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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The organizing role of the limb bud ectoderm in intrapouch embroyonal transplants in the hamster (Mesocricetus auratus)

Smith, Thomas Edward, Jr January 1958 (has links)
Thesis (Ph.D.)--Boston University / The potential usefulness of the membranous cheek pouch of the hamster as an investigative tool in experimental embryology has been explored* After preliminary studies involving the transplantation of ova, morulas, and various embryonal tissues, the anterior limb buds of embryos in the eighth to eleventh day of development were chosen for intensive study.
2

An experimental study of some effects of halothane and nitrous oxide anesthesia on the offspring of the golden hamster

Bussard, David Arthur January 1974 (has links)
This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).
3

Apoptose de linfócitos na imunossupressão da leismaniose visceral em hamsteres infectados com Leishmania (Leishmania) chagasi / Apoptosis of lymphocytes in immunosuppression leishmaniasis in hamsters infected with visceral Leishmania (Leishmania) chagasi

Fazzani, Camila 17 December 2010 (has links)
Hamsteres infectados com Leishmania (L.) chagasi são considerados um dos melhores modelos para estudo de fatores relacionados à imunossupressão que ocorre durante a leishmaniose visceral ativa, pois apresenta manifestações clínicas similares ao que ocorre no homem e não conseguem controlar a infecção. Neste estudo, hamsteres infectados intraperitonealmente com 2x107 parasitos foram utilizados para avaliação de possíveis fatores envolvidos na dinâmica da imunossupressão. Os parâmetros avaliados foram a produção de citocinas de padrão Th1 e Th2, produção de óxido nítrico por células esplênicas e detecção de apoptose em linfócitos esplênicos em tempos precoces (6, 20, 48 e 72 horas), intermediários (7 e 15 dias) e tardios (30 e 60 dias) de infecção. Inicialmente avaliamos a carga parasitária no baço e observamos aumento progressivo dependente do tempo de infecção, ratificando que hamster infectado é um bom modelo para desenvolvimento de doença. A resposta celular frente a mitógeno e antígeno de Leishmania foi o parâmetro utilizado para avaliação de imunossupressão. Observamos resposta preservada à concanavalina A em todos os tempos de infecção e resposta preservada ao antígeno de Leishmania nos tempos precoces, porém com ausência de resposta antígeno específica a partir do tempo de 7 dias de infecção. A quantificação de óxido nítrico foi determinada em sobrenadante de células esplênicas de cultura estimuladas com concanavalina A e antígeno de Leishmania, pelo método de Griess. Observamos inicialmente baixo nível de produção de óxido nítrico em todos os tempos de infecção, no entanto quando as células foram estimuladas com antígeno de Leishmania observamos níveis ainda menores nos tempos de 48 e 72 horas de infecção. O perfil de citocinas produzido foi determinado pela reação em cadeia da polimerase por transcrição reversa, sendo detectado RNA mensageiro tanto de citocinas Th1, quanto Th2 em todos os tempos de infecção (precoce, intermediária e tardia), em células ex-vivo e estimuladas; e também em animais controles não infectados; não havendo um padrão de dicotomização de produção de citocinas neste modelo experimental. Detecção de apoptose em células esplênicas não aderentes (prováveis linfócitos T) ex-vivo e em cultura estimuladas com concanavalina A e antígeno de Leishmania foi avaliada pelos seguintes métodos: Anexina V, caspase 3 clivada e TUNEL por citometria de fluxo. Houve marcação da exposição de fosfatidil serina pelo método da anexina V, nos tempos de 6 horas de infecção, quando as células foram estimuladas com mitogeno ou antígeno de Leishmania; e com 48 horas e 60 dias de infecção somente quando estimuladas com antígeno de Leishmania. Em células esplênicas em cultura estimuladas com concanavalina não houve marcação de caspase 3 clivada, porém em células esplênicas ex-vivo nos tempos 20, 48 e 72 horas de infecção houve detecção de apoptose, definida por marcação de caspase 3 clivada. A marcação de células esplênicas não aderentes para quebra de DNA foi baixa em todos os tempos analisados, porém observamos aumento de marcação em células esplênicas não aderentes, estimuladas com antígeno nos tempos de 20 horas e posteriormente de 7 dias até 60 dias de infecção. Nossos resultados sugerem que a imunossupressão na leishmaniose visceral no modelo de hamsteres infectados com Leishmania (L.) chagasi é antígeno dependente e instala-se nos tempos intermediários de infecção, a partir de 7 dias. Esta imunossupressão parece estar relacionada com aumento de apoptose em linfócitos já nos tempos precoces de infecção, que pode favorecer a progressão da infecção, por ocorrer principalmente em células esplênicas antígenos reativas. Nossos dados sugerem ainda, que a imunossupressão não é decorrente da dicotomização da produção de citocinas Th1 e Th2 / Hamsters infected by Leishmania (L.) chagasi are considered one of the most remarkable models to study several characteristics related to immunosuppression, raised during active visceral leishmaniasis especially because hamsters show similar clinical manifestations as it is found in humans without surmounting the infection. In this study, hamsters infected intraperitoneally with 2x107 parasites were used to evaluate the possible factors involved in the dynamic of immunosuppression that occurs during the disease development. The evaluated parameters were the production of Th1 and Th2 cytokines profile, nitric oxide production of splenic cells and detection of apoptosis in splenic lymphocytes at early (6,20, 48 e 72 hours), intermediate (7 e 15 days) and late times (30 e 60 days) of infection. Initially, we evaluate the parasite load in the spleen and observed a progressive increase dependent on the time of infection, ratifying that infected hamsters are good models to set up the disease development. Cellular response upon mitogen or Leishmania antigen was the parameter used to evaluate the immunosuppression showing a preserved response to concanavalin A at all period of infection and a preserved response to the Leishmania antigen at all early phases however with no specific antigen response from 7 day of infection until the late phase of infection. Nitric oxide quantification was determined in the splenic cells supernatant in culture stimulated upon concanavalin A and Leishmania antigen and we observed initially low level of nitric oxide production, measured by the Griess method. Nonetheless, when the cells were stimulated upon Leishmania antigen we observed a lower level nitric oxide production at 48 and 72 hours of infection. mRNA of Th1 e Th2 cytokines profile was determined by RT-PCR at all period of infection studied in infected or non infected hamsters showing no difference at the cytokine profile in this experimental model. Detection of apoptosis in the non adherent splenic cells (probably T lymphocytes) ex-vivo and in the stimulated culture with concanavalin A and Leishmania antigen was evaluated by the following methods: annexin V-FITC, cleaved caspase 3 and TUNEL by flow cytometry analysis. There was phosphatidilserine staining by annexin method, at 6 hour of infection when cells were stimulated by mitogen or Leishmania antigen at 48 hours and 60 days of infection only when stimulated by Leishmania antigen. Splenic cells in culture stimulated by concanavalin A showed no cleaved caspase 3 staining in all period of infection studied. Otherwise, apoptosis was detected in the ex-vivo splenic cells at 20, 48 and 72 hours of infection by cleaved caspase 3 staining. We observed a low DNA break staining of non adherent splenic cells in all period analyzed, although this staining was increased in non adherent cells stimulated upon Leishmania antigen at 20 hours from 7 day of infection until 60 day of infection. Our results suggest that a visceral leishmaniasis immunosuppression in the hamsters model infected by Leishmania (L.) chagasi is antigen dependent and sets up in the intermediate phases of infection from 7 days on. This immunosuppression seems to be related to the apoptosis increase in lymphocytes already in the early period of infection probably favoring its progression especially because of its occurrence in reactive splenic antigen. Our data also suggest that the immunosuppression is not provided by dichotomization in the Th1 and Th2 cytokines profile
4

