Relevant bibliographies by topics / Etiology

Academic literature on the topic 'Etiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 May 2024

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Contents

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

Journal articles on the topic "Etiology":

1

Pratama, Bangkit Ary, and Wahyuni. "LITERATURE REVIEW: IDENTIFIKASI PENYEBAB HEPATITIS AKUT TANPA ETIOLOGI PADA ANAK." KOSALA : Jurnal Ilmu Kesehatan 10, no. 2 (May 17, 2022): 63–75. http://dx.doi.org/10.37831/kjik.v10i2.233.

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Kasus hepatitis akut tanpa etiologi yang menyerang anak-anak telah dikaitkan dengan beberapa kemungkinan etiologi termasuk penyakit coronavirus 2019 (COVID-19), vaksinasi COVID-19, agen infeksi baru, racun, dan kemungkinan etiologi terkait makanan. Masih perlu banyak penelitian yang dilakukan untuk secara tepat mengidentifikasi agen penyebab hepatitis akut tanpa etiologi. Penelitian ini bertujuan untuk mengidentifikasi kemungkinan penyebab hepatitis akut tanpa etiologi pada anak. Penelitian ini menggunakan kajian literatur (literature review). Sumber data pada penelitian ini adalah jurnal ilmiah yang tersedia di PubMed dengan tema hepatitis akut tanpa etiologi pada anak. Berdasarkan pencarian jurnal menggunaan database di PubMed dengan menggunakan kata kunci “acute hepatitis of unknown aetiology” dan “children”, didapatkan 14 jurnal dan hanya 4 jurnal saja yang memenuhi kriteria dan selanjutnya dianalisis. Hasil penelitian menunjukkan terdapat beberapa kemungkinan penyebab kasus hepatitis akut tanpa etiologi meliputi infeksi Human Adenovirus 41 Subtipe F (HAdV41-F), infeksi coronavirus–2 (SARS-CoV-2), vaksinasi COVID-19, infeksi virus lainnya, dan faktor non-infeksi. Kesimpulan pada penelitian ini adalah etiologi hepatitis akut tanpa etiologi pada anak-anak belum dapat ditentukan sehingga perlu adanya penelitian lebih lanjut. Kata kunci : anak, hepatitis akut tanpa etiologi Cases of acute hepatitis with no etiology affecting children have been associated with several possible etiologies including coronavirus disease 2019 (COVID-19), COVID-19 vaccination, new infectious agents, toxins, and possible food-related etiologies. More research was needed to accurately identify the causative agent of acute hepatitis without an etiology. This study aimed to identify possible causes of acute hepatitis without etiology in children. This study used a literature review. The data sources in this study were scientific journals available on PubMed with the theme of acute hepatitis without etiology in children. Based on a journal search using the PubMed database using the keywords “acute hepatitis of unknown aetiology” and “children”, 14 journals were obtained and only 4 journals met the criteria and were then analyzed. The results showed that there were several possible causes of acute hepatitis cases without etiology including Human Adenovirus 41 Subtype F (HAdV41-F) infection, coronavirus-2 (SARS-CoV-2) infection, COVID-19 vaccination, other viral infections, and other factors. non-infectious. The conclusion in this study is that the etiology of acute hepatitis without an etiology in children has not been determined so that further research is needed. Keywords: acute hepatitis of unknown aetiologi, children Korespondensi: Bangkit Ary Pratama, Poltekkes Bhakti Mulia, Jl. Solo-Sukoharjo No.KM. 9, Sukoharjo, Jawa Tengah, email: bangkit@poltekkesbhaktimulia.ac.id, 085326333050
2

White, Keith C. "Etiology." Clinical Obstetrics and Gynecology 31, no. 1 (March 1988): 141–52. http://dx.doi.org/10.1097/00003081-198803000-00017.

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Crowther, Mark, and Jeffrey Weitz. "ETIOLOGY." Evidence-based Cardiovascular Medicine 3, no. 2 (June 1999): 34–35. http://dx.doi.org/10.1054/ebcm.1999.0207.

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Field, Teresa. "ETIOLOGY." Evidence-based Oncology 1, no. 2 (June 2000): 44–45. http://dx.doi.org/10.1054/ebon.2000.0021.

