Relevant bibliographies by topics / Hurler

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

Academic literature on the topic 'Hurler'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 June 2025

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Journal articles on the topic "Hurler"

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Gocer, Celil, and Fred H. Linthicum,. "Hurler Disease." Otology & Neurotology 25, no. 1 (2004): 81–82. http://dx.doi.org/10.1097/00129492-200401000-00016.

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Rao, Kalipatnam Seshagiri, Sudhir Adhikari, Sandeep Singh, Shankar Poudel, Sahisnuta Basnet, and Ganesh Bishwakarma. "Hurler Syndrome." Journal of Nepal Paediatric Society 36, no. 3 (2017): 295–97. http://dx.doi.org/10.3126/jnps.v36i3.16349.

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We report a case of Hurler syndrome in 10 years old boy diagnosed on the basis of classical clinical and radiological features. Early diagnosis, genetic counseling and regular follow up with recent modalities of treatment can decrease mortality significantly and the child may grow normally.J Nepal Paediatr Soc 2016;36(3):295-297
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Chamoles, Néstor A., Mariana B. Blanco, Daniela Gaggioli, and Carina Casentini. "Hurler-like Phenotype." Clinical Chemistry 47, no. 12 (2001): 2098–102. http://dx.doi.org/10.1093/clinchem/47.12.2098.

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Abstract Background: Clinical differentiation among mucopolysaccharidosis, oligosaccharidosis, and mucolipidosis II and III is difficult. We describe methods for the assay of 8 lysosomal enzymes in dried blood spots on filter paper that allow screening for 12 lysosomal storage diseases that present with a Hurler-like phenotype. Methods: To test tubes containing 3-mm blood spots, we added elution liquid and fluorescent or radioactive substrate solution. After incubation at 37 °C, the reaction was terminated by the addition of a stop buffer. The amount of hydrolyzed product was compared with a calibrator to allow the quantification of enzyme activity. Sample stability was studied during storage for 21 days and during shipment of samples. We measured enzyme activities in 85 healthy controls (35 newborn, 50 adult), 57 patients suffering from 11 lysosomal storage diseases, and 46 obligate carriers. Results: Intra- and interassay CVs were <9% and <15%, respectively. Mean activity losses during transportation or storage for up to 21 days at 4 °C were ≤27%. Enzyme activities in all patients were outside the ranges of values seen for carriers and controls. Conclusions: The described methodology distinguishes between patients and controls with samples that are sufficiently stable to be mailed to the testing laboratory.
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Buchinskaya, Nataliya V., Anastasiya O. Vechkasova, Ekaterina E. Shishunova, et al. "Differential Diagnosis of Hurler and Hurler–Scheie Syndromes: Clinical Case." Current Pediatrics 24, no. 2 (2025): 105–11. https://doi.org/10.15690/vsp.v24i2.2883.

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Background. Mucopolysaccharidosis type I (MPS I) is a disease known for over 100 years. Implementation of new management approaches for MPS I requires from doctor to clearly differentiate subtypes of this disease for the effective and rational use of treatment methods. Clinical case description. Girl B. with early MPS I onset during the neonatal period. Symptoms of musculoskeletal system damage were the following: feet adduction and hip joints dysplasia. Further follow-up at the age of 6 months has shown linear growth retardation, umbilical hernia, and exudative otitis. Psychomotor development up to 1 year of age was delayed. Coarse facial features by the age 1.5 years along with orthopedic problems, exudative otitis, and umbilical hernia led to mucopolysaccharidosis diagnosis. The diagnosis of mucopolysaccharidosis type I was established according to clinical findings, enzyme diagnostics (significant decrease in lysosomal enzyme alpha-L-iduronidase activity — 0.26 μmol/l/h; reference values from 1.96), and molecular genetic testing (pathogenic variant c.208C>T (Gln70Ter) in exon 2 and nucleotide variant of unknown clinical value c.1524G>C (p.Glu508Asp) in exon 10 of IDUA gene in compound heterozygous state). Echocardiography has revealed structural changes in the mitral valve and minimal aortic insufficiency. Abdominal ultrasound has revealed signs of hepatomegaly, hydrocalycosis, right-side pyelectasia, kidneys’ sizes lesser than the age norms. Abdominal magnetic resonance imaging has shown simple kidney cysts. Conclusion. The major feature of this clinical case is the complexity of differential diagnosis between the severe form of MPS I, Hurler syndrome, and milder form, Hurler–Scheie syndrome. Molecular genetic testing has revealed the presence of the frequent pathogenic variant c.208C>T (Gln70Ter) in the IDUA gene associated with severe disease course and nucleotide variant c.1524G>C (p.Glu508Asp) with undefined clinical significance, thus, additional examination is necessary. Functional analysis of the novel variant is required to establish its role in protein function. It will help more precisely determine the disease form and predict its severity. Combination of MPS I and polycystic kidney disease in the proband is unique case.
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Tam, David A. "Microcephaly in Hurler Syndrome." Clinical Pediatrics 36, no. 1 (1997): 51–52. http://dx.doi.org/10.1177/000992289703600107.

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Taylor, Colm, Philip Brady, Ann O'Meara, David Moore, Frank Dowling, and Esmond Fogarty. "Mobility in Hurler Syndrome." Journal of Pediatric Orthopaedics 28, no. 2 (2008): 163–68. http://dx.doi.org/10.1097/bpo.0b013e3181649e25.

