.10, which was selected for its ability to promote differentiation of the pro-B clones. rIL-7 alone stimulated some DNA synthesis (measured by [3H]thymidine uptake) but not actual growth (increase in cell number) of the pro-B clones. Antibodies against IL-4 and IL-6 or against receptors for IL-2, IL-3, and IL-5 did not inhibit this effect of rIL-7 on the pro-B clones. rIL-7 alone or in various combinations with other cytokines (from rIL-1 alpha to rIL-6) could not induce differentiation of the pro-B clones into IgM+ B cells regardless of the presence of lipopolysaccharide (LPS). The RP.0.10 marrow stroma cells by themselves do not support the growth of the pro-B clones. However, the pro-B clones grew when cultured with rIL-7 and monolayers of the RP.0.10 stroma cells. While the RP.0.10 stroma cells induced the pro-B clones to differentiate into IgM+ B cells but not T3+ T cells when cultured in the presence of LPS and rIL-3, the B-cell progenitor clones gave rise to significantly higher numbers of IgM+ B cells (up to 63%) and to many more B cells expressing higher levels of surface IgM when cocultured with rIL-7, LPS, and RP.0.10 stroma cells. The pro-B clones also generated IgM+ B cells (up to 20%) when cocultured with RP.0.10 stroma cells and rIL-7 in the absence of LPS. By using culture plates designed for testing requirements for cell-cell contact, we found that cell interactions between the pro-B cell and the marrow stroma cell are essential to induce rearrangement and expression of the immunoglobulin genes in the pro-B clones. Possible mechanisms to account for the remarkable effects of rIL-7 in the presence of RP.0.10 stroma cells on both growth and differentiation of the pro-B clones are discussed. Finally, rIL-7 alone or together with RP.0.10 stroma cells neither supported proliferation nor induced differentiation into T3+ T cells or IgM+ B cells of the marrow pro-T clones or the fetal thymocyte clones. In light of these findings, we postulate that the interaction of the pluripotential stem cell with marrow stroma cells like RP.0.10 and the availability of IL-7 could play a critical role in the commitment to develop along the B-lymphocyte pathway.
Elimination of the Immunogenicity of Therapeutic Antibodies (1999)

The immunogenicity of therapeutic Abs limits their long-term use. The processes of complementarity-determining region grafting, resurfacing, and hyperchimerization diminish mAb immunogenicity by reducing the number of foreign residues. However, this does not prevent anti-idiotypic and anti-allotypic responses following repeated administration of cell-binding Abs. Classical studies have demonstrated that monomeric human IgG is profoundly tolerogenic in a number of species. If cell-binding Abs could be converted into monomeric non-cell-binding tolerogens, then it should be possible to pretolerize patients to the therapeutic cell-binding form. We demonstrate that non-cell-binding minimal mutants of the anti-CD52 Ab CAMPATH-1H lose immunogenicity and can tolerize to the "wild-type" Ab in CD52-expressing transgenic mice. This finding could have utility in the long-term administration of therapeutic proteins to humans.
TGF-β: A Balancing Act (1998)

Regulation of developmental processes as well as host defense and repair mechanisms requires the maintenance of a delicate balance of positive and negative regulatory signals. TGF-beta, a molecule known for its many diverse activities, can promote or inhibit cell growth and function. Disruption of the balance between these opposing activities can contribute to aberrant development, malignancy, or pathogenic immune and inflammatory responses. TGF-beta transgenic mouse studies highlight the essential function(s) of TGF-beta and its receptors and provide insight to potential therapeutic approaches to manipulate TGF-beta expression.
A randomised, double blind, placebo controlled study of celecoxib, a selective cyclooxygenase 2 inhibitor, on duodenal polyposis in familial adenomatous polyposis (2002)

A panel of five endoscopists found a significant reduction in duodenal polyposis after six months of treatment with celecoxib 400 mg twice daily. COX-2 inhibition may help this otherwise untreatable condition.
Clinical patterns and complications of African diabetic patients: preliminary data from Kigali University Teaching Hospital, Rwanda (2012)

