Relevant bibliographies by topics / DYSF

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'DYSF'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "DYSF"

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Xiao, Yizhi, Honglin Zhu, Liya Li, Siming Gao, Di Liu, Bingying Dai, Qiuxiang Li, et al. "Global analysis of protein expression in muscle tissues of dermatomyositis/polymyosisits patients demonstrated an association between dysferlin and human leucocyte antigen A." Rheumatology 58, no. 8 (March 25, 2019): 1474–84. http://dx.doi.org/10.1093/rheumatology/kez085.

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Abstract Objectives DM and PM are characterized by myofibre damage with inflammatory cell infiltration due to the strong expressions of MHC class I HLA-A and monocyte chemoattractant protein-1 (MCP-1). Dysferlin (DYSF) is a transmembrane glycoprotein that anchors in the sarcolemma of myofibres. DYSF mutation is closely associated with inherited myopathies. This study aimed to determine the role of DYSF in the development of DM/PM. Methods Mass spectrometry was performed in muscle tissues from DM/PM patients and controls. The DYSF levels in muscle tissue, peripheral blood cells and serum were detected by Western blotting, IF, flow cytometry or ELISA. Double IF and co-immunoprecipitation were used to investigate the relationship between DYSF and HLA-A. Results Mass spectrometry and bioinformatics analysis findings suggested the dysregulated proteins in DM/PM patients participated in common biological processes and pathways, such as the generation of precursor metabolites and energy. DYSF was upregulated in the muscle tissue and serum of DM/PM patients. DYSF was mainly expressed in myofibres and co-localized with HLA-A and MCP-1. DYSF and HLA-A expressions were elevated in myocytes and endothelial cells after being stimulated by patient serum and IFN-β. However, no direct interactions were found between DYSF and HLA-A by co-immunoprecipitation. Conclusion Our study revealed the dysregulated proteins involved in common and specific biological processes in DM/PM patient samples. DYSF is upregulated and exhibits a potential role along with that of HLA-A and MCP-1 in inflammatory cell infiltration and muscle damage during the development of DM/PM.
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Michel Espinoza-Fonseca, L. "Pathogenic mutation R959W alters recognition dynamics of dysferlin inner DysF domain." Molecular BioSystems 12, no. 3 (2016): 973–81. http://dx.doi.org/10.1039/c5mb00772k.

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We have used atomistic simulations to demonstrate that the pathogenic mutation R959W alters recognition dynamics of dysferlin inner DysF domain. Based on these simulations, we propose a novel role for the inner DysF domain in muscle membrane repair through recruitment of dysferlin to plasma membrane.
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Mezzani, Alessandro, Ugo Corrà, Cristina Andriani, Andrea Giordano, Roberto Colombo, and Pantaleo Giannuzzi. "Anaerobic and aerobic relative contribution to total energy release during supramaximal effort in patients with left ventricular dysfunction." Journal of Applied Physiology 104, no. 1 (January 2008): 97–102. http://dx.doi.org/10.1152/japplphysiol.00608.2007.

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Energetic metabolism during effort is impaired in patients with left ventricular dysfunction (Dysf), but data have been lacking up to now on the relative anaerobic vs. aerobic contribution to total energy release during supramaximal effort. Recently, the maximal accumulated oxygen deficit (MAOD) has been shown to be measurable in Dysf patients, making it possible to evaluate the anaerobic/aerobic interaction under conditions of maximal stress of both anaerobic and aerobic metabolic pathways in this population. Nineteen Dysf patients and 17 normal patients (N) underwent one ramp cardiopulmonary, three moderate-intensity constant-power, and three supramaximal constant-power (1- to 2-min, 2- to 3-min, and 3- to 4-min duration) exercise tests. MAOD was the difference between accumulated O2demand (accO2dem; estimated from the moderate-intensity O2uptake/watt relationship) and uptake during supramaximal tests. Percent anaerobic (%Anaer) and aerobic (%Aer) energetic release were [(MAOD/accO2dem)·100] and 100 − %Anaer, respectively. MAOD did not vary between 1–2, 2–3, and 3–4 min supramaximal tests, whereas accO2dem increased significantly with and was linearly related to test duration in both Dysf and N. Consequently, %Anaer and %Aer decreased and increased, respectively, with increasing test duration but did not differ between Dysf and N in 1–2 min, 2–3 min, and 3–4 min tests. Our study demonstrates a similar relative anaerobic vs. aerobic contribution to total energy release during supramaximal effort in Dysf and N. This finding indicates that energetic metabolism during supramaximal exercise is exercise tolerance independent and that relative anaerobic vs. aerobic contribution in this effort domain remains the same within the physiology- or pathology-induced limits to individual peak exercise performance.
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Ganchinho Lucas, Sandra, Inês Vieira Santos, Filipe Jorge Pencas Alfaiate, and Ireneia Lino. "A new dysferlin gene mutation in a Portuguese family with Miyoshi myopathy." BMJ Case Reports 14, no. 7 (July 2021): e242341. http://dx.doi.org/10.1136/bcr-2021-242341.

