Relevant bibliographies by topics / M-NV RNA

Academic literature on the topic 'M-NV RNA'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "M-NV RNA"

1

Zeitler, Corinne E., Mary K. Estes, and B. V. Venkataram Prasad. "X-Ray Crystallographic Structure of the Norwalk Virus Protease at 1.5-Å Resolution." Journal of Virology 80, no. 10 (May 15, 2006): 5050–58. http://dx.doi.org/10.1128/jvi.80.10.5050-5058.2006.

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ABSTRACT Norwalk virus (NV), a member of the Caliciviridae family, is the major cause of acute, epidemic, viral gastroenteritis. The NV genome is a positive sense, single-stranded RNA that encodes three open reading frames (ORFs). The first ORF produces a polyprotein that is processed by the viral cysteine protease into six nonstructural proteins. We have determined the structure of the NV protease to 1.5 and 2.2 Å from crystals grown in the absence or presence, respectively, of the protease inhibitor AEBSF [4-(2-aminoethyl)-benzenesulfonyl fluoride]. The protease, which crystallizes as a stable dimer, exhibits a two-domain structure similar to those of other viral cysteine proteases with a catalytic triad composed of His 30, Glu 54, and Cys 139. The native structure of the protease reveals strong hydrogen bond interactions between His 30 and Glu 54, in the favorable syn configuration, indicating a role of Glu 54 during proteolysis. Mutation of this residue to Ala abolished the protease activity, in a fluorogenic peptide substrate assay, further substantiating the role of Glu 54 during proteolysis. These observations contrast with the suggestion, from a previous study of another norovirus protease, that this residue may not have a prominent role in proteolysis (K. Nakamura, Y. Someya, T. Kumasaka, G. Ueno, M. Yamamoto, T. Sato, N. Takeda, T. Miyamura, and N. Tanaka, J. Virol. 79:13685-13693, 2005). In the structure from crystals grown in the presence of AEBSF, Glu 54 undergoes a conformational change leading to disruption of the hydrogen bond interactions with His 30. Since AEBSF was not apparent in the electron density map, it is possible that these conformational changes are due to subtle changes in pH caused by its addition during crystallization.
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Vaughan, Kathleen, Lena Diaw, Wang Zhengyuan, Chia-Hao Liu, Marci Barr, Deepika Darbari, Kimberley A. Woodhouse, et al. "Comparative Clinical and Gene Expression Analysis of Sickle Cell Anemia and Hemoglobin SC Disease." Blood 124, no. 21 (December 6, 2014): 4059. http://dx.doi.org/10.1182/blood.v124.21.4059.4059.

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Abstract Homozygous hemoglobin (Hb) SS is the most common form of sickle cell disease (SCD), while HbSC represents a third of patients and has been less studied. Despite similarities in pathogenesis, there are significant clinical differences between genotypes. To elucidate any molecular differences, we compared gene expression profiles for HbSS and HbSC using microarrays. The Paxgene (PAX) blood RNA system was used to extract RNA from whole blood, which was then globin reduced. We also