Wyniki wyszukiwania - Biblioteka Nauki

1

Żywienie w chorobach wątroby i dróg żółciowych u osób starszych

100%

Zwolinska-Wcislo M.

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nr 2

EN

The process of aging predisposes to hepatic functional and structural impairment and metabolic risk. There are no specific age-related liver diseases but some of them are particularly more frequent in the elderly population, such as nonalcoholic fatty liver disease (NALFD), chronic hepatitis C and hepatocellular carcinoma. NAFLD is the most common liver disease, affecting about 30% of the overall population. Clinically NAFLD tends to be associated with the most typical geriatric syndromes, such as dementia, sarcopenia, dysfunction of the autonomic nervous system. The nutrition therapy for chronic liver diseases should be planned on an assessment of their complications, nutritional state and dietary intake. Non-pharmacological treatment including diet and physical activity should be individually tailored considering the physical limitations, typical geriatric syndromes, such as frailty, multimorbidity, polypharmacy and dementia. For malnourished patients with chronic liver disease oral and enteral nutrition is recommended. Parenteral nutrition should be reserved for those with moderate-to-se- vere malnutrition who cannot meet their caloric needs by oral or enteral routes. Daily caloric ESPEN recommendations for patients with chronic liver disease ran ges from 35 - 40 kcal/kg/ day. Daily protein requirement is 1,0 - 1,5 g/kg/day, and in acute encephalopathy is 0,6 - 0,6 g/ kg/day. Small meals evenly distributed through the day and a bedtime snack of complex carbohydrates minimize muscle loss. Branched-chain amino acids (BAA) supplementation may help to achieve daily protein goals in patients who are protein intolerant. Sodium restriction, 80 - 120 mmol sodium/day is recommended in the therapy of ascites. Restriction of fluids is not recommended until serum level of sodium decreases to 120-125 mmol/l.

2

Assessment of co-existence of Helicobacter pylori and Candida fungi in diseases of the upper gastrointestinal tract

38%

Karczewska E. , Wojtas I. , Sito E. , Trojanowska D. , Budak A. , Zwolinska-Wcislo M. , Wilk A.

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2009

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tom 60

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nr 6

3

Disturbances of autonomic nervous system activity and diminished response to stress in patients with celiac disease

38%

Przybylska-Felus M. , Furgala A. , Zwolinska-Wcislo M. , Mazur M. , Widera A. , Thor P. , Mach T.

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nr 6

4

Ocena przydatnosci chromogennych podlozy w diagnostyce mikrobiologicznej

38%

Budak A. , Tokarczyk M. , Nowak P. , Skalkowska M. , Bogusz B. , Zwolinska-Wcislo M. , Wilk M.

Medycyna Doświadczalna i Mikrobiologia

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2009

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tom 61

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nr 2

167-174

5

Effect of Candida colonization on human ulcerative colitis and the healing of inflammatory changes of the colon in the experimental model of colitis ulcerosa

26%

Zwolinska-Wcislo M. , Brzozowski T. , Budak A. , Kwiecien S. , Sliwowski Z. , Drozdowicz D. , Trojanowska D. , Rudnicka-Sosin L. , Mach T. , Konturek S. J. , Pawlik W. W.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 1

107-118

EN

The influence of fungal colonization on the course of ulcerative colitis (UC) has not been thoroughly studied. We determined the activity of the disease using clinical, endoscopic and histological index (IACH) criteria in UC patients with fungal colonization and the healing process of UC induced by an intrarectal administration of trinitrobenzene sulfonic acid (TNBS) in rats infected with Candida, without and with antifungal (fluconazole) or probiotic (lacidofil) treatment. The intensity of the healing of the colonic lesions was assessed by macro- and microscopic criteria as well as functional alterations in colonic blood flow (CBF). Myeloperoxidase (MPO) content and plasma proinflammatory cytokines IL-1ß and TNF- levels were evaluated. Candida more frequently colonized patients with a history of UC within a 5-year period, when compared with those of shorter duration of IBS. Among Candida strains colonizing intestinal mucosa, Candida albicans was identified in 91% of cases. Significant inhibition of the UC activity index as reflected by clinical, endoscopical and histological criteria was observed in the Candida group treated with fluconazole, when compared to that without antifungal treatment. In the animal model, Candida infection significantly delayed the healing of TNBS-induced UC, decreased the CBF and raised the plasma IL-1ß and TNF- levels, with these effects reversed by fluconazole or lacidofil treatment. We conclude that 1) Candida delays healing of UC in both humans and that induced by TNBS in rats, and 2) antifungal therapy and probiotic treatment during Candida infection could be beneficial in the restoration and healing of colonic damage in UC.