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Gordon, Neil. "THE PSEUDO - HURLER SYNDROMES." Developmental Medicine & Child Neurology 20, no. 3 (2008): 383–87. http://dx.doi.org/10.1111/j.1469-8749.1978.tb15230.x.

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van den Broek, Brigitte T. A., Jaap van Doorn, Charlotte V. Hegeman, et al. "Hurdles in treating Hurler disease: potential routes to achieve a “real” cure." Blood Advances 4, no. 12 (2020): 2837–49. http://dx.doi.org/10.1182/bloodadvances.2020001708.

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Abstract Mucopolysaccharidoses (MPSs) are multiorgan devastating diseases for which hematopoietic cell transplantation (HCT) and, to a lesser extent, enzyme replacement therapy have substantially altered the course of the disease. Furthermore, they have resulted in increased overall survival, especially for Hurler disease (MPS-1). However, despite the identification of clinical predictors and harmonized transplantation protocols, disease progression still poses a significant burden to patients, although at a slower pace. To design better therapies, we need to understand why and where current therapies fail. In this review, we discuss important aspects of the underlying disease and the disease progression. We note that the majority of progressive symptoms that occur in “hard-to-treat” tissues are actually tissues that are difficult to reach, such as avascular connective tissue or tissues isolated from the circulation by a specific barrier (eg, blood-brain barrier, blood-retina barrier). Although easily reached tissues are effectively cured by HCT, disease progression is observed in these “hard-to-reach” tissues. We used these insights to critically appraise ongoing experimental endeavors with regard to their potential to overcome the encountered hurdles and improve long-term clinical outcomes in MPS patients treated with HCT.
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Filippova, V. V., A. A. Gulenok, I. V. Levchenko, and T. V. Matafonova. "Common rare diseases: Hurler syndrome." Public health of the Far East Peer-reviewed scientific and practical journal 86, no. 4 (2020): 91–94. http://dx.doi.org/10.33454/1728-1261-2020-4-91-94.

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Oliveira Junior, Wilson Maia, Therezinha de Jesus Collares de Carvalho Paiva, and Daniela Dos Santos de Souza. "Manifestações da Síndrome de Hurler." ConScientiae Saúde 8, no. 2 (2009): 317–26. http://dx.doi.org/10.5585/conssaude.v8i2.1431.

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A Síndrome de Hurler é uma doença rara, decorrente da deficiência genética de enzimas lisossômicas responsáveis pela hidrólise de mucopolissacarídeos, acarretando o acúmulo dessa macromolécula em células do tecido conectivo, gerando, como consequência, várias características clínicas clássicas de tal síndrome. Os portadores apresentam deficiência visual (opacificação da córnea), hepatoesplenomegalia, retardo mental, doença cardíaca, alterações gengivais, macroglossia, retardo de erupção dentária, vários dentes impactados. As características mais comuns são impactação dentária e retardo de erupção. As alterações gengivais observadas pelos autores foram a fibrose e a hiperplasia gengival, decorrentes da higienização precária e respiração bucal. Em relação aos aspectos histológicos foram observadas características como acúmulo intracelular de mucopolissacarídeo em várias células do organismo, sendo afetados o fígado, o baço, o coração, a cartilagem, os ossos, bem como os fibroblastos que apresentam aspecto de células “claras” chamadas também de células de gárgula. Neste relato clínico, salienta-se a necessidade de fazer mais pesquisas sobre o assunto e fornecer aos cirurgiões-dentistas uma visão mais ampla a respeito da doença.
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Dissertations / Theses on the topic "Hurler"

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Amorín, Milagros, Andrea Carlina, and Ana Prötzel. "Mucopolisacaridosis de tipo I Hurler: Informe de un caso." Sociedad Argentina de Pediatría (SAP), 2014. http://hdl.handle.net/10757/313689.

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Mucopolysaccharidosis I (MPS I) is a rare, recessively inherited, lysosomal storage disorder caused by deficiency on the enzyme α-L-iduronidase. This defect results in accumulation of heparan and dermatan sulfate in different tissues and organs due to a deficiency in the catabolism of glycosaminoglycans. The overall incidence of MPS I is 0.99-1.99/100.000 live births. There are three clinical presentations: Hurler (severe), Hurler Scheie (mild) and Scheie (mild). We report the case of a 10-years-old male patient diagnosed with Hurler syndrome, the severe presentation, 5 years ago by enzyme α-L-iduronidase activity measurement in leukocytes; with a history of recurrent respiratory infections, umbilical hernia, corneal opacity, coarse facial features, macroglossia, hearing loss, stiffness of joints, cardiac compromise, claw hands, mental retardation and stunted growth. After enzyme replacement therapy the patient has shown improvement of visceral symptoms, but the neurological damage continuous in progress. Key words: mucopolysaccharidosis, Hurler syndrome, MPS 1, Hurler, genetic disorder, enzymatic replacement therapy, ERT.<br>Revisión por pares
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Nelson, John. "The mucopolysaccharidoses in Northern Ireland : a clinical, genetic and biochemical study." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357486.

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Hurler, Bernhard Alexander [Verfasser], and M. [Akademischer Betreuer] Zitterbart. "Dienstorientierte Sensornetze: Programmierabstraktionen und Dienstkomposition / Bernhard Alexander Hurler. Betreuer: M. Zitterbart." Karlsruhe : KIT-Bibliothek, 2012. http://d-nb.info/1033351539/34.