Apoptose de linfócitos na imunossupressão da leismaniose visceral em hamsteres infectados com Leishmania (Leishmania) chagasi / Apoptosis of lymphocytes in immunosuppression leishmaniasis in hamsters infected with visceral Leishmania (Leishmania) chagasi

Camila Fazzani 17 December 2010 (has links)
Hamsteres infectados com Leishmania (L.) chagasi são considerados um dos melhores modelos para estudo de fatores relacionados à imunossupressão que ocorre durante a leishmaniose visceral ativa, pois apresenta manifestações clínicas similares ao que ocorre no homem e não conseguem controlar a infecção. Neste estudo, hamsteres infectados intraperitonealmente com 2x107 parasitos foram utilizados para avaliação de possíveis fatores envolvidos na dinâmica da imunossupressão. Os parâmetros avaliados foram a produção de citocinas de padrão Th1 e Th2, produção de óxido nítrico por células esplênicas e detecção de apoptose em linfócitos esplênicos em tempos precoces (6, 20, 48 e 72 horas), intermediários (7 e 15 dias) e tardios (30 e 60 dias) de infecção. Inicialmente avaliamos a carga parasitária no baço e observamos aumento progressivo dependente do tempo de infecção, ratificando que hamster infectado é um bom modelo para desenvolvimento de doença. A resposta celular frente a mitógeno e antígeno de Leishmania foi o parâmetro utilizado para avaliação de imunossupressão. Observamos resposta preservada à concanavalina A em todos os tempos de infecção e resposta preservada ao antígeno de Leishmania nos tempos precoces, porém com ausência de resposta antígeno específica a partir do tempo de 7 dias de infecção. A quantificação de óxido nítrico foi determinada em sobrenadante de células esplênicas de cultura estimuladas com concanavalina A e antígeno de Leishmania, pelo método de Griess. Observamos inicialmente baixo nível de produção de óxido nítrico em todos os tempos de infecção, no entanto quando as células foram estimuladas com antígeno de Leishmania observamos níveis ainda menores nos tempos de 48 e 72 horas de infecção. O perfil de citocinas produzido foi determinado pela reação em cadeia da polimerase por transcrição reversa, sendo detectado RNA mensageiro tanto de citocinas Th1, quanto Th2 em todos os tempos de infecção (precoce, intermediária e tardia), em células ex-vivo e estimuladas; e também em animais controles não infectados; não havendo um padrão de dicotomização de produção de citocinas neste modelo experimental. Detecção de apoptose em células esplênicas não aderentes (prováveis linfócitos T) ex-vivo e em cultura estimuladas com concanavalina A e antígeno de Leishmania foi avaliada pelos seguintes métodos: Anexina V, caspase 3 clivada e TUNEL por citometria de fluxo. Houve marcação da exposição de fosfatidil serina pelo método da anexina V, nos tempos de 6 horas de infecção, quando as células foram estimuladas com mitogeno ou antígeno de Leishmania; e com 48 horas e 60 dias de infecção somente quando estimuladas com antígeno de Leishmania. Em células esplênicas em cultura estimuladas com concanavalina não houve marcação de caspase 3 clivada, porém em células esplênicas ex-vivo nos tempos 20, 48 e 72 horas de infecção houve detecção de apoptose, definida por marcação de caspase 3 clivada. A marcação de células esplênicas não aderentes para quebra de DNA foi baixa em todos os tempos analisados, porém observamos aumento de marcação em células esplênicas não aderentes, estimuladas com antígeno nos tempos de 20 horas e posteriormente de 7 dias até 60 dias de infecção. Nossos resultados sugerem que a imunossupressão na leishmaniose visceral no modelo de hamsteres infectados com Leishmania (L.) chagasi é antígeno dependente e instala-se nos tempos intermediários de infecção, a partir de 7 dias. Esta imunossupressão parece estar relacionada com aumento de apoptose em linfócitos já nos tempos precoces de infecção, que pode favorecer a progressão da infecção, por ocorrer principalmente em células esplênicas antígenos reativas. Nossos dados sugerem ainda, que a imunossupressão não é decorrente da dicotomização da produção de citocinas Th1 e Th2 / Hamsters infected by Leishmania (L.) chagasi are considered one of the most remarkable models to study several characteristics related to immunosuppression, raised during active visceral leishmaniasis especially because hamsters show similar clinical manifestations as it is found in humans without surmounting the infection. In this study, hamsters infected intraperitoneally with 2x107 parasites were used to evaluate the possible factors involved in the dynamic of immunosuppression that occurs during the disease development. The evaluated parameters were the production of Th1 and Th2 cytokines profile, nitric oxide production of splenic cells and detection of apoptosis in splenic lymphocytes at early (6,20, 48 e 72 hours), intermediate (7 e 15 days) and late times (30 e 60 days) of infection. Initially, we evaluate the parasite load in the spleen and observed a progressive increase dependent on the time of infection, ratifying that infected hamsters are good models to set up the disease development. Cellular response upon mitogen or Leishmania antigen was the parameter used to evaluate the immunosuppression showing a preserved response to concanavalin A at all period of infection and a preserved response to the Leishmania antigen at all early phases however with no specific antigen response from 7 day of infection until the late phase of infection. Nitric oxide quantification was determined in the splenic cells supernatant in culture stimulated upon concanavalin A and Leishmania antigen and we observed initially low level of nitric oxide production, measured by the Griess method. Nonetheless, when the cells were stimulated upon Leishmania antigen we observed a lower level nitric oxide production at 48 and 72 hours of infection. mRNA of Th1 e Th2 cytokines profile was determined by RT-PCR at all period of infection studied in infected or non infected hamsters showing no difference at the cytokine profile in this experimental model. Detection of apoptosis in the non adherent splenic cells (probably T lymphocytes) ex-vivo and in the stimulated culture with concanavalin A and Leishmania antigen was evaluated by the following methods: annexin V-FITC, cleaved caspase 3 and TUNEL by flow cytometry analysis. There was phosphatidilserine staining by annexin method, at 6 hour of infection when cells were stimulated by mitogen or Leishmania antigen at 48 hours and 60 days of infection only when stimulated by Leishmania antigen. Splenic cells in culture stimulated by concanavalin A showed no cleaved caspase 3 staining in all period of infection studied. Otherwise, apoptosis was detected in the ex-vivo splenic cells at 20, 48 and 72 hours of infection by cleaved caspase 3 staining. We observed a low DNA break staining of non adherent splenic cells in all period analyzed, although this staining was increased in non adherent cells stimulated upon Leishmania antigen at 20 hours from 7 day of infection until 60 day of infection. Our results suggest that a visceral leishmaniasis immunosuppression in the hamsters model infected by Leishmania (L.) chagasi is antigen dependent and sets up in the intermediate phases of infection from 7 days on. This immunosuppression seems to be related to the apoptosis increase in lymphocytes already in the early period of infection probably favoring its progression especially because of its occurrence in reactive splenic antigen. Our data also suggest that the immunosuppression is not provided by dichotomization in the Th1 and Th2 cytokines profile
5

Absence of accessory sex gland secretions in the ejaculate alters the profile of proteins in uterine fluid after mating and early pregnancy in the golden hamster (Mesocricetus auratus).

