Nematodes of the genus Meloidogyne are known as “root-knot” nematodes due to the characteristic knots or galls found on the roots of infected plants. Root-knot nematodes attack over 2000 species of plants and cause over 80 billion dollars lost annually. Giant cells are feeding sites of root-knot nematodes and are enlarged multinuclear cells induced by the nematodes in susceptible host roots and that function to provide nutrients to the nematode. This thesis presents data on two techniques of studying the nuclear condition in giant cells. Colchicine was used to arrest mitosis in giant cells in a previous study. Here we test the effect of colchicine on nematode activity. The results showed that colchicine did not affect nematode egg hatch, juvenile activity, or hatch of eggs produced by treated juveniles. These results confirm that colchicine can be used to arrest mitosis in giant cells without affecting the nematode parasite. A major obstacle to the study of giant cells is collecting tissue samples that are specific to giant cells. Laser capture microdissection (LCM) is a technique that allows one to sample a single giant cell. A focused laser beam was used to collect samples of giant cell cytoplasm from fixed and sectioned tissues. RNA was then extracted from those isolated samples. Using three tomato genes as test samples, specific primers were designed to measure expression level of Rb7, LHA4, and HXK1 gene by Real-Time PCR. Expression of LHA4 and Rb7 increased with time after inoculation, and immature giant cells reached levels that were 3 and 6 times, respectively, that of cortical cells, but which were not different from root meristem cells. Expression of HXK1 did not change with time after inoculation and has the same level of that in root tip and cortical tissues. These data confirmed that the techniques of LCM coupled with RT-real-time PCR can be used to quantitate expression of genes at different stages of giant cell development without contamination from surrounding cells.

Thesis (M.S.)--University of Michigan, 1970.

Thesis (M.S.)--University of Michigan, 1970.

Introduction: There are no validated strategies in the teaching of ultrasound as a diagnostic tool in undergraduate medicine students. Given the role that ultrasound plays in the diagnostic capacity of any clinician is currently undeniable, a teaching method is proposed based on the demonstration of the association between the histopathology of a large vessel vasculitis and the characteristic ultrasound finding, known as the «halo sign». Methods: The teaching strategy was imparted by means of a 10-minute video presentation. Twenty-one final-year students from a single medical school participated in a concordance study and a validation test, identifying images corresponding to the halo sign in 120 different cases. The overall sensitivity, specificity and likelihood ratio of the students were also determined. Results: The overall concordance test had a kappa coefficient of 0.749 (SD: 0.11). The kappa concordance was 0.76 with dynamic images, and 0.84 with cross-sectional slices. The overall sensitivity was 89.7%, and the positive predictive value was 92.3%. The likelihood ratio achieved was 7.28. Conclusions: It has been shown that the application of this pedagogical method is useful in teaching the identification of an ultrasound sign to medical students. This study also suggests conditions that could be useful to improve between-observer agreement in both teaching scenarios and multiple observer scientific studies. / Revisión por pares

Giant Cell arteritis (GCA) is a systemic inflammatory disease that affects arteries of medium- and large size. Symptoms of GCA such as headache and fever usually promptly improve with treatment of glucocorticoids. Apart from advanced age, female sex and Northern-European descent, risk factors for GCA are unknown. Most studies have found that life expectancy for patients with GCA is not reduced compared with the general population and studies on cardiovascular disease in GCA have provided conflicting results. Data for the studies of this thesis are drawn from the Reykjavik Study (RS) that is a general population-based cohort study with continuous surveillance for coronary heart disease and vital status. Subjects born in 1907–1934 and living in Reykjavik, Iceland or adjacent communities in 1966 were invited for study visit from 1967-1994. Information on cardiovascular risk factors were collected at study visit. Diagnosis of GCA for this study was based on re-examination of all temporal arteries biopsies (TAB) from members of the RS cohort; however, information was also obtained from the original pathology report. Of 19,360 subjects included in the RS, 194 developed GCA during the follow-up period. Body mass index was inversely associated with the occurrence of GCA. Among men, but not women, hypertension was associated and smoking inversely associated with the occurrence of GCA. Among women, but not men, GCA was associated with coronary heart disease. Subjects with GCA had approximately 50% increase in mortality risk compared with the general population. Increase mortality was mainly observed among GCA patients based on the diagnosis of re-examination of TAB; however, no such an association was found if diagnosis of GCA was made based on the original pathology report. Those subjects were likely not clinically diagnosed with GCA, signaling that treatment for GCA might be beneficial with respect to mortality risk.

No description available.

We describe the case of a patient with documented temporal arteritis, who presented two years into her course with acute digital ischemia, presumed secondary to small vessel vasculitis. To our knowledge, this complication of temporal arteritis has not been previously reported.

