181 |
Aspectos morfológicos da hipófise do macaco Cebus apella / Morphology Aspects of the Hipophisis of the monkey Cebus apellaRibeiro, Adriana Rodrigues 29 June 2006 (has links)
O conhecimento de diversos aspectos da Neuroanatomia de primatas não humanos - que atualmente é falho, pela falta de trabalhos a respeito - é importante não apenas pela importância intrínseca desse conhecimento como até pelo fato de contribuir para um melhor entendimento da própria evolução do grupo, o que representa um fator relevante para a sua preservação e proteção. O objetivo deste trabalho é efetuar estudos morfológicos da hipófise do macaco Cebus apella a fim de conhecer melhor esta estrutura, e oferecer subsídios para análises comparativas mais amplas. Utilizamos 11 animais sendo 7 deles constantes do acervo de pesquisa da Universidade Federal de Uberlândia e, os outros 4 exemplares, doados pelo IBAMA-MG. A preparação das peças anatômicas foi levada a efeito mediante cuidadosa dissecção dos espécimes, cujos encéfalos foram retirados das caixas cranianas, preservando-se ao máximo todas as suas estruturas. As hipófises, depois de registrada sua macroscopia, foram submetidas aos métodos histológicos de rotina para observações em microscopia de luz e eletrônica de transmissão. Dos resultados obtidos podemos citar que a hipófise, neste animal, é uma glândula intracraniana alojada na sela turcica, fixada à base do cérebro pelo infundíbulo, sendo este muito curto. Ela exibe forma odontóide, exibindo-se aparentemente, como uma massa única, pois macroscopicamente apenas é possível, a identificação de uma divisão discreta em um lobo anterior e outro posterior, além do infundíbulo. As análises histológicas mostram esta glândula dividida em três lobos: anterior (adenohipófise), intermédio e posterior (neurohipófise). À microscopia eletrônica de transmissão foi possível identificar e classificar 4 tipos celulares em relação á adenohipófise: células do tipo I, II, III e IV. O aspecto do núcleo dessas células, exibindo freqüentemente, invaginações profundas de sua membrana, confere à hipófise do macaco Cebus apella, características peculiares, o que nos instiga a realizar novas pesquisas sobre o assunto / The knowledge of many aspects of Neuroanatomy of non-human primates - which is currently poor due to the lack of studies on the subject - is very important not only for the intrinsic significance of the knowledge itself but also because it contributes for a better understanding of the evolution of the group, which represents a relevant factor for its preservation and protection. The objective of this study is to perform morphological researches on the hypophysis of the Cebus apella monkey in order to understand this structure better and to provide basis for wider comparative analyses. Eleven animals were used on this study. Seven of them were properties of the research collection of the Federal University of Uberlândia and the other four were donated by the IBAMA-MG. The preparation of the anatomical parts was carefully done through dissection of the specimens, whose encephalus were removed from their skulls preserving all their structures. The hypophysis, after having their macroscopy registered, were submitted to histological methods of routine for observation in light microscopy and electronic microscopy of transmission. We could conclude from the obtained results that the hypophysis, on this particular animal, is a intracranial gland lodged in the sela turcica fixed to the base of the brain by the infundibulum which is very short. It has in dens shape and it presents itself as a single mass, because, macroscopically, it is only possible the identification of a discrete division in an anterior lobe and another posterior one besides the infundibulum. The histological analyses show this gland divided in three lobes: anterior (adenohypophysis), intermediary and posterior (neurohypophysis). Through the electronic microscopy of transmission it was possible to identify and classify four cellular types related to the adenohypophysis: types I, II, III and IV. The aspect of the cores of these cells, frequently showing deep invaginations of their membranes, confers to hypophysis of the Cebus apella monkey, peculiar characteristics, which instigates us to carry on performing new studies on the subject
|
182 |
Repeated exposure to restraint but not social defeat leads to habituation of the pituitary-adrenal and stress-herthermic responsesBarnum, Christopher John. January 2006 (has links)
Thesis (M.A.)--State University of New York at Binghamton, Psychology Department, 2006. / Includes bibliographical references.
