Relevant bibliographies by topics / Rlnn1

Academic literature on the topic 'Rlnn1'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "Rlnn1"

Williams, K., S. Taylor, P. Bogacki, M. Pallotta, H. Bariana, and H. Wallwork. "Mapping of the root lesion nematode (Pratylenchus neglectus) resistance gene Rlnn1 in wheat." Theoretical and Applied Genetics 104, no. 5 (April 2002): 874–79. http://dx.doi.org/10.1007/s00122-001-0839-3.

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Marshall, Sarah A., Jonathan T. McGuane, Yu May Soh, Helen M. Gehring, Emma Simpson, and Laura J. Parry. "Abnormal extracellular matrix remodelling in the cervix of pregnant relaxin-deficient mice is not associated with reduced matrix metalloproteinase expression or activity." Reproduction, Fertility and Development 30, no. 9 (2018): 1214. http://dx.doi.org/10.1071/rd17544.

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Relaxin regulates cervical extracellular matrix (ECM) remodelling during pregnancy by modifying collagen and other ECM molecules by unknown mechanisms. We hypothesised that abnormal collagen remodelling in the cervix of pregnant relaxin-deficient (Rln1−/−) mice is due to excessive collagen (Col1a1 and Col3a1) and decreased matrix metalloproteinases (Mmp2, Mmp9, Mmp13 and Mmp7) and oestrogen receptors (Esr1 and Esr2). Quantitative polymerase chain reaction, gelatinase zymography, MMP activity assays and histological staining evaluated changes in ECM in pregnant wildtype (Rln1+/+) and Rln1−/− mice. Cervical Col1a1, Col3a1 and total collagen increased in Rln1−/− mice and were higher at term compared with Rln1+/+ mice. This was not correlated with a decrease in gelatinase (Mmp2, Mmp9) expression or activity, Mmp7 or Mmp13 expression, which were all significantly higher in Rln1−/− mice. In late pregnancy, circulating MMP2 and MMP9 were unchanged. Esr1 expression was highest in Rln1+/+ and Rln1−/− mice in late pregnancy, coinciding with a decrease in Esr2 in Rln1+/+ but not Rln1−/− mice. The relaxin receptor (Rxfp1) decreased slightly in late-pregnant Rln1+/+ mice, but was significantly higher in Rln1−/− mice. In summary, relaxin deficiency results in increased cervical collagen in late pregnancy, which is not explained by a reduction in Mmp expression or activity or decreased Rxfp1. However, an imbalance between Esr1 and Esr2 may be involved.

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Brandsen, Sarah, Kevin D. Stubbs, and Henry D. Pfister. "Reinforcement Learning with Neural Networks for Quantum Multiple Hypothesis Testing." Quantum 6 (January 26, 2022): 633. http://dx.doi.org/10.22331/q-2022-01-26-633.

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Reinforcement learning with neural networks (RLNN) has recently demonstrated great promise for many problems, including some problems in quantum information theory. In this work, we apply RLNN to quantum hypothesis testing and determine the optimal measurement strategy for distinguishing between multiple quantum states {ρj} while minimizing the error probability. In the case where the candidate states correspond to a quantum system with many qubit subsystems, implementing the optimal measurement on the entire system is experimentally infeasible. We use RLNN to find locally-adaptive measurement strategies that are experimentally feasible, where only one quantum subsystem is measured in each round. We provide numerical results which demonstrate that RLNN successfully finds the optimal local approach, even for candidate states up to 20 subsystems. We additionally demonstrate that the RLNN strategy meets or exceeds the success probability for a modified locally greedy approach in each random trial.While the use of RLNN is highly successful for designing adaptive local measurement strategies, in general a significant gap can exist between the success probability of the optimal locally-adaptive measurement strategy and the optimal collective measurement. We build on previous work to provide a set of necessary and sufficient conditions for collective protocols to strictly outperform locally adaptive protocols. We also provide a new example which, to our knowledge, is the simplest known state set exhibiting a significant gap between local and collective protocols. This result raises interesting new questions about the gap between theoretically optimal measurement strategies and practically implementable measurement strategies.