January 2004 (has links)
Ho Wing Ki Vicky. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (leaves 191-211). / Abstracts in English and Chinese. / Abstracts --- p.i / Abstracts in Chinese --- p.iii / Acknowledgements --- p.v / Table of Abbreviations --- p.vi / Table of Contents --- p.ix / List of Figures and Tables --- p.xiv / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter 1.1. --- The Male Accessory Sex Glands --- p.2 / Chapter 1.1.1. --- The Prostatic Complex --- p.4 / Chapter 1.1.2. --- The Coagulating Gland --- p.4 / Chapter 1.1.3. --- The Seminal Vesicles --- p.5 / Chapter 1.1.4. --- The Ampullary Gland --- p.6 / Chapter 1.1.5. --- The Cowper's gland --- p.6 / Chapter 1.1.6. --- The Littre's Gland --- p.7 / Chapter 1.2. --- The Uterus --- p.7 / Chapter 1.2.1. --- The Structure of Uterus --- p.7 / Chapter 1.2.2. --- The Endometrium --- p.8 / Chapter 1.3. --- Identifications of Proteins by Two Dimensional Gel Electrophoresis and Matrix-assisted Laser Adsorption / ionization Time-of-flight (MALDI-TOF) Mass Spectrometry --- p.9 / Chapter 1.3.1. --- Principle of Two Dimensional Gel Electrophoresis --- p.9 / Chapter 1.3.2. --- Principle of MALDI-TOF Mass Spectrometry --- p.11 / Chapter 1.4. --- Hypothesis and Aim of this Study --- p.12 / Chapter 1.4.1. --- Hypothesis --- p.13 / Chapter 1.4.2. --- Aim --- p.13 / Legends and Figures --- p.14 / Chapter Chapter 2 --- The Effect of Omission of Male Accessory Sex Gland Secretions on Post Coital Uterine Fluid --- p.17 / Chapter 2.1. --- Introduction --- p.18 / Chapter 2.1.1. --- Uterine Fluid at the Time of Mating --- p.18 / Chapter 2.1.2. --- Ventral Prostate Secretory Proteins --- p.20 / Chapter 2.1.3. --- Proteins Specifically Bind to Sperm Membrane --- p.22 / Aim of Study --- p.23 / Chapter 2.2. --- Materials and Methods --- p.24 / Chapter 2.2.1. --- Animal Model --- p.24 / Chapter 2.2.1.1. --- Female golden hamsters --- p.24 / Chapter 2.2.1.2. --- Male golden hamsters --- p.25 / Chapter 2.2.2. --- Collections of Biological Samples --- p.26 / Chapter 2.2.2.1. --- Female Hamster Serum --- p.26 / Chapter 2.2.2.2. --- Uterine Fluid --- p.26 / Chapter 2.2.2.3. --- Uterine Tissues --- p.27 / Chapter 2.2.2.4. --- Ejaculated Sperm in Uterus --- p.27 / Chapter 2.2.2.5. --- ASG Secretions --- p.27 / Chapter 2.2.2.6. --- ASG Tissues --- p.28 / Chapter 2.2.2.7. --- Epididymal Sperm --- p.28 / Chapter 2.2.3. --- Isolation and Purification of Sperm Binding Ventral Prostate Proteins (SBVPP) --- p.28 / Chapter 2.2.3.1. --- Plasma Membrane Protein from Epididymal Sperm --- p.28 / Chapter 2.2.3.2. --- Affinity Chromatography --- p.29 / Chapter 2.2.3.3. --- FPLC Gel Filtration --- p.30 / Chapter 2.2.4. --- Histology of Flushed Uterus --- p.30 / Chapter 2.2.5. --- Quantification of Protein --- p.31 / Chapter 2.2.6. --- Two dimensional Electrophoresis --- p.31 / Chapter 2.2.6.1. --- First DimensiońؤIsoelectric Focusing --- p.32 / Chapter 2.2.6.2. --- Second DimensiońؤSDS PAGE --- p.32 / Chapter 2.2.6.3. --- Visualization of Protein Spots --- p.33 / Chapter 2.2.7. --- Identification of Proteins --- p.34 / Chapter 2.2.7.1. --- Protein Spots Detection --- p.34 / Chapter 2.2.7.2. --- MALDI-TOF --- p.34 / Chapter 2.2.7.2.1. --- In-Gel Digestion for MALDI-TOF --- p.34 / Chapter 2.2.7.2.2. --- MALDI-TOF Analysis --- p.35 / Chapter 2.2.7.2.3. --- MALDI-TOF Data Analysis --- p.36 / Chapter 2.2.8. --- Confirmation of Prostate Specific Antigen (PSA) --- p.37 / Chapter 2.2.9. --- Confirmation of Prostatic Acid Phosphatase (PAP) --- p.37 / Chapter 