gebhart/patrepeval huggingface dataset:
Endogenous gibberellins in Arabidopsis thaliana and possible steps blocked in the biosynthetic pathways of the semidwarf ga4 and ga5 mutants. (1990)

Twenty gibberellins (GAs) have been identified in extracts from shoots of the Landsberg erecta line of Arabidopsis thaliana by full-scan gas chromatography-mass spectrometry and Kovats retention indices. Eight of them are members of the early-13-hydroxylation pathway (GA53, GA44, GA19, GA17, GA20, GA1, GA29, and GA8), six are members of the early-3-hydroxylation pathway (GA37, GA27, GA36, GA13, GA4, and GA34), and the remaining six are members of the non-3,13-hydroxylation pathway (GA12, GA15, GA24, GA25, GA9, and GA51). Seven of these GAs were quantified in the Landsberg erecta line of Arabidopsis and in the semidwarf ga4 and ga5 mutants by gas chromatography-selected ion monitoring (SIM) using internal standards. The relative levels of the remaining 13 GAs were compared by the use of ion intensities only. In comparison with the Landsberg erecta line, the ga4 mutant had reduced levels of the 3-hydroxy- and 3,13-dihydroxy-GAs, and it accumulated the 13-hydroxy-GAs, except GA53, and the non-3,13-hydroxy-GAs, except GA12. The GA4 gene encodes, therefore, a protein with 3 beta-hydroxylation activity. The ga5 mutant had reduced levels of the C19-GAs, which indicates that the product of the GA5 gene catalyzes the elimination of C-20 at the aldehyde level. The ga5 mutant also had increased levels of certain C20-GAs, which indicates existence of an additional control, possibly hydroxylation of C-20. The growth-response data, as well as the accumulation of GA9 in the ga4 mutant, indicate that GA9 is not active in Arabidopsis, but it must be 3 beta-hydroxylated to GA4 to become bioactive. It is concluded that the reduced levels of the 3 beta-hydroxy-GAs, GA1 and GA4, are the cause of the semidwarf growth habit of both mutants.
Allogeneic bone marrow transplantation for acute leukemia refractory to induction chemotherapy (1985)

This article compares the outcome of 14 patients with primary refractory acute leukemia who underwent bone marrow transplantation from human leukocyte antigen (HLA)-identical donors with that of 18 age-matched control patients who received chemotherapy. Complete clearing of leukemia was seen in all 14 transplanted patients. Five of the transplanted patients are alive 98 to 1790 days posttransplant, and four are free of leukemia. Nine patients have died, eight with severe graft-versus-host disease associated with interstitial pneumonia or systemic infections and one with relapse from chemotherapy-associated infections. Engraftment was seen in all patients. Severe graft-versus-host disease (grades III and IV) was seen in ten patients and resolved in three patients following high-dose corticosteroid treatment. Three of the 18 control patients are alive, none of them in complete remission. It appears that the combination of piperazinedione and total-body irradiation followed by allogeneic transplant is effective induction treatment for primary refractory acute leukemia and will be considered in the future as first salvage treatment for patients failing induction treatment.
ATM and satellite distribution of multimedia educational courseware (2002)

The Distributed and Interactive Courseware Environment (DICE) is a system for large-scale delivery of multimedia hypertext-based courseware to school sites without high-speed network connectivity using satellite technologies. DICE is being developed on a testbed consisting of (1) a network-resident architecture supported by a high-speed ATM WAN backbone, (2) a classroom-resident architecture consisting of PC LANs in participating school classrooms, and (3) a satellite communications infrastructure serving as a communications link between the network- and classroom-resident architectures. Based on real-time classroom performance evaluation, the network-resident architecture incrementally and adaptively delivers courseware segments to the receiving classroom-resident architecture via satellite.
De-Embedding and Unterminating (1974)

De-embedding is the process of deducing the impedance of a device under test from measurernents made at a distance, when the electrical properties of the intervening structure are known. Unterminating is the process of deducing the electrical properties of the intervening structure from a series of measurements with known embedded devices. The mathematical steps necessary for de-embedding and unterminating with theoretically redundant measurements in order to minimize the effect of experimental errors.
Serine Proteases in Rodent Hippocampus (1998)