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MONTAGNA, ANNA. "Induced pluripotent stem cells (IPSCS) for modelling mucopolysaccharidosis type I (Hurler syndrome)." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2016. http://hdl.handle.net/10281/113869.

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Mucopolysaccharidosis type I (MPS-IH or Hurler syndrome) is a rare lysosomal storage disease caused by mutations in the IDUA gene, resulting in the deficiency of alpha-L-iduronidase (IDUA) enzyme activity with a consequent intracellular accumulation of glycosaminoglycans (GAGs). Among a broad spectrum of clinical manifestations, MPS-IH is characterized by a range of skeletal abnormalities known as dysostosis multiplex. To date, the skeletal pathogenesis of the MPSs has been assumed to be directly related to the progressive storage of GAGs. It is now clear that more complex cellular and molecular mechanisms underlie the patient clinical symptoms. Therefore, an appropriate humanized in vitro model is highly recommended to highlight these mechanisms. Compared to mesenchymal stromal cells (MSCs), induced pluripotent stem cells (iPSCs) represent a useful tool to achieve this purpose, due to their high proliferation capability in culture and, mostly, to their ability to mimic development. Thus, they demonstrate great potential for investigating the osteogenic differentiation process. In this study, we generated MPS-IH patient-specific iPS cells (MPS-IH iPSCs) which maintained the genetic mutation in the IDUA gene and, as a consequence, reduced IDUA enzyme activity and GAGs intracellular accumulation. In order to assess if the osteogenic differentiation phenotype is already compromised in MPS-IH iPSCs cell, we focused on their bone differentiation capability. Thus, we developed an osteogenic differentiation protocol through the generation of mesenchymal stromal cells from iPSC (hereafter named MSCs-like cells). We designed a robust, multistep differentiation method to isolate MSCs-like cells, both from wild-type iPSCs (WT-iPSCs) and MPS-IH iPSCs. The process included: embryoid body (EB) formation, cell outgrowth from EBs, monolayer culture of sprouted cells from EBs, and a serial of passages in culture until they reached a fibroblast-like morphology and the full expression of mesenchymal surface markers. Firstly, we characterized WT and patient derived-MSCs-like cells in terms of morphology, phenotype, proliferation kinetics and differentiation capacity in mesodermal tissues. WT and patient derived-MSCs-like cells showed the capacity to differentiate in adipocytes, as confirmed by Oil Red O staining. Moreover, MSCs-like cells derived-chondrogenic pellets exhibited a spherical, compact morphology. Histological analysis revealed an initial chondrogenic differentiation, as confirmed by q-RT-PCR for key early chondrogenic markers, such as SOX9 and COLII. Subsequently, we developed an osteogenic differentiation protocol for the obtained MSC-like cells. In order to verify if the differentiation process was accomplished, we performed Alizarin Red staining and quantified the hydroxyapatite production by colorimetric detection at 405 nm both on WT and MPS-IH iPSCs-derived osteoblasts. At the same time, we examined the expression for key osteogenic markers, such as OPN, RUNX2 OTC, OTN, ALP and COL 1A2, through q-RT-PCR. Recently, our group isolated MSCs from bone marrow (BM-MSCs) of both healthy donors and MPS-IH patients, studying a possible involvement of MSCs in the skeletal abnormalities affecting Hurler patients. We previously observed the ability of WT, MPS-IH BM-MSCs and MSCs-derived osteoblasts to stimulate osteoclastogenesis in vitro by measuring the molecular levels of receptor activator of nuclear factor-Kb ligand (RANKL) and osteoprotegerin (OPG), two key partners of the system directly regulating osteoclast differentiation. MPS-IH MSCs and osteoblasts derived from MPS-IH MSCs, expressed a higher level of RANKL compared to HD-MSCs and osteoblasts. OPG level, instead, was similar. In the present study, the osteogenic differentiation protocol developed allowed us to assess if this altered phenotype is already evident in both MSCs-like cells MSCs-like derived osteoblasts, by evaluating the OPG and RANKL expression levels.
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Hurler, Wolfgang [Verfasser]. "Fusions- und seltene Lageanomalien der Niere: Symptome, Morbidität und klinische Relevanz / Wolfgang Hurler." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1022896393/34.

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Pitt, Cheryl Anne. "Psychosocial outcomes of bone marrow transplant for individuals affected by MPS I Hurler Disease." Thesis, Bucks New University, 2009. http://bucks.collections.crest.ac.uk/9769/.

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RATIONALE: A theoretical model was used to examine the impact of risk and resistance factors on the psychosocial adjustment of children and young people affected by Mucopolysaccharidosis Type I Hurler Disease post-bone marrow transplant. METHOD: A sequential exploratory mixed methods design was employed and the study carried out in two phases. In the initial phase qualitative methods were employed in an in-depth study of a small sample of parents of individuals affected by this condition (n=10). They were administered semi-structured interviews, which were analysed using Interpretative Phenomenological Analysis. The themes highlighted were used to inform the design of the second phase, which employed quantitative methods. In this phase forty-four families affected by MPS IH post-BMT participated (44 mothers, 36 fathers, 44 patient participants). This comprised almost the entire population of this patient group in the UK, whose ages ranged from 16 months to 25 years. A face-to-face survey method was used with the mothers, telephone-survey with the fathers and psychometric testing of the patient participants. The measures included risk factors (e.g. physical, cognitive, and adaptive functioning), resistance factors (intrapersonal, stress processing, and socialecological), and adjustment for both parent and patient participants. RESULTS: Data from the qualitative phase revealed a number of themes, highlighting numerous issues pertinent to parents of children affected by this condition. These included perceptions of child vulnerability, uncertainty, perceptions of stress and sources of support, and feeling that others do not understand their situation. Data from the second phase illustrate how stress processing and social-ecological factors make significant contributions to parent adjustment. They also illustrate how intrapersonal, socialecological, and maternal stress processing factors contribute significantly to patient adjustment. A theoretical path of the determinants of patient psychosocial outcomes was created to illustrate these relationships. CONCLUSION: The findings are indicative of how resistance factors moderate the effects that disease- and disability-related risk factors have on parent and patient adjustment as predicted by the model. The dynamic interplay between disease-related risk factors and intrapersonal, socialecological, and stress processing factors are discussed in relation to parent and patient adjustment outcomes, as are the implications these relationships pose for patient and family support.
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GATTO, FRANCESCA. "Exploring hurler syndrome through the study of disease-specific multipotent and pluripotent stem cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29890.