6

Antibiotic treatment with ampicillin accelerates the healing of colonic damage impaired by aspirin and coxib in the experimental colitis. Importance of intestinal bacteria, colonic microcirculation and proinflammatory cytokines

26%

Zwolinska-Wcislo M. , Krzysiek-Maczka G. , Ptak-Belowska A. , Karczewska E. , Pajdo R. , Sliwowski Z. , Urbanczyk K. , Drozdowicz D. , Konturek S. J. , Pawlik W. W. , Brzozowski T.

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nr 3

EN

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for their anti-inflammatory, analgesic and antipyretic effects, however their use is associated with the broad spectrum of side effects observed in human as well as the experimental animals. Despite damaging activity of NSAIDs in upper gastrointestinal (GI) tract, these drugs exert deleterious influence in lower GI tract, including colon. The role of GI microflora in the pathogenesis of NSAIDs-induced experimental colonic damage is not completely understood. The aim of this study was 1) to evaluate the relative importance of the GI microflora on the experimental colonic damage in the presence of caused by NSAID, and 2) to assess the efficacy of antibiotic treatment with ampicillin on the process of healing of colitis. We compared the effect of vehicle, ASA applied 40 mg/kg intragastrically (i.g.) or the selective cyclooxygenase (COX)-2 inhibitor, celecoxib (25 mg/kg i.g.) without or with ampicillin treatment (800 mg/kg i.g.) administered throughout the period of 10 days, on the intensity of TNBS-induced colitis in rats. The severity of colonic damage, the alterations in the colonic blood flow (CBF) and myeloperoxidase (MPO) activity, the mucosal expression of TNF-, IL-1ß, COX-2, VEGF and iNOS and the plasma concentration of TNF- and IL-1ß were assessed. In all rats, the faeces samples as well as those from the colonic mucosa, blood, liver and spleen underwent microbiological evaluation for intestinal bacterial species including Escherichia coli and Enterococcus spp. The administration of TNBS resulted in macroscopic and microscopic lesions accompanied by the significant fall in the CBF, an increase in tissue weight and 4-5-fold rise in the MPO activity and a significant increase in the plasma IL-1ß and TNF- levels. ASA or celecoxib significantly increased the area of colonic lesions, enhanced MPO activity and caused the marked increase in colonic tissue weight and plasma IL-1ß and TNF- levels, as well as an overexpression of mRNA for IL-1ß and TNF-, COX-2, VEGF and iNOS in the colonic tissue. ASA and coxib also resulted also in a significant increase of E. coli counts in the stool at day 3 and day 10 day of the observation compared with the intact rats. Moreover, E. coli translocation from the colon to the blood and extraintestinal organs such as liver and spleen in the group of rats treated without or with ASA and coxib. E. coli was the most common bacteria isolated from these organs. Treatment with ampicillin significantly attenuated the ASA- or celecoxib-induced increase in plasma levels of IL-1ß and TNF- and suppressed the mucosal mRNA expression for IL-1ß and TNF-ß, COX-2, iNOS and VEGF in the colonic mucosa. Ampicillin administration caused a significant fall in the number of E. coli in the faeces at day 3 and day 10 of observation in ASA- and coxib-treated rats with colitis. Antibiotic therapy markedly reduced bacterial translocation to the colonic tissue and the extraintestinal organs such as the liver and spleen. We conclude that administration of ASA and to lesser extent of celecoxib, delays the healing of experimental colitis and enhances the alterations in colonic blood flow, proinflammatory markers such as IL-1ß, TNF-, COX-2, iNOS and VEGF and increased intestinal mucosal permeability resulting in the intestinal bacterial translocation to the blood, spleen and liver. Antibiotic treatment with ampicillin is effective in the diminishing of the severity of colonic damage, counteracts both the NSAID-induced fall in colonic microcirculation and bacterial E.coli translocation to the extraintestinal organs.