Brain serine proteases are implicated in developmental processes, synaptic plasticity, and in disorders including Alzheimer's disease. The spectrum of the major enzymes expressed in brain has not been established previously. We now present a systematic study of the serine proteases expressed in adult rat and mouse hippocampus. Using a combination of techniques including polymerase chain reaction amplification and Northern blotting we show that tissue-type plasminogen activator (t-PA) is the major species represented. Unexpectedly, the next most abundant species were RNK-Met-1, a lymphocyte protease not reported previously in brain, and two new family members, BSP1 (brain serine protease 1) and BSP2. We report full-length sequences of the two new proteases; homologies indicate that these are of tryptic specificity. Although BSP2 is expressed in several brain regions, BSP1 expression is strikingly restricted to hippocampus. Other enzymes represented, but at lower levels, included elastase IV, proteinase 3, complement C2, chymotrypsin B, chymotrypsin-like protein, and Hageman factor. Although thrombin and urokinase-type plasminogen activator were not detected in the primary screen, low level expression was confirmed using specific polymerase chain reaction primers. In contrast, and despite robust expression of t-PA, the usual t-PA substrate plasminogen was not expressed at detectable levels.
Inhibition of protein kinase Cε prevents hepatic insulin resistance in nonalcoholic fatty liver disease (2007)

Nonalcoholic fatty liver disease is strongly associated with hepatic insulin resistance and type 2 diabetes mellitus, but the molecular signals linking hepatic fat accumulation to hepatic insulin resistance are unknown. Three days of high-fat feeding in rats results specifically in hepatic steatosis and hepatic insulin resistance. In this setting, PKCepsilon, but not other isoforms of PKC, is activated. To determine whether PKCepsilon plays a causal role in the pathogenesis of hepatic insulin resistance, we treated rats with an antisense oligonucleotide against PKCepsilon and subjected them to 3 days of high-fat feeding. Knocking down PKCepsilon expression protects rats from fat-induced hepatic insulin resistance and reverses fat-induced defects in hepatic insulin signaling. Furthermore, we show that PKCepsilon associates with the insulin receptor in vivo and impairs insulin receptor kinase activity both in vivo and in vitro. These data support the hypothesis that PKCepsilon plays a critical role in mediating fat-induced hepatic insulin resistance and represents a novel therapeutic target for type 2 diabetes.
Intrathecal HIV-1 Envelope Glycoprotein gp120 Induces Enhanced Pain States Mediated by Spinal Cord Proinflammatory Cytokines (2001)

Perispinal (intrathecal) injection of the human immunodeficiency virus-1 (HIV-1) envelope glycoprotein gp120 creates exaggerated pain states. Decreases in response thresholds to both heat stimuli (thermal hyperalgesia) and light tactile stimuli (mechanical allodynia) are rapidly induced after gp120 administration. gp120 is the portion of HIV-1 that binds to and activates microglia and astrocytes. These glial cells have been proposed to be key mediators of gp120-induced hyperalgesia and allodynia because these pain changes are blocked by drugs thought to affect glial function preferentially. The aim of the present series of studies was to determine whether gp120-induced pain changes involve proinflammatory cytokines [interleukin-1beta (IL-1) and tumor necrosis factor-alpha (TNF-alpha)], substances released from activated glia. IL-1 and TNF antagonists each prevented gp120-induced pain changes. Intrathecal gp120 produced time-dependent, site-specific increases in TNF and IL-1 protein release into lumbosacral CSF; parallel cytokine increases in lumbar dorsal spinal cord were also observed. Intrathecal administration of fluorocitrate (a glial metabolic inhibitor), TNF antagonist, and IL-1 antagonist each blocked gp120-induced increases in spinal IL-1 protein. These results support the concept that activated glia in dorsal spinal cord can create exaggerated pain states via the release of proinflammatory cytokines.
New effective gonadotropin releasing hormone antagonists with minimal potency for histamine release in vitro (1986)