isolated peripheral blood mononuclear cell (PBMC) RNA to assess transcript patterns in cell populations lacking erythrocytes and granulocytes. To demonstrate clinical differences, we compared HbSS and HbSC subjects from the Bethesda Sickle Cell Cohort Study (ClinicalTrials.gov identifier: NCT00011648). Hematologic parameters were significantly different, with HbSS having higher leukocytes, lower hematocrit, and higher platelets, reticulocytes and fetal hemoglobin. Significant differences were also observed for transaminases, LDH, bilirubin, creatinine kinase, ESR and ferritin. On the other hand, HbSC patients had higher diastolic blood pressure (P=0.0009), higher SpO2 (P<0.0001), less frequent leg ulcers (Odds Ratio 2.90, 95% CI 1.15-7.35, P=0.008) and more prevalent tricuspid jet velocity above 2.9 m/s (Odds Ratio 5.07, 95% CI 1.75-14.71, P=0.0006). These associations led us to hypothesize that these are distinct forms of SCD whose biological differences might be identified with gene expression profiling. RNA was isolated from ten subjects each with HbSS, HbSC or normal volunteers (NVs) using whole blood, PBMCs and Ficoll purified PBMCs (devoid of platelets). Microarray profiling showed that SCD subjects, regardless of genotype, have significant enrichment in glucose metabolism, cellular respiration, and mitochondrial energy generation pathways compared to NVs. Next, we used hierarchical clustering to distinguish SCD expression profiles from NVs, but we were unable to further distinguish HbSS from HbSC samples using this method. We attribute the above differences between SCD and NV samples to the erythroid cell RNA expression in whole blood. There is significant overlap between the 100 most abundantly expressed transcripts and a published signature in purified reticulocytes. However, no significant differences were observed when comparing SCD and NV samples using PBMCs and Ficoll purified PBMCs. We only observed expression differences comparing HbSS and HbSC at the gene level for ATP1B1 (1.3 fold change, P=1.04E-4), WSB1 (1.3 FC, P=3.64E-3) and IL6ST (1.3 FC, P=1.13E-4), despite the evident hematological and clinical differences. ATP1B1 encodes a small ATPase for Na+/K+ transport and has hardly been explored in hemoglobinopathies. Furthermore, ATP1B1 was highly up-regulated in HbSS patients (against controls) but showed less change in HbSC patients. Our results provide an important first step towards elucidating the molecular pathophysiology that might explain the differences in clinical symptoms and survival between these 2 common forms of SCD. Disclosures No relevant conflicts of interest to declare.
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Talarico, Christine L., Sterling Wu, Ojesh R. Upadhyay, Marty St Clair, Veerle Van Eygen, Krischan J. Hudson, Sandy Griffith, et al. "1021. HIV-1 RNA Blips and Low-Level Replication During Phase III/IIIb Cabotegravir + Rilpivirine Long-Acting Studies Are Similar to Oral 3-Drug Therapy and Not Associated with Week 48 Virologic Outcome." Open Forum Infectious Diseases 7, Supplement_1 (October 1, 2020): S540—S541. http://dx.doi.org/10.1093/ofid/ofaa439.1207.