Diabetes mellitus, and its complications and comorbidities form a major component of emerging non-communicable diseases (NCDs) in developing countries where they coexist with traditional infectious diseases. The potential cost of optimum management of complications arising from diabetes and other NCDs adds an additional burden to the economy of African countries already living in poverty, with limited affordability of treatment. We describe a prospective cross-sectional study carried out in Kigali University Teaching Hospital, Rwanda, between October 2008 and May 2010, to investigate the clinical patterns and complications profile of diabetic patients attending the Department of Internal Medicine. The study involved 294 patients (65% females, 40% of patients aged below 45 years). Co-morbidity with hypertension, overweight and dyslipidemia was found in 31%, 33%, and 28%, respectively. The mean diabetes duration was 6±6 years (mean ± SD). Microvascular complications were common: neuropathy (53%), retinopathy (23%), and nephropathy (20%). Macrovascular complications were less frequent: cerebrovascular disease (4%), coronary artery disease (3%), and peripheral vascular disease (15%). More efforts focused on education programmes, and early diagnosis through mass population screening, as well as the improvement of case management may help to reduce the burden of complications. prevalence and the related complications worldwide. 3 In sub-Saharan Africa, while communicable diseases such as HIV/AIDS, malaria, and tuberculosis have continued to pose great threats to the public health system, it is now apparent that NCDs such as diabetes are undoubtedly adding to the multiple burdens for people in this
Gemtuzumab Ozogamicin Therapy for Isolated Extramedullary AML Relapse after Allogeneic Hematopoietic Stem-Cell Transplantation (2010)

The treatment of isolated extramedullary relapse (IEMR) after allogeneic hematopoietic stem-cell transplantation (allo-HSCT) poses a challenge for which no standard approach exists. Gemtuzumab ozogamicin (GO) is a recombinant humanized monoclonal antibody, conjugated to calicheamicin, which targets the CD33 antigen that is expressed in acute myelogenous leukemia (AML) blasts. The selectivity of GO for CD33-positive leukemic cells makes it an attractive agent for use in patients with multiple sites of IEMR after allo-HSCT, because GO does not suppress cells responsible for the putative graft-versus-leukemia (GVL) effect. Herein, we describe a 54-year-old male patient who developed AML with multiple sites of extramedullary (EM) relapse after allo-HSCT, and who exhibited apparent donor-derived hematopoiesis in the bone marrow. At approximately 120 days after allo-HSCT, the patient complained of severe lumbago. T2-weighted magnetic resonance images and fluorodeoxyglucose-positron emission tomography showed multiple mass lesions in soft tissue and bone. A biopsy specimen from a lumbar soft tissue mass confirmed EM relapse, and revealed that donor T lymphocytes were present in the relapse site and that leukemic cells expressed CD33. Therefore, to maintain the GVL effect of donor T lymphocytes, the patient was treated with GO as a single agent. He achieved complete hematological remission, and has remained in remission, with only mild liver injury, for more than 10 months since GO treatment. GO can be an effective therapy for IEMR after allo-HSCT, especially when cytotoxic T lymphocytes react to leukemic cells at the site of EM relapse.
R de réel (2001)

Un carré noir et blanc sur papier glacé. La sobriété est l’écrin d’un alphabet insolite. R de réel, revue bimestrielle fondée en janvier 2000 par Raphaël Meltz et Laetitia Bianchi, décline numéro après numéro chacune des lettres de l’alphabet. « On a créé la revue qu’on aurait aimé lire, à mi-chemin entre le style universitaire et le style journalistique, et loin du jargon spécialisé ; une revue qu’on veut intellectuelle et sympathique, rigoureuse et rigolote, dotée d’une âme », expliquent d’...
Structure of the mouse glial fibrillary acidic protein gene: implications for the evolution of the intermediate filament multigene family (1985)

We report the complete sequence of the gene encoding mouse glial fibrillary acidic protein (GFAP), the intermediate filament (IF) protein specific to astrocytes. The 9.8 kb gene includes nine exons separated by introns ranging in size from 0.2 to 2.5 kb. A comparison of the organization of the GFAP gene with that of genes encoding other IF proteins reveals that the structure of IF genes is highly conserved in spite of considerable divergence at the amino acid level. Thus, most of the evolutionary events leading to the placement of introns in IF genes must have occurred prior to the duplication and subsequent divergence of IF genes from a presumptive common ancestral sequence. The conserved gene organization is unrelated to structural features of IF proteins. A curious feature of the GFAP gene is the large number of repeated sequences found in the introns. Six tracts of reiterated di- or trinucleotides are present, plus tandem repeats of two different novel sequences. One repeat is unique to the GFAP gene; the other occurs elsewhere in the mouse genome, although at relatively low frequency.
Mean Arterial Pressure at 11 <sup>+0</sup> to 13 <sup>+6</sup> Weeks in the Prediction of Preeclampsia (2008)