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Dysferlinopathies are autosomal recessive muscular dystrophies caused by mutations in the dysferlin gene (DYSF). A 33-year-old man was born to a non-consanguineous couple. At the age of 25 he stared to feel weakness of the distal lower limbs and also experienced episodes of rhabdomyolysis. Electromyography showed a myopathic pattern, and muscle biopsy revealed dystrophic changes with absence of dysferlin. Genetic analysis was positive for a mutation in the c3367_3368del DYSF gene (p.Lys1123GLUFS*2). After 8 years of disease evolution the symptomatology worsened. This is the first report of this mutation of the DYSF gene identified in a non-consanguineous Portuguese family, studied over 8 years. We believe the mutation is responsible for the Miyoshi myopathy. Disease progression cannot be predicted in either the patient or carrier family because there are no similar cases previously described in the literature.
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Bryant, Grace, Steven A. Moore, James S. Nix, Grace Rice, Murat Gokden, and Aravindhan Veerapandiyan. "Miyoshi Muscular Dystrophy Due to Novel Splice Site Variants in DYSF Gene." Child Neurology Open 9 (January 2022): 2329048X2211402. http://dx.doi.org/10.1177/2329048x221140298.

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Dysferlinopathies are a group of phenotypically heterogeneous disorders caused by pathogenic variants in the DYSF (DYStrophy-associated Fer-1-like) gene encoding dysferlin. The phenotypic spectrum includes Miyoshi muscular dystrophy (MMD), limb-girdle muscular dystrophy type R2, distal myopathy with anterior tibial onset, and isolated hyperCKemia. MMD is characterized by muscle weakness and atrophy predominantly affecting the calf muscles with symptoms onset between 14 and 40 years of age. There is no clear phenotype – genotype correlation for dysferlinopathy. We describe a 15-year-old girl who presented with a phenotype consistent with MMD. However, she was initially treated for presumed polymyositis without improvement. Subsequent genetic testing revealed two novel variants in DYSF: c.3225dup (p.Gly1076Trpfs*38) in exon 30 and c.3349-2A > G (Splice acceptor) in intron 30. No dysferlin was detected in a muscle biopsy using immunostains and western blots, a result consistent with dysferlinopathy that supports the pathogenicity of the DYSF variants.
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Kocherova, I., E. Pachera, D. Nurzynska, F. DI Meglio, O. Distler, P. Blyszczuk, and G. Kania. "POS0486 IDENTIFICATION OF NEW CANDIDATE TARGETS INVOLVED IN ACTIVATION OF CARDIAC FIBROBLASTS UNDER IMMUNOFIBROTIC CONDITIONS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 498.1–498. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4399.