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White, John W. "Etiology." Journal of Burn Care & Rehabilitation 7, no. 5 (September 1986): 446. http://dx.doi.org/10.1097/00004630-198609000-00037.

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Morgan, Rachel. "Etiology." Prairie Schooner 91, no. 2 (2017): 116. http://dx.doi.org/10.1353/psg.2017.0028.

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Dr. Nupur Sah, Dr Nupur Sah, Dr Hemant Bhutani, and Dr Priyadarshini Shetty. "Halitosis – Etiology and Diagnosis." Indian Journal of Applied Research 3, no. 11 (October 1, 2011): 352–54. http://dx.doi.org/10.15373/2249555x/nov2013/109.

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8

Nagai, Atsushi, and Kazutetsu Aoshiba. "2. Etiology." Nihon Naika Gakkai Zasshi 97, no. 6 (2008): 1177–83. http://dx.doi.org/10.2169/naika.97.1177.

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Davidson, Joseph. "Bacterial Etiology." Journal of the American Dental Association 122, no. 1 (January 1991): 28. http://dx.doi.org/10.14219/jada.archive.1991.0013.

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Gillison, M. "Viral etiology." Radiotherapy and Oncology 82 (February 2007): S4. http://dx.doi.org/10.1016/s0167-8140(07)80017-x.

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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Etiology":

1

Molina, Seguin Jessica. "Caracterización clínica, radiológica, pronóstica y del perfil de biomarcadores de los sujetos con ictus isquémico criptogénico no lacunar de mecanismo embólico." Doctoral thesis, Universitat de Lleida, 2019. http://hdl.handle.net/10803/665836.

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Introducció: L’interés per conèixer les característiques dels pacients amb ictus criptogènic no llacunar de mecanisme embòlic (de l’anglès ESUS) ha crescut últimament desde que es disposa de fàrmacs més segurs pel tractament preventiu. Ens planteguem que els ESUS presenten unes característiques clíniques, radiològiques, perfil de biomarcadors (BM) i pronòstic propis que difereixen de les altres etiologies. Metodologia: Analitzem dues cohorts. La primera cohort prospectiva analitza les característiques clíniques, de neuroimatge, ecocardiogràfiques, BM (NSE, IL-6, hs-CRP, troponina, NT-proBNP, fibrinogen, leucòcits, colesterol tradicional i no-tradicional) i recurrència. La segona cohort determina dades clíniques i de l’evolució intrahospitalaria. Ambdues van analitzar predictors de mal pronòstic en ESUS. Conclusions: Les característiques clíniques, radiològiques i perfil de BM que presenten els ESUS, els diferencien dels altres subtipus inclòs de la FA crònica i de novo. Això implicaria que no tots els ESUS regeixen el seu origen en una font cardioembòlica no detectada, establint diversos subtipus etiològics.
Introducción: El interés por conocer las características de los sujetos con ictus criptogénico no lacunar de mecanismo embólico (del inglés ESUS) ha crecido últimamente tras disponer de fármacos más seguros para el tratamiento preventivo. Nos planteamos que los ESUS presentan características clínicas, radiológicas, perfil de biomarcadores (BM) y pronóstico propios que difieren de las otras etiologías. Metodología: Analizamos dos cohortes. La primera cohorte prospectiva analiza características clínicas, de neuroimagen, ecocardiográficos, BM (NSE, IL-6, hs-CRP, troponina, NT-proBNP, fibrinógeno, leucocitos, colesterol tradicional y no-tradicional) y recurrencia. La segunda cohorte determina datos de la clínica y evolución intrahospitalaria. Ambas analizaron predictores de mal pronóstico en ESUS. Conclusiones: Las características clínicas, radiológicas y perfil de BM que presentan los ESUS, los diferencia de los otros subtipos incluso de la FA crónica y de novo. Esto implicaría que no todos los ESUS rigen su origen en una fuente cardioembólica no detectada, pudiéndose establecer varios subtipos etiológicos.
Introduction: The interest in knowing the characteristics of subjects with embolic source undetermined stroke (ESUS) has increased recently, following the release of safer drugs for preventive treatment. We propose that ESUS subjects exhibit specific clinical and radiological characteristics, biomarker (BK) patterns and a prognosis that differentiates them from other etiologies. Methodology: Two cohorts were analysed. The first prospective cohort analysed clinical, neuroimaging, echocardiography characteristics, BK (NSE, IL-6, hs-CRP, troponin, NT-proBNP, fibrinogen, leukocytes, traditional and non-traditional cholesterol) and recurrence. The second cohort established the clinical and intra-hospital evolution data. In both cohorts, the predictors of poor prognosis in ESUS were analysed. Conclusions: The clinical, radiological and BK profile characteristics of the ESUS differentiates them from the other subtypes, including chronic and the new diagnosis of AF. These results suggest that not all ESUS subjects originate from an undetected cardioembolic source, but in fact could establish several etiological subtypes.
2