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Abstract Background Phase III/IIIb studies demonstrated cabotegravir (CAB) + rilpivirine (RPV) long-acting (LA) dosed every 4 weeks (Q4W) was noninferior to current antiviral regimen (CAR) (FLAIR and ATLAS) and CAB + RPV LA dosed every 8 weeks (Q8W) was noninferior to Q4W (ATLAS-2M) through Week 48 (W48). HIV-1 ribonucleic acid (RNA) blips (viral load [VL] ≥50 to &lt; 200 c/mL) are common during antiretroviral therapy (ART) and generally not associated with subsequent virologic failure (2 consecutive HIV-1 RNA ≥200 c/mL). We compared the frequency of HIV-1 RNA blips and low-level qualitative and quantitative HIV-1 RNA replication among participants treated with CAB+RPV LA and oral CAR and assessed impact on virologic outcome. Methods Plasma samples collected at study visits were analyzed for HIV-1 RNA viral load using the Abbott RealTime HIV-1 assay and qualitative target detected (TD) or target not detected (TND) outcomes were provided for HIV-1 RNA &lt; 40 c/mL. The HIV-1 SuperLow assay (bioMONTR Labs) was used to measure HIV-1 RNA &lt; 2 c/mL at Baseline and W48. Results The proportion of participants with HIV-1 RNA blips was similar overall between Q4W CAB + RPV LA and CAR arms in FLAIR (38/283 [13%] vs 39/283 [14%]) and ATLAS (17/308 [6%] vs 23/308 [7%]). Presence of HIV-1 RNA blips in either arm was not associated with virologic non-response at W48 (HIV-1 RNA ≥50 c/mL per US Food and Drug Administration Snapshot). In ATLAS-2M, HIV-1 RNA blips were observed in 32/523 (6%; Q4W) and 18/522 (3%; Q8W) of participants, with W48 virologic nonresponse in 2 Q4W and 0 Q8W participants. TD outcomes at individual study visits were comparable between study arms for the 3 studies. At W48, the proportion of participants with HIV-1 RNA &lt; 2 c/mL was similar to Baseline and similar between treatment groups in all studies. Conclusion The proportions of study participants with HIV-1 RNA blips, TD viral load results, and HIV-1 &lt; 2 c/mL were similar between the Q4W and Q8W CAB+RPV LA and the oral 3-drug CAR arms through W48 in phase III/IIIb studies. HIV-1 RNA blips did not predict virologic nonresponse (Snapshot analysis) at W48. Disclosures Christine L. Talarico, M.S, GlaxoSmithKline (Shareholder)ViiV Healthcare (Employee) Sterling Wu, PhD, GlaxoSmithKline (Employee, Shareholder) Marty St. Clair, GlaxoSmithKline (Shareholder)ViiV Healthcare (Employee) Veerle Van Eygen, MSc, Janssen Pharmaceutica NV (Employee) Krischan J. Hudson, PhD, MPH, GlaxoSmithKline (Shareholder)ViiV Healthcare (Employee) Sandy Griffith, PharmD, GlaxoSmithKline (Shareholder)ViiV Healthcare (Employee) Conn M. Harrington, BA, ViiV Healthcare (Employee) Jan van Lunzen, MD, PhD, GlaxoSmithKline (Shareholder)ViiV Healthcare (Employee) David Margolis, MD, MPH, GlaxoSmithKline (Shareholder)ViiV Healthcare (Employee) William Spreen, PharmD, ViiV Healthcare (Employee, Shareholder)
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Woods, D. M., M. J. Pitcairn, D. G. Luster, and W. L. Bruckart. "First Report of Musk Thistle Rust (Puccinia carduorum) in California and Nevada." Plant Disease 86, no. 7 (July 2002): 814. http://dx.doi.org/10.1094/pdis.2002.86.7.814b.