In order to minimize the adverse effect of histamine release in the rat of some gonadotropin releasing hormone (GnRH) antagonists, such as [Ac-D2Nal1,D4FPhe2,DTrp3,DArg6]-GnRH, new structures with modifications at positions 1, 2, 3, 5, 6, 7, and 10 were synthesized and tested in several biological systems. In vitro: the affinity for the pituitary GnRH receptor was measured as was the ability of the analogues to inhibit GnRH-stimulated release of luteinizing hormone (LH) by dispersed anterior pituitary cells in culture and to release histamine from rat mast cells. In vivo: inhibition of ovulation in the cycling rat was determined after subcutaneous (sc) injection of the peptides at noon on the day of proestrus; the duration of action of the peptides was evaluated by measuring LH levels in the castrated male rat after sc injection of some selected analogues. [Ac-D2Nal1,D4ClPhe2,D3Pal3,Arg5,D-4-p-methoxy benzoyl-2-aminobutyric acid6,DAla10]-GnRH was found to be one of the most potent analogues of this series, causing a 100% inhibition of ovulation at 5 micrograms/kg or less. Release of histamine was observed at doses 10-25 times that required for [Ac-D2Nal1,D4FPhe2,DTrp3,DArg6]-GnRH. Thus, introduction of arginine in position 5 with a hydrophobic amino acid in position 6 is compatible with high potency in several biological systems and results in compounds with lowered potency to release histamine compared to homologous peptides with tyrosine in position 5 and D-arginine in position 6.
Targeted therapies in CLL: mechanisms of resistance and strategies for management (2015)

The therapy of relapsed chronic lymphocytic leukemia (CLL) has changed dramatically in the past year with the regulatory approval of idelalisib and ibrutinib, with other therapeutic small molecules likely to become widely available in the next few years. Although durable remissions are being seen in many patients with these agents, it is becoming apparent that some patients with high genomic risk disease will relapse. Next-generation sequencing in patients as well as in vitro models is affording us the opportunity to understand the biology behind these relapses, which is the first step to designing rational therapies to prevent and treat targeted therapy-resistant CLL. These strategies are critical, as these relapses can be very difficult to manage, and a coordinated effort to put these patients on clinical trials will be required to efficiently determine the optimal therapies for these patients. In this review, we will describe mechanisms of resistance, both proven and hypothesized, for idelalisib, ibrutinib, and venetoclax, describe patterns of resistance that have been described with ibrutinib, and discuss potential strategies for management of disease resistant to these drugs as well as potential strategies to prevent resistance.
Improvements in Laboratory Rearing of the Southern Corn Rootworm,Diabrotica undecimpuncta howardiBarber (Coleoptera: Chrysomelidae), on an Artificial Diet and Corn (1985)

Journal Article Improvements in Laboratory Rearing of the Southern Corn Rootworm, Diabrotica undecimpuncta howardi Barber (Coleoptera: Chrysomelidae), on an Artificial Diet and Corn Get access P. G. Marrone, P. G. Marrone Monsanto Agricultural Products Company, 800 North Lindbergh Boulevard, St. Louis, Missouri 63167 Search for other works by this author on: Oxford Academic PubMed Google Scholar F. D. Ferri, F. D. Ferri Monsanto Agricultural Products Company, 800 North Lindbergh Boulevard, St. Louis, Missouri 63167 Search for other works by this author on: Oxford Academic PubMed Google Scholar T. R. Mosley, T. R. Mosley Monsanto Agricultural Products Company, 800 North Lindbergh Boulevard, St. Louis, Missouri 63167 Search for other works by this author on: Oxford Academic PubMed Google Scholar L. J. Meinke L. J. Meinke Monsanto Agricultural Products Company, 800 North Lindbergh Boulevard, St. Louis, Missouri 63167 1North Carolina State Univ., Raleigh, N.C. Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Economic Entomology, Volume 78, Issue 1, 1 February 1985, Pages 290–293, https://doi.org/10.1093/jee/78.1.290 Published: 01 February 1985 Article history Received: 11 June 1984 Accepted: 23 October 1984 Published: 01 February 1985
Inhibitory effect of Bifidobacterium longum on colon, mammary, and liver carcinogenesis induced by 2-amino-3-methylimidazo[4,5-f]quinoline, a food mutagen. (1993)