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Feng, Shu, Natalia V. Bogatcheva, Aparna A. Kamat, Anne Truong, and Alexander I. Agoulnik. "Endocrine Effects of Relaxin Overexpression in Mice." Endocrinology 147, no. 1 (January 1, 2006): 407–14. http://dx.doi.org/10.1210/en.2005-0626.

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Relaxin is a small peptide hormone with a variety of biological functions. To investigate the systemic endocrine effects of relaxin, we produced mice with transgenic overexpression of the Rln1 gene, Tg(Rln1), driven by rat insulin 2 promoter. The expression of relaxin was detected in the pancreas of the transgenic animals. An analysis of the sera from the transgenic animals revealed at least 20-fold elevation of the level of bioactive relaxin. Transgenic animals had normal viability and fertility in both sexes. Transgenic overexpression of Rln1 did not rescue the undescended testis phenotype in Insl3-deficient males, suggesting that in vivo relaxin does not interact with the insulin-like 3 factor receptor, leucine-rich repeats-containing G protein-coupled receptor 8, Lgr8. Phenotypically, the excess of relaxin resulted in hypertrophic nipple development in virgin female mice. Deletion of the relaxin receptor, leucine-rich repeats-containing G protein-coupled receptor 7, Lgr7, in Tg(Rln1) animals abrogated the development of enlarged nipples in females, indicating that relaxin exerts its effect through Lgr7 alone. The levels of previously defined targets of relaxin signaling, such as matrix metalloproteinases 2 and 9, vascular endothelial growth factor, or nitric oxide, were similar in the sera of the transgenic and wild-type mice. However, the total plasma protein concentration in male Tg(Rln1) mice was lower than that in control animals. The livers of male Tg(Rln1) mice exhibited significantly higher hydroxyproline content, indicative of increased collagen deposition. Our results indicate that relaxin overexpression causes gender-specific changes in liver collagen metabolism.

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Quang Huy, Đặng, Nguyen Minh Ngoc, and Le Ngoc Thanh. "RỐI LOẠN NHỊP NHĨ Ở BỆNH NHÂN THÔNG LIÊN NHĨ: TỈ LỆ MẮC BỆNH, DIỄN BIẾN, TIÊN LƯỢNG VÀ CHỈ ĐỊNH ĐIỀU TRỊ." Tạp chí Phẫu thuật và Tim mạch và Lồng ngực Việt Nam 27 (October 26, 2020): 37–48. http://dx.doi.org/10.47972/vjcts.27.2019.147.

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RLNN trong bệnh TLN bao gồm: rung nhĩ, cuồng nhĩ và nhịp nhanh nhĩ. Tỉ lệ mắc bệnh tăng theo tuổi, sự khác biệt có ý nghĩa thống kê ở độ tuổi 40. Đường kính nhĩ trái, mức độ hở van hai lá và mức độ hở van ba lá là những yếu tố tiên lượng của RLNN. Mặc dù RLNN giảm đi sau khi đóng TLN bằng can thiệp hoặc phẫu thuật, có thể xuất hiện rối loạn nhịp mới với thời gian theo dõi lâu dài.Phẫu thuật Maze với mục đích điều trị hoặc dự phòng rối loạn nhịp giúp làm giảm nguy cơ nhồi máu não và biến chứng chảy máu do thuốc chống đông. Các bằng chứng khoa học cho thấy RLNN nên được chẩn đoán xác định trước mổ. Phẫu thuật Maze nên được kết hợp với đóng TLN đem lại hiệu quả điều trị toàn diện cho bệnh nhân.

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Huy, Đặng Quang, Nguyen Minh Ngoc, and Le Ngoc Thanh. "RỐI LOẠN NHỊP NHĨ Ở BỆNH NHÂN THÔNG LIÊN NHĨ: TỈ LỆ MẮC BỆNH, DIỄN BIẾN, TIÊN LƯỢNG VÀ CHỈ ĐỊNH ĐIỀU TRỊ." Tạp chí Phẫu thuật Tim mạch và Lồng ngực Việt Nam 27 (November 3, 2020): 37–48. http://dx.doi.org/10.47972/vjcts.v27i.147.