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Musk thistle, Carduus nutans L., is an introduced weed of pastures, rangelands, and natural areas in much of North America. Puccinia carduorum Jacky, an autoecious rust fungus from Turkey, has been evaluated for biological control of musk thistle since 1978, including a field study near Blacksburg, VA, from 1987 to 1990. After release of the fungus in Virginia, rusted musk thistle was found in eight eastern states by 1992, in Missouri by 1994 (1), and in Oklahoma by 1997 (2). A rust disease was discovered on musk thistle near Mt. Shasta, CA, on 22 September 1998, and near Mogul, NV, on 12 August 1999. The pathogen was identified as P. carduorum on the basis of pathogenicity on musk thistle and urediniospore morphology (ovate spores, 21 μm diameter, three germ pores equatorial in location, and echinulations over the upper two-thirds to three-quarters of urediniospores). Ribosomal RNA internal transcribed spacer DNA sequences (ITS1 and ITS2) were identical to those from the isolate obtained after the field release in Virginia, verifying that the California isolate is P. carduorum. The initial California infestation was observed on a few plants late in the season, and by September 2000, nearly 100% of plants were infected. The occurrence of P. carduorum in California is apparently the result of natural, unaided spread of the fungus on musk thistle from the East Coast of the United States. References: (1) A. B. A. M. Baudoin and W. L. Bruckart. Plant Dis. 80:1193, 1996. (2) L. J. Littlefield et al. Plant Dis. 82:832, 1998.
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Bag, S., J. Singh, R. M. Davis, W. Chounet, and H. R. Pappu. "Iris yellow spot virus in Onion in Nevada and Northern California." Plant Disease 93, no. 6 (June 2009): 674. http://dx.doi.org/10.1094/pdis-93-6-0674c.

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The disease caused by thrips-transmitted Iris yellow spot virus (IYSV; genus Tospovirus, family Bunyaviridae) has become a major constraint to bulb and seed onion crops in several parts of the country and the world (1,3). As part of an ongoing survey for IYSV incidence in onion in the western United States, commercial fields in Lyon County, Nevada and several commercial fields in the northern Californian counties of Colusa, San Benito, Sutter, and Yolo were surveyed during the summer of 2008. Symptomatic plants were found widespread in northern California, especially in seed-production fields. In Lyon County, NV, symptoms were observed only on volunteer onions in one commercial field. Symptoms on leaves and scapes included characteristic diamond-shaped lesions with or without green islands. Four samples from Nevada and fourteen from northern California were tested by double-antibody sandwich (DAS)-ELISA using a commercially available kit (Agdia Inc., Elkhart, IN). All tested samples were found positive in ELISA. IYSV infection was verified by reverse transcription (RT)-PCR. Total nucleic acids were prepared from symptomatic tissue, and primers specific to the small (S) RNA of IYSV were used to amplify an approximate 1.2-kb region of the S-RNA. This region included the complete nucleoprotein (N) gene (2). The amplicons from one sample each from Nevada and northern California were sequenced (GenBank Accession Nos. FJ713699 and FJ713700, respectively). Sequence analysis showed that the amplicons contained a single open reading frame of 822 bp, coding for a 273-amino acid N protein, and the gene shared 96 to 98% identity with known IYSV N gene sequences. To our knowledge, this is the first report of IYSV in onion in Nevada. In California, outbreaks of IYSV had been reported earlier in Imperial Valley and Antelope Valley in southern California (4), and the disease has been increasing in incidence in bulb and seed crops in northern California, as well. California and Nevada are major onion-producing states in the United States and regular surveys to determine the incidence and impact on yield are needed to develop an integrated disease management program. References: (1) D. H. Gent et al. Plant Dis. 90:1468, 2006. (2) H. R. Pappu et al. Arch. Virol. 151:1015, 2006. (3) H. R. Pappu and M. E. Matheron. Online publication. doi:10.1094/PHP-2008-0711-01-BR. Plant Health Progress, 2008. (4) G. J. Poole et al. Online publication. doi:10.1094/PHP-2007-0508-01-BR. Plant Health Progress, 2007.
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Houtman, M., X. Ge, A. Mcgovern, K. Klein, G. Orozco, M. Frank Bertoncelj, M. Marks, et al. "OP0016 IDENTIFICATION OF FUNCTIONAL VARIANTS IN THE RHEUMATOID ARTHRITIS ASSOCIATED JAZF1 LOCUS IN SYNOVIAL FIBROBLASTS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 9.1–9. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1400.