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Mucopolysaccharidosis type I (or Hurler syndrome) is a rare genetic disorder, caused by mutations in the idua gene, resulting in the deficiency of α-L-iduronidase enzyme activity and intra-cellular accumulation of glycosaminoglycans. The aim of the present project was focused on the isolation and characterization of two different stem cell populations, multipotent and pluripotent, derived from patients affected by Hurler syndrome. We aim to use Mesenchymal Stem Cells (MSCs) and induced Pluripotent Stem Cells (iPSCs) as a tool to explore still unknown disease mechanisms involved in the genetic metabolic disorder of our interest. Our recently published study focused on the characterization of MSCs isolated from bone marrow of Hurler patients. The MSCs were characterized for their expansion rate, phenotype, telomerase activity, IDUA activity and differentiation capacity towards adipocytes, osteoblasts, chondrocytes and smooth muscle cells in vitro. Interestingly, affected MSCs displayed increased capacity to support osteoclastogenesis according to the upregulation of the RANKL/RANK/OPG molecular pathway in Hurler MSCs. The second study describes the isolation of iPSCs from fibroblasts of Hurler patients. The generated cell lines were fully characterized for their pluripotency markers, gene expression profile, viral copy number integration and differentiation potential both in vitro and in vivo. As a proof of principle, we are attempting to gene correct patient-derived iPSCs with an alternative and safer method than viral vectors, using a Zinc Finger Nucleases-mediated approach for gene targeting of pluripotent cells.
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Federhen, Andressa. "Mucopolissacaridose tipo I: avaliação de um novo instrumento para classificação fenotípica." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/52961.

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Introdução: A mucopolissacaridose tipo I é comumente classificada em três síndromes clínicas (Hurler, Hurler-Scheie e Scheie), de acordo com a gravidade do fenótipo. Devido à alta heterogeneidade da doença e à sobreposição de sintomas em pacientes, alguns autores consideram esta forma de classificação ultrapassada e defendem que a doença apresenta um espectro fenotípico mais amplo. Para tanto, seria muito útil o desenvolvimento de novas ferramentas que possam contribuir para uma melhor classificação dos pacientes. Objetivo: Avaliar um novo instrumento para a classificação fenotípica da MPS I e verificar a correlação dos resultados obtidos com o mesmo com as características bioquímicas e moleculares dos pacientes avaliados. Materiais e Método: Um instrumento elaborado por um grupo de especialistas foi por nós adaptado para avaliar a gravidade do fenótipo ao diagnóstico de 43 pacientes brasileiros com MPS I. Uma nota de zero a 14 foi obtida com a aplicação deste instrumento pela avaliação da presença ou ausência dos seguintes sinais e sintomas ao diagnóstico: atraso no desenvolvimento neuropsicomotor e/ou declínio cognitivo, rigidez articular/artropatia/contraturas articulares, cifose, disostose multiplex, macrocefalia e bossa frontal. Os pacientes incluídos foram também avaliados em relação aos mesmos parâmetros do instrumento e quanto ao seu fenótipo por três geneticistas com reconhecida experiência com essa doença. Dados bioquímicos e moleculares também foram utilizados para comparação com os resultados da aplicação do instrumento. Resultados: Os pontos de corte com melhor balanço de sensibilidade e especificidade encontrados a partir da aplicação do instrumento e a partir da avaliação dos geneticistas foram, respectivamente 7 e 9. Os parâmetros do instrumento para os quais foi observada diferença estatisticamente significativa foram atraso do desenvolvimento neuropsicomotor/declínio cognitivo (entre o fenótipo Hurler e os fenótipos Hurler-Scheie e Scheie) e disostose múltipla (entre os fenótipos Hurler e Scheie). Não foi observada correlação entre a nota obtida no instrumento e os valores de GAGs urinários, nos diferentes fenótipos. A maior parte dos pacientes com mutações sem sentido foi classificada como grave, tanto a partir do instrumento quanto pela avaliação dos geneticistas. Conclusões: Os pontos de corte encontrados podem ser úteis para a classificação dos pacientes em dois grupos distintos – grave e atenuado. O atraso no dsenvolvimento neuropsicomotor/declínio cognitivo e a disostose múltipla são achados importantes para predizer a gravidade da doença. Mutações sem sentido parecem determinar o fenótipo mais grave da síndrome. Não foi possível distinguir os diferentes fenótipos a partir dos valores de GAGs na urina. A ferramenta desenvolvida parece ser útil para auxiliar na classificação da gravidade da MPS I, mas é recomendável sua aplicação em um número maior de pacientes para melhor dimensionar sua potencial aplicação.<br>Introduction: Mucopolysaccharidosis type I is usually classified into three clinical syndromes (Hurler, Hurler-Scheie and Scheie) according to the severity of the phenotypic expression. Some authors believe this classification is not accurate because of disease variation and overlapping findings in some patients, and suggest that its phenotypic spectrum is wider. With this view, it would be useful the development of new tools which could contribute to a better classification of patients. Objective: To evaluate a new tool the phenotypic classification of MPS I and investigate whether the results obtained are correlated with biochemical and molecular characteristics of the patients. Material and methods: A tool developed by a group of specialists was adapted by us for the evaluation of the phenotypic severity at diagnosis in 43 Brazilian patients with MPS I. A score of zero to 14 was obtained using this tool, which evaluated presence or absence of the following signs and symptoms: delay in neurological and psychomotor development and cognitive decline; joint stiffness, arthropathy and joint contractures; kyphosis; dysostosis multiplex; macrocephaly; and frontal bossing. The same patients had the same parameters evaluated by three MDs with expertise in MPS who also provided their impression about the phenotype. Biochemical and molecular findings were also compared with the results obtained in the proposed tool. Results: The cut-off points with better balance of sensitivity and specificity found with the use of the tool and according to the experts' evaluations were 7 and 9, respectively. The tool parameters with statistically significant differences were neurological and psychomotor development delay and cognitive decline (when the Hurler phenotype was compared with the Hurler-Scheie and Scheie phenotypes), and dysostosis multiplex (for the comparison between the Hurler and Scheie phenotypes). There was no correlation between the scores obtained when using the tool and the urinary GAG values across the different phenotypes. Most patients with nonsense mutations were classified as severe according to the tool scores and to the experts’ evaluations. Conclusions: The cut-off points found in this study may be useful for the classification of patients into two distinct groups - severe and attenuated. Neurological and psychomotor developmental delay and cognitive decline, as well as dysostosis multiplex, are important findings to predict disease severity. Nonsense mutations seem to determine the most severe syndrome phenotype. The urinary GAG values do not allow differentiating the different phenotypes. The tool developed seems to be useful to help in the classification of the severity of MPS I, but it would be advisable its application in a larger number of patients to better evaluate its potential application.
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PENNA, SARA. "Development of novel cell based therapeutic approaches to correct primary and secondary bone defects." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/304794.