The inhibitory effect of lyophilized cultures of Bifidobacterium longum on 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)-induced carcinogenesis was investigated in male and female F344 rats. Beginning at 5 weeks of age, male and female rats were divided into various experimental groups and fed one of the high-fat, semipurified diets containing 0 and 0.5% lyophilized cultures of B. longum with or without 125 ppm IQ in the diet. All animals were continued on this regimen until the termination of the study. All animals were necropsied during the 58th week. The results indicated that dietary B. longum significantly inhibited the IQ-induced incidence (percentage of animals with tumors) of colon (100% inhibition) and liver (80% inhibition) tumors and multiplicity (tumors/animal) of colon, liver, and small intestinal tumors in male rats. In female rats, dietary supplementation of Bifidobacterium cultures also suppressed the IQ-induced mammary carcinogenesis to 50% and liver carcinogenesis to 27% of those observed in animals fed the control diet, but the differences did not reach a statistical significance at P < 0.05; however, the mammary tumor multiplicity (tumors/animal) was significantly (P < 0.05) inhibited in female rats fed the diet containing Bifidobacterium cultures. These findings suggest that Bifidobacterium supplements in the diet inhibit IQ-induced colon and liver tumors and to a lesser extent mammary tumors in F344 rats.
Revised Airlie House consensus guidelines for design and implementation of ALS clinical trials (2019)

The revised Airlie House ALS Clinical Trials Consensus Guidelines should serve to improve clinical trial design and accelerate the development of effective treatments for patients with ALS.
Atrial Natriuretic Hormone, Vessel Dilator, Long-Acting Natriuretic Hormone, and Kaliuretic Hormone Decrease the Circulating Concentrations of Total and Free T4 and Free T3 with Reciprocal Increase in TSH (2001)

The present investigation was designed to determine whether atrial natriuretic peptides (ANPs) consisting of amino acids 1-30 [i.e. long-acting natriuretic hormone (LANH)], 31-67 (vessel dilator), 79-98 (kaliuretic hormone), and 99-126 (atrial natriuretic hormone [ANH]) of the 126-amino acid ANH prohormone decrease the circulating concentrations of total and free T4 and/or free T3 in healthy humans (n = 30). Vessel dilator, kaliuretic hormone, LANH, and ANH decreased the circulating concentrations of total T4 by 61%, 58%, 47%, and 55% and of free T4 by 60%, 67%, 79%, and 79%, whereas free T3 decreased 72%, 67%, 71%, and 67% (P < 0.05 for each), respectively, when infused at 100 ng/kg BW x min for 60 min. Vessel dilator, kaliuretic hormone, LANH, and ANH simultaneously increased circulating TSH concentrations 4- to 12.5-fold (P < 0.004). The decreases in T4 and T3 with reciprocal increases in TSH lasted 2-3 h after cessation of the respective ANP infusions. The reciprocal increase in TSH with the decreases in T4 and T3 suggests that their modulation of T4 and T3 concentrations occurs in the thyroid rather than in the pituitary or hypothalamus, because TSH would be decreased in the circulation if their inhibitory effects were in either the hypothalamus or pituitary.
Kronecker-product gain-shape vector quantization for multispectral and hyperspectral image coding (1998)

This paper proposes a new vector quantization based (VQ-based) technique for very low bit rate encoding of multispectral images. We rely on the assumption that the shape of a generic spatial block does not change significantly from band to band, as is the case for high spectral-resolution imagery. In such a hypothesis, it is possible to accurately quantize a three-dimensional (3-D) block-composed of homologous two-dimensional (2-D) blocks drawn from several bands-as the Kronecker-product of a spatial-shape codevector and a spectral-gain codevector, with significant computation saving with respect to straight VQ. An even higher complexity reduction is obtained by representing each 3-D block in its minimum-square-error Kronecker-product form and by quantizing the component shape and gain vectors. For the block sizes considered, this encoding strategy is over 100 times more computationally efficient than unconstrained VQ, and over ten times more computationally efficient than direct gain-shape VQ. The proposed technique is obviously suboptimal with respect to VQ, but the huge complexity reduction allows one to use much larger blocks than usual and to better exploit both the statistical and psychovisual redundancy of the image. Numerical experiments show fully satisfactory results whenever the shape-invariance hypothesis turns out to be accurate enough, as in the case of hyperspectral images. In particular, for a given level of complexity and image quality, the compression ratio is up to five times larger than that provided by ordinary VQ, and also larger than that provided by other techniques specifically designed for multispectral image coding.
Inactivation of the ATM Gene in T-Cell Prolymphocytic Leukemias (1998)