|
183 |
Epidemiology and Genetics of Pituitary Tumors Épidémiologie et génétique des adénomes hypophysairesDaly, Adrian Francis 18 January 2008 (has links)
Pour avoir une parfaite compréhension dune maladie, il est nécessaire den
connaitre la fréquence, la symptomatologie et les causes dapparition. Dans le
cas des adénomes hypophysaires, les données de la littérature concernant
lépidémiologie de ces tumeurs sont contradictoires certaines études
suggérant une haute prévalence, et dautres affirmant quelles sont plutôt
rares. En parallèle, la compréhension de la physiopathologie des tumeurs
endocrines telles que les adénomes hypophysaires a fait un bond en avant
avec lavènement des techniques de biologie moléculaire. Pourtant, leur
physiopathologie reste encore très floue. Le fait de se concentrer sur les
causes familiales permet dapprocher plus efficacement les causes des
tumeurs endocrines. Concernant les adénomes hypophysaires, mis à part les
Néoplasies endocriniennes multiples de type I (MEN1) et le Complexe de
Carney (CNC), le domaine des adénomes hypophysaires familiaux est peu
compris. En effet, mise à part lacromégalie familiale, il ny a eu aucune étude
sur dautres types dadénomes hypophysaires entrant dans le cadre familial.
Les buts du travail contenu dans cette thèse étaient de décrire des aspects
épidémiologiques et génétiques des adénomes hypophysaires. Tout dabord,
nous avons étudié la discordance entre les taux de prévalence dadénomes
hypophysaires provenant détudes radiologiques/autopsiques (les
incidentalomes étant très fréquents) et dautre part ceux provenant de
registres de cancers et plus rarement de données de population. Une étude
intensive et complète de la prévalence des adénomes hypophysaires a été
réalisée dans 3 régions géographiquement parfaitement délimitées dans la
province de Liège. Dans cette étude qui a concerné une population de plus de
70 000 habitants, les adénomes hypophysaires diagnostiqués lont été en
collaboration avec toute la communauté médicale de ces régions. Les données
démographiques, cliniques, hormonales, radiologiques et pathologiques de
tous les patients ont été confirmées de façon indépendante. A une date fixe,
nous avons montré que les adénomes hypophysaires diagnostiqués suite à des
symptômes cliniques surviennent avec une prévalence de 1 cas par 1064
habitants résidants dans les limites géographiques déterminées pour cette
étude. Ces résultats montrent que la prévalence des adénomes hypophysaires
évidents sur le plan clinique est de 3.5 à 5 fois plus haute que les estimations
précédentes se rapportant à des populations ou des registres. Cela suggère
que les adénomes hypophysaires significatifs sur le plan clinique surviennent
assez fréquemment dans la pratique de tous les jours et ceci peut avoir des
implications importantes sur la distribution des ressources de santé. Une
étude épidémiologique internationale appliquant la même méthodologie est
actuellement en cours.
Létude des adénomes hypophysaires familiaux en-dehors du contexte de la
polyendocrinopathie de type I ou du Complexe de Carney constitue la
deuxième partie de ce travail. Jusquà présent, seule lacromégalie familiale
avait été rapportée dans la littérature. Nous avons réalisé une étude
internationale pour démontrer que tous les types dadénomes hypophysaires
pouvaient survenir dans le cadre dune pathologie familiale différente de la
polyendocrinopathie de type I et du complexe de Carney. La suspicion de cette
pathologie est née à Liège au cours de la dernière décennie. Cette étude a
démontré que les adénomes hypophysaires familiaux isolés (Familial Isolated
Pituitary Adenoma ou FIPA) constituent 2% des adénomes hypophysaires et
64 familles FIPA ont été caractérisées cliniquement. Cette étude a démontré
pour la première fois que tous les phénotypes dadénomes hypophysaires
peuvent survenir dans les mêmes familles. Quelques familles montrent
seulement un phénotype parmi les membres atteints (familles FIPA
homogènes) et dautres familles montrent différents types de tumeurs chez
les patients atteints (famille FIPA hétérogène). Dans les familles FIPA, les
adénomes hypophysaires étaient plus agressifs et tendaient à survenir à un
âge plus jeune que dans les cas sporadiques. Les familles FIPA montrent une
grande proximité familiale entre les membres atteints suggérant un mode
dominant de transmission. Les études ultérieures ont été réalisées sur les
aspects génétiques et anatomo-pathologiques des adénomes hypophysaires et
particulièrement ceux qui survenaient dans le contexte FIPA. La découverte
dun gène nouveau aryl hydrocarbon receptor interacting protein (AIP), dont
quelques mutations ont été associées avec des adénomes hypophysaires nous
a conduit à entreprendre la première étude génétique dans les FIPA. Des
mutations AIP ont été découvertes dans 15 % des familles et 50% des familles
homogènes dacromégales dans le contexte FIPA. Ceci suggère que dautres
gènes peuvent également être responsables du contexte FIPA. Dans les
familles FIPA qui portent la mutation AIP, les tumeurs étaient plus
importantes et survenaient à un âge plus jeune que dans les familles FIPA
sans mutation AIP. Neuf nouvelles mutations AIP ont été identifiées, dont la
majorité permet de prédire la perte du ligand ou de la région de AIP qui
interagit avec son récepteur. Une mutation AIP dans les FIPA était associée
avec différents types dadénomes hypophysaires incluant acromégalie,
prolactinomes, adénomes mixtes à GH-prolactine et adénomes nonsécrétants.