Vranjac, Alexandre. "Meningites de etiologia indeterminada no município de São Paulo, 1960 a 1977." Universidade de São Paulo, 1988. http://www.teses.usp.br/teses/disponiveis/6/6132/tde-05012018-092602/.

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E realizado o estudo epidemiológico das meningites de etiologia indeterminada no Municlpio de São Paulo, no período de 1960 a 1977. O trabalho é apresentado em quatro partes. Na primeira parte são apresentados e discutidos os diferentes modos de diagnóstico etiológico das meningites (presuntivos e de certeza) e é enfatizada a necessidade do estudo das meningites indeterminadas. Na segunda parte é apresentado o comportamento epidemiológico da doença meningocócica no Município de São Paulo, no período 1960 a 1977. Esta apresentação é feita visando comparar e procurando verificar a influência da doença meningocócica no comportamento epidemiológico das meningites de etiologia indeterminada. Na terceira e quarta partes são apresentados os caracteres epidemiológicos das meningites de etiologia indeterminada. Inicialmente os casos são classificados em meningites indeterminadas de provavel etiologia bacteriana ou viral, utilizando-se como parâmetro para a classificação o percentual de neutrófilos no liquor. Em seguida são apresentados e analisados os comportamentos segundo variaveis da pessoa (idade e sexo), do local de residência (segundo distritos e areas homogêneas do município), do tempo (variação anual e mensal), modo diagnóstico, evolução clinica, tempo de hospitalização. O estudo mostra que entre 1972 e 1977 ocorreu no Município de São Paulo um aumento significativo de casos de meningite de etiologia indeterminada; grande parte dos casos, provavelmente, era constituída por casos de meningite meningocócica, dos quais não foi possivel a determinação etiológica. Ocorreu também, concomitantemente, um aumento significativo de meningites de provável etiologia viral. O percentual de neutrófilos no liquor (primeiro exame) em épocas epidêmicas, pode ser utilizado como parâmetro para classificacão epidemiológica meningites segundo etiologia provavelmente bacteriana ou viral.
The epidemiological behaviour of the meningitis of undetermined etiology within the Municipality of São Paulo, during the period from 1860 to 1977, is studied. The work consists of four parts. In the first part, the different forms of etiological diagnosis of meningitis (either presumptives ar certain) are submitted and discussed, as well as the need study of the undetermined meningitis. In the second part the epidemiological behaviour of the meningococcal diseases within the Municipality of São Paulo, during the period from 1960 to 1977, is submitted. Such a presentation is made with the purpose of comparison, and trying to verify the influence of the meningococcal disease on the epidemiological behaviour of the meningitis of undetermined etiology. In the third and fourth parts, the epidemiologic characters of the meningitis of undetermined etiology are submitted. At first, the cases are classified as undetermined meningitis of probable bacterial or viral etiology, using as parameter for the classification the percentile number of neutrophiles in the liquor (first examination). Then, there are submitted and analysed the behaviour as per the variables of the person (age and sex), place of residence (according to districts and homogeneous areas within the Municipality), time (annual and monthly variation), form of diagnosis, clinic evolution, and hospitalization period. It is concluded that between 1972 and 1977 there was in the Municipality of São Paulo, an epidemics of meningitis of undetermined etiology; most of the cases were, probably, constituted by cases of meningococcic meningitis, of which it was not possible to make the etiologic determination. There was, also, al the same time, an important increase of diagnosis of meningitis of probable viral etiology. The percentile number of neutrophiles in the Liquor (first examination), in epidemic times, may be used as an epidemiological parameter for the classification of the meningitis, as per the etiology, probably bacterial or viral.
3

Nilsson, Magnus. "Etiology of gastroesophageal reflux /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-852-1/.