2.2.10. --- Confirmation of Tumor Necrosis Factor Stimulated Gene-6 (TSG-6) --- p.37 / Chapter 2.2.11. --- Scanning Electron Microscopy (SEM) --- p.38 / Chapter 2.3. --- Results --- p.39 / Chapter 2.3.1. --- Morphology of Flushed Uterus --- p.39 / Chapter 2.3.2. --- Protein Concentration --- p.39 / Chapter 2.3.3. --- "Serum, Pre and Post Coital Uterine Fluid Protein Profiles" --- p.39 / Chapter 2.3.4. --- ASG Secretory Proteins and Their Fate After mating --- p.40 / Chapter 2.3.4.1. --- ASG Secretory Proteins and 1 hp.c. Uterine Fluid --- p.40 / Chapter 2.3.4.2. --- VP Secretory Proteins and SBVPP --- p.40 / Chapter 2.3.4.3. --- PAP and PSA --- p.41 / Chapter 2.3.5. --- Protein Profile at 1 h p.c --- p.41 / Chapter 2.3.6. --- Protein Profile at 4 h p. c --- p.42 / Chapter 2.3.7. --- Identification of Proteins Differentially Expressed by the Three Groups at 1 h p .c --- p.43 / Chapter 2.3.7.1. --- Confirmation of TSG-6 --- p.43 / Chapter 2.3.8. --- SEM --- p.44 / Chapter 2.4. --- Discussion --- p.45 / Chapter 2.5. --- Conclusion --- p.55 / Legends and Figures --- p.56 / Chapter Chapter 3 --- The Effect of Omission of Male Accessory Sex Glands Secretions on Periimplanation Uterine Fluid Proteins --- p.114 / Chapter 3.1. --- Introduction --- p.115 / Chapter 3.1.1. --- Cytokine & Growth Factor --- p.115 / Chapter 3.1.1.1. --- Vascular Endothelial Growth Factor (VEGF) --- p.115 / Chapter 3.1.1.2. --- Leukaemia Inhibitory Factor (LIF) --- p.116 / Chapter 3.1.1.3. --- Insulin-like Growth Factors (IGFs) --- p.116 / Chapter 3.1.1.4. --- Interleukin 1 (IL-1) --- p.117 / Chapter 3.1.1.5. --- Adhesion Molecule --- p.118 / Chapter 3.1.2. --- Uterine Secretory Proteins --- p.118 / Chapter 3.1.2.1. --- Estrogen Dependent Protein --- p.119 / Chapter 3.1.2.2. --- Progestin-Dependent Endometrial Protein --- p.120 / Chapter 3.1.2.3. --- Uteroglobin --- p.121 / Chapter 3.1.2.4. --- Uteroferrin --- p.122 / Chapter 3.1.2.5. --- Prolactin --- p.123 / Chapter 3.1.2.6. --- Glycodelin --- p.123 / Chapter 3.2. --- Aim of Study --- p.124 / Chapter 3.3. --- Method and Materials --- p.124 / Chapter 3.3.1. --- Animal and Surgery --- p.125 / Chapter 3.3.2. --- Collection of Biological Samples --- p.125 / Chapter 3.3.2.1. --- Uterine Fluid --- p.125 / Chapter 3.3.2.2. --- Uterine Tissue --- p.125 / Chapter 3.3.3. --- Quantification of Protein --- p.125 / Chapter 3.3.4. --- Two Dimensional Electrophoresis --- p.125 / Chapter 3.3.5. --- Identification of Proteins --- p.126 / Chapter 3.3.6. --- Confirmation of Growth Differentiation Factor-8 (DGF-8) by PCR --- p.126 / Chapter 3.3.7. --- Confirmation of GDF-8 by Western Blotting --- p.126 / Chapter 3.4. --- Results --- p.128 / Chapter 3.4.1. --- Protein Concentration --- p.128 / Chapter 3.4.2. --- 60 Hours Post Coitum --- p.128 / Chapter 3.4.2.1. --- Protein Profile --- p.128 / Chapter 3.4.2.2. --- Differentially Expressed Protein Spots and Proteins Identification --- p.129 / Chapter 3.4.3. --- 72 Hours Post Coitum --- p.129 / Chapter 3.4.3.1. --- Protein Profile --- p.129 / Chapter 3.4.3.2. --- Differentially Expressed Protein Spots and Proteins Identification --- p.130 / Chapter 3.4.3.3. --- Confirmation of Growth differentiation factor 8 (GDF-8) --- p.130 / Chapter 3.5. --- Discussion --- p.132 / Chapter 3.6. --- Conclusion --- p.139 / Legends and Figures --- p.140 / Chapter Chapter 4 --- General Conclusion --- p.186 / Chapter 4.1. --- Conclusion --- p.187 / Chapter 4.2. --- Further Studies --- p.190 / References --- p.191 / Appendices --- p.212
6