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BackgroundInflammatory dilated cardiomyopathy (iDCM) often leads to heart failure (HF), which is the main cause of mortality in patients with systemic diseases. Fibroblast activation, driven by the activator protein 1 family member Fos-related antigen 2 (FOSL2), represents a critical step in cardiac fibrogenesis. The existing antifibrotic therapies, based on known fibrotic markers, failed to demonstrate efficacy against myocardial fibrosis.ObjectivesTo identify new candidate targets implicated in cardiac fibrogenesis under immunofibrotic conditions.MethodsCardiac fibroblasts were isolated from the left atria of patients (n=5) undergoing heart transplantation due to HF associated with iDCM and from unaffected hearts of brain-dead donors (UDs, n=5). Protein identification and quantification was performed using liquid chromatography tandem-mass spectrometry (LC–MS/MS). The data were analysed with MaxQuant v1.6.2.3 software. Bulk RNA sequencing (RNA-seq) was conducted using the Illumina HiSeq platform. Differentially expressed genes were identified using DESeq2. Additionally, we analysed publicly available single-cell (sc) RNA sequencing datasets (GSE109816, GSE121893) [1] on adult hearts from HF patients (n=6) and UDs (n=14) using Seurat package (V.2.3.4). Specific gene knockdown was achieved by siRNA transfection of human foetal cardiac fibroblasts (HCFs, Sigma), untreated or stimulated with TGF-β for 48-72h. The profibrotic marker expression was assessed using RT-qPCR and Western Blot. Cell viability was measured using PrestoBlue HS reagent (Invitrogen), and ATP production was quantified with CellTiter-Glo assay (Promega) in untreated and TGF-β-stimulated HCFs 48h after transfection.ResultsThe LC–MS/MS analysis revealed 14 differentially expressed proteins (absolute log2FC>1, adj. p<0.05) in the HF group compared to UDs. The most upregulated protein in HF fibroblasts was dysferlin (DYSF, log2FC=5.78, adj. p<0.004), which is known to play a role in the sarcolemma repair of both skeletal muscle fibres and cardiomyocytes. Bulk RNA-seq analysis identified a total of 67 significantly differentially expressed genes (absolute log2FC>1, adj. p<0.05). The comparative analysis of bulk RNA-seq results and publicly available scRNA-seq datasets revealed two commonly upregulated genes in HF fibroblasts or their subclusters, encoding transcription factor FOXF1 (log2FC=3.51, adj.p<0.05) and matrix remodelling-associated protein MXRA5 (log2FC=2.91, adj. p<0.05).Further in vitro studies on HCFs (n=4) showed that TGF-β upregulated DYSF (p<0.001) and MXRA5 (p<0.01) but downregulated FOXF1 (p<0.05). DYSF silencing in HCFs (n=4) upregulated MXRA5 after 48h of TGF-β stimulation (p<0.05), downregulated ACTA2 (48h and 72h of TGF-β stimulation, p<0.05), and upregulated FOSL2 protein levels in untreated HCFs and 72h after TGF-β stimulation (n=3, p<0.05). MXRA5 knockdown (n=8) resulted in the upregulation of DYSF (p<0.05), ACTA2 (p<0.05) and COL1A1 (p<0.001) in untreated HCFs, and also upregulated DYSF (p<0.01) and COL1A1 (p<0.05) after 48h of TGF-β stimulation. FOXF1 silencing in HCFs (n=8) followed by 48h of TGF-β stimulation downregulated MXRA5 (p<0.01) and ACTA2 (p=0.06), and upregulated DYSF (p<0.001) and COL1A1 (p=0.05). Candidate targets knockdown reduced cell viability in untreated (n=4, DYSF: p<0.01, MXRA5: p<0.001, FOXF1: p<0.01) and TGF-β stimulated (n=4, DYSF: p<0.05, MXRA5: p<0.05, FOXF1: p<0.01) HCFs. ATP levels were decreased in TGF-β-stimulated HCFs after DYSF silencing (n=6, p=0.05).ConclusionBased on transcriptomics, proteomics and in vitro analysis of human cardiac fibroblasts, we identified DYSF, MXRA5 and FOXF1 as candidate targets implicated in profibrotic phenotype development, including profibrotic transcription factor FOSL2 regulation. These newly proposed candidates may serve as potential therapeutic targets for the treatment of cardiac fibrosis.References[1]Wang, L. et al. Nat. Cell Biol. 2020.Disclosure of InterestsIevgeniia Kocherova: None declared, Elena Pachera: None declared, Daria Nurzynska: None declared, Franca Di Meglio: None declared, Oliver Distler Speakers bureau: Bayer, Boehringer Ingelheim, Janssen, Medscape, Consultant of: Abbvie, Acceleron, Alcimed, Amgen, AnaMar, Arxx, AstraZeneca, Baecon, Blade, Bayer, Boehringer Ingelheim, Corbus, CSL Behring, 4P Science, Galapagos, Glenmark, Horizon, Inventiva, Kymera, Lupin, Miltenyi Biotec, Mitsubishi Tanabe, MSD, Novartis, Prometheus, Roivant, Sanofi and Topadur, Grant/research support from: Kymera, Mitsubishi Tanabe, Boehringer Ingelheim, Przemyslaw Blyszczuk: None declared, Gabriela Kania: None declared.
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Rubi, Lena, Vaibhavkumar S. Gawali, Helmut Kubista, Hannes Todt, Karlheinz Hilber, and Xaver Koenig. "Proper Voltage-Dependent Ion Channel Function in Dysferlin-Deficient Cardiomyocytes." Cellular Physiology and Biochemistry 36, no. 3 (2015): 1049–58. http://dx.doi.org/10.1159/000430278.