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Schildt, Elsy-Britt. "Etiology of oral cancer." Doctoral thesis, Umeå universitet, Onkologi, 1998. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96907.

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Zinkevičienė, Auksė. "Yeast in atopic dermatitis etiology." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2012. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2012~D_20121107_091213-63157.

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Isolation and identification of all yeast species found on skin affected by atopic dermatitis, evaluation of their influence to the synthesis of IgE antibodies, and assessment of the possible cross-reactivity between different yeast species was performed. It was shown that in 36.9 % of the cases of atopic dermatitis, the affected skin was colonized with yeast belonging to three genera: Candida, Malassezia and Rhodotorula. Systematic and phylogenetic analysis of sequences from atypical Malassezia restricta strain M8 indicated that this isolate could be a member of a new yeast species. Three atypical Malassezia isolates M47, M54 and M235 were identified as non-lipid-dependent variants of Malassezia furfur. It was shown that in atopic dermatitis, cutaneous colonization with yeast is two-fold higher in adults than in children. The sera of atopic dermatitis patients have specific IgE antibodies to cross-reactive intracellular yeast antigens. Candida pelliculosa and house dust mites Dermatophagoides pteronyssinus and Dermatophagoides farinae might share some allergenic epitopes. The results of this study suggest that attention should be given to a cutaneous colonization by saprophytic yeast since the immune response to the allergens could further exacerbate allergic inflammation due to cross-reactive epitopes.
Išskirtos ir identifikuotos atopinio dermatito pažeistą odą kolonizuojančios mielių rūšys, įvertinta jų įtaka specifinių IgE antikūnų sintezei bei kryžminių reakcijų tarp skirtingų mielių rūšių galimybė. Nustatyta, kad 36,9 % atvejų atopinio dermatito pažeista oda yra kolonizuojama Candida, Malassezia ir Rhodotorula genties mielėmis. Išskirtas netipinėmis fiziologinėmis savybėmis pasižymintis Malassezia restricta kamienas M8 gali būti naujos rūšies atstovas. Išskirti netipinėmis fiziologinėmis savybėmis pasižymintys Malassezia genties kamienai M47, M54 ir M235 identifikuoti kaip nuo išorinio lipidų šaltinio nepriklausantys Malassezia furfur. Įrodyta, kad mielės suaugusių asmenų atopinio dermatito pažeistą odą kolonizuoja du kartus dažniau negu vaikų. Įrodyta, kad atopiniu dermatitu sergančių asmenų kraujo serume aptinkama prieš kryžmiškai reaguojančius mielių viduląstelinius antigenus nukreiptų specifinių IgE antikūnų. Taip pat nustatyta, kad Candida pelliculosa ir namų dulkių erkių Dermatophagoides pteronyssinus ir Dermatophagoides farinae alergenai gali turėti panašius epitopus. Darbo rezultatai patikimai rodo, kad atopinio dermatito pažeistą odą kolonizuojančios komensalinės mielės gali pasunkinti atopinio dermatito eigą dėl kryžmiškai reaguojančių epitopų tarp skirtingų biologinių rūšių antigenų.
6

Tabatabaei, Ali Reza. "Parkinson's disease : etiology, prevention and treatment." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30382.

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This thesis consists of three chapters dealing with different aspects of Parkinson's disease (PD). 3-Acetylpyridine (3-AP), a naturally occurring neurotoxin, was studied for its neurodegenerative properties on the mesostriatal dopaminergic system in rats as a possible environmental cause of idiopathic PD. Chronic administration of this compound to rats caused a moderate but insignificant reduction of striatal dopamine (determined by HPLC measurement of striatal dopamine) and a more substantial degeneration of cerebellar neurons and their neurotransmitters (determined by amino acid analysis of cerebellum). Prophylactic use of a high dose of nicotinamide prevented the reduction of dopamine in the striatum as well as the severe behavioural manifestations induced by 3-AP in rats. The cerebellar damage, however, was not affected. Different mechanisms of damage by 3-AP in these structures were presumed based on the protective effects of nicotinamide in the substantia nigra but not in the cerebellum. Possible protective properties of MK-801 (a noncompetitive NMDA antagonist) and nicotinamide against MPTP neurotoxicity were also examined in mice. MK-801 treatment provided a substantial protection against MPTP-induced reduction of striatal dopamine. Nicotinamide on the other hand provided no such protection. Finally, a new controversial approach to the treatment of parkinsonism was evaluated. Nervous tissue from 13-15 day-old fetuses was transplanted into MPTP-treated mice. The transplanted material was harvested from different areas of the fetal brain and was prepared by various procedures to examine the possible bases of any improvement in the host animal. After two studies, we did not find a biochemical improvement in transplanted mice treated with MPTP regardless of the nature of the transplanted materials.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
7