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Yamasato, Kelly, Pai-Jong Stacy Tsai, James Davis, Sandra Y. Yamamoto, and Gillian D. Bryant-Greenwood. "Human relaxins (RLNH1, RLNH2), their receptor (RXFP1) and fetoplacental growth." Reproduction 154, no. 1 (July 2017): 67–77. http://dx.doi.org/10.1530/rep-17-0039.

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Relaxin, a systemic and placental hormone, has potential roles in fetoplacental growth. Human placenta expresses two RLN genes, RLNH1 and RLNH2. Maternal obesity is common and is associated with abnormal fetal growth. Our aims were to relate systemic and cord blood RLNH2, placental RLNs and their receptor (RXFP1) with fetoplacental growth in context of maternal body mass index, and associations with insulin-like growth factor 2 (IGF2) and vascular endothelial growth factor A (VEGFA) in the same placentas. Systemic, cord blood and placental samples were collected prior to term labor, divided by prepregnancy body mass index: underweight/normal (N = 25) and overweight/obese (N = 44). Blood RLNH2 was measured by ELISA; placental RLNH2, RLNH1, RXFP1, IGF2 and VEGFA were measured by quantitative immunohistochemistry and mRNAs were measured by quantitative reverse transcription PCR. Birthweight increased with systemic RLNH2 only in underweight/normal women (P = 0.036). Syncytiotrophoblast RLNH2 was increased in overweight/obese patients (P = 0.017) and was associated with placental weight in all subjects (P = 0.038). RLNH1 had no associations with birthweight or placental weight, but was associated with increased trophoblast and endothelial IGF2 and VEGFA, due to female fetal sex. Thus, while systemic RLNH2 may be involved in birthweight regulation in underweight/normal women, placental RLNH2 in all subjects may be involved in placental weight. A strong association of trophoblast IGF2 with birthweight and placental weight in overweight/obese women suggests its importance. However, an association of only RLNH1 with placental IGF2 and VEGFA was dependent upon female fetal sex. These results suggest that both systemic and placental RLNs may be associated with fetoplacental growth.

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Kamat, Aparna A., Shu Feng, Natalia V. Bogatcheva, Anne Truong, Colin E. Bishop, and Alexander I. Agoulnik. "Genetic Targeting of Relaxin and Insulin-Like Factor 3 Receptors in Mice." Endocrinology 145, no. 10 (October 1, 2004): 4712–20. http://dx.doi.org/10.1210/en.2004-0515.

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Abstract Relaxin (RLN) is a small peptide hormone that affects a variety of biological processes. Rln1 knockout mice exhibit abnormal nipple development, prolonged parturition, agerelated pulmonary fibrosis, and abnormalities in the testes and prostate. We describe here RLN receptor Lgr7-deficient mice. Mutant females have grossly underdeveloped nipples and are unable to feed their progeny. Some Lgr7−/− females were unable to deliver their pups. Histological analysis of Lgr7 mutant lung tissues demonstrates increased collagen accumulation and fibrosis surrounding the bronchioles and the vascular bundles, absent in wild-type animals. However, Lgr7-deficient males do not exhibit abnormalities in the testes or prostate as seen in Rln1 knockout mice. Lgr7-deficient females with additional deletion of Lgr8 (Great), another putative receptor for RLN, are fertile and have normal-sized litters. Double mutant males have normal-sized prostate and testes, suggesting that Lgr8 does not account for differences in Rln1−/− and Lgr7−/− phenotypes. Transgenic overexpression of Insl3, the cognate ligand for Lgr8, does not rescue the mutant phenotype of Lgr7-deficient female mice indicating nonoverlapping functions of the two receptors. Our data indicate that neither Insl3 nor Lgr8 contribute to the RLN signaling pathway. We conclude that the Insl3/Lgr8 and Rln1/Lgr7 actions do not overlap in vivo.

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Xu, Qi, Edna D. Lekgabe, Xiao-Ming Gao, Ziqiu Ming, Geoffrey W. Tregear, Anthony M. Dart, Ross A. D. Bathgate, Chrishan S. Samuel, and Xiao-Jun Du. "Endogenous Relaxin Does Not Affect Chronic Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis." Endocrinology 149, no. 2 (November 8, 2007): 476–82. http://dx.doi.org/10.1210/en.2007-1220.