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Le malattie scheletriche pediatriche compromettono fortemente la durata della vita. Disturbi monogenici rari e gravi come l'osteopetrosi autosomica recessiva (ARO) e la mucopolisaccaridosi di tipo 1 Hurler (MPSIH) sono causati rispettivamente da difetti ossei primari e secondari. In particolare, i pazienti con ARO soffrono di elevata densità e fragilità ossea, difetti neurologici e fibrosi del midollo osseo che portano ad un aumento del numero di cellule CD34+ circolanti. La forma più frequente di ARO è dovuta alle mutazioni del gene TCIRG1, che codifica per una pompa protonica necessaria per l'attività di riassorbimento osseo degli osteoclasti. La sindrome MPSIH è uno dei disturbi da accumulo lisosomiale più frequenti, causato da mutazioni del gene IDUA, che codifica per l'enzima alfa-L-iduronidasi. L'enzima IDUA difettoso causa un ingolfamento lisosomiale dovuto al ridotto turnover dei glicosaminoglicani (GAG), portando a gravi disfunzioni degli organi e ad anomalie scheletriche. La patogenesi dei difetti ossei in MPSIH è ancora ampiamente dibattuta. Il trapianto allogenico di cellule staminali ematopoietiche (HSCT) è l'approccio standard per i pazienti ARO e MPSIH, ma l'alta incidenza di esiti avversi e la scarsa disponibilità di donatori compatibili, aprono la strada allo sviluppo di strategie di terapia genica (GT) per curare queste malattie. Nella presente tesi abbiamo sviluppato una nuova strategia di GT basata su vettori lentivirali clinicamente ottimizzati esprimenti il gene TCIRG1. Abbiamo testato il nostro protocollo di GT sul modello di topo oc/oc, molto simile alla malattia umana, con un'aspettativa di vita di 2-3 settimane. I topi GT hanno raggiunto fino a quattro mesi di età, mostrando un miglioramento del fenotipo osseo e dello stato clinico generale. In parallelo, le cellule CD34+ isolate dal sangue di pazienti ARO sono state caratterizzate fenotipicamente in termini di composizione di cellule staminali e progenitori ematopoietici e analizzate dal punto di vista del trascrittoma. Inoltre, le cellule CD34+ circolanti di pazienti ARO sono state trasdotte ed espanse, applicando un protocollo che consente il mantenimento della staminalità. Abbiamo inoltre eseguito test in vitro per valutare la capacità di riassorbimento degli osteoclasti derivati dai pazienti ARO e abbiamo valutato il potenziale di ripopolamento multi-lineage a lungo termine delle cellule CD34+ espanse mediante trapianto primario e secondario in topi NSG. Per quanto riguarda MPSIH, la sperimentazione clinica per la GT è in corso presso SR-Tiget (NCT03488394), e ha mostrato miglioramenti nei difetti scheletrici e nell'attività dell’enziama IDUA dei pazienti MPSIH. Abbiamo studiato la funzionalità degli osteoclasti e il loro ruolo nel fornire l'enzima IDUA nel microambiente osseo, correggendo le cellule stromali mesenchimali e la loro progenie dopo la GT. A tal fine, abbiamo differenziato gli osteoclasti dal sangue o dal midollo osseo di pazienti con MPSIH pre e post-GT, osservando che gli osteoclasti trasdotti producono livelli sovrafisiologici di IDUA, creando così un modello per lo studio del cross talk osteoblasto-osteoclasto. I nostri risultati suggeriscono che la GT rappresenta un trattamento alternativo possibile ed efficace per la cura dell’osteopetrosi TCIRG1-dipendente e della sindrome di Hurler.<br>Pediatric skeletal diseases strongly impair the lifespan of young children. Rare and severe monogenic disorders like Autosomal Recessive osteopetrosis (ARO) and Mucopolysaccharidosis type 1 Hurler (MPSIH) are caused by primary and secondary bone defects, respectively. In particular, ARO patients suffer from high bone density and fragility, neurological defects and bone marrow fibrosis leading to increased number of circulating CD34+ cells. The most frequent form of ARO is due to mutations in TCIRG1 gene, that encodes for a proton pump necessary for bone resorptive activity of osteoclasts. MPSIH syndrome is one of the most frequent lysosomal storage disorders, caused by mutations of IDUA gene, that encodes for the alpha-L-iduronidase enzyme. Defective IDUA enzyme causes lysosomal engulfment due to impaired turnover of glycosaminoglycans (GAGs), leading to severe organ dysfunctions and skeletal abnormalities. The pathogenesis of bone defects in MPSIH is still largely debated. Allogeneic haematopoietic stem cells transplantation (HSCT) is the standard approach for ARO and MPSIH patients, but the high incidence of adverse outcomes and the low availability of compatible donors, pave the way for the development of gene therapy (GT) strategies to cure these diseases. In the present thesis we developed a novel GT strategy based on clinically-optimized lentiviral vectors, driving TCIRG1 expression. We tested our GT protocol on the oc/oc mouse model, closely resembling the human disease, with a life expectancy of 2-3 weeks. GT mice reached up to four months of age, showing an amelioration of the bone phenotype and an improved clinical status. In parallel, CD34+ cells isolated from the blood of ARO patients were phenotypically characterized in terms of hematopoietic stem and progenitor cells composition and analysed for transcriptome profile. Moreover, ARO circulating CD34+ were transduced and expanded, applying a protocol that allows stemness maintenance. We performed in vitro assays to evaluate resorption capacity of patient-derived osteoclasts and we evaluated the long-term multilineage repopulating potential of expanded CD34+ cells by primary and secondary transplant into NSG mice. With regard to MPSIH, GT clinical trial is ongoing at SR-Tiget (NCT03488394), ameliorating skeletal defects and rescuing IDUA activity of MPSIH patients. We investigated the functionality of osteoclasts and their role in delivering IDUA enzyme in the bone microenvironment, cross-correcting mesenchymal stromal cells and their progeny after GT. To this end, we differentiated osteoclasts from the blood or bone marrow of MPSIH patients pre- and post-GT, observing that transduced osteoclasts produce supraphysiological levels of IDUA thus modulating osteoblast-osteoclast cross talk. Our results suggest that GT represents a feasible alternative treatment for TCIRG1-dependent ARO and Hurler syndrome.
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Dusing, Stacey Chapman Thorpe Deborah E. "Gross motor and gait abilities of children with Hurler syndrome, pre and post umbilical cord blood transplant." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,266.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.<br>Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree Doctor of Philosophy in the School of Medicine (Curriculum in Human Movement Science)." Discipline: Human Movement Science; Department/School: Medicine.
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Books on the topic "Hurler"

