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BACKGROUND: Diet plays a key role in the pathogenesis of nonalcoholic fatty liver disease. Limited data exist regarding specific nutrients and food groups and liver fat continuously, particularly among different ethnicities. OBJECTIVES: We aimed to determine the relationship between usual dietary intake and accurately measured liver fat content in a multiethnic population. METHODS: Participants from the Multiethnic Cohort were recruited into the cross-sectional Adiposity Phenotype Study including women and men aged 60–77 y and 5 race/ethnic groups (African American, Japanese American, Latino, Native Hawaiian, and white). They filled out a detailed FFQ and underwent abdominal MRI for liver fat quantification and whole-body DXA for total adiposity. Intake of a priori–selected dietary factors (total and macronutrient energy, specific micronutrients, and food groups) was analyzed in relation to liver fat by estimating the mean percentage liver fat for quartiles of each dietary factor in a general linear model that adjusted for age, sex, race/ethnicity, percentage body fat, and daily energy intake (kcal/d). RESULTS: In total, 1682 participants (mean age: 69.2 y; 51% female) were included. Mean ± SD liver fat percentage was 5.7 ± 4.6. A significant positive association with liver fat was found across quartiles of percentage energy from fat, saturated fat, cholesterol, total red meat, red meat excluding processed red meat, and coffee (Bonferroni-adjusted P-trend

This review explores the role of diet in the pathogenesis and treatment of inflammatory bowel disease and highlights various contemporary dietary options in the treatment of adult and pediatric inflammatory bowel disease. The role of diet in inflammatory bowel disease has become clearer through epidemiologic, basic science, and interventional studies. Multiple dietary treatment strategies are used as primary or adjunctive therapy in inflammatory bowel disease to varying degrees of success. While the field of nutrition and nutritional therapy in inflammatory bowel disease has evolved with supporting evidence from basic science and clinical research, further studies are necessary to fully understand the impact and potential of diet and dietary therapy in the management of IBD.

Ulcerative colitis is an inflammatory condition of the colon. The diagnosis of ulcerative colitis is based on clinical presentation, endoscopic evaluation, and histologic parameters in the absence of demonstrable alternate etiology. The differential diagnosis remains broad, and infection in particular must be considered and excluded. Although laboratory and radiographic findings can aid in the diagnosis of ulcerative colitis, endoscopy remains the gold standard for diagnosis. A correct diagnosis and disease staging are imperative because these factors affect treatment options and prognosis.

Short bowel syndrome (SBS) is the most common cause of intestinal failure resulting in the need for long-term parenteral nutrition. Treatment for SBS involves the close management of parenteral and...

Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a life-long relapsing and remitting condition characterized by inflammation of the intestine. While the exact pathogenesis of IBD is unclear, the current belief is that both genetic and environmental factors play a role in development of disease. Management options include nutritional, pharmacological, and surgical therapies. In particular, nutritional therapies for IBD have garnered significant interest due to their limited side effect profile, bowel-sparing nature, and naturalistic approach. This review will examine the role of diet in the pathogenesis and malnutrition in IBD, and will discuss dietary approaches to management of IBD, including exclusive enteral nutrition, specific carbohydrate diet, anti-inflammatory diet, and food supplements (specifically curcumin and long-chain n-3 polyunsaturated fatty acids). Past and recent literature on these subjects were reviewed in Medhub and Scopus databases for this review article with a focus on pediatric and high-quality publications. At this time, these approaches seem to be safe and show promise of an efficacious sole or supplemental role in the treatment of IBD, but randomized, prospective studies are lacking. Additional studies investigating these diets and food supplements are needed to provide more information on their efficacy, mechanism, applicability, and safety.

Purpose of review Despite improvement in short-term outcomes after intestinal transplantation in the last 20 years, long-term rates of graft attrition and patient survival remain unchanged, with worse outcomes compared with other solid organ transplants. This review investigates the multiple causes of late graft loss, including chronic rejection, infection, graft-versus-host disease, posttransplant lymphoproliferative disorder and postsurgical complications. Recent findings New insights into immunology of the intestine and evolution of immunosuppression, as well as review of current persistent causes of late graft loss, shed light on findings that may help improve long-term intestinal allograft survival. Summary Although intestinal transplantation remains a life-saving intervention with significant advancements since its inception, further understanding of mechanisms of injury is needed to improve long-term outcomes and prevent late intestinal graft loss.

Ulcerative colitis is an inflammatory condition of the colon. The diagnosis of ulcerative colitis is based on clinical presentation, endoscopic evaluation, and histologic parameters in the absence of demonstrable alternate etiology. The differential diagnosis remains broad, and infection in particular must be considered and excluded. Although laboratory and radiographic findings can aid in the diagnosis of ulcerative colitis, endoscopy remains the gold standard for diagnosis. A correct diagnosis and disease staging are imperative because these factors affect treatment options and prognosis.

Posttraumatic osteoarthritis (PTOA) is the most common form of osteoarthritis (OA) of the ankle joint. PTOA occurs as a result of several factors, including the poor regenerative capacity of hyaline articular cartilage as well as increased contact stresses following trauma. The purpose of this article is to review the epidemiology, pathogenesis, and potential targets for treatment of PTOA in the ankle joint. Previous reviews primarily addressed clinical approaches to ankle PTOA, while the focus of the current article will be specifically on the newly acquired knowledge of the cellular mechanisms that drive PTOA in the ankle joint and means for potential targeted therapeutics that might halt the progression of cartilage degeneration and/or improve the outcome of surgical interventions. Three experimental treatment strategies are discussed in this review: (1) increasing the anabolic potential of chondrocytes through treatment with growth factors such as bone morphogenetic protein-7; (2) limiting chondrocyte cell death either through the protection of cell membrane with poloxamer 188 or inhibiting activity of intracellular proteases, caspases, which are responsible for cell death by apoptosis; and (3) inhibiting catabolic/inflammatory responses of chondrocytes by treating them with anti-inflammatory agents such as tumor necrosis factor-α antagonists. Future studies should focus on identifying the appropriate timing for treatment and an appropriate combination of anti-inflammatory, chondro- and matrix-protective biologics to limit the progression of trauma-induced cartilage degeneration and prevent the development of PTOA in the ankle joint.