Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 4 uppsatser.

Diss. (sammanfattning) Linköping : Univ., 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.

Thesis (M.Sc. (Physiology))--Mahidol University, 1982.

Thesis (Ph.D.)--University of Alabama at Birmingham, 2009. / Title from PDF title page (viewed on Sept. 9, 2009). Includes bibliographical references.

O desmame precoce (DP) consiste na abrupta substituição do leite pela dieta sólida e este padrão de alimentação pode ter impacto sobre o crescimento do estômago. Esta situação é também estressante para os filhotes e eleva os níveis de corticosterona que age ligando-se ao receptor de glicocorticoide (GR). Estudamos a expressão e a distribuição do GR na mucosa gástrica de ratos amamentados (C) e em DP. A expressão de GR foi maior aos 17 dias no grupo C e aumentou do 17º para o 18º dia no grupo em DP (p<0,05). O DP diminuiu o nível de GR, principalmente aos 18 dias (p<0,05), porém não alterou sua distribuição tecidual. Em termos de localização subcelular o GR, ficou mais concentrado no citoplasma no C (p<0,05), enquanto no DP, a distribuição foi similar entre os compartimentos, com uma redução no citoplasma (p<0,05), e um sutil aumento no núcleo. Sugerimos que a resposta de GR ao DP indica a alteração um elemento essencial na atividade da corticosterona, e essa modificação pode ser importante na coordenação do crescimento da mucosa gástrica durante o desmame precoce. / Early weaning (EW) is the abrupt change from suckling (S) to solid food and it can impair stomach development. This is a stressful situation for pups and it augments corticosterone levels, which acts through glucocorticoid receptor (GR). We studied GR expression, tissue and subcellular distribution in the gastric mucosa of S and EW pups. GR expression was higher at 17 d in S pups (p<0,05), whereas in EW group, it increased from the 17th to 18th d (p<0,05). GR protein levels decreased throughout EW, mainly at 18 d (p<0,05). However, EW did not alter tissue distribution of GR along the gastric gland. As for GR subcellular distribution, we found that in S group GR was more concentrated in the cytoplasm, (p<0,05), whereas in EW pups, GR was similarly distributed between compartments, though we detected a decrease in the cytoplasm (p<0.05) and a slight increase in the nucleus. We suggest that GR response to EW indicates the change of an essential element of corticosterone cascade, and such alteration might be important in the coordination of gastric mucosa growth.

Sucralfate is a drug that effectively heals duodenal, gastric and oesophageal ulcers. It is not absorbed systemically and it has been shown to act locally by coating the ulcer base. However when it was also shown to prevent stress ulcers and ethanolinduced gastric mucosa! lesions, it seemed likely that it acted in some way to improve the effectiveness of the gastric mucosa! barrier. Some investigators suggested that it did so by stimulating local prostaglandin release. The Slomiany group, on the basis of in vitro work on the effects of Sucralfate on pig gastric mucus, claimed that Sucralfate acted by altering the physico-chemical properties of mucus to increase the viscosity and retard the back diffusion of H+ ions. The work described in this dissertation set out to verify, in vivo, these claimed effects on mucus, using an experimental porcine model of peptic ulceration, the bile duct ligated pig. In addition, the effects of Sucralfate were compared with those of Famotidine and Misoprostol, and changes in mucous prostaglandins, gastric juice pepsin and gastric flora were sought. By way of introduction, the known and postulated actions of Sucralfate, current understanding of gastric mucus physiology and pathogenesis of peptic ulceration, have been reviewed, as have experimental animal models of peptic ulceration, in order to justify using the bile duct ligated pig model.

