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The effects of variable dose methotrexate infusion in the laboratory rat /Dodridge, M. E. January 1987 (has links) (PDF)
Thesis (M.D.S.)--University of Adelaide, 1988. / Includes bibliographical references (leaves 186-211).
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Qualitative and quantitative assessment of cytochromes P450 mRNA in human : studies in the liver, blood and gastrointestinal mucosa /Thörn, Mari, January 2005 (has links)
Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.
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Sulfasalazin ve bileşenlerinin, amonyak ile oluşturulan mide mukoza lezyonlarına koruyucu etkisi /Aksakal, Gökhan. İşler, Mehmet. January 2003 (has links) (PDF)
Tez (Tıpta Uzmanlık) - Süleyman Demirel Üniversitesi, Tıp Fakültesi, İç Hastalıkları Anabilim Dalı, 2003. / Bibliyografya var.
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Biochemical characterisation of human gastric mucin in normal and diseased statesMcLeod, Heather Alison January 1992 (has links)
Thesis (Masters Diploma (Medical Technology) -- Cape Technikon, Cape Town, 1992 / Gastric cancer, a fatal malignancy, is endemic in the Coloured population of the Western Cape region of South
Africa. Diagnosis is based mainly on histologic
investigation with patients of either sex being mainly
between 40-60 years of age. The extent to which genetic and
environmental influences play a role in the aetiology of the
disease is unknown.
This study is an attempt to biochemically characterise
gastric mucins or mucus glycoproteins, (the main gel forming
components of crude mucus scrapings off the mucosal surface),
in carcinoma of the stomach (HCA), as compared to those in
ulcer disease (HGU), post mortem specimens (PM) and samples
obtained from organ transplant donor stomachs (HD). The aim
of this study is the development of a diagnostic marker
within mucus secretions for the detection of pre-malignant
disease amongst the high risk population of the Western Cape
region of South Africa.
Mucins were extracted from crude mucus gel scrapings
according to a carefully designed technique in which
proteolytic inhibitors were used to minimise the possibility
of endogenous proteolysis in the laboratory through possible
contamination. Two density gradient ultra-centrifugation
steps for 48 hours each at 105,000g in caesium chloride, a
well established standard isolation procedure for mucins,
gave a yield of pure mucins which fractionated at a density
of approximately 1.41gjml in all groups. These mucins, from
the HO, PH, HGU and HCA groups eluted mainly in the included
volume of a Sepharose 2B column as broad, polydisperse peaks,
suggesting that they were degraded and comprised mainly
lower molecular weight PAS positive material in relation to
large polymeric gel forming mucin.
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Studies on intrinsic factor in manBardhan, Karna Dev January 1968 (has links)
No description available.
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Localization and characterization of phosphodiesterase II in intestinal mucosaFlanagan, Peter Rutledge January 1974 (has links)
PDase II activity was determined using a synthetic substrate, the 2,4-dinitrophenyl ester of thymidine 3'-phosphate. The enzyme activity was estimated in fractions obtained by differential centrifugation of homogenates of epithelial cells fromt.the small intestinal mucosa of guinea pigs and rats. In guinea pig preparations PDase II occurred with highest specific activity in those fractions rich in succinate dehydrogenase and acid phosphatase. A lysosomal location for the guinea pig enzyme was indicated by its structure-linked latency and by its association with particles which underwent a characteristic
decrease in equilibrium density when Triton WR-1339 was injected into the animals. With rat preparations a much greater proportion of the PDase II activity was found in the soluble fraction after uult-ra;c;entrifugation. The rat enzyme exhibited a lower degree of latency and administration