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1952-, Farley Randall K., and Farley Cynthia Bee 1952-, eds. Hungry hurler: The homecoming. Broadman & Holman Publishers, 2002.

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1898-, Kessel Joseph, and Ponfilly Christophe de, eds. Lettre ouverte à Joseph Kessel sur l'Afghanistan: Suivi de, Une envie de hurler. Bibliophane/Daniel Radford, 2002.

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Hurter, Eric. Hurter. Jérôme Do Bentzinger, 2011.

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Kitchen-Hurle, Michael. Michael Kitchen-Hurle. Chris Beetles Limited, 1986.

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Hurley, W. N. Hurley families in America. Heritage Books, 1995.

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King, Donald E. Arrivederci, Hurley--halo, Hamtramck. Vantage Press, 1992.

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McGregor, Alasdair. Frank Hurley: A photographer's life. Viking, 2004.

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Hurter, Werner. Werner Hurter: Malerei, Zeichnungen, Aquarelle. Kunstmuseum, 2007.

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Hurley, Margaret. Margaret Hurley: An oral history. Washington State Oral History Program, Office of the Secretary of State, 1995.

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Hurley, Wilson. Wilson Hurley: A retrospective exhibition. Published by the Lowell Press of Kansas City in association with the Albuquerque Museum and the Buffalo Bill Historical Center, 1985.

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Book chapters on the topic "Hurler"

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Kaltofen, Heike, Uta Emmig, Dierk A. Vagts, and Peter Biro. "Hurler-Syndrom." In Anästhesie bei seltenen Erkrankungen. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-44368-2_141-1.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, et al. "Hurler Syndrome." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6300.

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Idrees, Sana. "Hurler-Scheie Syndrome." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_560-1.