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Background/Aims: Dysferlin plays a decisive role in calcium-dependent membrane repair in myocytes. Mutations in the encoding DYSF gene cause a number of myopathies, e.g. limb-girdle muscular dystrophy type 2B (LGMD2B). Besides skeletal muscle degenerative processes, dysferlin deficiency is also associated with cardiac complications. Thus, both LGMD2B patients and dysferlin-deficient mice develop a dilated cardiomyopathy. We and others have recently reported that dystrophin-deficient ventricular cardiomyocytes from mouse models of Duchenne muscular dystrophy show significant abnormalities in voltage-dependent ion channels, which may contribute to the pathophysiology in dystrophic cardiomyopathy. The aim of the present study was to investigate if dysferlin, like dystrophin, is a regulator of cardiac ion channels. Methods and Results: By using the whole cell patch-clamp technique, we compared the properties of voltage-dependent calcium and sodium channels, as well as action potentials in ventricular cardiomyocytes isolated from the hearts of normal and dysferlin-deficient (dysf) mice. In contrast to dystrophin deficiency, the lack of dysferlin did not impair the ion channel properties and left action potential parameters unaltered. In connection with normal ECGs in dysf mice these results suggest that dysferlin deficiency does not perturb cardiac electrophysiology. Conclusion: Our study demonstrates that dysferlin does not regulate cardiac voltage-dependent ion channels, and implies that abnormalities in cardiac ion channels are not a universal characteristic of all muscular dystrophy types.
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Malcher, Jakub, Leonie Heidt, Aurélie Goyenvalle, Helena Escobar, Andreas Marg, Cyriaque Beley, Rachid Benchaouir, et al. "Exon Skipping in a Dysf-Missense Mutant Mouse Model." Molecular Therapy - Nucleic Acids 13 (December 2018): 198–207. http://dx.doi.org/10.1016/j.omtn.2018.08.013.

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Sula, Altin, Ambrose R. Cole, Corin Yeats, Christine Orengo, and Nicholas H. Keep. "Crystal structures of the human Dysferlin inner DysF domain." BMC Structural Biology 14, no. 1 (2014): 3. http://dx.doi.org/10.1186/1472-6807-14-3.

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Liewluck, Teerin, Sunsanee Pongpakdee, Rawiphan Witoonpanich, Tumtip Sangruchi, Theeraphong Pho-iam, Chanin Limwongse, Wanna Thongnoppakhun, et al. "Novel DYSF mutations in Thai patients with distal myopathy." Clinical Neurology and Neurosurgery 111, no. 7 (September 2009): 613–18. http://dx.doi.org/10.1016/j.clineuro.2009.05.001.

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Dissertations / Theses on the topic "DYSF"

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Patel, Pryank. "Structural studies of the inner DysF domain of human myoferlin." Thesis, Birkbeck (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479383.

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Heidt, Leonie Victoria [Verfasser]. "Proteinfehlfaltung als Ursache der Muskeldystrophie Dysferlinopathie: Das Mausmodell Dysf-MMex38 / Leonie Victoria Heidt." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1176637223/34.

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Slaviero, André. "Konstruktionsoptimering av självrensande dysa." Thesis, Högskolan i Gävle, Avdelningen för Industriell utveckling, IT och Samhällsbyggnad, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-8064.

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Lie, Gustavsson Victor. "Konstruktion av infästning till dysa." Thesis, Karlstads universitet, Fakulteten för hälsa, natur- och teknikvetenskap (from 2013), 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-33641.