This study aimed to determine the performance of screening for preeclampsia (PE) by maternal medical history and mean arterial pressure (MAP) at 11(+0) to 13(+6) weeks. In 5590 women with singleton pregnancies attending for routine care at 11(+0) to 13(+6) week's gestation we recorded maternal variables and measured the MAP. We excluded 397 because they had missing outcome data or the pregnancies resulted in miscarriage or termination. In 104 patients there was subsequent development of PE, 97 developed gestational hypertension, 574 delivered small-for-gestational-age newborns, and 4418 were unaffected by PE, gestational hypertension, or small for gestational age. A multivariate Gaussian model was fitted to the distribution of log multiple of the median MAP in the PE and unaffected groups. Likelihood ratios for log multiple of the median MAP were computed and used together with maternal variables to produce patient-specific risks for each case. Detection rates and false-positive rates were calculated by taking the proportions with risks above a given risk threshold. In the unaffected group, log MAP was influenced by maternal age, ethnic origin, smoking, family and personal history of PE, and fetal crown-rump length. In the prediction of PE, significant contributions were provided by log multiple of the median MAP, ethnic origin, body mass index, and personal history of PE. The detection rate of PE by log multiple of the median MAP and maternal variables was 62.5% for a false-positive rate of 10%. Maternal variables, together with MAP, at 11(+0) to 13(+6) weeks identify a group at high risk for development of PE.
The family of G‐protein‐coupled receptors (1995)

The family of G-protein-coupled receptors can be defined by their similar structural and functional characteristics. Although their primary sequences are quite diverse, these proteins share several common structural features that reflect their common mechanism of action. Mutagenesis and biophysical analysis of several of these receptors indicate that small molecule agonists and antagonists bind to a hydrophobic pocket buried in the transmembrane core of the receptor. In contrast, peptide ligands bind to both the extracellular and transmembrane domains. The mechanisms by which these peptide and small molecule agonists cause receptor activation are being explored by various approaches, but are not yet well defined. A deeper understanding of structural basis for the functional activity of this large family of receptors will have important implications for drug design in a variety of therapeutic areas.
Limbal epithelial stem cell therapy (2006)

Restoring vision in patients suffering from previously intractable blinding ocular surface disease has become possible with the advent of techniques for ex vivo expansion and transplantation of limbal epithelial stem cells onto the cornea. This approach represents one of the few adult stem cell therapies presently in the clinic. This article highlights several key research areas where progress will be made to specifically understand the biology and therapeutic potential of limbal epithelial stem cells, which may have an applicability to the understanding of other adult stem cell populations.
A New Mechanism of the Maillard Reaction Involving Sugar Fragmentation and Free Radical Formation (1983)

Analyses of the hyperfine structures of ESR spectra found at an early stage of the Maillard reaction led to the assignment that the radical products are N,N'-disubstituted pyrazine cation radicals. Quantitative product determination at the reaction stage involving the free radicals indicates a sequential formation of glucosylamine, a 2-carbon and other sugar fragmentation products, then certain reducing products and the free radical, the Amadori product, and finally, glucosones. N,N'-dialkylpyrazines, or mixtures of glycolaldehyde with amino compounds, are shown to be highly active in free radical formation as well as in browning. Thus we propose the existence of a new pathway to browning in the Maillard reaction, involving sugar fragmentation and free radical formation prior to the Amadori rearrangement.
Evidence That 3-Phosphoinositide-dependent Protein Kinase-1 Mediates Phosphorylation of p70 S6 Kinase in Vivoat Thr-412 as well as Thr-252 (1999)