The microanatomy and ultrastructure of the developing thymus in the hamster

Weakley, Brenda Shaw January 1965 (has links)
Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Recent experimental work has indicated that the thymus in late fetal and early neonatal life plays a major role in the development of mechanisms of immunity. To date, however, no study of the ultrastructure of the prenatal thymus has been reported in the literature, and histochemical and cytochemical studies of this early period are fragmentary. Therefore, in an effort to extend present knowledge of thymic differentiation and function during its early development, the thymus in the golden hamster (Mesocricetus auratus) was studied by selected histochemical methods and by electron microscopy from 9 1/2 days post coitum through 24 hours post partum. Histochemical techniques for the light microscopy included the periodic acid-Schiff technique with salivary digestion control for glycogen, the methyl green-pyronin technique as an indicator for protein synthesis, the sudan black B technique for determination of total unbound lipid, the Nile blue and oil r ed 0 techniques for deter mination of neutral lipid, and the Elftman t echnique for determination of phospholipid. Material was prepared for electron microscopy by fixation for one hour in l% osmium tetroxide (Millonig, 1963), dehydration in graded acetones followed by propylene oxide, and embedding in Maraglas epoxy resin (Freeman and Spurlock, 1962). Grids prepared from these specimens were stained either with 1% phosphotungstic acid in 95% alcohol, or with lead citrate (Reynolds, 1963). They were scanned with either an R.C.A. EMU 2-B electron microscope or a Siemens Elmiskop I. [TRUNCATED] / 2031-01-01
7

Regional lymph node response to homologons and heterologous transplants of tumor and normal tissues in the cheek pouch of the hamster