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The goal of this thesis is to design an attachment between a duct and a pod. A pod is what could be compared to an outboard engine for larger vessels. The pod is placed on the outside of the ship’s hull and can rotate 360 ̊. A duct is a large steel ring that can be placed around the propeller on the pod to increasethe propulsion force of the ship in lower velocities. The thesis is written for Rolls Royce AB in Kristinehamn.The demanded requirements of the design are: it must be easy to adapt to different sizes and shapes of pod houses, the duct must be able to bemounted and dismounted from the pod.The result from this thesis is that anupper and a lower attachment weredesigned. The upper attachment consists of two parallel steel plates which arebolted together with a screw plate that is welded to the pod house.The lower attachment is basically a wing with a streamlined profile which is bolted to a stay. Both attachments consist of bolted joints, two guide pins and bursting screws.The design is controlled by parameters in CAD, meaning that if you change the size of the duct the attachments automatically adapts themselves to the new dimensions.The total result from this thesis is a design suggestion and not an actual manufactured product.The design is dimensioned by a load analysis and strength calculations. The dimensions of the bolts are determined by basic load calculation and the guide pins aredimensioned to withstand the shear forces that occur.The conclusion of this thesis is that the developed attachment solution is a good way to solve this problem andthe personal recommendation is that it should be developed further.Further design work that needs to be done with the attachment is a more thorough analysis of the strength and especially with fatigue, since no account has been taken considering fatigue.
Målet med detta arbete är att konstruera en infästning mellan en dysa och en pod. En pod är vad som kan liknasen utombordsmotor för stora fartyg som sitter på utsidan av skrovet och kan rotera 360 ̊. En dysa är en stor stålring som kan sättas runt propellern, dysan ger förenklaten ökad framdrivningskraft och är lämplig för användning vid fartygstillämpningar där det handlar om låga hastigheter.Arbetet utförs på uppdrag av Rolls Royce AB i Kristinehamn.Kraven som ställdes på konstruktionen var att den skulle vara lätt att anpassa och att det skulle gå att montera och demontera dysan.Problemformuleringen för arbetet är att en ny infästning behövs för att kunna fästa dysan i poden.Resultatet av arbetet blev en övre och en nedre infästning på dysan. Den övre infästningen består av två parallella plåtar som skruvas ihop med en svetsad infästning på dysan. Den nedre infästningen består av en vinge med en strömningsvänlig profil som skruvas fast på ett stag. Båda infästningarna består av ett skruvförband, två styrpinnar och sprängskruv.Konstruktionen parametriserades i CAD så attomdysans storlekändrasså följer infästningarna med.Hela arbetet resulterade i ett konstruktionsförslag.Konstruktionen har dimensionerats med hjälp av en lastanalys och hållfasthetsberäkningarför att uppskatta infästningarnas nedböjning. Skruvförbanden har dimensionerats med enklare beräkningar och styrpinnarna har dimensioneratför att uppta skjuvspänningar.Slutsatsen som dras av arbetet är att konstruktionen är en lämplig lösning på problemet och rekommendationen är att det är värt att undersöka denna lösning vidare.Vidarearbete som behöver utföras är nogrannare dimensionering av konstruktionen, ingen hänsynhar tagits till utmattning eller vridning då det inte fanns tid inom arbetets tidsram för detta.
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Storm, Josef. "Termisk utmattning : Hur termiska belastningar avgör livslängden på en Pressure seal-dysa och en bultad dysa." Thesis, Karlstads universitet, Fakulteten för hälsa, natur- och teknikvetenskap (from 2013), 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-85207.

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Thermal fatigue is a major problem in various mechanical constructions. Details with strict boundary conditions subjected to cyclic thermal loadings experience significant internal stresses. Due to the capability of materials to expand or contract differently, components in separate materials, assembled, behave in their own ways. The cyclic thermal loads result in strains that cause stresses in the exposed materials. The magnitude of the resulted stresses is commonly dependent on the thermal loads and the material properties, and even if the magnitude of the stresses is too low to cause an immediate failure of the material, these stresses applied repeatedly will eventually result in localized plastic deformation. In the heavily deformed locations, stresses might reach the ultimate tensile strength of the material and thus initiate a fatigue crack. Repeated exposure to stresses will lead to crack growth and failure of components. In the present work a stress computational model in Abaqus was built up to calculate the stresses generated when components are subjected to thermal loads. The stress analysis was performed on two different spray nozzles attached to a steam pipe. The nozzles work under cyclic conditions, they start at a rather high temperature which decreases while cold water is passed through. This occurrence is repeated since the water flow runs sporadically. Cold water runs only when the temperature is too high, it is applied to regulate the temperature inside the steam pipe. The nozzle covers are the main differences between them, one is called a Pressured seal nozzle while the other nozzle is sealed with bolts. The results of the stress analysis showed that the highest stresses were found in the welding between the nozzle and the steam pipe. The Pressured sealnozzle’s stresses were more uniformly distributed around the welding compared to the nozzle with the bolts, which experienced stresses a little more varying in its welding. Worth to remark, the nozzle with bolts had one smaller area in the welding where the stresses were significantly higher than what appeared to be the average value of the stress in the welding of the Pressured seal nozzle. These results indicate that the Pressured seal nozzle’s welding should experience a more uniform fatigue while the other nozzle might get larger fatigue symptoms in a smaller area, while the rest of the part is not so heavily stressed.
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Huguenel, Colin John. "Ciliated Sensory Neuron Defects in Caenorhabditis elegans." Thesis, Boston College, 2008. http://hdl.handle.net/2345/573.