Protein kinase B and p70 S6 kinase are members of the cyclic AMP-dependent/cyclic GMP-dependent/protein kinase C subfamily of protein kinases and are activated by a phosphatidylinositol 3-kinase-dependent pathway when cells are stimulated with insulin or growth factors. Both of these kinases are activated in cells by phosphorylation of a conserved residue in the kinase domain (Thr-308 of protein kinase B (PKB) and Thr-252 of p70 S6 kinase) and another conserved residue located C-terminal to the kinase domain (Ser-473 of PKB and Thr-412 of p70 S6 kinase). Thr-308 of PKBalpha and Thr-252 of p70 S6 kinase are phosphorylated by 3-phosphoinositide-dependent protein kinase-1 (PDK1) in vitro. Recent work has shown that PDK1 interacts with a region of protein kinase C-related kinase-2, termed the PDK1 interacting fragment (PIF). Interaction with PIF converts PDK1 from a form that phosphorylates PKB at Thr-308 alone to a species capable of phosphorylating Ser-473 as well as Thr-308. This suggests that PDK1 may be the enzyme that phosphorylates both residues in vivo. Here we demonstrate that PDK1 is capable of phosphorylating p70 S6 kinase at Thr-412 in vitro. We study the effect of PIF on the ability of PDK1 to phosphorylate p70 S6 kinase. Surprisingly, we find that PDK1 bound to PIF is no longer able to interact with or phosphorylate p70 S6 kinase in vitro at either Thr-252 or Thr-412. The expression of PIF in cells prevents insulin-like growth factor 1 from inducing the activation of the p70 S6 kinase and its phosphorylation at Thr-412. Overexpression of PDK1 in cells induces the phosphorylation of p70 S6 kinase at Thr-412 in unstimulated cells, and a catalytically inactive mutant of PDK1 prevents the phosphorylation of p70 S6K at Thr-412 in insulin-like growth factor 1-stimulated cells. These observations indicate that PDK1 regulates the activation of p70 S6 kinase and provides evidence that PDK1 mediates the phosphorylation of p70 S6 kinase at Thr-412.
Synthesis and Deuteration of Some Halogenoquinoli-zinium Bromides (1981)

Syntheses and H-nrm spectra are reported for the hitherto mhom 1-br-, 3-broro, 4-bnmo, 2-&lo-, 4-chlom, 1.2-dib-, 3,4-diband 2,7-dibrorrquinolizinim branide.These axpwds, quimllzinim brcmide, 1-hydroxy-, 2-hylroxy-, 3-hydraq-, 2-pipendmo-and 2-d~ethylHninoquimlizinim b r m d e and 2and 4-quinolizone were deuterated by heating with D20 (Table I ) . Intrductlon and resultsGuinolizin~m s a l t s form a class of capmr& whose -=tieshave not yet been studied ex- 1tenslvely .The special interest in t h i s laboratory in the behaviour of halqemhetarenes and hetarinim s a l t s tcwards nucleophiles induced us t o prepare several halogenaqrunolizinim branides and t o s t q their reactivity tcwards nucleophiles.In t h i s paper we report on the synthesis of 1-broro, 2-br-, 3-br-, 4-br-, 2-&lo-, 4-chlom, 1,2-dibronr, 3 .4 -d i b m and 2.7-dibroro 2 qlunolizlnium brcmide (quinolizinim b r m d e f m here on abbreviated as QB) .Only 2-brorcQB and 3 4 -c h l o r ~n o l i z i r u u m perchlorate have been described i n the literature thus f a r .Since structure 1 identification of the QB's is based rminly on their H-rmn spectra, we prepred deuterium labelled ccmpounds in order t o support the assigrvrents of the peaks i n the s-a.Ihe parent carq2und : qrunolizinim b r d d e (1) ha^ been synthesized by several methd.5;we obtained the best overall yield (24%) by a 4-step synthesis starting f n m pyridine-2-carboxylic 4 acid .0 1-er-B(2) was prepared i n 69% p e l d by heating quinolizinim perbranide (2) a t 200 C for 6 h
Type 1 Diabetes in Young Adulthood (2015)

Type 1 diabetes has traditionally been studied as a chronic illness of childhood. However, young adulthood is a critical time for the development and integration of lifelong diabetes management skills, and research is starting to identify unique challenges faced by youth with diabetes as they age into adulthood. Most young adults experience multiple transitions during this unstable developmental period, including changes in lifestyle (e.g., education, occupation, living situation), changes in health care, and shifting relationships with family members, friends, and intimate others. Young adults with type 1 diabetes must navigate these transitions while also assuming increasing responsibility for their diabetes care and overall health. Despite these critical health and psychosocial concerns, there is a notable lack of evidence-based clinical services and supports for young adults with type 1 diabetes. We review relevant evolving concerns for young adults with type 1 diabetes, including lifestyle considerations, health care transitions, psychosocial needs, and changes in supportive networks, and how type 1 diabetes impacts and is impacted by these key developmental considerations. Specific avenues for intervention and future research are offered.