Nous avons également observé que la même mutation AIP pouvait
être responsable de différents phénotypes dans 2 familles FIPA différentes.
Un suivi détaillé dune famille FIPA avec mutation AIP a permis de montrer
pour la première fois quune anomalie endocrinienne différente dune tumeur
hypophysaire pouvait survenir chez des porteurs de mutation AIP (élévation
de lIGF1). Une analyse détaillée de lADN germinal et somatique provenant
dun grand groupe international européen dadénomes hypophysaires
sporadiques (non familiaux) a montré que les mutations AIP surviennent
rarement dans cette condition.
En conclusion : Le travail entrepris a apporté une nouvelle compréhension de
la vraie prévalence des adénomes hypophysaires diagnostiqués de façon
clinique dans une population et il a permis de codifier et de caractériser le
désordre FIPA, une nouvelle entité clinique qui représente une aire de
recherche potentielle pour des études cliniques et génétiques impliquant la
fonction de AIP et dautres gènes non encore identifiés.
To have a full understanding of a disease, it is necessary to at least know how frequently it occurs, its clinical features and by what means it is caused. In the case of pituitary adenomas, data in the literature on the epidemiology of
these tumors is conflicting, with some studies suggesting a high frequency,
others that they occur rarely in the clinical setting. In parallel, the
understanding of the pathophysiology of endocrine tumors like pituitary
adenomas has advanced greatly with the advent of molecular genetic
techniques. However, much remains unclear regarding pathophysiology. A
valuable avenue for studying the causes of endocrine tumors has been to
focus on the familial setting. With respect to pituitary adenomas, apart from
multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC), the
field of familial pituitary tumors is poorly understood. Indeed, apart from
familial acromegaly, there have been virtually no studies on other pituitary
adenomas occurring in the familial setting.
The aims of the work described in this thesis were based on addressing
aspects of the epidemiology and genetics of pituitary tumors. Firstly, the
disconnect between the prevalence rates for pituitary adenomas from
autopsy/radiology studies (incidentalomas being very common) and cancer
registries/population data (rare) was studied. An intensive, comprehensive,
case-finding study of the prevalence of pituitary adenomas was performed in
three tightly-defined geographical areas in the Province of Liège. In this
study, which involved a population of more than 70,000 people, diagnosed
pituitary adenomas were sought in collaboration with the entire group of
community medical practitioners in the study areas, and the demographics
and clinical, hormonal, radiological and pathological features of all patients
were confirmed independently. On a fixed date, it was found that clinically
diagnosed pituitary adenomas occurred with a prevalence of 1 case per 1064
individuals residing within the geographic boundaries of the study. These
results report a clinical prevalence of pituitary adenomas that is 3.5 to 5
times higher than previous population/registry estimates. It suggests that
clinically relevant pituitary adenomas occur frequently in the everyday
clinical setting, which may have important implications for health resource
allocations. Also, it is possible to undertake detailed, comprehensive, crosssectional
epidemiological studies in well-defined geographic areas, and this
methodology can be applied internationally
Studying the familial occurrence of pituitary adenomas outside of MEN1 and
CNC was the next aim of the work described. Up to this time, only the
familial occurrence of acromegaly had been reported with any frequency in
the literature. An international study was undertaken to assess whether
isolated pituitary adenomas of all types could occur in the familial setting, a
suspicion raised in Liège over the past decade. This study demonstrated that
familial isolated pituitary adenomas (FIPA) occur in about 2% of pituitary
adenoma populations, and 64 FIPA families were characterized clinically.