of Triton WR-1339 had no effect. The rat enzyme activity in these crude preparations further differed from that of the guinea pig in other respects; it was more labile at 60°C, exhibited a slightly lower pH optimum, had a higher molecular weight as determined by gel filtration chromatography and displayed a much smaller tendency to aggregate under Llow salt conditions. Both enzymes were purified by chromatography on DEAE-cellulose, CM-cellulose and agarose, the extensive
purification (550 fold) of the rat enzyme being largely due to its behaviour oh the latter material where it was found to bind tenaciously in low ionic strength solutions. On the other hand, only a fifteen-fold purification of the guinea pig enzyme was obtained because of its tendency tofform insoluble aggregatesdduring the chromatographic steps. In the main, the properties of the partially purified enzymes were quite similar. Both displayed pH optima between pH 6 and 7, were inhibited in solutions of high ionic strength, were unaffected' by divalent cations or EDTA, were similarly inactivated by heating at a temperature
of 60°G displayed discontinuous Arrhenius plots _5 and exhibited Km values of the order 2-5x10 M for dTpDNP. In most casestfche differences between the enzymes were just differences of degree and could probably be accounted for byethe different extents to which the enzymes were purified. A more extensive characterization of the highly purified rat PDase was carried out. The fall-off in PDase II reaction rate observed at high enzyme levels with dTpDNP as substrate was found to be due to competitive inhibition of the enzyme by dTp, a reaction product which showed a of 2x10 M. The isoelectric point of PDase II was estimated by electrofocusing but since multiple peaks of activity were found at pH 3.4, 4.2-4.5, and pH 7.2 a conclusive result was not obtained. Polyacrylamide gel electrophoresis of purified rat PDase II indicated that the pattern obtained
was, in part, dependent on whether the preparation was fresh or not; freshly purified PDase II contained up to 10 bands in gels stained for protein whereas only 1-2 bands were obtained when the preparations were "aged". A molecular weight of 150000-170000 for the enzyme was estimated in experiments performed by gel-filtration chromatography on dextran and agarose gels. Investigation of the interaction with, and hydrolysis by, rat PDase II of a number of possible phosphodiester substrates indicated that'-, the enzyme required a nucleoside 3'-phosphoryl residue for the initiation of hydrolysis which then proceeded in a 5'+3' direction. Finally, the effect of some enzyme inhibitors was investigated. PDase II activity was inhibited in the presence; of NEM, PCMB, PCMPS and iodoacetic acid. It was further found that the inactivation by iodoacetic acid could be prevented by the presence of a PDase substrate or, better still, by dTp. This is good evidence that iodoacetate alkylates an essential residue at the active center of PDase II and is the first time that such an effect has been shown for a PDase. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate
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Distribuição do receptor de glicocorticoide na mucosa gástrica de ratos submetidos ao desmame precoce. / Distribution of glucocorticoid receptor in the gastric mucosa of rats submitted to early weaning.Ghizoni, Heloisa 21 August 2012 (has links)
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.
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Effects of somatostatin and glucagon on portal pressure, gastric mucosal blood flow and gastric mucosal injury in portal hypertension.January 1998 (has links)
by Tsui, Chi Ping. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 106-119). / Abstract also in Chinese. / ABSTRACT --- p.1 / INTRODUCTION --- p.4 / Chapter 1. --- Portal Hypertension --- p.5 / Chapter 1.1 --- Introduction --- p.5 / Chapter 1.2 --- Anatomy of Normal Portal System --- p.5 / Chapter 1.3 --- Classification and Causes of Portal Hypertension --- p.8 / Chapter 1.4 --- Pathophysiology of Portal Hypertension --- p.9 / Chapter 1.4.1 --- Vascular Change in Portal Hypertension --- p.9 / Chapter 1.4.2 --- Hemodynamic Changes in Portal Hypertension --- p.12 / Chapter 1.4.3 --- Gastric Abnormalities in Portal Hypertension --- p.17 / Chapter 2. --- Somatostatin --- p.22 / Chapter 2.1 --- Introduction --- p.22 / Chapter 2.2 --- Somatostatin