Reed, Daniel. "Assessment of fifth metatarsal fracture etiology." Connect to this title online, 2008. http://etd.lib.clemson.edu/documents/1219855425/.

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Hanna, Courtney Wood. "Recurrent miscarriage : unraveling the complex etiology." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44347.

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Recurrent miscarriage (RM), defined as 3 or more consecutive spontaneous losses of pregnancy before 20 weeks gestation, affects 1-2% of couples and has a complex etiology. Half of miscarriages from RM cases are caused by chromosomal abnormalities in the embryo and while there are several associated maternal factors, underlying causes and clinically relevant biomarkers have been elusive. I hypothesized that genetic and/or epigenetic factors associated with maternal meiotic non-disjunction, reproductive aging and endocrinological profile, or placental functioning will contribute to the etiology of RM. In these case-control studies, I investigated the association between RM and 1) maternal mutations in synaptonemal complex protein 3 (SYCP3), 2) maternal telomere lengths, 3) maternal polymorphisms in genes in the hypothalamus-pituitary-ovarian (HPO) axis and 4) placental DNA methylation patterns. The findings suggest that maternal mutations in SYCP3 and polymorphisms in HPO axis genes may not contribute significantly to risk for RM. No mutations in SYCP3 were identified in women with RM with at least one trisomic conception. While associations between polymorphisms within the estrogen receptor β, activin receptor 1, prolactin receptor and glucocorticoid receptor genes and RM were identified, these were not significant after correction for multiple comparisons. Aspects of chromosomal biology may be important factors in the etiology of RM. Women with RM had significantly shorter telomeres compared to controls, suggesting altered rates of biological aging. In the placental villi of RM samples, there were few differences in DNA methylation at targeted sites when compared to isolated miscarriages and elective terminations. However, gene ontology analysis showed that imprinted genes and immune response pathways were overrepresented among those sites differentially methylated between RM and elective termination placentas. The RM group additionally had an increase in the number of outlier cases at a select number of imprinted loci. Furthermore, several placental samples from both cases and controls showed aberrant DNA methylation profiles at many loci investigated, suggesting these samples may have global dysregulation of DNA methylation and/or differences in placental composition/functioning. These studies have improved our understanding of mechanisms involved in RM and will contribute to the direction of future research.
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Lancaster, Johnathan Mark. "Molecular genetic etiology of ovarian cancer." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/55576/.

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Ovarian cancer is the fifth leading cause of cancer death among women in Western Europe and the United States and has the highest mortality rate of all gynecologic cancers. Approximately 75% of cases of epithelial ovarian carcinoma are diagnosed at advanced-stage (III/IV) with disseminated intra-peritoneal metastases, such that the majority of patients succumb to the disease within 5 years. Mortality from the disease has changed little over the last several decades. Despite such dismal statistics, our understanding of the molecular etiology that underlies ovarian cancer development, progression and response to therapy remains incomplete. The recent development of DNA microarrays enables the simultaneous measurement of expression of thousands of genes in a single sample, providing a molecular phenotyping not evident by traditional clinical, molecular or histopathologic methods. This thesis outlines the characterization of genome-wide expression patterns that underlie ovarian cancer development and metastasis, as well as clinical behavior relating to likelihood of optimal surgical resection, response to chemotherapy, and ultimate survival. Individual genes that contribute to the expression profiles are analysed further to delineate their specific role in ovarian cancer development and progression. Additionally, the contribution of a low penetrance polymorphic allele in the progesterone receptor gene as a risk factor for the development of the disease is examined in a large population-based case-control trial. Our data suggest that microarray analysis can facilitate the characterization of the molecular basis to ovarian cancer development, metastasis, and response therapy. Specific genes identified in this analysis represent not only potential biomarkers for the presence and clinical behavior of ovarian cancers, but appealing therapeutic targets. Our findings suggest that gene-expression profiles can be developed that can be applied in the clinic to not only provide prognostic information, but predict response to specific chemotherapeutic agents, enabling treatments to be tailored to individual patients with ovarian cancer.
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Haemer, Joseph Michael. "Mechanical etiology of osteoarthritis after meniscectomy /." May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Books on the topic "Etiology":

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Schneider, Hans-Joachim, ed. Urolithiasis: Etiology · Diagnosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70579-3.