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Agemy, Steven. "Pseudo-Hurler Polydystrophy." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_767-1.

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Idrees, Sana. "Hurler-Scheie Syndrome." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_560.

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Agemy, Steven. "Pseudo-Hurler Polydystrophy." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_767.

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Brown, Michael B., and Paul S. Trivette. "Mucopolysaccharide disorders (Hurler, Scheie, Hurler- Scheie, Hunter, Morquio, and Sanfilippo syndromes)." In Health-related disorders in children and adolescents: A guidebook for understanding and educating. American Psychological Association, 1998. http://dx.doi.org/10.1037/10300-062.

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Davies, D. L., G. N. Dutton, J. Farquharson, R. W. Logan, and J. L. Tolmie. "Hurler-Scheie Phenotype Associated with Consanguinity." In Studies in Inherited Metabolic Disease. Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1069-0_53.

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Böhles, Hansjosef. "Mukopolysaccharidose Typ 1 (Morbus Hurler), 1920." In Historische Fälle aus der Medizin. Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-662-59833-7_24.

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Schroeder, L., P. Orchard, C. B. Whitley, et al. "Cardiac Ultrasound Findings in Infants with Severe (Hurler Phenotype) Untreated Mucopolysaccharidosis (MPS) Type I." In JIMD Reports. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/8904_2012_208.

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Conference papers on the topic "Hurler"

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Dharmadasa, Ruvini, Dustin Williams, Kevin Elmer, et al. "High Temperature Copper Metallization: Demand, Hurdles and Reliability." In 2024 IEEE 52nd Photovoltaic Specialist Conference (PVSC). IEEE, 2024. http://dx.doi.org/10.1109/pvsc57443.2024.10749130.

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Singh, Agampreet, Kanwarpartap Singh Gill, Mukesh Kumar, and Ruchira Rawat. "Addressing Bone Marrow Classification Hurdles Using EfficientNetB5 Technique." In 2024 Global Conference on Communications and Information Technologies (GCCIT). IEEE, 2024. https://doi.org/10.1109/gccit63234.2024.10862078.

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Villicaña, Ana, and Bailey Reichelt. "The Nuclear Space Age: Solving for Regulatory Hurdles." In Nuclear and Emerging Technologies for Space (NETS 2025). American Nuclear Society, 2025. https://doi.org/10.13182/xyz-47503.

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Barbour, Andrew J. "Telecommunications Fiber for Sensing Earthquake Aftershocks: Progress and Hurdles." In 2024 IEEE Photonics Society Summer Topicals Meeting Series (SUM). IEEE, 2024. http://dx.doi.org/10.1109/sum60964.2024.10614569.

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MOHAMAD, ARIFHA, MOHD ASAMDI MOHD ANGSOR, MOHD NAZIR MOHD ADI, and Angeline Tan Jia Min. "Malaysia's e-commerce landscape: legal structures and operational hurdles." In International Conference on Medical Imaging, Electronic Imaging, Information Technologies, and Sensors (MIEITS 2025), edited by Kamal Jadidy Aval, Lazim Abdullah, and Samad Rashid. SPIE, 2025. https://doi.org/10.1117/12.3059023.

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Islam, Md Ashraful, Khusbu Rahman, M. M. Naushad Ali, et al. "Overcoming Hurdles: A Comprehensive Analysis of Renewable Energy in Bangladesh." In 2024 International Conference on Computational Intelligence for Green and Sustainable Technologies (ICCIGST). IEEE, 2024. http://dx.doi.org/10.1109/iccigst60741.2024.10717611.

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Wang, Jinguang, Yuexi Yin, Haifeng Sun, et al. "QoKV: Comprehending and Surpassing the Hurdles of KV Cache Quantization." In ICASSP 2025 - 2025 IEEE International Conference on Acoustics, Speech and Signal Processing (ICASSP). IEEE, 2025. https://doi.org/10.1109/icassp49660.2025.10890716.

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Namazova-Baranova, Leyla, Nato Vashakmadze, Elena Vishneva, Anait Gevorkyan, Liliya Selimzyanova, and Ludmila Kuzenkova. "Respiratory system impairments in children with mucopolysaccharidoses: Hurler and Hunter syndromes." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3345.

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Gutev, Grigor. "MODELLING COMPETITION PERIODIZATION DURING THE OLYMPIC YEAR IN THE DISCIPLINE 110 M HURDLES (MEN)." In INTERNATIONAL SCIENTIFIC CONGRESS “APPLIED SPORTS SCIENCES”. Scientific Publishing House NSA Press, 2022. http://dx.doi.org/10.37393/icass2022/18.

