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| 1 | Diet and nutritional factors in inflammatory bowel diseases显示文摘Inflammatory bowel disease(IBD) development is affected by complex interactions between environmental factors, changes in intestinal flora, various predisposing genetic properties and changes in the immune system. Dietary factors seem to play an underestimated role in the etiopathogenesis and course of the disease. However, research about food and IBD is conflicting. An excessive consumption of sugar, animal fat and linoleic acid is considered a risk factor for IBD development, whereas a high fiber diet and citrus fruit consumption may play a protective role. Also, appropriate nutrition in particular periods of the disease may facilitate achieving or prolonging remissions and most of all, improve the quality of life for patients. During disease exacerbation, a low fiber diet is recommended for most patients. In the remission time, an excessive consumption of alcohol and sulfur products may have a negative effect on the disease course. Attempts are also made at employing diets composed in detail in order to supplement IBD therapy. A diet with a modified carbohydrate composition, a semi-vegetarian diet and a diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols are under investigation. Due to chronic inflammation as well as side effects of chronically used medications, patients with IBD are also at increased risk of nutritional factor deficiencies, including iron, calcium, vitamin D, vitamin B12, folic acid, zinc, magnesium and vitamin A. It should also be remembered that there is no single common diet suitable for all IBD patients; each of them is unique and dietary recommendations must be individually developed for each patient, depending on the course of the disease, past surgical procedures and type of pharmacotherapy. | Danuta Owczarek Tomasz Rodacki Renata Domagała-Rodacka Dorota Cibor Tomasz Mach | 2016 | World Journal of Gastroenterology2016，22，3： | 19 |
| 2 | Inflammatory bowel disease:Epidemiology,pathology and risk factors for hypercoagulability显示文摘Hypercoagulability observed in patients with inflammatory bowel diseases(IBD)may lead to thromboembolic events(TE),which affect the venous and arterial systems alike and are an important factor in patients’morbidity and mortality.The risk of TE in IBD patients has been demonstrated to be approximately threefold higher as compared to the general population.The pathogenesis of thrombosis in IBD patients is multifactorial and not fully explained.The most commonly listed factors include genetic and immune abnormalities,disequilibrium between procoagulant and anticoagulant factors,although recently,the role of endothelial damage as an IBD-triggering factor is underlined.Several studies report that the levels of some coagulation enzymes,including fibrinogen,factorsⅤ,Ⅶ,Ⅷ,active factorⅪ,tissue factor,prothrombin fragment 1+2and the thrombin-antithrombin complex,are altered in IBD patients.It has been demonstrated that there is a significant decrease of tissue plasminogen activator level,a marked increase of plasminogen activator inhibitor type 1 and thrombin-activable fibrinolysis inhibitor,a significantly lower level of antithrombinⅢand tissue factor pathway inhibitor.IBD patients have been also observed to produce an increased amount of various anticoagulant antibodies.Hyperhomocysteinemia,which is a potential risk factor for TE was also observed in some IBD patients.Further studies are necessary to assess the role of coagulation abnormalities in IBD etiology and to determine indications for thromboprophylactic treatment in patients at high risk of developing TE. | Danuta Owczarek Dorota Cibor Mikolaj K Glowacki Tomasz Rodacki Tomasz Mach | 2014 | World Journal of Gastroenterology2014，20，1： | 16 |
