Search results: Found 3

Listing 1 - 3 of 3
Sort by
Recent advances in Pancreatology

Author:
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193332 Year: Pages: 69 DOI: 10.3389/978-2-88919-333-2 Language: English
Publisher: Frontiers Media SA
Subject: Nutrition and Food Sciences --- Medicine (General) --- Physiology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
License:

Loading...
Export citation

Choose an application

Abstract

Pancreatic diseases include intractable ones including acute and chronic pancreatitis, and pancreatic cancer. In recent years, great advances have been made in the field of pancreatology, including the pathogenesis, diagnostic modalities, and development of novel therapeutic interventions. It has been established that pancreatic stellate cells play a pivotal role in the development of pancreatic fibrosis in chronic pancreatitis as well as in pancreatic cancer known as desmoplastic reaction. Although it might be still controversial, accumulating evidence has shown that interaction between pancreatic stellate cells-cancer cells contribute to the progression of pancreatic cancer through the increased proliferation and migration, and production of cytokines and extracellular matrix components. In addition, pancreatic stellate cells lead to the resistance to chemotherapy and radiation therapy. Pancreatic stellate cells attract the researchers as a novel therapeutic target of pancreatic cancer. Genetic studies have shown that mutations in the trypsin-related genes such as cationic trypsinogen (PRSS1) gene and the serine protease inhibitor, Kazal type 1 (SPINK1) gene are associated with pancreatitis. In general, each of these factors appears to limit trypsin activation or enhance inactivation, and is believed to increase intrapancreatic trypsin activity and predispose to pancreatitis when the gene is mutated. These results have supported a concept that pancreatic protease/anti-protease plays pivotal roles in the pathogenesis of pancreatitis. In addition, genetic studies focusing on phenotypic variances would provide us with important information how genetic variants would affect the phenotypic variances. Autophagy is an intracellular bulk degradation system in which cytoplasmic components are directed to the lysosome/vacuole by a membrane-mediated process. Recent studies have highlighted a role of autophagy in acute pancreatitis. Using a conditional knockout mouse that lacks the autophagy-related (Atg) gene Atg5 in the pancreatic acinar cells, autophagy exerts a detrimental effect in pancreatic acinar cells by activation of trypsinogen to trypsin. A theory in which autophagy accelerates trypsinogen activation by lysosomal hydrolases under acidic conditions, thus triggering acute pancreatitis in its early stage. The epithelial-mesenchymal transition is a developmental process that allows a polarized epithelial cell to undergo multiple biochemical changes that enable it to assume a mesenchymal phenotype. The phenotype associated with epithelial-mesenchymal transition includes enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased production of extracellular matrix components. In addition to its role in development, tissue regeneration, and fibrosis, epithelial-mesenchymal transition is now considered as a critical process in cancer progression. Induction of epithelial-mesenchymal transition in cancer cells results in the acquisition of invasive and metastatic properties. Epithelial-mesenchymal transition could be an important mechanism in the progression of pancreatic cancer and its poor prognosis. Autoimmune pancreatitis is a unique form of pancreatitis in which autoimmune mechanisms are suspected to be involved in the pathogenesis. There is accumulating study to deal with this new disease concept. In addition to these topics, we have selected several topics in pancreatology, focusing on recent studies increasingly deepening our knowledge in both basic and clinical researches.

Risk Factors for Pancreatic Cancer: Underlying Mechanisms and Potential Targets

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194681 Year: Pages: 115 DOI: 10.3389/978-2-88919-468-1 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
License:

Loading...
Export citation

Choose an application

Abstract

Pancreatic Cancer has been and still is one of the deadliest types of human malignancies. The annual mortality rates almost equal incidence rates making this disease virtually universally fatal. The 5-year survival of patients with pancreatic cancer is a dismal 5% or less. Therapeutic strategies are extremely limited with gemcitabine extending the survival by a disappointing few weeks. The failure of several randomized clinical trials in the past decade investigating the therapeutic efficacy of different mono- and combination therapies reflects our limited knowledge of pancreatic cancer biology. In addition, biomarkers for early detection are sorely missing. Several pancreatic cancer risk factors have been identified. Unfortunately, the underlying mechanisms linking these risk factors to cancer development are poorly understood. Well known possible and probable risk factors for the development of pancreatic cancer are age, smoking, chronic pancreatitis, obesity, and type-2 diabetes mellitus. Age is certainly of the most important risk factors as most cases of pancreatic cancer occur in the elderly population. Smoking ten cigarettes a day increases the risk by 2.6 times and smoking a pack per day increases it by 5 folds. Chronic pancreatitis increases the risk of pancreatic cancer by up to 13 times. Patients with hereditary forms of chronic pancreatitis have an even higher risk. Obesity, a growing global health problem, increases the risk of pancreatic cancer by about 1.5 fold. Type-2 diabetes mellitus is also associated with an increased risk of pancreatic cancer by at least two-fold. The more recent the onset of diabetes, the stronger the correlation with pancreatic cancer is. In addition, heavy alcohol drinking, a family history of the disease, male gender and African American ethnicity are other risk factors for pancreatic cancer. Pancreatic cancer is characterized by several genetic alterations including mutations in the Kras proto-oncogene and mutations in the tumor suppressor genes p53 and p16. While Kras mutations are currently thought as early events present in a certain percentage of pancreatic intraepithelial neoplasias (PanINs), known precursor lesions of pancreatic ductal adenocarcinomas, mutations in tumor suppressor genes, e.g. p53, seem to accumulate later during progression. In addition, several intracellular signaling pathways are amplified or enhanced, including the MAPK/ERK and PI3K/AKT signaling modules. Overall, these genetic alterations lead to enhanced and sustained proliferation, resistance to cell death, invasive and metastatic potential, and angiogenesis, all hallmarks of cancers. The scope of this Research Topic is to collect data and knowledge of how risk factors increase the risk of initiation/progression of pancreatic cancer. Of particular interest are potential underlying molecular mechanisms. Understanding the molecular mechanisms and driving signaling pathways will ultimately allow the development of targeted interventions to disrupt the risk factor-induced cancer development. This Research Topic is interested in a broad range of risk factors, including genetic and environmental, and welcomes original papers, mini and full reviews, and hypothesis papers. Manuscripts that address the effect of combination of risk factors on pancreatic cancer development and progression are of great interest as well.

