939 resultados para Gastrointestinal-tract


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http://digitalcommons.colby.edu/atlasofmaine2008/1015/thumbnail.jpg

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Purpose Combination of COL-3, a matrix metalloproteinase inhibitor, and doxorubicin (DOX) might be a promising anticancer regimen. The present study was to examine the potential pharmacokinetic interactions and toxicity profile following their coadministration in rats.
Methods Normal rats were treated with single agent or different combinations with oral or intravenous COL-3 and DOX, and the bile-duct cannulated (BDC) rats received oral COL-3 plus DOX. In a separate disposition study, the effects of DOX on the biliary, urinary, and fecal excretion of COL-3 were examined. In addition, the effects of DOX on in vitro protein binding, metabolism, and transport of COL-3 across Caco-2 monolayers were investigated.
Results COL-3 did not affect the pharmacokinetics of DOX in rats. However, treatment with DOX significantly decreased the oral absorption, and prolonged the elimination, of COL-3 in the normal rats, but not in the BDC rats. DOX did not alter the biliary and urinary excretion of COL-3, but significantly decreased the fecal excretion of COL-3. DOX significantly enhanced the basolateral to apical flux of COL-3 across Caco-2 monolayers, but had no apparent effects on the protein binding and metabolism of COL-3. The combination of DOX with oral COL-3 did not significantly (p > 0.05) increase the acute diarrhea score and intestinal damage compared to rats receiving DOX alone.
Conclusions These results indicated that DOX altered the oral absorption and elimination of COL-3, largely resulting from gastrointestinal toxicity caused by biliary excretion of DOX. Further studies are required to explore the efficacy and optimized dosage regimen of this promising combination.

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A 30-year-old HIV-infected intravenous drug user presented with sepsis, acute renal failure, oedema, proteinuria and iron deficiency anaemia. After extensive investigation, a diagnosis of reactive systemic AA (amyloid, serum amyloid A protein) amyloidosis was made on the basis of renal, gastric and duodenal biopsies.

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Background: Malnutrition and its associated complications are a considerable issue for surgical patients with upper gastrointestinal and colorectal cancer.The present study aimed to determine whether specific perioperative nutritional practices and protocols are associated with improved patient outcomes in this group.
Methods: Patients admitted for elective upper gastrointestinal or colorectal cancer surgery (n = 95) over a 19-month period underwent a medical history audit assessing weight changes, nutritional intake, biochemistry, post-operative complications and length of stay. A subset of patients (n = 25) underwent nutritional assessment by subjective global assessment prior to surgery in addition to assessment of post-operative medical outcomes, nutritional intake and timing of dietetic intervention.
Results: Mean (SD) length of stay for patients was 14.0 (12.2) days, with complication rates at 35%. Length of stay was significantly longer in patients who experienced significant preoperative weight loss compared to those who did not [17.0 (15.8) days versus 10.0 (6.8) days, respectively; P < 0.05]. Low albumin and post-operative weight loss were also predictive of increased length of stay. Of patients who underwent nutritional assessment, 32% were classified as mild–moderately malnourished and 16% severely malnourished. Malnourished patients were hospitalised twice as long as well-nourished patients [15.8 (12.8) days versus 7.6 (3.5) days; P < 0.05]. Time taken [6.9 (3.6) days] to achieve adequate nutrition post surgery was a factor in post-operative outcomes, with a positive correlation with length of stay (r = 0.493; P < 0.01), a negative correlation with post-operative weight change (r = —0.417; P < 0.05) and a greater risk of complications (52% versus 13%; P < 0.01).
Conclusions: Malnutrition is prevalent among surgical patients with gastrointestinal cancer. Poor nutritional status coupled with delayed and inadequate post-operative nutrition practices are associated with worse clinical outcomes.

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Despite the enormous amount of data available on the importance of the gastrointestinal (GI) microbiota in vertebrate (especially mammals), information on the GI microbiota of seabirds remains incomplete. As with many seabirds, penguins have a unique digestive physiology that enables them to store large reserves of adipose tissue, protein, and lipids. This study used quantitative real-time polymerase chain reaction (qPCR) and 16S rRNA gene pyrosequencing to characterize the interspecific variations of the GI microbiota of four penguin species: the king, gentoo, macaroni, and little penguin. The qPCR results indicated that there were significant differences in the abundance of the major phyla Firmicutes, Bacteroides, Actinobacteria, and Proteobacteria. A total of 132,340, 18,336, 6324, and 4826 near full-length 16S rRNA gene sequences were amplified from fecal samples collected from king, gentoo, macaroni, and little penguins, respectively. A total of 13 phyla were identified with Firmicutes, Bacteroidetes, Proteobacteria, and Fusobacteria dominating the composition; however, there were major differences in the relative abundance of the phyla. In addition, this study documented the presence of known human pathogens, such as Campylobacter, Helicobacter, Prevotella, Veillonella, Erysipelotrichaceae, Neisseria, and Mycoplasma. However, their role in disease in penguins remains unknown. To our knowledge, this is the first study to provide an in-depth investigation of the GI microbiota of penguins.

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Cases of autism have frequently been reported in association with gastrointestinal problems. These observations have stimulated investigations into possible abnormalities of intestinal microbiota in autistic patients. The objectives of this paper were to review the possible involvement and mechanisms of gastrointestinal microbiota in autistic spectrum disorder and explain the possible role of gastrointestinal microbiota in the condition. This review addresses the possible involvement of bacteria, viruses and fungi, and their products in autism. Direct viral damage of neurons or disruption of normal neurodevelopment by immune elements such as cytokines, nitric oxide and bacterial products, including lipopolysaccharides, toxins and metabolites, have been suggested to contribute to autistic pathology. Numerous intestinal microbial abnormalities have been reported in individuals with autism. Research to date exploring possible gastrointestinal problems and infection in autism has been limited by small and heterogeneous samples, study design flaws and conflicting results. Furthermore, interventions designed to modify the intestinal microbial population of autistic patients are few and limited in their generalisation. In order to bring clarity to this field, high-quality and targeted investigations are needed to explore the role of gastrointestinal microbiology in autism. To this end, several promising avenues for future research are suggested.