Shepro, David January 1959 (has links)
Thesis (Ph.D.)--Boston University / The golden hamster, Mesocricetus auratus, is unique in that it frequently accepts not only homografts but even heterografts of normal and malignant tissues. One of the many theories a tterpting an explanation of this phenomenon, namely that lymphatic tissues that drain the sites of imphntation do not respond in a t;rpicol fashion, motivated this study. Thus, the weight changes ,and the c;'tolof'ical variations of the superficial cervical nodes in response to homologous and heterologous normal and malignant tissue transplants in the cheek pouch of the hamster were studied. The major objectives were: (1) to determine if there be any "defect" in the hamster's lymphatic tissue response to the various transplants; (2) to investigate the effects of the grafts on the large lymphoid cells of the cortex and on the plasma cells of the medulla; and ( 3) to investigate the feasibility of employing the histological picture of a regional node draining the site of a tumor heterotransplant as a base line for anti-tumor studies during the cortisone conditioning. [TRUNCATED]
8

Diferenças entre sexos repercutem na carga parasitária e parâmetros bioquímicos na infecção experimenta l por Leishmania infantu

Marinho, Ananda Isis Lima 11 1900 (has links)
Submitted by Pós Imunologia (ppgimicsufba@gmail.com) on 2017-03-14T18:58:18Z No. of bitstreams: 1 dissertação Ananda Isis Lima de Marinho.pdf: 1076899 bytes, checksum: 21e99adf683c19eda3cf6952ccc97d03 (MD5) / Approved for entry into archive by Delba Rosa (delba@ufba.br) on 2017-04-24T13:08:50Z (GMT) No. of bitstreams: 1 dissertação Ananda Isis Lima de Marinho.pdf: 1076899 bytes, checksum: 21e99adf683c19eda3cf6952ccc97d03 (MD5) / Made available in DSpace on 2017-04-24T13:08:50Z (GMT). No. of bitstreams: 1 dissertação Ananda Isis Lima de Marinho.pdf: 1076899 bytes, checksum: 21e99adf683c19eda3cf6952ccc97d03 (MD5) / CNPq / Nas infecções parasitárias alguns fatores estão associados com a susceptibilidade do hospedeiro, dentre eles o sexo, a idade, condição genética, fatores ambientais e o estado imunológico. Diferenças entre os sexos são observadas em diversas infecções. Acredita- se que isto ocorra devido a ações de hormônios sexuais, podendo afetar os diferentes tipos de resposta imune. A Leishmaniose é um grave problema de saúde pública apresentando aumento da prevalência e afetando grande parte da população mundial. No Brasil é endêmica e o Nordeste é a região mais afetada. A forma visceral é a mais grave podendo levar o indivíduo a óbito se não tratada. Objetivamos determinar se existe diferença entre sexos no modelo experimental de LV. Hamsters (Mesocricetus auratus) machos e fêmeas foram infectados com L. infantum/chagasi através da injeção intradérmica e comparados com animais controles, após 5 meses de infecção. Após eutanásia sangue, baço e fígado foram coletados para as análises de carga parasitária, histológicas e de parâmetros bioquímicos. As fêmeas infectadas apresentaram um maior tamanho de baço que os machos infectados. Porém, foram os machos que apresentaram maior carga parasitária. As alterações bioquímicas foram maiores nas fêmeas, podendo estar relacionadas às alterações histológicas observadas no fígado das mesmas. As fêmeas infectadas apresentaram concentrações séricas inferiores de estradiol quando comparadas com fêmeas não infectadas. Essa redução não foi detectada nos machos. Nossos resultados indicam que existem diferenças entre sexos na LV experimental. A determinação de diferenças entre os sexos nas respostas às infecções é de fundamental importância na escolha da melhor abordagem terapêutica para o tratamento das enfermidades, incluindo as leishmanioses. / In parasitic infections some factors are associated with the susceptibility of the host, including sex, age, genetic condition, environmental factors and immune status. Gender differences are observed in various infections. It is believed it occurs due to sex hormones, which may affect different types of immune responses. Leishmaniasis is a serious public health problem presenting increased prevalence and affecting much of the world population. In Brazil it is endemic and the Northeast is the most affected region. The visceral form is the most severe and may cause death if left untreated. We aimed to determine whether there is gender difference in the experimental model of LV. Hamsters (Mesocricetus auratus) males and females were infected with L. infantum / chagasi by intradermal injection and compared with control animals after 5 months of infection. After euthanasia, blood, spleen and liver were collected for parasite load, histological and biochemical parameters analysis. Infected females showed an increase in the size of spleen compared to infected males. However, males had higher parasite burden. Biochemical changes were higher in females, which may be related to the histological changes observed in their liver. Infected females had lower serum concentrations of estradiol compared to uninfected females. This reduction was not detected in males. Our results indicate that there are gender differences in experimental LV. The determination of sex differences in responses to infection is very important in choosing the best therapeutic approach for the treatment of diseases, including leishmaniasis.
9

Quantitative studies of flow in small blood vessels of the frog, Rana Pipiens, and of the hamster, Mesocricetus Auratus