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The effect of endogenous relaxin on the development of cardiac hypertrophy, dysfunction, and fibrosis remains completely unknown. We addressed this question by subjecting relaxin-1 deficient (Rln1−/−) and littermate control (Rln1+/+) mice of both genders to chronic transverse aortic constriction (TAC). The extent of left ventricular (LV) remodeling and dysfunction were studied by serial echocardiography over an 8-wk period and by micromanometry. The degree of hypertrophy was estimated by LV weight, cardiomyocyte size, and expression of relevant genes. Cardiac fibrosis was determined by hydroxyproline assay and quantitative histology. Expression of endogenous relaxin during the course of TAC was also examined. In response to an 8-wk period of pressure overload, TAC mice of both genotypes developed significant LV hypertrophy, fibrosis, hypertrophy related gene profile, and signs indicating congestive heart failure when compared with respective sham controls. The severity of these alterations was not statistically different between the two genotypes of either gender. Relaxin mRNA expression was up-regulated, whereas that of its receptor was unchanged in the hypertrophic myocardium of wild-type mice. Collectively, the extent of pressure overload-induced LV hypertrophy, fibrosis, and dysfunction were comparable between Rln1+/+ and Rln1−/− mice. Thus, although up-regulated in its expression, endogenous relaxin had no significant effect on the progression of cardiac maladaptation and dysfunction in the setting of chronic pressure overload.

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Bennasar García, Miguel Israel, Vilma Del Valle Lanza Castillo, and Rainier Vicente Sánchez Camacho. "Formación docente universitaria, desde una mirada diversa y crítica de sus actores." Educación Superior, no. 30 (December 4, 2020): 11–28. http://dx.doi.org/10.56918/es.2020.i30.pp11-28.

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En el presente artículo se presentan los resultados del estudio sobre la formación docente universitaria, desde una perspectiva crítica de sus actores, cuyo objetivo fue comparar los programas de formación docente en el Recinto Luis Napoleón Núñez Molina (RLNNM), de República Dominicana y a la Universidad Pedagógica Experimental Libertador- Instituto Pedagógico de Maturín (UPEL-IPM), Venezuela. Su pertinencia e importancia se justifica, porque son los protagonistas quienes precisan las evidencias a partir de las cuales se basan los resultados. La metodología empleada fue la fenomenología, para ello se eligieron al azar 5 docentes de manera intencional, 3 del RLNNM, y 2 de la UPEL-IPM, a quienes se les aplicó un cuestionario indagatorio sobre el proceso de formación. Los principales resultados fueron: la mayoría opina que los programas, en ambas instituciones, es adecuado; existe una marcada vinculación, entre los programas de formación docente, y el entorno social. La calidad de los programas de formación, en las dos instituciones, están en una relación estrecha con los aprendizajes de los estudiantes; los discursos evidencian el predominio de una práctica pedagógica que enfatiza los resultados, en lugar de los procesos de formación y adquisición de conocimientos.

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Dissertations / Theses on the topic "Rlnn1"

Jayatilake, Dimanthi Vihanga. "Fine mapping of nematode resistance genes Rlnn1 and Cre8 in wheat (Triticum aestivum)." Thesis, 2014. http://hdl.handle.net/2440/97789.