The study demonstrated for the first time that all phenotypes of pituitary
adenomas can occur together in families; some families exhibit only one
phenotype among affected members (homogeneous FIPA kindreds), others
have multiple tumor types among affected family members (heterogeneous
FIPA). In FIPA families, pituitary tumors were more aggressive and tended
to occur at a younger age than sporadic pituitary adenomas. FIPA families
display a high degree of familiality, suggesting a dominant mode of
inheritance. Subsequent studies were performed on the genetic and
pathological features of pituitary adenomas, particularly those occurring as
FIPA. The discovery of a novel gene, aryl hydrocarbon receptor interacting
protein ( AIP), mutations in which were associated with isolated pituitary
adenomas, led us to undertake the first such genetic studies in FIPA. AIP
mutations account for a minority (15%) of FIPA families and 50% of familial
acromegaly kindreds in FIPA. This suggests that other genetic causes for
FIPA also exist. In AIP mutation carrying FIPA families, tumors were larger
and had a younger age at diagnosis than non- AIP mutated FIPA kindreds. A
series of 9 novel AIP mutations were identified, the majority of which led to
predicted loss of vital ligand and receptor interacting regions of the AIP
protein. AIP mutations in FIPA were associated with multiple pituitary
adenoma types, including acromegaly, prolactinomas, mixed growth
hormone/prolactin secreting adenomas and non-secreting tumors. It was also
found that the same AIP mutation was responsible for different pituitary
adenoma types in two separate FIPA families. A detailed follow-up study of
an individual FIPA kindred with an AIP mutation found for the first time
that non-pituitary tumor-associated endocrine abnormalities (elevated
circulating insulin-like growth factor-1) occur in AIP mutation carriers. A
detailed analysis of germline and somatic DNA from a large international
European cohort of sporadic (non-familial) pituitary adenoma cases showed
that AIP mutations occur rarely in this setting.
In conclusion, the work undertaken has provided new understanding of the
true prevalence of clinically-relevant pituitary adenomas in the population, in
addition to codifying and characterizing FIPA, a new clinical entity that
represents a potentially valuable area for genetic and clinical studies
involving the function of AIP and other as yet unidentified associated genetic
causes.
|
184 |
Early rearing experience, hypothalamic-pituitary-adrenal (HPA) activity, and serotonin transporter genotype influences on the development of anxiety in infant rhesus monkeys (Macaca mulatta) /Dettmer, Amanda M., January 2009 (has links)
Thesis (Ph. D.)--University of Massachusetts Amherst, 2009. / Open access. Includes bibliographical references (p. 89-87). Print copy also available.
|
185 |
Optical Investigations of Neurohypophysial Excitability and Amyloid Fibril FormationFoley, Joseph Leo 01 January 2013 (has links)
This dissertation describes the work done on two distinct projects. In the first part I sought to unravel the mechanisms that underlie the activity-dependent modulation of response in the excitation-secretion coupling of the neurohypophysis. In the second part, I optically monitored and analyzed the secondary structure changes accompanying amyloid fibril formation along multiple pathways, under both denaturing and near-physiological conditions.
Neuronal plasticity plays an important role in regulating various biological systems by modulating release of hormones or neurotransmitters. The changing response to the same stimulus, depending on the context and previous stimulation events, is also the basis of learning and all higher order brain functions. The mechanisms behind this modulation are widely varied, and are often poorly understood in specific tissues. In this work, we examined excitation-secretion coupling in the neurohypophysis, a tissue composed of densely packed axons that secretes the hormones arginine vasopressin and oxytocin. The release of hormones depends not only on the overall level of activity in the gland, but also upon the specifics of the temporal pattern of stimulation. By optically monitoring the electrical activity using voltage sensitive dyes, we were able to investigate this plasticity in the intact gland. Varying extracellular potassium concentration in the bath, increasing interstitial space via hypertonic saline, and retarding potassium reuptake with ouabain all showed that extracellular potassium accumulation drives the depression of excitability. This effect is hidden from glass micro-electrode recordings because of the inevitable damage sustained by the surrounding tissue. Furthermore, no calcium mediated release mechanism played any significant role in the depression. Numerical simulations confirmed the findings and give more insight to the details of the mechanism.