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Background:Over the past decade, genome wide association studies (GWAS) have identified the JAZF1 locus as a risk locus for several autoimmune diseases, including rheumatoid arthritis (RA)1. However, the exact causal variants in the JAZF1 locus and their underlying regulatory events contributing to RA are still not known. Here, we focus on the effect of these variants on gene expression in synovial fibroblasts (SF).Objectives:To characterize the functional consequences of RA-causal variants in the JAZF1 locus in SF.Methods:Genetic fine-mapping of RA loci was conducted by computing sets of credible variants driving GWAS signals. These credible variant sets were integrated with DNA architecture (ChIP-seq), 3D chromatin interactions (3C, HiC and capture HiC), DNA accessibility (ATAC-seq) and gene expression (RNA-seq and CAGE-seq) datasets to select putative RA-causal variants in SF. Selected variants in the JAZF1 locus were tested for regulatory function by luciferase reporter assays and electrophoretic mobility shift assays (EMSA) in the fibrosarcoma cell line HT1080. The JASPAR2020 database was used to identify putative transcription factors (TF) binding to the selected variants. The expression of HOTTIP was measured by quantitative PCR in hand SF (n=23). Genotyping was done by pyrosequencing.Results:Genetic fine mapping revealed 47 variants in the JAZF1 locus. Integration of these variants with the chromatin datasets prioritized rs2158624, rs57585717 and rs186735625 as the top candidates (posterior probability of causality >0.1) in the JAZF1 locus. We found that rs2158624 and rs186735625 are located in the vicinity of enhancer elements in SF as determined by ATAC-seq. In addition, the region of rs2158624 exhibited strong chromatin interactions with the genomic region of HOTTIP and HOXA13. Both these transcripts were previously shown to be specifically expressed in SF isolated from hands and feet2. Based on this, we selected rs2158624 as the most promising candidate in the JAZF1 locus. We found that the rs2158624-C allele (risk) is associated with lower expression of HOTTIP, but not HOXA13, in hand SF compared to the rs2158624-T allele (non-risk) (p=0.02). Luciferase assays in HT1080 cells demonstrated enhancer activity with both the rs2158624-C allele (p=0.006) and T allele (p=0.04), with no significant difference in enhancer activity between the rs2158624-C and T allele. EMSAs identified stronger specific binding of HT1080-cell nuclear extract for the rs2158624-T allele than for the C allele (risk). Based on the JASPAR2020 database, we identified NFAT5 as a potential TF that can bind to rs2158624 and may regulate the expression of HOTTIP.Conclusion:We were able to substantially narrow down the potential functional variants in the JAZF1 locus using our data integration approach and functional assays. We suggest that the risk allele of rs2158624 influences the binding of TFs controlling the expression of the long non-coding RNA HOTTIP in SF, which might confer specific risk to develop RA in hands.References:[1]Okada Y et al. Genetic of rheumatoid arthritis contributes to biology and drug discovery. Nature 2014;506:376.[2]Frank-Bertoncelj M et al. Epigenetically-driven anatomical diversity of synovial fibroblasts guides joint-specific fibroblast functions. Nat Commun 2017;8:14852.Disclosure of Interests:Miranda Houtman: None declared, Xiangyu Ge: None declared, Amanda McGovern: None declared, Kerstin Klein: None declared, Gisela Orozco: None declared, Mojca Frank Bertoncelj: None declared, Miriam Marks: None declared, Oliver Distler Speakers bureau: Bayer, Boehringer Ingelheim, iQone, Medscape, MSD, Novartis, Pfizer and Roche, Consultant of: Abbvie, Acceleron Pharma, Amgen, AnaMar, Arxx Therapeutics, Bayer, Baecon Discovery, Boehringer, CSL Behring, ChemomAb, Corbus Pharmaceuticals, Galapagos NV, GSK, Glenmark Pharmaceuticals, Horizon Pharmaceuticals, Inventiva, Italfarmaco, iQvia, Kymera, Lilly, Medac, Medscape, Mitsubishi Tanabe Pharma, MSD, Pfizer, Roche, Roivant Sciences, Sanofi and UCB, Grant/research support from: Kymera Therapeutics and Mitsubishi Tanabe, Paul Martin: None declared, Stephen Eyre: None declared, Caroline Ospelt: None declared
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Islabão, Gláucia Oliveira, Ledemar Carlos Vahl, Luís Carlos Timm, Donald Luiz Paul, and Aline Hernandez Kath. "Rice husk ash as corrective of soil acidity." Revista Brasileira de Ciência do Solo 38, no. 3 (June 2014): 934–41. http://dx.doi.org/10.1590/s0100-06832014000300025.