| 3 | Endothelial dysfunction in inflammatory bowel diseases:Pathogenesis,assessment and implications显示文摘Endothelial dysfunction is considered one of the etiological factors of inflammatory bowel disease(IBD). An inflammatory process leads to functional and structural changes in the vascular endothelium. An increase of leukocyte adhesiveness and leukocyte diapedesis, as well as an increased vascular smooth muscle tone and procoagulant activity is observed. Structural changes of the vascular endothelium comprise as well capillary and venule remodeling and proliferation of endothelial cells. Hypoxia in the inflammatory area stimulates angiogenesis by upregulation of vascular endothelial growth factor, fibroblast growth factor and tumor necrosis factor-α. Inflammatory mediators also alter the lymphatic vessel function and impair lymph flow, exacerbating tissue edema and accumulation of dead cells and bacteria. The endothelial dysfunction might be diagnosed by the use of two main methods: physical and biochemical. Physical methods are based on the assessment of large arteries vasodilatation in response to an increased flow and receptors stimulation. Flowmediated vasodilatation(FMD) is the method that is the most widely used; however, it is less sensitive in detecting early changes of the endothelium function. Most of the studies demonstrated a decrease of FMD in IBD patients but no changes in the carotic intima-media thickness. Biochemical methods of detecting the endothelial dysfunction are based on the assessment of the synthesis of compounds produced both by the normal and damaged endothelium. The endothelial dysfunction is considered an initial step in the pathogenesis of atherosclerosis in the general population. In IBD patients, the risk of cardiovascular diseases is controversial. Large, prospective studies are needed to establish the role of particular medications or dietary elements in the endothelial dysfunction as well to determine the real risk of cardiovascular diseases. | Dorota Cibor Renata Domagala-Rodacka Tomasz Rodacki Artur Jurczyszyn Tomasz Mach Danuta Owczarek | 2016 | World Journal of Gastroenterology2016，22，3： | 10 |
| 4 | A reviewon the basketball jump shot显示文摘 | OKAZAKI V H A RODACKI A L SATERN M N | 2015 | Sports Biomech’2015，14，2： | 1 |
| 5 | NK cells and type 1 diabetes 显示文摘 | Rodacki M Milech A de Oliveira JE | 2006 | Clin Dev Immuno12006，13，24： | 1 |
| 6 | Vertical jumpcoordination:fatigue effects显示文摘 | RODACKI A L FOWLER N E BENNETT S J | 2002 | Med Sci Sports Exe2002，34，1： | 1 |
| 7 | Changes in lipid profile after treatment of women with gestational diabetes mellitus 显示文摘 | Kern Pessoa V N Rodacki M Negrato C A | 2016 | J Clin Lipidol2016，10，2： | 1 |
| 8 | Transient effects of stretching exercises on gait parameters of elderly women显示文摘 | Rodacki AL Souza RM Ugrinowitsch C | 2009 | Man Ther2009，14，2： | 1 |
| 9 | Altered natural killer cells in type 1 diabetic patients显示文摘 | Rodacki M Svoren B Butty V | 2007 | Diabetes2007，56，1： | 1 |
| 10 | Altered natural killer cells in type 1 diabetic patients显示文摘 | Rodacki M Svoren B Butty V | | 0，，： | 1 |
| 11 | Impact of advanced and basic carbohydrate counting methods on metabolic control in patients with type 1 diabetes 显示文摘 | Souto DL Zajdenverg L Rodacki M | 2014 | Nutrition2014，30，： | 1 |
| 12 | Altered natural killer cells in type I diabetic patients显示文摘 | Rodacki M Svoren B Butty V | 2007 | Diabetes2007，56，1： | 1 |
| 13 | Nk cells and type 1 diabetes 显示文摘 | Rodacki M Milech A De Oliveira J | 2006 | Clin Develop Immunol2006，13，24： | 1 |
| 14 | Altered natural killer cells in type 1 diabetic patients显示文摘 | Rodacki M Svoren B Butty V | | 0，，1： | 1 |
| 15 | Altered natural killer cells in type 1 diabetic patients显示文摘 | Rodacki M Svoren B Burry V | 2007 | Diabetes2007，56，1： | 1 |
| 16 | Fish-oil supplementation enhances the effects of strength training in elderly women 显示文摘 | Rodacki CL Rodacki AL Pereira G | 2012 | Am J Clin Nutr2012，95，2： | 1 |
| 17 | Altered natural killer cells in type 1 diabetic patients显示文摘 | Rodacki M Svoren B Butty V | 2007 | Diabetes2007，56，1： | 1 |
| 18 | Fish-oil supplementation enhances the effects of strength training in elderly women显示文摘 | Rodacki CL Rodacki AL Pereira G | 2012 | Am J Clin Nutr2012，95，： | 1 |
| 19 | et al Bodymass as a factor in stature change 显示文摘 | RodackiAL FowlerNE ProvensiCL | 2005 | Clinical Biomechanics2005，20，79： | 1 |
| 20 | NK ceils and type 1 diabetes 显示文摘 | Rodacki M Milech A de Oliveira JE | 2006 | Clin Dev Immunol2006，13，24： | 1 |
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