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ABSTRACT Competition periodization in contemporary sports is a difficult task composed of basic rules of training periodization, adaptation, and a busy competition calendar. Influence on the process has many outer factors. Establishing the competition calendar in the year of the main competition (Olympic Games) and secondary ones is a great difficulty. These difficulties are compounded by aggravating factors such as a fading global pandemic and travel difficulties. In addition, participation in commercial tournaments is another major part of the competition calendar. The main aim of the following study is to analyze and model the competition periodization of elite 110 m hurdles during the Olympic year (2021). Respondents are all participants in the Olympic tournament in the chosen discipline – in total, 39 athletes. We found different tactics regarding participation in competitions during the Olympic year. Also, we found a different pattern of sports result utilization before a major competition. All finalists do not take part in the competition 20 days before the heats of the Olympic games. Some athletes participate in 60 m hurdles discipline just to check their sports form, others search for top performance in indoor competitions. The number of race days varies between 10 and 21 an (average of 16) for the finalists. After participating in the Olympic games, most of the athletes participated in a few commercial tournaments and no later than the middle of September, they finished race season. Based on the results, we can improve the training process and competition planning based on the experience of world-class hurdlers. We must consider that sometimes participation in the competition is canceled due to other factors such as injuries or travel problems. Also, we propose annual competition models based on elite hurdler performance during the Olympic year.
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Fonseca, Karolina Pinheiro, LETÍCIA MARIA ALVES PESSOA SOARES, LARA FERREIRA CHAVES GOMES DE CASTRO, SARAH CAROLINY OLIVEIRA SERRA MAGALHÃES, and SAMARA TATIELLE M. GOMES. "OBSERVAÇÃO IMUNOLÓGICA E GENÉTICA DAS MUCOPOLISSACARIDOSES." In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6913.

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Introdução: As Mucopolissacaridoses (MPS) são doenças hereditárias e progressivas de acúmulo lisossomal de glicosaminoglicanos (GAGs). Esse acúmulo de GAGs é decorrente da deficiente ação metabolizadoras das enzimas lisossomais, gerando o depósito nos lisossomos de diversos tecidos e órgãos, desencadeando modificações morfofuncionais. O início das manifestações das mucopolissacaridoses ocorrem nos primeiros meses de vida, com piora progressiva e, em geral, com comprometimento em ossos, articulações, via respiratória, sistema cardiovascular e sistema nervoso. Objetivo: Compreender os aspectos imunogenéticos envolvidos nas Mucopolissacaridoses. Métodos: Revisão bibliográfica dos aspectos imunológicos e genéticos da Mucopolissacaridose a partir de artigos e revistas, publicados entre os anos de 2017 e 2021, no idioma português, selecionados em fontes como: Pubmed, Google Scholar e Scielo. Foram selecionados 8 artigos entre os 8 encontrados. Resultados: As MPS podem ser classificadas em seis tipos, diferenciadas pela enzima defeituosa: Tipo I ou Síndrome de Hurler, Tipo II ou Síndrome de Hunter, Tipo III ou Síndrome de Sanfilippo, Tipo IV ou Síndrome de Mórquio, Tipo VI ou Síndrome de Maroteaux-Lamy e tipo VII ou Síndrome de Sly. Essas síndromes decorrem devido a defeitos em um dos 22 pares de cromossomos não ligados ao sexo, ou seja, é considerada uma herança autossômica recessivas, com exceção da MPS Tipo II ligada ao cromossomo X, sendo mais incidente em recém-nascidos do sexo masculino. Apenas três tipos de GAGs são acumulados, mas nem todos encontram-se relacionados a todas MPS, sendo eles: dermatan sulfato, heparan sulfato e queratan sulfato. O acúmulo desses mucopolissacarídeos ocorre por variações genéticas que acarretam a não produção das enzimas ou a formação de enzimas defeituosas que não conseguem metabolizá-los. A ação imunológica, apesar de existirem evidências da participação do sistema imune no desenvolvimento, o mecanismo pelo qual isso ocorre ainda não foi esclarecido completamente, existindo apenas indícios que a Terapia de Reposição Enzimática possa induzir uma resposta inflamatória. Conclusão: As MPS podem se manifestar de formas mais brandas e agressivas, no entanto, todas sem cura ou tratamento efetivo comprovado. Quanto à resposta imune, estudos abrangem apenas camundongos, onde a formação de resposta autoimune foi provada ser pequena ou inexistente, não contribuindo com a aparição de sintomas.
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Reports on the topic "Hurler"

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Handy, Robert. Patrick J. Hurley and China, 1944-1945. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.1461.

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Dinehart, Timothy, Steven Booth, and Gasper Toole. Conclusions of Arch Hurley Conservancy District Irrigation Project--Summary. Office of Scientific and Technical Information (OSTI), 2014. http://dx.doi.org/10.2172/1164451.

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Booth, Steven, Gasper Toole, and Timothy Dinehart. Feasibility of Renewable Energy Development at Arch Hurley Conservancy District. Office of Scientific and Technical Information (OSTI), 2014. http://dx.doi.org/10.2172/1164440.

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Luchtman, Fredrick R. Counterland Doctrine - An Integration Hurdle. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada422711.

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VonBerge, Gerald C. Empowerment: Quality Air Force's Biggest Hurdle. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada329394.

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Lugano, Geoffrey. ICC hurdles more than just legal. Edited by Reece Hooker. Monash University, 2022. http://dx.doi.org/10.54377/6c2a-0b74.

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Jaishankar, Dhruva. Four hurdles to brighter India–US relations. East Asia Forum, 2019. http://dx.doi.org/10.59425/eabc.1564005630.

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Kaplan, Robert, Wilfred Drath, and Joan Kofodimos. High hurdles: The challenge of executive self-development. Center for Creative Leadership, 1985. http://dx.doi.org/10.35613/ccl.1985.1084.

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Hastiadi, Fithra. Ten years on, China’s grand scheme faces hurdles. Edited by Ria Ernunsari and Ilaria Walker. Monash University, 2023. http://dx.doi.org/10.54377/406c-e648.

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Pokharel, Kushal. Overcoming hurdles to effective sub-national governance in Nepal. East Asia Forum, 2024. http://dx.doi.org/10.59425/eabc.1711404000.

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