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La disputa sulle origini della neoscolastica italiana: Salvatore Roselli, Vincenzo Buzzetti e Gaetano Sanseverino
La disputa sulle origini della neoscolastica italiana: Salvatore Roselli, Vincenzo Buzzetti e Gaetano Sanseverin
Letter: use of collagen proportionate area to quantify liver fibrosis and predict clinical outcomes non‐alcoholic fatty liver disease—authors' reply
Editorial: collagen proportionate area as a prognostic indicator in NAFLD—authors’ reply
Oxidative stress management in elite athletes
It is well known that strenuous exercise training can induce an overproduction of reactive oxygen species with subsequent impairment of cellular macromolecules and metabolism, leading to cellular dysfunction. In elite athletes, reactive oxygen species can add to other injurious factors for muscle tissue; therefore special precautions are required to avoid an increase in injury risk
Intestinal hormones, gut microbiota and non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome and has a complex pathophysiology with multiple pathways of development and progression implicated. Intestinal hormones regulate multiple biological functions and may play a role in the pathogenesis of non alcoholic fatty liver disease (NAFLD) by affecting food intake, body weight and insulin resistance. Bacterial products can affect the secretion of these hormones and thus have an effect on metabolism. Gut microbiota are normally involved in the intestinal energy harvest and their role has been increasingly been implicated in the pathogenesis of obesity and NAFLD. The intestinal hormone pathways as well as the intestinal microbiota populations are potential therapeutic targets in the management of NAFLD. We review the evidence on the associations of the intestinal hormones and gut microbiota in the development, progression and treatment of NAFLD
The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD)
Nonalcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. Despite its high prevalence, only a small minority of affected patients develops inflammation and subsequently fibrosis and chronic liver disease, while most of them only exhibit simple steatosis. In this context, the full understanding of the mechanisms underlying the development of NAFLD and non-alcoholic steatohepatitis (NASH) is of extreme importance; despite advances in this field, knowledge on the pathogenesis of NAFLD is still incomplete. The ‘two-hit’ hypothesis is now obsolete, as it is inadequate to explain the several molecular and metabolic changes that take place in NAFLD. The “multiple hit” hypothesis considers multiple insults acting together on genetically predisposed subjects to induce NAFLD and provides a more accurate explanation of NAFLD pathogenesis. Such hits include insulin resistance, hormones secreted from the adipose tissue, nutritional factors, gut microbiota and genetic and epigenetic factors. In this article, we review the factors that form this hypothesis
Genetic iron overload disorders
Due to its pivotal role in orchestrating vital cellular functions and metabolic processes, iron is an essential component of the human body and a main micronutrient in the human diet. However, excess iron causes an increased production of reactive oxygen species leading to cell dysfunction or death, tissue damage and organ disease. Iron overload disorders encompass a wide spectrum of pathological conditions of hereditary or acquired origin. A number of ‘iron genes’ have been identified as being associated with hereditary iron overload syndromes, the most common of which is hemochromatosis. Although linked to at least five different genes, hemochromatosis is recognized as a unique syndromic entity based on a common pathogenetic mechanism leading to excessive entry of unneeded iron into the bloodstream. In this review, we focus on the pathophysiologic basis and clinical aspects of the most common genetic iron overload syndromes in humans
Thrombolisis versus PTCA in patients with recent myocardial infarction: exercise stress echocardiography study
Pancreatic cancer
Pancreatic cancer is the fourth leading cause of death for neoplasm in western countries. Surgery still remains the treatment of choice although almost 80% of patients are not resectable at diagnosis because of liver metastases and the 5-year overall survival of patients treated with surgery is only (20%). During the last two decades we have witnessed an overall improvement in terms of survival, mostly due to the advances in therapy and strategies for a more accurate patient selection for surgery. Specific preoperative criteria, mostly linked to the biological features of the tumour, have been proposed to better identify those patients who will benefit from surgical resection, such as duration of symptoms and serum level of CA19-9 in resectable disease. Oncological therapy plays a central role in the management of pancreatic cancer. In patients undergone surgical resection, adjuvant therapy might increase the overall survival and reduce the rate of early relapse. Patients with locally advanced pancreatic cancer can be treated with neoadjuvant treatment. Chemotherapy or chemoradiotherapy are usually used with the aim to downstage the disease but whether one specific strategy or drug is the treatment of choice is still under debate
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