Deposits of amyloid fibrils, long, unbranched polymeric protein aggregates, are the molecular hallmark for a variety of human diseases, including Alzheimer's disease, Parkinson's disease, and type II diabetes. While the amyloid fibrils all share a characteristic cross-beta sheet structure, the proteins that make up the aggregates have no unifying theme in either native structure or function. In this research, I characterized the structural reordering that accompanies this aggregation using Fourier transform infrared spectroscopy (FTIR). Hen egg white lysozyme forms fibrillar aggregates with two distinct morphologies, depending on the growth conditions. At acidic pH with low ionic concentrations, lysozyme forms the fibrils with standard amyloid morphology. These aggregates are long and stiff but with the cross sectional area of a single monomer. At higher salt concentrations, the aggregation follows another pathway, under which oligomers initially form and later assemble into protofibrils. The oligomeric protofibrils are thicker than the monomeric filaments, but are much more curvilinear. These fibrils are not universally recognized as amyloidogenic aggregates. Using FTIR, I showed that both this aggregates are indeed amyloid structures, but that they are structurally distinct. While it is generally accepted that partial unfolding of the protein is a prerequisite for amyloid fibril formation, we found that native protein can be the substrate for amyloid growth when seeded with preformed oligomeric or protofibrillar aggregates. These seeded fibrils grown under near-physiological conditions are structurally indistinguishable from those grown from partially unfolded protein under denaturing conditions. This incorporation and restructuring of native monomers is characteristic of prion-like assembly.
|
186 |
Molecular cloning and functional characterization of a goldfish pituitary adenylate cyclase activating polypeptide receptor謝齡祥, Shea, Ling-cheung, William. January 1998 (has links)
published_or_final_version / Zoology / Master / Master of Philosophy
|
187 |
Regulation of the content of met-enkephalin, beta-endorphin and substance P and of the gene expression of their precursors byhaloperidol in the rat striatum and pituitary during aging劉思文, Lau, See-man. January 1997 (has links)
published_or_final_version / Physiology / Master / Master of Philosophy
|
188 |
Effects of endocrine manipulation on the peptide levels and the gene expression of {221}-endorphin, met-enkephalin, somatostatin, substanceP and cholecystokinin in the rat hypothalamus and pituitary張頌恩, Cheung, Chung-yan. January 1998 (has links)
published_or_final_version / Physiology / Master / Master of Philosophy
|
189 |
EFFECT OF REDUCED ENERGY INTAKE ON PITUITARY RESPONSE TO GONADOTROPIN RELEASING HORMONEChipepa, Joseph Augustine Shangosa January 1981 (has links)
An experiment was conducted with Brangus cows to evaluate the effect of loss of body weight and condition on pituitary responsiveness to gonadotropin releasing hormone (GnRH) stimulation during late lactation. The treatment groups were lactating intact (LI), lactating ovariectomized (LO), nonlactating intact (NLI), and nonlactating ovariectomized (NLO). The study was carried out in two separate blocks, each one consisting of 3 periods. During period 1 the cows were fed a ration that supplied 90% and 88% of the NRC recommendations for TDN in lactating and nonlactating cows, respectively. This period lasted 170 in block 1 and 130 days in block 2. During period 2 the TDN was reduced to 55% or 52% for lactating and nonlactating cows, respectively. Period 2 lasted 100 days for cows in block 1 and 63 days for cows in block 2. At the beginning of period 3 TDN was further reduced to 25% or 27% for the lactating and nonlactating cows, respectively. Cows in block 1 were challenged with GnRH 40 days after the beginning of the 1st energy reduction, 30 days later and 7 days after the 2nd energy reduction. The cows in block 2 were challenged with GnRH 30 days after the 1st energy reduction, 30 days later and 25 days after the 2nd energy reduction. At the end of the study body composition parameters and organ gland weights were determined. No significant differences in the weights of the cows among the treatment groups were found. All cows were, however, losing weight through the course of this study. The nonlactating cows maintained higher body condition (P < .05) than lactating cows from 31 days after ovariectomies were performed until the end of the study. The pituitary glands were significantly heavier in the lactating ovariectomized (2.3 g vs. 1.7 g, P < .05) than the nonlactating intact cows. The weight of the adrenals per unit of body weight of LO cows was significantly higher (.057 g/kg vs. .040 g, P < .05) than among NLO cows. The percent of carcass lipid was significantly higher (P < .05) in nonlactating as compared to lactating cows. Percent moisture and protein were higher (P < .05) in lactating cows. Amount of LH released after GnRH stimulation tended to be higher in lactating than nonlactating cows. The magnitude of the LH peak did not differ significantly among the treatment groups at each of the dates GnRN was injected. Ovariectomized cows (LO and NLO) responded more rapidly (P < .05) to GnRH stimulation than intact cows (LI and NLI). Time on reduced TDN did not affect cow's response pattern after GnRH injection.
|
190 |
Cortisol and mood as a function of luteal progesterone change : a prospective cohort study in Cambridge using diary methods and biological samplesSteele, Amber January 2012 (has links)
No description available.
|
Page generated in 0.0337 seconds