Grillo, Gene Patrick January 1964 (has links)
Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Quantitative relationships between blood flow velocity, vessel diameter, width of the peripheral plasma layer and induction of thrombus formation were studied in small blood vessels of the retrolingual membrane and intestinal mesentery of the frog, Rana Pipiens, and of the cheek pouch of the golden hamster, Mesocricetus auratus. Blood flow velocity was measured by a modification of the technique described by Hugues (Arch. Int. de Physiol. 61: 565, 1953). Internal vessel diameters and widths of the total peripheral plasma layer were measured with an ocular micrometer. Thrombus thresholds were determined by graded electrical stimulation. Determinations were made on 202 vessels in retrolingual membranes of frogs prepared by single pithing. In 95 arterioles (diameters from 10 to 40 microns), the mean flow velocity was 2.84 mm/sec. and the mean volume flow rate, 1.68xl0-3 cu mm/sec. The mean width of the total peripheral plasma layer was 3.6 microns and its ratio to mean vessel diameter was 1:6. In 107 venules (diameters from 10 to 50 microns), the mean flow rate was 1.20 mm/sec. The mean volume flow rate was 1.02x10-3 cu mm/sec. The mean width of the total peripheral plasma layer was 4.1 microns and its ratio to mean vessel diameter was 1:7.4. The ratios of mean arterial to mean venous velocity and volume flow were 1:2.3 and 1:1.6 respectively. Measurements were made on 100 mesenteric vessels of frogs prepared by single pithing. In 50 arterioles (diameters from 15 to 45 microns), the mean velocity was 3.77 mm/sec. The mean volume flow was 3.05xlo-3 cu mm/sec. The mean width of the total peripheral plasma layer was 2. 7 microns and its ratio to mean vessel diameter was 1:11.5. In 50 venules (diameters from 20 to 50 microns), the mean velocity was 1.55 mm/sec. and the mean volume flow rate, 1.76x10-3 cu mm/sec. The mean width of the total peripheral plasma layer was 6.7 microns and its ratio to mean vessel diameter was 1:5.3. The ratios of mean arterial to mean venous velocity and volume flow were 1:2.3 and 1:1.7 respectively. A total of 109 mesenteric vessels were studied in frogs anesthetized with urethane. In 55 arterioles (diameters from 15 to 45 microns), the mean velocity was 3.28 mm/sec. The mean volume flow was 2.87x10-3 cu mm/sec. The mean width of the total peripheral plasma layer was 3.2 microns and its ratio to mean vessel diameter was 1:9.3. In 54 venules (diameters from 20 to 50 microns), the mean flow rate was 1.61 mm/sec. and the mean volume flow, 1.83x10-3 cu mm/sec. The mean width of the total peripheral plasma layer was 5.6 microns and its ratio to mean vessel diameter was 1:5.9. The ratios of mean arterial to mean venous velocity and volume flow were 1:2.0 and 1:1.5 respectively. In these three series of studies in the frog, no relationship was clearly apparent between velocity and either vessel diameter or width of the peripheral plasma layer in arterioles. Suggestions of a direct relationship between velocity and peripheral plasma layer in veins, however, were evident. In all cases, and in both arterioles and venules, vessel diameter and peripheral plasma layer were clearly and directly related. The effects of flow velocity changes on width of the total peripheral plasma layer in individual vessels were studied in 26 arterioles of the hamster cheek pouch. Blood flow was varied by means of a cuff described by Copley (Biorheology 1: 3, 1962). A direct relationship between velocity and width of the peripheral plasma layer was clearly demonstrated. Thrombus thresholds were determined in mesenteric vessels of the frog. In 103 arterioles (diameters from 20 to 140 microns), the mean strength of stimulus necessary to produce a platelet thrombus was 24.8 volts with an amperage of 0.18 milliamperes. In 100 venules (diameters from 20 to 140 microns), the mean strength of stimulus necessary was 20.7 volts with an amperage of 0.12 milliamperes. Possible relationships of thrombus thresholds to flow velocity in mesenteric arterioles and venules are discussed. / 2031-01-01
10