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M, Peacock, and Schneider Hans-Joachim 1931-, eds. Urolithiasis: Etiology, diagnosis. Berlin: Springer-Verlag, 1985.

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Segal, Bernard. Alcoholism Etiology and Treatment. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003290773.

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Jarrett, Ruth F., ed. Etiology of Hodgkin’s Disease. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-0339-8.

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H, Ellenberg Jonas, Koller William C. 1945-, and Langston J. W, eds. Etiology of Parkinson's disease. New York: Dekker, 1995.

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F, Jarrett Ruth, North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Research Workshop on the Aetiology of Hodgkin's Disease (1994 : Loch Lomond, Scotland), eds. Etiology of Hodgkin's disease. New York: Plenum Press, 1995.

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L, Dellarco Vicki, Voytek Peter E, Hollaender Alexander 1898-, and Symposium on Aneuploidy: Etiology and Mechanisms (1985 : Carnegie Institution of Washington), eds. Aneuploidy: Etiology and mechanisms. New York: Plenum Press, 1985.

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Schad-Somers, Susanne P. Sadomasochism: Etiology and treatment. Northvale, N.J: Jason Aronson, 1996.

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V, Patterson Alina, and Yeager Pauline N, eds. Asthma: Etiology, pathogenesis & treatment. New York: Nova Science Publishers, 2008.

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Levine, Arthur S., ed. Etiology of Cancer in Man. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2532-8.

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Book chapters on the topic "Etiology":

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Steele, Sonya U., and Ellen M. Mowry. "Etiology." In Multiple Sclerosis and CNS Inflammatory Disorders, 1–9. Chichester, UK: John Wiley & Sons, Ltd., 2014. http://dx.doi.org/10.1002/9781118298633.ch1.

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Thrusfield, Michael. "Etiology." In Diseases of Coral, 16–27. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828502.ch3.

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Molina, J. Ernesto. "Etiology." In New Techniques for Thoracic Outlet Syndromes, 47–49. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5471-7_13.

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Sameshima, Glenn T. "Etiology." In Clinical Management of Orthodontic Root Resorption, 27–31. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58706-2_3.

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Cheli, Rodolfo, Alessandro Perasso, and Attilio Giacosa. "Etiology." In Gastritis, 81–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71845-8_6.

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Sturmey, Peter, and Don E. Williams. "Etiology." In Pica in Individuals with Developmental Disabilities, 29–38. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30798-5_3.

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Kar, Sujita Kumar, and Sarvodaya Tripathy. "Etiology." In Encyclopedia of Evolutionary Psychological Science, 1–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-16999-6_767-1.

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Aravalli, Rajagopal N., and Clifford J. Steer. "Etiology." In Hepatocellular Carcinoma, 3–6. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09414-4_2.

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Willis, Diane J., and C. Eugene Walker. "Etiology." In Handbook of Child Psychopathology, 29–51. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-1162-2_2.

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Suzuki, Jiro. "Etiology." In Moyamoya Disease, 131–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-95483-2_11.

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Conference papers on the topic "Etiology":

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Lehman, Lyle V., and John L. Brumley. "Etiology of Multiple Fractures." In SPE Production Operations Symposium. Society of Petroleum Engineers, 1997. http://dx.doi.org/10.2118/37406-ms.

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Rallis, Efstathios, Eleni Sfyri, and Vasiliki Kefala. "Etiology of chronic pruritus." In 1st Conference of the Hellenic Scientific Society of Aesthetics. PHARMAKON-Press, 2024. http://dx.doi.org/10.61873/zefl9915.

