by Ho Cheong-Yip. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 198-222). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

A hipersensibilidade dentinária (HD) é descrita na literatura como uma dor aguda, de curta duração, provocada por estímulos térmico, tátil, osmótico, químico ou evaporativo em região de exposição dentinária, não sendo atribuída à dor causada pela presença de defeito ou doença de origem dentária. Esse tipo de acometimento tem sido cada vez mais reportado pelos pacientes, em vista disso, o objetivo desse estudo foi avaliar a extensão e gravidade de HD, bem como sua associação com indicadores periodontais [índice de placa (IP), índice gengival (IG) e recessão gengival (RG)] em uma amostra composta por 132 indivíduos com HD diagnosticada por meio de estímulo térmico/evaporativo (jato de ar) associada à escala Schiff. Análises descritivas foram feitas e as porcentagens médias de IP e IG foram estimadas considerando 6 sítios por dente e também 3 sítios das faces vestibulares. Além disso, os dados foram analisados através de modelos uni e multivariados utilizando análises de regressão linear. A média de idade foi de 30.66±10.33, sendo o sexo feminino mais afetado pela HD (83.3%). Foi possível observar que a HD esteve associada à recessão gengival. A prevalência de dentes com recessão gengival foi de 17.17%, enquanto que a prevalência de recessão em dentes com HD foi de 77.1% e a média de recessão vestibular foi de 1.58±0.87. Quando considerada a média de dentes com 1 ou mais milímetros de recessão, observou-se que, em média, 4.48 dos dentes apresentaram esta condição. Um maior número médio de dentes com recessão e menores escores médios de IP nos sítios vestibulares apresentaram-se signicativamente associados ao número médio de dentes com HD. A gravidade da HD nos pacientes foi significativamente influenciada por maior média de recessão gengival e foi maior nos pacientes do sexo feminino. Dentes que possuíam maiores médias de recessão e maiores escores médios de IP e menores de IG nos sítios vestibulares apresentaram maiores valores na escala Schiff (p<0.05). Frente aos achados, é possível observar que portadores de HD têm um grande número de dentes afetados por esta condição e que estes apresentam recessão. Além disto, nos dentes que apresentam HD, a gravidade desta está associada a presença de mais placa e melhor condição gengival, além da extensão da recessão. / Dentin hypersensitivity (DH) is described in the literature as an acute short-term pain caused by thermal, tactile, osmotic, chemical or evaporative stimuli in the region of dentin exposure and not attributed to pain caused by the presence of defect or disease of dental origin. Therefore, the aim of this study was to evaluate the extent and severity of DH, as well as its correlation with periodontal indicators [plaque index (PI), gingival index (GI) and gingival recession (GR)] in 132 individuals with DH diagnosed by thermal/evaporative (air blast) stimulation associated with the Schiff scale. Descriptive analyzes were made and the mean percentages of PI and GI were estimated considering 6 sites per tooth and also 3 buccal sites. In addition, the data were analyzed using univariate and multivariate models using linear regression analysis. The mean age was 30.66 ± 10.33, female sex being more affected by DH (83.3%). It was possible to observe that DH was associated to gingival recession. The prevalence of teeth with gingival recession was 17.17%, while the prevalence of recession in teeth with DH was 77.1%. The mean of vestibular recession was 1.58 ± 0.87, and when considered the mean teeth with 1 or more millimeters recession, it was observed that, a mean of 4.48 teeth presented this condition. A higher mean number of teeth with recession and lower mean PI scores in the vestibular sites were associated (p<0.001) with the mean number of teeth with DH. The severity of DH in number of patients was significantly influenced by the higher mean of gingival recession and was higher in the female patients. Teeth that had higher recession mean and higher mean PI scores at the buccal sites, but lower GI scores at this sites, presented significantly higher values on the Schiff scale (p <0.05). In view of the findings, it is possible to observe that DH patients have a large number of teeth affected by this condition and that these present gingival recession. In addition, in the teeth that present DH, the severity is associated with the presence of more plaque and better gingival condition, in addition to the extent of the recession.