T-cell prolymphocytic leukemia (T-PLL) is a rare form of mature leukemia that occurs both in adults as a sporadic disease and in younger patients suffering an hereditary condition, ataxia telangiectasia (AT). The ATM gene, located in the 11q22-23 chromosomal region, is consistently mutated in AT patients. The strong predisposition of AT patients to develop T-PLL and the high frequency of T-cell leukemias/lymphomas observed in atm-deficient mice, together with the known functions of the ATM protein, led us to evaluate the ATM gene as a potential tumor suppressor gene involved in T-PLL. Paired leukemic and nonleukemic cells were obtained from a series of 15 patients suffering sporadic T-PLLs, allowing loss of heterozygosity (LOH) analysis. LOH of the 11q22-23 region was detected in 10 of these 15 cases (67%). The minimal deleted region was defined as an approximately 2.5 Mb interval that contained the ATMgene. No ATM rearrangement or biallelic deletion was detected by Southern blotting in the T-PLL series. However, in five T-PLLs with LOH of the 11q22-23 region, Western blot analysis showed either undetectable (3 cases) or decreased levels (1 case) of ATM protein, whereas ATM was present at high levels in cases without LOH. The protein truncation test (PTT) was then used to search for mutations in the ATM gene. Four mutations (1 nonsense, 2 aberrant splicings, and 1 missense) were detected in patients with LOH and none in patients without LOH of the region. The acquired character of these ATM mutations was demonstrated in three patients. Altogether, allelicATM inactivations by large deletions or mutations were found in approximately two thirds of T-PLL. ATM is thus a tumor suppressor gene whose inactivation is a key event in the development of T-cell prolymphocytic leukemias.
Dental arch analysis: arch form A review of the literature (1981)

The literature of dental arch analysis is reviewed outlining the methods that have been used to evaluate dental arch form. The theory, practical applications and problems of these methods are described.
Histone deacetylase 3 regulates the inflammatory gene expression programme of rheumatoid arthritis fibroblast-like synoviocytes (2016)

Inhibition of HDAC3 in RA FLS largely recapitulates the effects of pan-HDACi in suppressing inflammatory gene expression, including type I IFN production in RA FLS. Our results identify HDAC3 as a potential therapeutic target in the treatment of RA and type I IFN-driven autoimmune diseases.
Dico: Um Modelo Conceitual de Recursos de Busca Avançada para Pesquisa Exploratoria na Web (2014)

Com a abundância de informacao disponivel na Web e a necessidade de filtra-la em quantidade compativel com a atencao limitada do ser humano, recursos de busca avancada tornam-se uma opcao para essa tarefa. Entretanto, sua utilizacao e baixa por nao ser contextualizada e intuitiva. Este trabalho investiga aspectos de Information Seeking e Pesquisa Exploratoria para fundamentar um modelo conceitual para ferramentas que permitam ao usuario expressar melhor suas consultas de forma incremental com recursos de busca avancada. O modelo sera avaliado por especialistas e posteriormente instanciado em uma ferramenta de Pesquisa Exploratoria que sera avaliada empiricamente por usuarios.
Post-transcriptional Regulation of α-Synuclein Expression by mir-7 and mir-153 (2010)

Genetic and biochemical studies have established a central role for alpha-synuclein accumulation in the pathogenesis of Parkinson disease. Here, two microRNAs, namely mir-7 and mir-153, have been identified to regulate alpha-synuclein levels post-transcriptionally. These microRNAs bind specifically to the 3'-untranslated region of alpha-synuclein and down-regulate its mRNA and protein levels, with their effect being additive. They are expressed predominantly in the brain with a pattern that mirrors synuclein expression in different tissues as well as during neuronal development, indicating that they play a tuning role in the amount of alpha-synuclein produced. Overexpression of mir-7 and mir-153 significantly reduces endogenous alpha-synuclein levels, whereas inhibition of mir-7 and mir-153 enhances translation of a luciferase construct bearing the alpha-synuclein 3'-untranslated region in primary neurons. These findings reveal a significant additional mechanism by which alpha-synuclein is regulated and point toward new therapeutic regimes for lowering endogenous alpha-synuclein levels in patients with familial or sporadic Parkinson disease.