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Thesis advisor: John Wing
Presented here is research investigating genes that are involved in the development and maintenance of ciliated nerve endings in the nematode Caenorhabditis elegans. C. elegans utilizes a subset of neurons, referred to as ciliated sensory neurons, to sense certain changes in its environment. There are two amphid sensilla (sense organs) that mediate exposure of these ciliated endings to the animal's external environment. Those ciliated endings that penetrate the cuticle are responsible for a myriad of behaviors that range from chemotaxis to osmotic avoidance, but in general function for the reception of environmental cues and stimuli. The intraflagellar transport (IFT) process facilitates the morphogenesis of these ciliated endings, and animals lacking intact ciliated endings may not be able to detect nourishment, hazardous environments, or other worms for mating. Mutant strains used in this study were generated by EMS mutagenesis of wild-type N2 animals and a subsequent screen of those worms displaying significant cilia dysfunction as evidenced by their dye-filling defective (Dyf) phenotype. Cilia-mediated uptake of lipophilic DiI into six pairs of amphid sensory neurons and two pairs of phasmid sensory neurons is expected in wild-type (N2) animals, but in Dyf animals, this dye-filling is disrupted, either through morphological defects, or deleterious mutations in the IFT process. To investigate the morphogenesis of cilia in C. elegans, we analyzed two specific mutant strains, WX737 dyf-3(og022)IV and PK841 dyf-15(pk841)V, that are defective in the uptake of fluorescent dye DiI and abnormal in sensory cilium structure. Through a variety of genetic mapping techniques, we were able to successfully map experimental gene dyf-15(pk841) to an interval of 2.84cM on chromosome V, and identify og022 as an allele of the gene dyf-3. It has been previously shown that dyf-3 expression is detected in 26 chemosensory neurons, including six IL2 neurons, eight pairs of amphid neurons (ASE, ADF, ASG, ASH, ASI, ASJ, ASK and ADL) and two pairs of phasmid neurons (PHA and PHB). Analysis of cilium malformation and the presence of a recognition sequence for the DAF-19 transcription factor suggest that dyf-3 is involved in the intraflagellar transport system complex B
Thesis (BS) — Boston College, 2008
Submitted to: Boston College. College of Arts and Sciences
Discipline: Biology
Discipline: College Honors Program
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Vadamootoo, Kavi. "Theory of art therapy : dys-embodiment and embodiment." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418942.

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Knapek, Olga. "Opowiadanie, błąd, dys-kurs : naruszenie reguły jako praktyka literacka." Doctoral thesis, Katowice : Uniwersytet Śląski, 2015. http://hdl.handle.net/20.500.12128/5873.

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This work presents an error as a literary practice in contemporary prose. The error is understood here as crossing the literary rules and a change that comes from genre deformation showed in analyzed texts. The functioning of the error is depicted via the examples of works by Dorota Masłowska, Jerzy Pilch, Andrzej Stasiuk and Jacek Dehnel. Furthermore I examine the term - error - s a literary practice using foreign articles and research on deception and error from all over the world. In the introductory chapters, I concentrate on the theoretical thesis of the substance of the error. I try to determine the semantics of the main term of this dissertation basing on explored aberrations in composition and genres. I do not attempt to generate any catalogue of norms or to analyze their transgressions. The genre matters are not an issue here. Taking into consideration the norms, however, I notice crossing the rules, yet I do not assume it comes solely from the convention. For me it is the result of the contemporary qualities of writing. The novels mentioned (and novels in general) are the mirror of their times and as such they become metatextual comment to the changes in literature. The immense part of my work is dedicated to the presentation of the difference between being mistaken and misleading somebody. I associate being mistaken with the motive of a labyrinth. Trying to go through it, we often meet blind spots that are the effect of being mistaken. If we apply a certain procedure, we can either go back or go forward breaking the order and the norms. When it comes to misleading, we can notice a peculiar stimulation of the matter of the text and subjective correlation of components. Taking that into account, misleading is presented through the selectivity of description and the special function of representation. Moreover, I analyze the matter of a novel and its status in the contemporary literature. I apply my findings to examine the latest Polish literature. I set together the critical diagnosis and the characteristics of the book market. I consider the phenomena composed of transgressing the rules, for example mosaic character of prose, the end of the great narratives, diversity of text, modifications of realism and innovation, as a normative state for the error. I show such practices as the origin of the new genders in literature. To sum up, my work is an attempt to prove that error as a literary practice is not a new phenomenon – it only requires systematization and theoretical discussion.
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Galli, Ursula. "Stress and pain (dys)regulation in chronic orofacial pain." Göttingen Cuvillier, 2008. http://d-nb.info/99103158X/04.

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Eby, Christine A. "Pediatric Cochlear Implant Outcomes in Auditory Neuropathy/Auditory Dys-Synchrony." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1085691784.

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Books on the topic "DYSF"

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Diryff-dyff-dyff der Vogel Gryff--. Basel: Buchverlag Basler Zeitung, 1987.

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Dyf, Marcel. Marcel Dyf. London: Frost and Reed, 1989.

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3

Evans, D. J. Goronwy. Gwell dysg na golud. [Llanbedr Pont Steffan]: [Goronwy Evans], 2003.