過敏性疾病的患病率一直上升，約30%至40%的世界人口受到一個或多個過敏疾病影響。然而，現時仍然缺乏有效治療過敏性疾病的方法，大多數傳統療法只能改善臨床症狀，卻沒有針對導致過敏性炎症的主要因素。嗜酸性粒細胞浸入和積累於局部炎症部位以及延緩了的細胞凋亡是過敏性炎症的標誌，而嗜酸性粒細胞亦被認為是過敏性炎症的主要效應細胞。因此，針對嗜酸性粒細胞，抑制其活性和衍生產物，是一個有潛力和有效地治療過敏性炎症的策略。發展針對嗜酸性粒細胞的療法需要詳細了解嗜酸性粒細胞介導炎症反應的機制。 / 在第三章中，我們把嗜酸性粒細胞與皮膚成纖維細胞一起培養，建立了一個體外的皮膚炎症模型，用以研究嗜酸性粒細胞在過敏性皮炎發病病理中的作用。我們發現，嗜酸性粒細胞和成纖維細胞的共培養顯著誘導促炎性的細胞因子IL-6和濕疹相關趨化因子CXCL1，CXCL10，CCL2和CCL5的釋放。這些炎症介質的釋放在能導致皮膚瘙癢的細胞因子IL-31和內源性警報因子IL-33的刺激下進一步加強。 IL-31和IL-33可顯著引起嗜酸性粒細胞和成纖維細胞釋放CXCL8，而當兩種細胞共培養後，CXCL8的釋放進一步增強。在共培養系統中，嗜酸性粒細胞是釋放CCL5的主要來源，而成纖維細胞則是釋放IL-6，CXCL1, CXCL8，CXCL10和CCL2的主要來源。嗜酸性粒細胞和成纖維細胞之間的直接相互作用是CXCL1，CXCL10，CXCL8和CCL5的釋放所必需的。在IL-31和IL-33的刺激下，共培養系統中嗜酸性粒細胞和成纖維細胞的細胞表面粘附分子ICAM-1的表達上調。而嗜酸性粒細胞和成纖維細胞間的互作用，以及IL-31和IL-33對兩種細胞的激活，是經由p38、ERK、JNK，NF-κB和PI3K-AK訊息傳遞徑路所調節的。另外，我們亦發現1,25-二羥維生素D3能顯著抑製共培養系統在IL-31或IL-33激活下IL-6，CCL2和CXCL8的釋放。 / 在第四章中，我們探討在嗜酸性粒細胞和支氣管上皮細胞BEAS-2B的共培養系統中，兩種細胞的細菌相關模式識別受體成員NOD1和NOD2激活機制。我們發現NOD配體iE-DAP和NOD2配體MDP能激活嗜酸性粒細胞內的ERK和NF-κB信號傳導通路，而MDP可以激活嗜酸性粒細胞和BEAS-2B細胞的ERK信號傳導通路。當嗜酸性粒細胞和BEAS-2B細胞共培養時，iE-DAP和MDP均可激活嗜酸性粒細胞和BEAS-2B細胞的ERK和NF-κB信號傳導通路，而且與單獨培養的細胞相比，激活的程度更強。此外，我們還探討了iE-DAP和MDP對 BEAS-2B細胞和嗜酸性粒細胞的核轉錄因子的激活作用。我們發現iE-DAP和MDP可以激活嗜酸性粒細胞和BEAS-2B細胞的某些轉錄因子，包括因子NF-κB、STAT-3和NFAT等，而多數被激活的轉錄因子都跟過敏性炎症和哮喘的發病有關。除了體外研究，我們還建立了過敏性肺部炎症的小鼠模型，用以研究iE-DAP和MDP的生理效應。iE-DAP和MDP均可激活第二型輔助性T細胞相關的免疫球蛋白E生產，以及誘導嗜酸性粒細胞趨化因子CCL5。 / 上述的研究結果表明IL-31與IL-33在過敏性皮炎的發病病理中發揮關鍵作用，通過不同的信號傳導機制激活嗜酸性粒細胞與成纖維細胞的相互作用。另外，我們探討了在嗜酸性粒細胞和BEAS-2B細胞中，調節NOD1和NOD2激活的信號傳導機制，加上動物實驗，所得的結果有助了解細菌感染在哮喘發作中所發揮的影響。這些關於細胞之間和細胞內調控機制的研究結果，進一步增強我們對嗜酸性粒細胞介導炎症的理解，並為發展更高專一性、效用和更少副作用的消炎藥提供了新的標靶和方向。 / The prevalence of allergic diseases has been steadily increased, with about 30-40% of the world population being affected by one or more allergic conditions. Effective treatments on allergic diseases are still lacking, as most of the traditional therapies aim at clinical improvement without targeting the factors that primarily promote the allergic inflammation. Infiltration, delayed apoptosis and accumulation of eosinophils at the local inflammatory sites are the hallmarks of allergic inflammation and eosinophils are considered as the principal effector cells in allergic inflammation. Anti-eosinophils therapeutics inhibit eosinophil activity and eosinophil-derived products are thus potential strategies in treating allergic inflammation effectively. Elucidation of the detailed mechanisms of eosinophil-mediated inflammation is therefore necessary for the development of anti-eosinophils therapeutics. / In Chapter 3, we established an in vitro skin inflammation model by co-culturing eosinophils with dermal fibroblasts in order to study the pathophysiology of eosinophils’ involvement in the pathogenesis of atopic dermatitis (AD). We revealed that co-culture of eosinophils and fibroblasts significantly induced release of pro-inflammatory cytokine IL-6 and AD-related chemokines CXCL1, CXCL10, CCL2 and CCL5. Such inductions