O leite é essencial para o desenvolvimento pós-natal da mucosa gástrica e durante o período de aleitamento, o jejum estimula a proliferação celular. Mostramos que o TGF<font face=\"Symbol\">b, reverte este efeito e p27 está envolvida neste mecanismo. Os níveis de p27 oscilam durante o ciclo celular, devido à sua fosforilação na Thr187, que leva à degradação pelo sistema UPS. Diferentes estudos relatam que TGF<font face=\"Symbol\">b pode aumentar p27, através do controle de sua degradação. Este estudo visa analisar o efeito do jejum e TGF<font face=\"Symbol\">b1, na regulação de p27 no epitélio gástrico de ratos lactentes. Para tanto, filhotes de 14 dias foram submetidos a jejum durante 90 min e receberam uma dose única de TGF<font face=\"Symbol\">b ou PBS, por gavagem. As amostras foram coletadas após 2 e 14 horas de tratamento. Analisamos a concentração proteica de p27, fosfo-p27, Skp2 e Cdh1. Observamos que durante o jejum houve a diminuição de p27 e Cdh1, paralelamente ao aumento de fosfo-p27 e Skp2. Enquanto que o tratamento com TGF<font face=\"Symbol\">b1, reverteu os efeitos do jejum em 2h e 14h em todas as proteínas analisadas. Além disso, o jejum aumentou a ubiquitinação e degradação de p27 e o tratamento com TGF<font face=\"Symbol\">b1 reverte esses efeitos. Desta forma, o TGF<font face=\"Symbol\">b1 do leite materno estabiliza os níveis de p27 e assim, influenciar a progressão do ciclo celular no epitélio gástrico. / Milk is essential for postnatal development of the gastric mucosa and during the suckling period fasting stimulates cell proliferation. We have shown that TGF<font face=\"Symbol\">b reverses this effect and p27 is involved in this mechanism. The levels of p27 oscillate during the cell cycle due to its phosphorylation at Thr187, which leads to its degradation by the UPS. Different studies reported that TGF<font face=\"Symbol\">b can increase p27, by controlling its degradation. This study aims to analyze the effect of fasting and TGF<font face=\"Symbol\">b1 in regulating p27 in lactating rats gastric epithelium. For such, the 14 days rats were fasted for 90 min and received a single dose of TGF<font face=\"Symbol\">b or PBS by gavage. Samples were collected after 2 and 14 hours of treatment. We analyzed the p27 protein concentration, phospho-p27, Skp2 and Cdh1. We found that during fasting, p27 and Cdh1 a decreased, at the same time to the increment of phospho-p27 and Skp2. The treatment with TGF<font face=\"Symbol\">b1, reversed the effects of fasting on 2h and 14h in all proteins analyzed. Moreover, the fasting increased the ubiquitination and the degradation of p27, while TGF<font face=\"Symbol\">b1 treatment reversed these effects. Thus the milk born TGF<font face=\"Symbol\">b1 can stabilize p27 levels and thus influences cell cycle progression in lactent rat gastric epithelium.

O Sistema nervoso entérico está localizados entre as camadas constituintes das paredes do trato gastrintestinal, entre as camadas musculares longitudinal e circular, que se estende por todo o trato digestório, desde o esôfago até o reto. Desordens gastrintestinais são complicações comuns causadas pela lesão térmica. A presente pesquisa avalia, em estômagos de ratos alterações na mucosa e no plexo mioentérico submetidos à lesão térmica corporal. O número de neurônios NADH-d e NADPH-d aumentaram significativamente nos animais queimados. Analisando a média da área do perfil dos neurônios NADH-dr e NADPH-dr evidenciaram uma diminuição significativa de 26% e 24%, respectivamente, na área do perfil dos neurônios dos animais queimados. Assim, associados o VIP o NO e a acetilcolina se apresentaram de maneira a interferir no esvaziamento gástrico causando ulcerações que foram observadas pela técnica da MEV na mucosa gástrica. Com esses dados, pode-se concluir que a LTC interfere no plexo mioentérico do estômago de ratos causando uma gastroparesia. / The enteric nervous system is located among the layer constituents of the gastrintestinal tract. Between the longitudinal and circular muscle layers, which extend throughout the digestory tract from the esophagus to the rectum. Gastrintestinal disorders are common complications caused by burn injury. This research evaluates, in stomach of rats changes in the mucosal and myenteric plexus, subjected burn injury. The number of neurons NADH-d and NADPH-d significantly increased in burned animals. Analyzing the average area of the profile of the neurons NADH-dr and NADPH-dr, showed a significant decrease of 26% and 24%, respectively, in the area of the profile of the neurons of the burned animals. Thus, the association of VIP, NO and acetylcholine is presented so as to interfere with gastric emptying causing changes in the mucosal wich were observed by the technique of MEV. With this data, it can be conclude that the burn injury interferes in the myenteric plexus of the stomach of rats causing a gastroparesis.