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Aspra-JR, Oficyna Wydawnicza, ed. Pędzę do ciebie co dysk wyskoczy. Warszawa: Oficyna Wydawnicza Aspra-Jr, 2014.

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Hoi logioi tou Vyzantiou stē Dysē. Iōannina: Panepistēmio Iōanninōn, 2004.

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Debiel, Tobias, and Andrea Gawrich, eds. (Dys-)Functionalities of Corruption. Wiesbaden: Springer Fachmedien Wiesbaden, 2014. http://dx.doi.org/10.1007/978-3-658-04633-0.

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Alun, Mathias W., and James E. Wyn, eds. Dysg a dawn: Cyfrol goffa Aneirin Lewis. (Caerdydd): Cylch Llyfryddol Caerdydd, 1992.

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1959-, Langlais Rick, ed. Dys-functional: The Rick Langlais story. Saskatoon: R. Langlais, 2010.

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Blom, Ida. Den haarde dyst: Fødsler og fødselshjelp gjennom 150 år. [Oslo]: J.W. Cappelen, 1988.

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Huws, Bleddyn Owen. Delfryd dysg cymeriad: Canmlwyddiant Ysgol Dyffryn Nantlle 1898-1998. Caernarfon: Cyngor Sir Gwynedd, 1998.

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Book chapters on the topic "DYSF"

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Bährle-Rapp, Marina. "dys..., Dys..." In Springer Lexikon Kosmetik und Körperpflege, 174. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_3451.

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Suski, W., and T. Palewski. "DySe-TlSe." In Pnictides and Chalcogenides II, 1147–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_345.

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Suski, W., and T. Palewski. "(DyS)1.21TaS2." In Pnictides and Chalcogenides II, 627–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_166.

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Suski, W., and T. Palewski. "(DyS)1.22NbS2." In Pnictides and Chalcogenides II, 631–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_167.

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Suski, W., and T. Palewski. "(DyS)1.22TaS2." In Pnictides and Chalcogenides II, 633–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_168.

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Suski, W., and T. Palewski. "(DyS)1.2NbS2." In Pnictides and Chalcogenides II, 636–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/10713485_169.

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Rinnerthaler, Peter. "U-/Dys-/Heterotopie?" In Parole(n) - Politische Dimensionen von Kinder- und Jugendmedien, 241–54. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-04848-6_17.

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Clack, Chris, and Colin Myers. "The Dys-functional student." In Funtional Programming Languages in Education, 289–309. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/3-540-60675-0_51.

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Debiel, Tobias, and Andrea Gawrich. "(Dys-)Functionalities of corruption: comparative perspectives and methodological pluralism." In (Dys-)Functionalities of Corruption, 1–11. Wiesbaden: Springer Fachmedien Wiesbaden, 2014. http://dx.doi.org/10.1007/978-3-658-04633-0_1.

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Göbel, Christian. "Warriors unchained: critical junctures and anticorruption in Taiwan and South Korea." In (Dys-)Functionalities of Corruption, 219–42. Wiesbaden: Springer Fachmedien Wiesbaden, 2014. http://dx.doi.org/10.1007/978-3-658-04633-0_10.

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Conference papers on the topic "DYSF"

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Farias, Igor Braga, Bruno de Mattos Lombardi Badia, Gustavo Carvalho Costa, Roberta Ismael Lacerda Machado, Carolina Maria Marin, Wladimir Bocca Vieira de Rezende Pinto, Paulo Victor Sgobbi de Souza, and Acary Souza Bulle Oliveira. "Clinical and genetic profile of Brazilian patients with dysferlinopathies – A retrospective study." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.054.

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Introduction: Dysferlinopathies are a group of conditions that are caused by mutations in the dysferlin gene. Objectives: To characterize the clinical phenotypes and genotypic spectrum of dysferlinopathies patients and to estimate the progression of functional and motor decline. Design and setting: Retrospective analysis of the medical records of patients followed up at our institution between 1995 and 2020. Methods: Patients were selected based on the following inclusion criteria:(i) Identification of a mutation defined as pathogenic in homozygosis or compound heterozygosis in the Dysf gene;or (ii)compatible clinical manifestations and decreased expression of dysferlin in immunohistochemistry on muscle biopsy. Classification of the phenotype was based on the first symptoms. Functionality was defined by the Gardner–Medwin & Walton(GMW) scale modified for dysferlinopathy. Results: 23 patients were included in the study. 16 were classified as limb-girdle muscular dystrophy autosomal recessive 2 (LGMDR2), 4 as Miyoshi muscular dystrophy, 2 as proximo-distal onset and 1 as asymptomatic hyperCKemia. Thighs adduction was the most affected movement in the first evaluation (mean strength=3). Plantar flexion was the movement with the greatest decline in strength(mean=-0.10 points on MRC/year;pT, Arg2042Cys and c.2643+1G>A, p.?(splicing), found 3 times each. There was no statistical difference in muscle strength in the first evaluation, motor and functional decline between the phenotypes. Conclusion: While LGMDR2 was the most common phenotype at onset, with the exception of asymptomatic hyperCKemia, there were not a clear difference in the pattern of progression between them.
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Csallner, Christoph, Nikolai Tillmann, and Yannis Smaragdakis. "DySy." In the 13th international conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1368088.1368127.