were further enhanced with pruritogenic cytokine IL-31 and endogenous alarmin IL-33 stimulation. IL-31 and IL-33 could significantly provoke the release of CXCL8 from eosinophils and fibroblasts, respectively, which was further enhanced upon co-culture. In co-culture, eosinophils and fibroblasts were the main source for the release of CCL5, and IL-6, CXCL1, CXCL8, CXCL10 and CCL2, respectively. Direct interaction between eosinophils and fibroblasts was required for CXCL1, CXCL10, CXCL8 and CCL5 release. Cell surface expression of intercellular adhesion molecule-1 on eosinophils and fibroblasts was upregulated in co-culture upon IL-31 and IL-33 stimulation. The interaction between eosinophils and fibroblasts under IL-31 and IL-33 stimulation differentially activated ERK, JNK, p38 MAPK, NF-κB and PI3KAkt pathways. 1,25-dihydroxy vitamin D3 exerted in vitro suppressive effect on the release of IL-6, CCL2 and CXCL8 release from IL-31 or IL-33 activated co-culture of eosinophils and fibroblasts. / In Chapter 4, we revealed the mechanisms underlying bacterial-related pattern recognition receptor members NOD1 and NOD2 activation in eosinophils and bronchial epithelial cells BEAS-2B from the co-culture system and animal model experiment. NOD1 ligand iE-DAP and NOD2 ligand MDP could activate ERK and NF-κB pathways in eosinophils, while MDP stimulation could activate ERK in both eosinophils and BEAS-2B cells. When the eosinophils and BEAS-2B cells were co-cultured together, both iE-DAP and MDP could induce ERK and NF-κB activation in the two cells, and the activation was enhanced when compared with that in cells cultured alone. Besides, we also investigated the transcription factors activation in eosinophils and BEAS-2B cells by iE-DAP and MDP. iE-DAP and MDP could also activate a panel of transcription factors in eosinophils and BEAS-2B cells, including NF-κB, STAT-3 and NFAT etc, the nuclear transcription factors commonly involved in allergic inflammation and related to the pathogenesis of asthma. Apart from in vitro study, we also established an in vivo allergic pulmonary inflammation mice model to study the physiological effects of iE-DAP and MDP. Both iE-DAP and MDP could activate the Th2 related IgE production and induce eosinophil chemokine CCL5. / The above findings suggest a crucial immunopathological role of IL-31 and IL-33 in AD through the activation of eosinophils-fibroblasts interaction via differential intracellular signaling mechanisms. The intracellular signaling mechanisms regulating NOD1 and NOD2 activation in eosinophils and bronchial epithelial cells and animal experiment were also revealed and give implications of the role of bacterial infections in the exacerbation of asthma. Such information further enhances our understandings on both the intercellular and intracellular mechanisms of eosinophil-mediated inflammation, and gives implications for new targets for the development of anti-inflammatory drugs with higher specificity, potency, and less side effects. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Leung, Ming Lam. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 136-153). / Abstracts also in Chinese. / ACKNOWLEDGEMENTS --- p.I / ABSTRACT --- p.III / 摘要 --- p.VI / PUBLICATIONS --- p.IX / ABBREVIATIONS --- p.XI / TABLE OF CONTENTS --- p.XIV / Chapter Chapter 1 --- : General Introduction / Chapter 1.1 --- Allergy --- p.1 / Chapter 1.1.1 --- Definition and characteristics of allergy --- p.1 / Chapter 1.1.2 --- Allergic diseases and their prevalence --- p.2 / Chapter 1.1.3 --- Allergic inflammation --- p.2 / Chapter 1.2 --- Biology of eosinophils --- p.8 / Chapter 1.2.1 --- Development of eosinophils --- p.8 / Chapter 1.2.2 --- Cellular characteristics of eosinophils --- p.9 / Chapter 1.2.3 --- Eosinophils surface and intracellular markers --- p.10 / Chapter 1.2.4 --- Eosinophil-derived mediators --- p.13 / Chapter 1.2.5 --- Accumulation and activation of eosinophils at inflammatory sites --- p.16 / Chapter 1.3 --- Adhesion molecules in allergic inflammation --- p.19 / Chapter 1.3.1 --- Selectins --- p.19 / Chapter 1.3.2 --- Integrins --- p.20 / Chapter 1.3.3 --- Immunoglobulin gene super family --- p.21 / Chapter 1.4 --- Cytokines in allergic inflammation --- p.23 / Chapter 1.4.1 --- Pro-inflammatory cytokines --- p.23 / Chapter 1.4.2 --- Anti-inflammatory cytokines --- p.25 / Chapter 1.5 --- Chemokines in allergic inflammation --- p.27 / Chapter 1.6 --- Signal transduction in allergic inflammation --- p.29 / Chapter 1.6.1 --- Intracellular signaling mechanisms --- p.29 / Chapter 1.6.2 --- Transcription factors activation --- p.33 / Chapter 1.7 --- Perspective treatments --- p.36 / Chapter 1.7.1 --- Inhibition of pro-inflammatory cytokines --- p.36 / Chapter 1.7.2 --- Inhibition of chemokines --- p.37 / Chapter 1.7.3 --- Small interfering (si)RNA against transcription factor --- p.37 / Chapter 1.7.4 --- Signaling pathway inhibitors --- p.38 / Chapter 1.8 --- Aim of study --- p.39 / Chapter Chapter 2 --- : Materials and Methods / Chapter 2.1 --- Materials --- p.42 / Chapter 2.2 --- Methods --- p.60 / Chapter 2.2.1 --- Purification of human eosinophils --- p.60 / Chapter 2.2.2 --- Cell culture --- p.61 / Chapter 2.2.3 --- Cell surface and intracellular immunofluorescence staining --- p.63 / Chapter 2.2.4 --- Western blot --- p.64 / Chapter 2.2.5 --- Allergic asthmatic mice model --- p.64 / Chapter 2.2.6 --- Statistical analysis --- p.65 / Chapter Chapter 3 --- : Activation of Eosinophils Interacting with Dermal Fibroblasts by Pruritogenic Cytokine IL-31 and Alarmin IL-33: Implications in Atopic Dermatitis / Chapter 3.1 --- Introduction --- p.66 / Chapter 3.1.1 --- Atopic dermatitis --- p.66 / Chapter 3.1.2 --- Eosinophils