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Rice husk ash (RHA) is a by-product from the burning of rice husk that can have favorable effects on the soil in terms of acidity correction. The objectives of this study were to determine the effective calcium carbonate equivalent (ECC) of RHA under field conditions, and establish technical criteria as a basis for estimating the overall ECC of RHA. The 12 treatments of the experiment consisted of 10 RHA dosages (0, 10, 20, 30, 40, 60, 80, 100, 120, and 140 Mg ha-1) and two references, one of which was an absolute control (AC) and the other a plot limed and fertilized according to official recommendations (recommended fertilization - RF). The soil was sampled twice (15 and 210 days after incorporating RHA), in the layers 0.00-0.10 and 0.10-0.20 m, to determine the pH(H2O) and base saturation (V%). The ECC and neutralizing value (NV) of RHA were also determined. The results showed that RHA neutralizes soil acidity, in a faster reaction than conventional limestone, despite a low ECC (around 3 %).
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Jongmans, Marjolijn C. "Clonal Reversion in Genetic Syndromes: Gene Therapy at Its Best." Blood 126, no. 23 (December 3, 2015): SCI—42—SCI—42. http://dx.doi.org/10.1182/blood.v126.23.sci-42.sci-42.

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Abstract Many genetic syndromes are characterized by a wide spectrum of clinical severity. Even within one family clinical presentations can show extreme variation. Mosaic tissue distribution caused by spontaneous correction of a germline pathogenic allele is one of multiple explanations for variety in phenotypic expression of an inherited mutation. This phenomenon, called somatic reversion, is infrequently observed and can be easily overlooked. Reversion needs to be considered if a person presents with a milder than expected clinical course or with a mixture of phenotypically normal and abnormal cells.1 Mechanisms that may explain reversion include mitotic gene conversion, back mutation, intragenic mitotic recombination and the occurrence of compensatory mutations. A mosaic pattern of somatic reversion only becomes apparent if several criteria are met. The non-mutant cells need to have a selective growth advantage over surrounding mutant cells. Furthermore, to facilitate expansion of the revertant clone the affected genes need to be expressed in regenerating organ systems like skin and blood.1 The chance of spontaneous correction of a pathogenic allele is likely increased in diseases with an underlying mechanism resulting in genomic instability or high mutation rates, like Bloom syndrome and Fanconi anemia, which are both caused by gene defects in DNA repair pathways.2,3 In skin disorders an evolving mosaic revertant pattern is easily visible. Ichthyosis with confetti, caused by mutations in KRT10, is an example of a skin disorder displaying multiple events of reversion.4 In this condition, normal skin spots appear early in life and increase in number and size over time. Each normal spot results from a separate event of loss of heterozygosity on chromosome 17q, which harbors KRT10, via mitotic recombination. Also in the genetic skin fragility disorder epidermolysis bullosa revertant mosaicism has been described repeatedly.5,6 We have observed reversion, caused by mitotic recombination of mutant TE RC (telomerase RNA component) alleles in a family affected by dyskeratosis congenita (DC).7 DC is a multisystem disorder characterized amongst others by bone marrow failure and lung fibrosis. The observation of mosaic stretches of uniparental disomy (UPD) of chromosome 3q as an indication of revertant mosaicism encouraged us to develop a highly sensitive method for detecting genomic regions with low mosaic UPD in SNP array data. Indeed this tool supported us in identifying additional cases of DC and a mosaic reversion pattern in blood cells. Revertant mosaicism being a recurrent event in DC related conditions was recently confirmed by others.8 Awareness of revertant mosaicism is important for improving diagnostic testing. In DC for instance it is common practice that analysis of the DC genes is performed on DNA isolated from peripheral blood cells. In case no pathogenic mutation is found, an obvious conclusion can be that the phenotype in the family is caused by an aberration in an as yet to be identified DC gene. Based on our findings, we recommend sequence analysis on DNA extracted from other cells, such as skin fibroblasts, particularly in individuals without bone marrow failure. The observation of reversion in hematological conditions is also of importance for the development of future therapies: Isolation of autologous reverted stem cells can probably circumvent more toxic and harmful therapies, like allogeneic stem cell transplantation, in a subset of individuals. 1. Hirschhorn R. In vivo reversion to normal of inherited mutations in humans. J Med Genet 2003;40 (10):721-728. 2 Ellis NA, Ciocci S, German J. Back mutation can produce phenotype reversion in Bloom syndrome somatic cells. Hum Genet 2001;108 (2):167-173. 3 Waisfisz Q, Morgan NV, Savino M, et al. Spontaneous functional correction of homozygous fanconi anaemia alleles reveals novel mechanistic basis for reverse mosaicism. Nat Genet 1999;22 (4):379-383. 4 Choate KA, Lu Y, Zhou J, et al. Mitotic recombination in patients with ichthyosis causes reversion of dominant mutations in KRT10. Science 2010;330 (6000):94-97. 5 Jonkman MF, Scheffer H, Stulp R, et al. Revertant mosaicism in epidermolysis bullosa caused by mitotic gene conversion. Cell 1997;88 (4):543-51. 6 Kiritsi D, Garcia M, Brander R, et al. Mechanisms of natural gene therapy in dystrophic epidermolysis bullosa. J Invest Dermatol 2014;134 (8):2097-104. 7 Jongmans MC, Verwiel ET, Heijdra Y, et al. Revertant somatic mosaicism by mitotic recombination in dyskeratosis congenita. Am J Hum Genet 2012;90 (3):426-33. 8 Alder JK, Stanley SE, Wagner CL, et al. Exome Sequencing Identifies Mutant TINF2 in a Family With Pulmonary Fibrosis. Chest 2015;147 (5):1361-8. Disclosures No relevant conflicts of interest to declare.
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Aguiar, Eugenia Miranda. "ALTERA��ES GENOT�XICAS COMO BIOMARCADORES EM PEIXES DE UMA �REA PROTEGIDA DO SUL DO MARANH�O." Revista Brasileira de Engenharia de Pesca 11, no. 1 (October 8, 2018): 13. http://dx.doi.org/10.18817/repesca.v11i1.1485.