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Pruritus is considered a very frequent symptom and defined as chronic when its duration is longer than 6 weeks. The prevalence and the etiology of chronic pruritus (CP) are associated with various factors such as, age, atopy, underly- ing diseases, ethnicity, climate and humidity, as well as access to local healthcare system. The CP significantly affects the patients’ quality of life. Over time, patients often report sleep and mood disorders, with a negative psycho-social impact. From skin to brain, pruritus transmission occurs via multiple pathways, which are regulated by numerous cells, mediators, and receptors. A complete history and careful clinical examination are the keys to the diagnostic approach and determining treatment steps. Dermatological examination is essential and sometimes, an extensive laboratory testing must be carried out. The complexity in the presentation of this symptom, its obscure pathophysiology and multifactorial etiology, and the absence of clearly defined therapeutic goals, make CP a diagnostic and therapeutic challenge.
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Zainettinova, D. B., M. N. Julanov, and N. N. Mukhamadiyeva. "Etiology of mastitis in cows." In Scientific achievements of the third millennium. SPC "LJournal", 2018. http://dx.doi.org/10.18411/scc-05-2018-11.

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Gilemkhanova, D. R., L. A. Gaynutdinova, and N. F. Sharifullina. "FEATURES OF POLYNEUROPATHY OCCUPATIONAL ETIOLOGY." In The 4th «OCCUPATION and HEALTH» International Youth Forum (OHIYF-2022). FSBSI «IRIOH», 2022. http://dx.doi.org/10.31089/978-5-6042929-6-9-2022-1-58-62.

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Polyneuropathy (PNP) is a common disease of peripheral nervous system, manifested by symptoms of sensory and motor nerve fibers damage. The main etiological factors of occupational PNP syndrome are physical overload and occupational vibration (local, whole-body – total). When diagnosing PNP, it is necessary to conduct electroneuromyography (ENMG). The article presents the results of developmental conditions and clinical and functional features of occupational PNP study according to 43 patients with occupational PNP examination by Ishteryakova O.A. developed registration card, statistical assessment. All patients underwent ENMG. When assessing the state of sensitive fibers, a decrease in the amplitude of the sensory response to 3.51±0.42μV (with PNP from vibration) and 3.09±0.15μV - with PNP from physical overload was noted. According to ENMG results, statistically significant (p<0.05) decrease in the nerve conduction velocity along the sensitive fibers was established median nerve on both sides in individuals with PNP from physical overload compared with PNP from vibration. When stimulating motor fibers of median nerve at the wrist and in the ulnar region in patients with PNP from vibration, the value of residual latency averaged 2.62±0.9 ms, with PNP from overload - 4.06±0.70 ms. According to work results, it was revealed that changes in ENMG parameters are more pronounced in people with PNP from physical overload.
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Mäntylä, Jarkko, Witold Mazur, Arja Viinanen, Minna Purokivi, and Paula Kauppi. "Etiology of bronchiectasis in Finland." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4506.

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Cheema, M., C. Gearges, A. Adial, M. Patel, S. Usman, and A. Iftikhar. "Unusual Etiology of Spontaneous Pneumomediastinum." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1539.

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CASSONE, ANTONIO. "Etiology of vascular related infections." In Frontiers in Imaging Science: High Performance Nuclear Medicine Imagers for Vascular Disease Imaging (Brain and Heart). Trieste, Italy: Sissa Medialab, 2008. http://dx.doi.org/10.22323/1.039.0006.

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KLÖPPEL, GÜNTER. "ALCOHOLIC CHRONIC PANCREATITIS ETIOLOGY AND PATHOGENESIS." In Proceedings of the 92nd Course of the International School of Medical Sciences. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814447249_0002.

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Hamdi, Besma, Iness Moussa, Anissa Berraies, Ameni Touil, Jamel Ammar, and Agnes Hamzaoui. "Exacerbations of bronchiectasis: Etiology and outcome." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3906.

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Hyde, R., and N. Moguillansky. "A Unique Etiology of Lipoid Pneumonia." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1870.

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Reports on the topic "Etiology":

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Petrova, S. G., and M. P. Neustroev. Salmonella abortion of horses (ETIOLOGY, PREVENTION). Yakut State Agricultural Academy, 2019. http://dx.doi.org/10.18411/978-5-6042744-2-2-253-255.

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Bordey, Angelique. Understanding the Etiology of Tuberous Sclerosis Complex. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566455.

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Young, J., Eitan Bogin, Donald Beitz, and A. McGillard. Etiology of Fatty Liver of Dairy Cows. United States Department of Agriculture, October 1986. http://dx.doi.org/10.32747/1986.7566851.bard.