in AD --- p.68 / Chapter 3.1.3 --- IL-31 --- p.68 / Chapter 3.1.4 --- IL-33 --- p.70 / Chapter 3.1.5 --- Vitamin D --- p.71 / Chapter 3.1.6 --- Hypothesis and aim of study --- p.73 / Chapter 3.2 --- Results --- p.74 / Chapter 3.2.1 --- Surface expression of receptors for IL-31 and IL-33 on human eosinophils and dermal fibroblasts --- p.74 / Chapter 3.2.2 --- Cytokine and chemokine release upon the interaction of eosinophils and dermal fibroblasts activated by IL-31 and IL-33 --- p.77 / Chapter 3.2.3 --- Source of the release of cytokines and chemokines in the co-culture system upon IL-31 and IL-33 stimulation --- p.80 / Chapter 3.2.4 --- Effect of transwell inserts on cytokine and chemokine release in IL-31 and IL-33-treated co-culture --- p.83 / Chapter 3.2.5 --- Effect of IL-31 and IL-33 on adhesion molecule expression on eosinophils and dermal fibroblast in co-culture system --- p.86 / Chapter 3.2.6 --- Intracellular signaling pathways involved in the interaction of eosinophils and dermal fibroblasts under IL-31 and IL-33 stimulation --- p.88 / Chapter 3.2.7 --- Surface expression of vitamin D receptor on human eosinophils and dermal fibroblasts --- p.96 / Chapter 3.2.8 --- Suppressive effects of 1,25-dihydroxy vitamin D₃ (calcitriol) on cytokine and chemokine release from IL-31 and IL-33-treated co-culture --- p.97 / Chapter 3.3 --- Discussion --- p.100 / Chapter Chapter 4 --- :Intracellular Signal Transduction Mechanisms of NLR Activation in Human Eosinophils and Bronchial Epithelial Cells: Implication for Bacterial Infection in Allergic Asthma / Chapter 4.1 --- Introduction --- p.107 / Chapter 4.1.1 --- Allergic asthma --- p.107 / Chapter 4.1.2 --- Eosinophils in allergic asthma --- p.108 / Chapter 4.1.3 --- NOD-like receptors --- p.109 / Chapter 4.1.4 --- Hypothesis and aim of study --- p.110 / Chapter 4.2 --- Results --- p.112 / Chapter 4.2.1 --- Intracellular signaling pathways involved in the interaction of eosinophils and BEAS-2B cells under iE-DAP and MDP stimulation --- p.112 / Chapter 4.2.2 --- Transcription factors activation in eosinophils and BEAS-2B cells under iE-DAP and MDP stimulation --- p.119 / Chapter 4.2.3 --- In vivo activating effect of NOD1,2 ligands on the IgE and chemokine concentration in serum and BALF in allergic asthmatic mice --- p.122 / Chapter 4.3 --- Discussion --- p.125 / Chapter Chapter 5 --- : Concluding Remarks and Future Studies / Chapter 5.1 --- Concluding remarks --- p.130 / Chapter 5.2 --- Future studies --- p.131 / REFERENCES --- p.136

Primary Objective: To confirm the findings of several small studies conducted in the southeastern United States showing hypersensitivity infusion reaction (HIR) rates as high as 22% with the monoclonal antibody, cetuximab. Although well known for a risk of HIRs, early clinical studies showed much lower reaction rates of 3%.

No description available.