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Neste estudo, objetivou-se utilizar biomarcadores genot�xicos para avalia��o de impacto ambiental em peixes do Parque Nacional da Chapada das Mesas (PNCM). Exemplares de Leporinus fasciatus (piau) e Hypostomus pusarum (cascudo) foram coletados em duas cachoeiras do PNCM: Cachoeira S�o Rom�o e Prata. As esta��es foram georreferenciadas por GPS (Global Position System) e em cada regi�o foram registradas vari�veis abi�ticas: pH, temperatura, s�lidos totais dissolvidos (TDS), oxig�nio dissolvido (OD) e condutividade. Os dados biom�tricos foram medidos em campo. Para tanto, as l�minas com esfrega�os de sangue foram deixadas em temperatura ambiente por 2 horas para secagem e em seguida fixadas em etanol absoluto por 30 minutos. Depois de secas, as l�minas foram coradas em corante Giemsa. Para a quantifica��o dos eritr�citos, foram utilizadas 2000 c�lulas. Foram identificadas altera��es morfol�gicas nucleares (AMN) nas duas esp�cies amostradas para os dois pontos de coleta. Dentre as AMN encontradas destacam-se: nucl�os binucleados (NB), n�cleos vacuolizados (NV). Os micron�cleos (MN) tamb�m foram encontrados em ambas as esp�cies, por�m, em L. fasciatus a frequ�ncia de MN e AMN foram maiores em rela��o a Hypostomus sp. Provavelmente, o cascudo (H. pusarum) por ser considerado uma esp�cie bent�nica e resistente aos condi��es ambientais apresentou uma frequ�ncia menor de altera��es genot�xicas em rela��o ao L. fasciatus que � uma esp�cie que apresenta um h�bito migrat�rio e sens�vel as vari�veis ambientais. Al�m disso, a frequ�ncia de MN e AMN n�o foram significativas para indicativo de poss�veis impactos ambientais nas duas �reas amostradas. Os dados apresentados mostram que as metodologias baseadas em biomarcadores em esp�cies residentes podem ser utilizadas em futuros programas de biomonitoramento e gest�o do parque.
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Yu, X. L., X. Q. Liu, P. S. Wang, and Y. Z. Wang. "First Report of Cherry Stem Rot and Leaf Necrosis Disease Caused by Phytophthora nicotianae in Yantai, China." Plant Disease 99, no. 2 (February 2015): 284. http://dx.doi.org/10.1094/pdis-05-14-0489-pdn.

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Cherry (Cerasus avium (Linn.) Moench) is the third most economically important fruit in Yantai, Shandong Province, China. In August 2012, brown spots or necrosis on cherry seedling leaves, with an incidence of 8.2 to 34.3%, were observed in some fields of cherry seedlings in Yantai. Our survey indicated that the economic losses could reach up to 15.3% if disease conditions, such as a cool rainy summer season, were favorable. Conspicuous watery lesions on the stems turned to brown streaks; the leaves all wilted; and finally the plants collapsed. Diseased stem and leaf samples were surface-disinfected in 1% sodium hypochlorite for 1 min, rinsed three times in sterile water, which was absorbed with filter paper, and then transferred to 10% V8 juice agar medium containing 50 μg/ml ampicillin and 5 μg/ml carbendazim (1). The plates were incubated at 22°C in the dark for 5 days. The colonies consisted of white, loose, fluffy aerial mycelia. Eight isolates were obtained, and all were identified as Phytophthora nicotianae based on morphological characteristics and the sequence of the internal transcribed spacer (ITS) region of rDNA. The sporangia were ovoid/spherical, obturbinate with rounded bases and prominent papillae that were 37.5 to 62.5 × 30 to 50 μm (average 46.4 × 37.8 μm, n = 100) in size, with an average length-to-breadth ratio of 1.2. Chlamydospores were terminal, intercalary, and measured 19 to 42 μm (average 30.4 μm), which is typical of P. nicotianae (2). The genomic DNA of the eight isolates was extracted from mycelia. The ITS region of all eight isolates was amplified using primers ITS1 and ITS4, producing specific products that were directly sequenced. The sequence of a representative isolate P1401 (895 bp) was submitted to GenBank (Accession No. KJ754387). It was 100% similar to P. nicotianae strains NV-20T and TARI 22073 (KC768775 and GU111667). To confirm the pathogenicity, at least 10 cherry leaves and new stems were inoculated with mycelial plugs (5 × 5 mm) from each isolate. Necrosis of leaves and stems was observed 4 and 7 days after inoculation, respectively. No symptoms were observed on the control leaves and stems that were inoculated with blank agar plugs. P. nicotianae was re-isolated from the infected leaves, and the ITS sequence was analyzed to confirm its identity. Phytophthora species, such as P. cambivora, P. megasperma, and P. drechsleri, had been previously isolated from cherry (3), but to the best of our knowledge this is the first report of stem rot and leaf necrosis disease caused by P. nicotianae on cherry. Since the economic loss caused by this disease could reach 15% if an outbreak occurred in a rainy summer, control measures should be implemented. References: (1) Y. Balci et al. Mycol. Res. 112:906, 2008. (2) D. C. Erwin and O. K. Ribeiro. Phytophthora Diseases Worldwide. The American Phytopathological Society, St Paul, MN, 1996. (2) S. M. Mircetich and M. E. Matheron. Phytopathology 66:549, 1976.
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Book chapters on the topic "M-NV RNA"

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