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The root lesion nematode Pratylenchus neglectus and the cereal cyst nematode Heterodera avenae cause significant yield damage to wheat (Triticum aestivum L.) and crops that are grown in rotation with wheat. The focus of this thesis is on two loci in wheat, Rlnn1and Cre8, which confer resistance against P. neglectus and H. avenae, respectively, with an overall scientific goal of characterizing these two resistance loci as an initiative towards isolation of the causal gene(s) and identification of diagnostic molecular markers for the use in marker-assisted selection in wheat breeding programmes. The thesis presents improvements to an existing Excalibur/Kukri linkage map of chromosome 7A by adding Lr20 (a gene for resistance against leaf rust caused by Puccinia triticina), Sr15 (a gene for resistance against stem rust caused by P. graminis), Psy-A1 (a phytoene synthase gene), Cat3-A1 (a catalase gene) and 59 new molecular markers. The genomic location of the Rlnn1 quantitative trait locus (QTL) was confirmed as the distal end of long arm of chromosome 7A (7AL). It coincides with the position of Lr20/Sr15, Psy-A1, Cat3-A1 and 34 molecular markers. Based on the findings that 1) some markers that collocate with the resistance genes Lr20/Sr15 and Rlnn1 are widely separated in mapping populations that do not segregate for these genes; 2) when anchored to a chromosome 7A syntenic build, these markers spanned a 0.9-Mb region; and 3) no recombinants were found in a large population of recombinant inbred lines, it is suggested that the clustering of molecular markers/genes/QTL at the distal end of 7AL is due to suppressed recombination. The suppressed recombination in Excalibur may be a result of a translocation. This suggestion is based on 1) phylogenetic analysis of Psy-A1 alleles; 2) marker amplification patterns that suggested that sequences at the distal end of 7AL in Excalibur are very different from those in Kukri and Chinese Spring; 3) amplicons observed for a normally 7B-specific marker that collocates with Rlnn1 on 7AL, and 4) FISH images that revealed an unknown putative translocation in Excalibur that is absent in Kukri. It seems likely that the Rlnn1-containing segment of 7AL may have been translocated from a 7B-like chromosome arm with an unknown ancestry. Such a translocation could have pre-dated hexaploidisation and occurred in a tetraploid or diploid ancestor. The thesis also presents a high-resolution genetic linkage map for a Trident/Molineux population. This map was used to confirm the locations of three previously reported QTL for H. avenae, including the Cre8 locus mapped as a large-effect QTL at the distal end of the long arm of chromosome 6B (6BL), with an estimated position 0.9 cM from the closest markers. A cross was designed and made to develop a population for future use in fine mapping. With these materials and with the closely-linked molecular markers developed here, Cre8 seems amenable to positional cloning. In the research conducted for this thesis, the Rlnn1 and Cre8 resistance loci were mapped at the distal ends of 7AL and 6BL, respectively and diagnostic markers were identified for the use in marker-assisted selection. A suppressed recombination at the end of 7AL impedes the prospects of cloning Rlnn1, while the research reported here have identified suitable markers and genetic resources for cloning the Cre8 gene with a forward genetics approach.
Thesis (Ph.D.) -- University of Adelaide, School of Agriculture, Food and Wine, 2014

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Book chapters on the topic "Rlnn1"

Waldvogel, Herman Hans. "Probenecid rlNN, BAN, USAN." In Analgetika Antinozizeptiva Adjuvanzien, 668–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56710-0_97.

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Conference papers on the topic "Rlnn1"

Das, Milton Kumar, Parthasarathi Bera, Partha Pratim Sarkar, and Krishnendu Chakrabarty. "MOGOA Based RLNN Controller for LFC of Three Area Deregulated HDG Power System." In 2021 IEEE 4th International Conference on Computing, Power and Communication Technologies (GUCON). IEEE, 2021. http://dx.doi.org/10.1109/gucon50781.2021.9573671.

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Das, Milton Kumar, Parthasarathi Bera, Partha Sarkar, and Krishnendu Chakrabarty. "PI-RLNN Controller for LFC of Hybrid Deregulated Power System Based on SPOA." In 2021 IEEE 18th India Council International Conference (INDICON). IEEE, 2021. http://dx.doi.org/10.1109/indicon52576.2021.9691741.

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Huang, Xianwei, Fazel Naghdy, Haiping Du, Golshah Naghdy, and Catherine Todd. "Reinforcement learning neural network (RLNN) based adaptive control of fine hand motion rehabilitation robot." In 2015 IEEE Conference on Control Applications (CCA). IEEE, 2015. http://dx.doi.org/10.1109/cca.2015.7320733.

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Academic literature on the topic 'Rlnn1'

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Journal articles on the topic "Rlnn1"

Dissertations / Theses on the topic "Rlnn1"

Book chapters on the topic "Rlnn1"

Conference papers on the topic "Rlnn1"