No description available.

by Cheng Yuen Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves [106]-113). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.iv / Research out puts --- p.v / Abbreviations --- p.vii / List of Figures --- p.viii / List of Tables --- p.xiii / Table of contents --- p.xiv / Chapter Chapter 1 --- Introduction & Hypothesis / Chapter 1.1. --- General Introduction --- p.1 / Chapter 1.2. --- Hypothesis --- p.4 / Chapter 1.3. --- Objectives --- p.4 / Chapter Chapter 2 --- An Overview of Giant Cell Tumour of Bone / Chapter 2.1. --- Introduction --- p.5 / Chapter 2.2. --- Pathobiological features of GCT --- p.6 / Chapter 2.2.1. --- Radiological appearances and clinical classifications of GCT --- p.7 / Chapter 2.2.2. --- Histological characteristics --- p.10 / Chapter 2.2.3. --- Metastatic GCT --- p.13 / Chapter 2.3. --- Histogenesis of GCT --- p.14 / Chapter 2.4. --- Treatment --- p.19 / Chapter 2.5. --- Summary --- p.22 / Chapter Chapter 3 --- Pharmacological aspect of bisphosphonates / Chapter 3.1. --- Introduction --- p.23 / Chapter 3.2. --- Chemical structures of bisphosphonates --- p.28 / Chapter 3.3. --- Mechanisms and actions --- p.28 / Chapter 3.3.1. --- Bisphosphonates induce osteoclast apoptosis --- p.30 / Chapter 3.3.2. --- Bisphosphonates induce cell apoptosis --- p.32 / Chapter 3.3.3. --- Apoptosis --- p.33 / Chapter 3.3.3.1. --- Morphological characteristic of apoptosis --- p.35 / Chapter 3.4. --- Clinical applications of bisphosphonates --- p.36 / Chapter 3.5. --- Bisphosphonates used in this study --- p.38 / Chapter 3.6. --- Summary --- p.43 / Chapter Chapter 4 --- Materials and methods / Chapter 4.1. --- Introduction --- p.44 / Chapter 4.2. --- Primary GCT cell culture and maintenance --- p.46 / Chapter 4.3. --- Drug preparation --- p.46 / Chapter 4.4. --- MTT assay --- p.47 / Chapter 4.5. --- Annexin-V-flous staining assay --- p.48 / Chapter 4.6. --- Haematoxyline and Eosin staining --- p.51 / Chapter 4.7. --- TUNEL assay (Terminal deoxynucleotidyltrasferase - mediated dUTP-biotin nick end labelling) --- p.52 / Chapter 4.8. --- TEM (Transmission Electron Microscopy) --- p.54 / Chapter 4.9. --- Statistical analysis --- p.54 / Chapter Chapter 5 --- Bisphosphonates induce apoptosis in giant cell tumour of bone -in vitro study / Chapter 5.1. --- Introduction --- p.56 / Chapter 5.2. --- Experimental design --- p.57 / Chapter 5.3. --- Results / Chapter 5.3.1. --- Bisphosphonates reduce cell viability of GCT stromal tumour cell --- p.59 / Chapter 5.3.2. --- Bisphosphonates induce morphological changesin GCT primary culture --- p.59 / Chapter 5.3.3. --- Bisphosphonate significantly induce apoptosis in GCT stromal cells in a dose dependent manner --- p.62 / Chapter 5.4. --- Discussions and Summary --- p.68 / Chapter Chapter 6 --- Bisphosphonates induce apoptosis in giant cell tumour of bone -in vivo study / Chapter 6.1. --- Introduction --- p.73 / Chapter 6.2. --- Experiment design --- p.74 / Chapter 6.3. --- Results / Chapter 6.3.1. --- H & E observations / Chapter 6.3.2. --- Pamidronate significantly induce apoptosis in both osteoclast-like giant cells and stromal tumour cells by TUNEL labelling assay --- p.79 / Chapter 6.3.3. --- Pamidronate induced cellular ultrastructural changes of GCT by TEM examination --- p.83 / Chapter 6.3.4. --- Pamidronate reduce the recurrent characteristic of GCT --- p.95 / Chapter 6.4. --- Discussions and Summary --- p.97 / Chapter Chapter 7 --- Summary and Future Study / Chapter 7.1. --- Summary --- p.101 / Chapter 7.2. --- Future directions --- p.103 / Chapter Chapter 8 --- Reference --- p.105 / Chapter Chapter 9 --- Appendix - solution preparation

Different species are separated by pre-zygotic reproductive barriers which impede gene flow between them. Rarely, when pre-zygotic barriers break down, interspecific hybrids are produced that display abnormal phenotypes, collectively called hybrid dysgenesis effects. Interspecies hybrid placental dysplasia (IHPD) in the genus Mus is a very consistent X-linked hybrid dysgenesis effect. Reproductive cloning and mutation of the gene Esx1 lead to placental hyperplasias with phenotypic similarities to IHPD. Comparative gene expression analysis of these three different models of placental hyperplasia showed that different mechanisms underlie these placental hyperplasias. We also identified several genes for which roles in placentation had not been studied earlier. We screened five of these genes, Car2, Ncam1, Fbln1, Cacnb3 and Cpe for their functions in placentation. Analysis of the spatio-temporal expression patterns of these genes during mouse placental development showed that they are ectopically expressed in IHPD placentas. Placental phenotype and gene expression was then studied in mice mutant for these genes. Our results show that complicated by the expression of functional counterparts, deletion of these genes failed to produce any consistent phenotype. Incompletely penetrant phenotypes were found in Cacnb3 and Cpe mutants. The Cpe mutant placentas recapitulated some IHPD phenotypes, despite co-expression of Cpd, a functionally redundant gene. Deregulated expression of Cpe and Cpd prior to manifestation of IHPD phenotype indicated that these are causally involved in IHPD and might be speciation genes in the genus Mus. We found that AT24 placentas also exhibit deregulated expression of these genes and could be used as a model to study IHPD. We tried rescuing the AT24 placental phenotype, by decreasing the expression of the over expressed genes. Normalization of transcript levels of these genes did not rescue the AT24 phenotype, thus indicating that up-regulation of these genes is a down-stream event in the generation of IHPD.