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Kerr, Nancy J., and Robert A. Dailey. Occurrence, etiology and management of ringwomb in ewes. West Virginia University Agricultural Experiment Station, January 1999. http://dx.doi.org/10.33915/agnic.720.

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Ng, Vicky, Michelle Science, Jordan Feld, Hemant Shah, Ari Bitnun, Laura Bourns, Aaron Campigotto, et al. Severe Acute Hepatitis in Children of Unknown Etiology. Ontario COVID-19 Science Advisory Table, June 2022. http://dx.doi.org/10.47326/ocsat.2022.03.63.1.0.

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Davis, Irene M. Biomechanical Factors in the Etiology of Tibial Stress Fractures. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409645.

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Davis, Irene S. Biomechanical Factors in the Etiology of Tibial Stress Fractures. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada458411.

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Freeman, Stanley, and Daniel Legard. Epidemiology and Etiology of Colletotrichum Species Causing Strawberry Diseases. United States Department of Agriculture, September 2001. http://dx.doi.org/10.32747/2001.7695845.bard.

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Abstract:
Diseases caused by Colletotrichum spp. are one of the most important limitations on international strawberry production, affecting all vegetative and fruiting parts of the plant. From 1995 to 1997, C. acutatum infections reached epidemic levels in Israeli strawberry nurseries, causing extensive loss of transplants in fruit-bearing fields and additional reductions in yield. Although C. acutatum also occurs on strawberry in Florida, recent crown rot epidemics have been primarily caused by C. gloeosporioides. Little is known about the basic epidemiology of these important diseases on strawberry. The source of initial inoculum for epidemics in Israel, Florida (other US states including California) and the rest of the world is not well understood. Subspecies relationships between Colletotrichum isolates that cause the different diseases on strawberry (i.e. attack different tissues) are also not well understood. Objectives of this proposal were to detennine the potential of infested soil, strawberry debris and other hosts as sources of primary inoculum for strawberry diseases caused by Colletotrichum spp. in Israel and Florida. In addition, traditional (ie. morphological characteristics, benomyl sensitivity, vegetative compatibility grouping) and DNA based methods were used to investigate the etiology of these diseases in order to resolve epidemiologically important subspecies variation. In Israel it was found that C. gloeosporioides and C. acutatum infecting strawberry could remain viable in sterilized soil for up to one year and in methyl-bromide fumigated soil for up to 4 months; inoculum in mummified fruit remained viable for at least 5 months under field conditions whereas that in infected crowns was not recovered. Therefore, the contribution of these inocula to disease epidemics should be considered. The host range and specificity of C. acutatum from strawberry was examined on pepper, eggplant, tomato, bean and strawberry under greenhouse conditions. The fungus was recovered from all plant species over a three-month period but caused disease symptoms only on strawberry. C. acutatum was also isolated from healthy looking, asymptomatic plants of the weed species, Vicia and Conyza, growing in infected strawberry fruiting fields. Isolates of C. acutatum originating from strawberry and anemone infected both plant species in artificial inoculations. The habitation of a large number of plant species including weeds by C. acutatum suggests that although it causes disease only on strawberry and anemone in Israel, these plants may serve as a potential inoculum source for strawberry infection and pennit survival of the pathogen between seasons. In Florida, isolates of Colletotrichum spp. from diseased strawberry fruit and crowns were evaluated to detennine their etiology and the genetic diversity of the pathogens. Only C. acutatum was recovered from fruit and C. gloeosporioides were the main species recovered from crowns. These isolates were evaluated at 40 putative genetic loci using random amplified polymorphic DNA (RAPD). Genetic analysis of RAPD markers revealed that the level of linkage disequilibrium among polymorphic loci in C. gloeosporioides suggested that they were a sexually reproducing population. Under field conditions in Florida, it was detennined that C. gloeosporioides in buried crowns survived
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Qin, Yi-Xian. Stress Fracture Etiology as Dependent on Mechanically Induced Fluid Flow. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada419689.

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Sauter, R. W. Etiology of Early Lifestage Diseases, Project 84-44, 1985 Final Report. Office of Scientific and Technical Information (OSTI), October 1986. http://dx.doi.org/10.2172/7166620.

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