Toxocaríase experimental em hamster / Experimental toxocariasis in hamsters

Silva, Ana Maria Gonçalves da 08 April 2015 (has links)
INTRODUÇÃO: Toxocaríase é uma infecção parasitária de distribuição global, causada pela fase larval de Toxocara spp. Os hospedeiros naturais são cães e gatos, nos quais o parasita completa o ciclo chegando a fase adulta. Outros hospedeiros podem ser infectados pela fase larval do parasita, após ingestão de ovos embrionados do solo, mãos contaminadas, fomites, ou ingestão de carne ou vísceras de animais infectados. Em hospedeiros paratênicos o parasita não completa o ciclo, invadindo em estágio larval vísceras ou outros tecidos, onde podem sobreviver e induzir a patologia. O presente estudo teve como objetivo caracterizar o hamster (Mesocricetus auratus), como modelo experimental de toxocaríase, inicialmente através do estudo das lesões histopatológicas em fígado, pulmão e rim. A caracterização da resposta imunológica do modelo, foi feita através do estudo de citocinas envolvidas nas respostas Th1 e Th2, e foi sugerida uma correlação entre alterações glomerulares e depósitos de complexos antígenos-anticorpo pré-formados na circulação. MÉTODOS: Hamsters foram inoculados com ovos embrionados de Toxocara canis, e mantidos no biotério do Instituto de Medicina Tropical de São Paulo. O estudo histopatológico foi desenvolvido utilizando-se cortes parafinados corados por hematoxilina e eosina. Para detecção de antígenos nos tecidos foram realizadas reações imunohistoquímicas, utilizando-se anticorpo monoclonal e policlonal anti- Toxocara canis. Utilizando-se o soro dos animais infectados e animais controle, foi realizada pesquisa de antígeno e anticorpo por ELISA. Para pesquisa de imunoglobulinas IgG e IgM e complemento, foram utilizados cortes congelados de rins para realização de reação de Imunofluorescência. Fragmentos de rins foram incluídos para utilização em microscopia eletrônica, para detecção de antígenos de toxocara e de imune complexos. Para caracterização de resposta imunológica foram estudadas citocinas envolvidas na resposta Th1 e Th2 por técnica de RT-PCR. RESULTADOS: Os achados histopatológicos demonstraram desde o início da infecção, presença de larvas em maior número no fígado, seguido de pulmão e raramente rins. Em fígado remanescentes larvares foram visualizados cercados por reação inflamatória granulomatosa. Logo no início da infecção foi encontrado pneumonite intersticial e intraalveolar focal, e lesão renal com glomérulo apresentando hiperplasia focal de células mesangiais (glomerulite mesangio-proliferativa). Houve marcação de antígenos em todos os grupos de animais infectados, tanto pelo anticorpo monoclonal, como pelo policlonal. Depósitos de imunoglobulinas e complemento foram marcados em glomérulo por imunofluorescência A análise dos soros por ELISA, demonstrou na pesquisa de anticorpos aumento gradativo no decorrer da infecção, acompanhado de diminuição de antígenos. Depósitos de antígenos em glomérulos foram detectados por microscopia imonoeletrônica. No RT-PCR foi detectado aumento significativo do nível de IL-4, com tendência de elevação de IL-10 e IFN-?. CONCLUSÃO: O hamster demonstrou ser um modelo experimental eficiente para toxocaríase. Entretanto este modelo é mais adequado para infecções de curto prazo. A resposta imunológica avaliada por RT-PCR, com elevado nível da expressão de IL-4, sugere uma resposta Th2, mas a tendência de aumento de IL-10 e IFN-? poderia sinalizar uma resposta mista Th1 e Th2. Achados de depósitos de imunoglobulinas no glomérulo sugerem a possibilidade de que as manifestações renais com síndrome nefrótica em humanos possa vir a ter como base a toxocaríase / INTRODUCTION: Toxocariasis is a parasitic infection of global distribution, caused by the larval stage of Toxocara spp. The natural hosts are dogs and cats, in which the parasite completes the cycle reaching adulthood. Other hosts can be infected with the larval stage of the parasite, after ingestion of embryonated eggs from the soil, contaminated hands, fomites, or ingestion of meat or viscera of infected animals. In paratenics hosts the parasite not complete the cycle, encroaching on larval stage in viscera or other tissues where they can survive and induce pathology. The present study aimed to characterize the hamster, Mesocricetus auratus, as experimental model of toxocariasis, initially through the study of histopathological lesions in the liver, lung and kidney. The characterization of immune response model, was made through the study of cytokines Th1 and Th2 responses involved, and a correlation was suggested between glomerular changes and antibody-antigen complexes deposits preformed in the circulation. METHODS: Hamsters were inoculated with embryonated eggs of Toxocara canis, and kept in the bioterium of the Institute of Tropical Medicine of the São Paulo. The histopathologic study was developed using paraffin slides stained by hematoxylin and eosin. For detection of antigens in tissues immunohistochemistry reactions were performed using monoclonal and polyclonal anti-Toxocara canis sera. Using the serum of infected and control animals, search has been carried out of antigen and antibody by ELISA. For the search of immunoglobulins IgG, IgM and complement, were used slides prepared from frozen fragments of kidneys and a immunofluorescence reaction. Fragments of kidneys were included for electron microscopy to detect antigens of Toxocara and immune complexes. For characterization of Th1 and Th2 response cytokines involved were detected by RT-PCR technique. RESULTS: Histopathological findings demonstrated since the beginning of the infection the presence of larvae in greater numbers in the liver, followed by lung and rarely kidneys. In the liver larval remnants were surrounded by a granulomatous inflammatory reaction. Early in the infection was found interstitial pneumonitis with intraalveolar focal inflammatory infiltrate and renal injury with glomerulus showing mesangial cell focal hyperplasia (mesangioproliferative glomerulonephritis). There were the presence of antigens in all groups of animals infected detected by both the monoclonal and polyclonal antibodies. Deposits of immunoglobulin and complement were present in glomerulus by immunofluorescence analysis. ELISA, showed that the presence of antibodies increased gradually in the course of infection, accompanied by progressive diminution of antigens. Clusters of antigen/s were detected by immunoelectron microscopy. RT-PCR showed a significant increase of IL-4, with a tendency of increase of IL- 10 and IFN-?. CONCLUSION: The hamster has proved to be an efficient experimental model for toxocariasis. However this model is best suited for short-term infections. The immune response evaluated by RT-PCR, with high level of expression of IL-4, suggests a Th2 response, but the trend of increase of IL-10 and IFN-? might suggest a Th1 and Th2 mixed response. Findings of immunoglobulin deposits in glomeruli suggests the possibility that the renal manifestations with nephrotic syndrome in humans might have, in certain circunstances, as a basis the toxocariasis

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