<p>After finishing a human genome reference sequence in 2002, the genomics community has</p><p>turned to the task of interpreting it. A primary focus is to identify and characterize not only</p><p>protein-coding genes, but all functional elements in the genome. The effort has identified</p><p>millions of regulatory elements across species and in hundreds of human cell-types. Nearly</p><p>all identified regulatory elements are found in non-coding DNA, hypothesizing a function</p><p>for previously unannotated sequence. The ability to identify regulatory DNA genome-wide</p><p>provides a new opportunity to understand gene regulation and to ask fundamental questions</p><p>in diverse areas of biology.</p><p>One such area is the aim to understand the molecular basis for phenotypic differences</p><p>between humans and other primates. These phenotypic differences are partially driven</p><p>by mutations in non-coding regulatory DNA that alter gene expression. This hypothesis</p><p>has been supported by differential gene expression analyses in general, but we have not</p><p>yet identified specific regulatory variants responsible for differences in transcription and</p><p>phenotype. I have worked to identify regulatory differences in the same cell-type isolated</p><p>from human, chimpanzee, and macaque. Most regulatory elements were conserved among</p><p>all three species, as expected based on their central role in regulating transcription. How-</p><p>ever, several hundred regulatory elements were gained or lost on the lineages leading to</p><p>modern human and chimpanzee. Species-specific regulatory elements are enriched near</p><p>differentially expressed genes, are positively correlated with increased transcription, show</p><p>evidence of branch-specific positive selection, and overlap with active chromatin marks.</p><p>ivSpecies-specific sequence differences in transcription factor motifs found within this regu-</p><p>latory DNA are linked with species-specific changes in chromatin accessibility. Together,</p><p>these indicate that species-specific regulatory elements contribute to transcriptional and</p><p>phenotypic differences among primate species.</p><p>Another fundamental function of regulatory elements is to define different cell-types in</p><p>multicellular organisms. Regulatory elements recruit transcription factors that modulate</p><p>gene expression distinctly across cell-types. In a study of 112 human cell-types, I classified</p><p>regulatory elements into clusters based on regulatory signal tissue specificity. I then used</p><p>these to uncover distinct associations between regulatory elements and promoters, CpG-</p><p>islands, conserved elements, and transcription factor motif enrichment. Motif analysis</p><p>identified known and novel transcription factor binding motifs in cell-type-specific and</p><p>ubiquitous regulatory elements. I also developed a classifier that accurately predicts cell-</p><p>type lineage based on only 43 regulatory elements and evaluated the tissue of origin for</p><p>cancer cell-types. By correlating regulatory signal and gene expression, I predicted target</p><p>genes for more than 500k regulatory elements. Finally, I introduced a web resource to</p><p>enable researchers to explore these regulatory patterns and better understand how expression</p><p>is modulated within and across human cell-types.</p><p>Regulation of gene expression is fundamental to life. This dissertation uses identified</p><p>regulatory DNA to better understand regulatory systems. In the context of either evolution-</p><p>ary or developmental biology, understanding how differences in regulatory DNA contribute</p><p>to phenotype will be central to completely understanding human biology.</p> / Dissertation

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2010.

<p>Understanding the mechanisms whereby the sequence of the human genome is interpreted into diverse cellular phenotypes is a critical endeavor in modern biology. A major determinant of cellular phenotype is the spatial and temporal pattern gene expression, which is regulated in part by epigenomic properties such as histone post-translational modifications, DNA methylation, chromatin accessibility and the 3-dimensional architecture of the genome within the nucleus. These properties regulate the dynamic assembly of transcription factors and their co-regulatory proteins upon chromatin. To properly understand the interplay between the epigenomic framework of a cell and transcription factors, integrated analysis of transcription factor-DNA binding, chromatin status, and transcription is required. This work integrates information about chromatin accessibility, as measured by DNaseI hypersensitivity, transcription factor binding, as measured by chromatin immunoprecipitation, and transcription, as measured by microarray or transcriptome sequencing, to further understand the functional role of two important transcription factors, the androgen receptor (AR) and CTCF, in cancer cell line models. Data gathered from a prostate cancer cell line model demonstrate that the AR does not exclusively bind accessible chromatin upon ligand-activation, and induces significant changes in chromatin accessibility upon binding. Regions of quantitative change in chromatin accessibility contain motifs corresponding to potential collaborators for AR function, and are also significantly associated with AR-regulated transcriptional changes. Furthermore, base pair resolution of the DNaseI cleavage profile revealed three distinct patterns of AR-DNA interaction, suggesting multiple modes of AR interacting with the genome. A novel role for the nuclear receptor REV-ERB&#945; in AR-mediated transcription was explored within the same model system. Though preliminary, results thus far indicate that REV-ERB&#945; is required for AR-induced increases in target gene transcription in a manner that is likely dependent on HDAC3. Genetic knockdown of REV-ERB&#945; resulted in notable changes in chromatin accessibility around AR-target genes both before and after AR activation. The function of CTCF was interrogated using stable knockdown in a breast cancer cell line model. CTCF knockdown led to widespread changes in chromatin accessibility that were dependent on DNA sequence. Further analysis suggested that AP-1 and FOXA1 are involved in CTCF function. Together, the work presented in this dissertation offers novel insight into the behavior of two critical transcription factors in cancer cell lines, and describe a framework of analysis that can be extended and applied to any transcription factor within any desired cellular context.</p> / Dissertation

No description available.