Receptors --- p.23 / Chapter 2.3 --- Mechanism of Action --- p.26 / Chapter 2.4 --- Actions of Somatostatin in the Gastrointestinal Tract --- p.28 / Chapter 2.4.1 --- Somatostatin Action in the Stomach --- p.29 / Chapter 2.4.2 --- Somatostatin Action in the Intestine --- p.30 / Chapter 2.4.3 --- Somatostatin Action in the Pancreas --- p.30 / Chapter 2.5 --- Effects of SMT on Hemodynamics in Portal Hypertension --- p.31 / Chapter 2.5.1 --- Splanchnic Circulation --- p.31 / Chapter 2.5.2 --- Systemic Circulation --- p.33 / Chapter 2.5.3 --- Collateral Blood Flow --- p.33 / Chapter 2.5.4 --- Gastric Blood Flow --- p.33 / Chapter 2.6 --- Somatostatin and its analogues in management of acute variceal bleeding --- p.34 / Chapter 3. --- Glucagon --- p.35 / Chapter 3.1 --- Introduction --- p.35 / Chapter 3.2 --- Glucagon Receptor and Mechanism of Action --- p.35 / Chapter 3.3 --- Actions of Glucagon on Circulatory System --- p.38 / Chapter 3.3.1 --- Actions on the Heart --- p.38 / Chapter 3.3.2 --- Vascular Effects --- p.38 / Chapter 3.3.3 --- Hemodynamic Effects --- p.39 / Chapter 3.4 --- Glucagon in Portal Hypertension --- p.40 / Chapter 3.4.1 --- Hyperglucagonemia and portal hypertension --- p.40 / Chapter 3.4.2 --- Hyperglucagonemia and hemodynamic disturbance in portal hypertension --- p.40 / Chapter 4 --- Interaction of somatostatin and glucagon in portal hypertension --- p.41 / Chapter 5. --- Acute Gastric Mucosal Injury --- p.43 / Chapter 5.1 --- Introduction --- p.43 / Chapter 5.2 --- Acute Gastric Mucosal Injury due to Acid and/or Alcohol --- p.43 / Chapter 5.3 --- Gastric Mucosal Defense Mechanisms --- p.45 / Chapter 5.3.1 --- Pre-epithelial Protection --- p.46 / Chapter 5.3.2 --- Epithelial Protection --- p.46 / Chapter 5.3.3 --- Subepithelial Protection --- p.47 / Chapter 5.4 --- Portal Hypertension and Gastric Mucosal Injury --- p.48 / OBJECTIVES --- p.50 / EXPERIMENTAL DESIGN --- p.52 / Chapter 1. --- Effects of Somatostatin and Glucagon on Gastric Mucosal Blood Flow in Portal Hypertension --- p.53 / Chapter 2. --- Effects of Somatostatin and Glucagon on Mucosal Injury Induced by Acid Alcohol in Portal Hypertension --- p.55 / MATERIALS AND METHODS --- p.57 / Chapter 1. --- Induction of portal hypertension --- p.58 / Chapter 2. --- Measurement of blood glucagon levels --- p.60 / Chapter 3. --- "Measurement of Gastric Mucosal Blood Flow, Systemic and Portal Blood Pressures" --- p.62 / Chapter 4. --- Induction of Gastric Mucosal Lesions by Acid Alcohol --- p.65 / Chapter 5. --- Assessment of the Gastric Mucosal Injury after Acid Alcohol Administration --- p.65 / Chapter 6. --- Effects of Somatostatin and Glucagon on Acid Alcohol-Induced Gastric Mucosal Injury --- p.66 / Chapter 7. --- Statistical Analysis --- p.68 / RESULTS --- p.69 / Chapter 1. --- Portal Hypertension Induction by Portal Vein Ligation --- p.70 / Chapter 2. --- Effect of Portal Vein Ligation on Glucagon Level --- p.74 / Chapter 3. --- Effect of Somatostatin and glucagon on Arterial Pressure --- p.77 / Chapter 4. --- Effect of Somatostatin and Glucagon on Portal Pressure --- p.80 / Chapter 5. --- Effect of Somatostatin and Glucagon on Gastric Mucosal Blood Flow --- p.85 / Chapter 8. --- Effect of Somatostatin and Glucagon on Acid Alcohol-induced Gastric Mucosal Injuryin Portal Hypertensive Rats --- p.92 / DISCUSSION --- p.95 / Chapter 1. --- Animal Model --- p.96 / Chapter 2. --- Glucagon Level in Portal Hypertension --- p.98 / Chapter 3. --- Effects of Somatostatin and Glucagon on Systemic and Portal Blood Pressure --- p.99 / Chapter 4. --- Effects of Somatostatin and Glucagon on Gastric Mucosal Blood Flow --- p.102 / Chapter 5. --- Effects of Somatostatin and Glucagon on Gastric Mucosal Injury --- p.103 / CONCLUSION --- p.104 / REFERENCES --- p.106
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The effects of variable dose methotrexate infusion in the laboratory ratDodridge, M. E. (Miles Edward) January 1987 (has links) (PDF)
Bibliography: leaves 186-211.
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Pharmacological therapy of Helicobacter pylori infection /Unge, Peter January 2002 (has links) (PDF)
Diss. (sammanfattning) Linköping : Univ., 2002. / Härtill 5 uppsatser.
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