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Norvag, K., and A. O. N. Nybo. "DyST: Dynamic and Scalable Temporal Text Indexing." In Thirteenth International Symposium on Temporal Representation and Reasoning (TIME'06). IEEE, 2006. http://dx.doi.org/10.1109/time.2006.12.

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Munawar, Ahmed Umar, and Uwe Schulz. "Microstructural Evolution of GdZ and DySZ Based EB-PVD TBC Systems After Thermal Cycling at High Temperature." In ASME Turbo Expo 2013: Turbine Technical Conference and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/gt2013-94061.

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Lower thermal conductivity and high temperature stability are the two properties which are highly desired from ceramic top coat materials in TBC systems. Gadolinium Zirconate, Gd2Zr2O7, (GdZ) and Dyprosia Stabilized Zirconia (DySZ) are two of the candidate materials with such properties and consequently the TBC system would be able to work at higher turbine inlet temperature (TIT) or the lifetime can be increased. In the present study, life time measurements are done for single and double layered Electron Beam Physical Vapor Deposition (EB-PVD) GdZ and DySZ samples by thermal-cycling tests. The double layered TBCs consisted of a thin 7YSZ layer and, on top, the new candidate material. Both single and double layered samples of GdZ and DySZ have shown similar or better lifetimes than the standard 7YSZ samples. However, single layered TBCs showed better lifetime results than the respective double layers. In this study, changes in the microstructure, diffusion of elements and sintering of the TBC materials with aging are observed.
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Van Der Smissen, Benjamin, Tom E. Claessens, Ernst R. Rietzschel, Marc L. De Buyzere, Dirk De Bacquer, Thierry C. Gillebert, Peter Van Ransbeeck, Pascal R. Verdonck, and Patrick Segers. "Noninvasive Assessment of Diastolic Intraventricular Pressure Gradients in a Large General Population (the Asklepios Study)." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19328.

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Accurate assessment of diastolic (dys)function by non-invasive techniques has important therapeutic and prognostic implications but remains a challenge to the cardiologist. A promising parameter to evaluate diastolic (dys)function more accurately is the early diastolic intraventricular pressure gradient (IVPGe) which is considered representative of the active relaxation of the left ventricle. It has been shown that IVPGe can be estimated non-invasively by measuring blood velocities along a base-to-apex scan line using color M-mode Doppler (CMD) echography [1]. Although this technique is known for about 20 years, IVPGe is still not used in daily clinical practice because its approach is complicated and too laborious [2].
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Zainulabdeen, Iman H., and Osamah I. Alzaidiki. "Comparison between different types of woods sawdust in the adsorption of blue dyse." In PROCEEDINGS OF THE 2020 2ND INTERNATIONAL CONFERENCE ON SUSTAINABLE MANUFACTURING, MATERIALS AND TECHNOLOGIES. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0030642.

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Tzouveli, Paraskevi, Andreas Schmidt, Michael Schneider, Antonis Symvonis, and Stefanos Kollias. "Adaptive Reading Assistance for the Inclusion of Students with Dyslexia: The AGENT-DYSL Approach." In 2008 Eighth IEEE International Conference on Advanced Learning Technologies. IEEE, 2008. http://dx.doi.org/10.1109/icalt.2008.236.

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"An energy landscape view of protein structure, dynamics, and (Dys) function." In 2017 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2017. http://dx.doi.org/10.1109/bibm.2017.8217613.

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Bidaut, Luc M., Roberto Pascual-Marqui, Jacqueline Delavelle, Margitta Seeck, Daniel Slosman, and Daniel Ruefenacht. "Assessment of neurological (dys)function through multidimensional and fully multisensor biomedical imaging." In Medical Imaging 1996, edited by Eric A. Hoffman. SPIE, 1996. http://dx.doi.org/10.1117/12.237872.

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FOWLER, J., and J. LEE. "An extended Kalman filter in a dynamic spherical coordinate (DYSC) system for space based satellite tracking." In 23rd Aerospace Sciences Meeting. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1985. http://dx.doi.org/10.2514/6.1985-289.

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