Extraintestinal Manifestations of Coeliac Disease

Authors: ---
ISBN: 9783038977988 9783038977995 Year: Pages: 270 DOI: 10.3390/books978-3-03897-799-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology --- Nutrition and Food Sciences
Added to DOAB on : 2019-04-25 16:37:17
License:

Loading...
Export citation

Choose an application

Abstract

Coeliac Disease (CD) affects at least 1% of the population. “Classical” CD refers to gastrointestinal presentations with anaemia and gastrointestinal symptoms. CD can, however, present with extraintestinal manifestations, the commonest of which are dermatitis herpetiformis and neurological presentations (e.g., ataxia, neuropathy, encephalopathy). Recognition and research into the pathophysiology of such manifestations is likely to enhance our understanding of this complex autoimmune disorder.

Keywords

dermatitis herpetiformis --- coeliac disease --- fracture --- bone health --- quality of life --- Gilles de la Tourette syndrome (GTS) --- children and adults --- motor and vocal/phonic tics --- obsessive-compulsive disorder (OCD) --- non-coeliac gluten sensitivity (NCGS) --- gluten-free diet --- one-year adherence --- dermatitis herpetiformis --- coeliac disease --- prevalence --- epidermal transglutaminase --- gluten-free diet --- long-term prognosis --- dermatitis herpetiformis --- coeliac disease --- gluten-free diet --- small bowel --- villous atrophy --- prognosis --- gluten neuropathy --- coeliac disease --- gluten free diet --- quality of life --- male --- extra-intestinal --- gastrointestinal --- celiac disease --- celiac disease --- dermatitis herpetiformis --- urticaria --- atopic dermatitis --- psoriasis --- recurrent aphtous ulceration --- rosacea --- alopecia areata --- cutaneous vasculitis --- gluten-free diet --- celiac disease --- glandular autoimmunity --- autoimmune thyroid disease --- type 1 diabetes --- polyglandular autoimmune syndrome --- coeliac disease --- osteoporosis --- fractures --- celiac disease --- non-celiac gluten sensitivity --- psychiatric disorders --- depression --- anxiety disorders --- eating disorders --- ADHD --- autism --- psychosis --- autoimmunity --- celiac hepatitis --- gut–liver axis --- liver immunity --- non-alcoholic fatty liver disease --- tolerance --- intestinal barrier --- celiac disease --- extraintestinal --- recognition --- diagnosis --- clinical presentation --- gluten-free diet --- prognosis --- movement disorders --- coeliac disease --- gluten --- gluten free diet --- celiac disease --- gluten --- gliadin --- autoantibody --- B cell --- T cell --- transglutaminase --- synapsin --- ganglioside --- gluten sensitivity --- gastrointestinal symptoms --- molecular mimicry --- intermolecular help --- biomarker --- autoimmune pancreatitis --- coeliac disease --- pancreatic disorders --- screening --- Gluten ataxia --- antigliadin antibodies --- coeliac disease --- MR spectroscopy --- gluten sensitive enteropathy --- antigliadin antibody titre --- gluten sensitivity --- coeliac disease --- gluten free diet --- migraine --- headache --- fatigue --- energy --- celiac disease --- extra-intestinal manifestations --- gluten --- latent celiac disease --- potential celiac disease --- extra-intestinal manifestations --- mild enteropathy --- early developing celiac disease --- genetic gluten intolerance --- natural history --- celiac trait --- celiac disease --- gluten neuropathy --- gluten ataxia --- prevalence --- incidence --- gluten-free diet

Listing 1 - 3 of 3
Sort by
Narrow your search
-->