Šunų I tipo padidinto jautrumo reakcijos klinikinė ir laboratorinė diagnostika. Darbo apimtis 42 puslapiai, sudarytos 8 lentelės, 6 paveikslai, naudoti 62 literatūros šaltiniai. Darbo tikslas - klinikiniais ir laboratoriniais tyrimo metodais įvertinti I tipo alerginės reakcijos atvejus šunų tarpe, kurie pasitaiko nedidelės smulkių gyvūnų klinikos praktikoje. Tyrimas buvo atliekamas veterinarijos klinikoje „Pas pumą“ 2012 – 2013 m. Buvo užregistruoti 38 šunų susirgimai, susiję su I tipo padidinto jautrumo reakcijos klikiniais požymiais, iš savininkų surinkta išsami anamnezė ir atlikti hematologiniai (morfologija) tyrimai. Imunologiniam tyrimui surinkti 13 alergiškų ir 12 sveikų šunų kraujo serumo mėginiai. Imunologinis IFA (ELISA) tyrimas, nustatyti tiriamųjų šunų IgE koncentracijai kraujo serume, buvo atliktas Lietuvos sveikatos mokslų universiteto veterinarijos fakulteto anatomijos ir fiziologijos katedros imunologijos laboratorijoje. Tyrimo metu nustatyta, kad dažniausiai pasitaikanti I tipo padidinto jautrumo reakcijos forma šunų tarpe buvo atopinis dermatitas (63,2 proc.), kurios ryškiausias požymis buvo niežulys (57,9 proc.), daugiausiai apimantis ausis ir pilvo ventralinę sieną. Šunų lytis ir veislė neturėjo reikšmingos įtakos I tipo padidinto jautrumo reakcijos pasireiškimui, o amžiaus tendencija ryški – alergijos pirmieji požymiai pasireiškia 6 mėn. – 2 m. šunims (62,5 – 78,57 proc.), o šunims iki 6 metų amžiaus alergijos pasikartoja dažniau. Kraujo neutrofilų... [toliau žr. visą tekstą] / Master thesis: Clinical and laboratory diagnosis of type I hypersensitivity reaction in dogs. Master thesis volume 41 pages, consisting of 8 tables, 6 pictures, 61 references used. The main aim of the thesis is to evaluate type I hypersensitivity reaction cases in dogs in small animal veterinary practice using clinical and laboratory methods. The study was carried out in veterinary practise “Pas pumą” in 2012 – 2013. 38 cases of dogs associated with type I hypersensitivity reaction were registered and a detailed medical history was collected from these dogs owners. Haematological examination was performed. Blood samples were collected from 13 dogs with type I hypersensitivity and from 12 healthy dogs. Immunological test ELISA was done to evaluate canine serum IgE levels concentration. Testing was performed in Lithuanian University of Health Sciences , Faculty of Veterinary Anatomy and Physiology, Department of Immunology laboratory. The analysis of clinical findings has shown the most common type I hypersensitivity clinical presentation among dogs is atopic dermatitis (63.2 percent). The most common clinical features were pruritus (57.9 percent) mainly of the ears and the ventral abdominal wall. Dog gender and breed had no significant effect on type I hypersensitivity reactions. The analysis showed that first signs of allergy for dogs commonly occur from 6 months until 2 years of age (62.5 – 78.57 percent of dogs). Allergies had a higher incidence of recurrence in dogs up... [to full text]