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| 1 | Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?显示文摘AIM: To study the possible association between chronic pancreatitis (CP) and liver cirrhosis (LC) of alcoholic etiology,after excluding any other causes.METHODS: One hundred and forty consecutive alcoholic patients were subdivided into three groups: CP (n = 53),LC (n = 57),and asymptomatic alcoholic (n = 30).Clinical,biochemical and morphological characteristics,Child-Pugh index,indocyanine green test,and fecal pancreatic elastase-1 test were assessed.RESULTS: In patients with cirrhosis,major clinical manifestations of CP such as pancreatic pain and steatorrhea,as well as imaging alterations of CP such as calcifications,duct dilation and pseudocysts were absent; insulin-dependent diabetes was present in 5.3% of cases,and elastase-1 test was altered in only 7%,and severely altered in none.In patients with CP,clinical characteristics of cirrhosis such as ascites,encephalopathy and gastrointestinal hemorrhage were present in one case,Child-Pugh grade > A in 5.7%,and altered indocyanine green test in 1.9% cases.In asymptomatic alcoholism,there was only a non-coincident alteration of elastase-1 test and indocyanine test in 14.8% and 10%,respectively,but other characteristics of cirrhosis or CP were absent.An inverse correlation (r = -0.746) between elastase-1 test and indocyanine test was found in alcoholic patients.CONCLUSION: There is a scarce coincidence in clinical and morphological alterations among patients with CP or LC of alcoholic etiology,but an inverse correlation between pancreatic and liver function tests.These findings support that these alcoholic diseases evolve in a different manner and have different etiopathogenesis. | Luis Aparisi Luis Sabater Juan Del-Olmo Juan Sastre Miguel-Angel Serra Ricardo Campello Daniel Bautista Abdalla Wassel José-Manuel Rodrigo | 2008 | World Journal of Gastroenterology2008，14，40： | 4 |
| 2 | Protein phosphatases and chromatin modifying complexes in the inflammatory cascade in acute pancreatitis显示文摘Acute pancreatitis is an inflammation of the pancreas that may lead to systemic inflammatory response syndrome and death due to multiple organ failure. Acinar cells, together with leukocytes, trigger the inflammatory cascade in response to local damage of the pancreas. Amplification of the inflammatory cascade requires up-regulation of proinflammatory cytokines and this process is mediated not only by nuclear factor κB but also by chromatinmodifying complexes and chromatin remodeling. Among the different families of histone acetyltransferases, the p300/CBP family seems to be particularly associated with the inflammatory process. cAMP activates gene expression via the cAMP-responsive element (CRE) and the transcription factor CRE-binding protein (CREB). CREB can be phosphorylated and activated by different kinases, such as protein kinase A and MAPK, and then it recruits the histone acetyltransferase co-activator CREB-binding protein (CBP) and its homologue p300. The recruitment of CBP/p300 and changes in the level of histone acetylation are required for transcription activation. Transcriptional repression is also a dynamic and essential mechanism of down-regulation of genes for resolution of inflammation, which seems to be mediated mainly by protein phosphatases (PP1, PP2A and MKP1) and histone deacetylases(HDACs) .Class HDACs are key transcriptional regulators whose activities are controlled via phosphorylationdependent nucleo/cytoplasmic shuttling. PP2A is responsible for dephosphorylation of class HDACs, triggeringnuclear localization and repression of target genes, whereas phosphorylation triggers cytoplasmic localization leading to activation of target genes. The potential benefit from treatment with phosphodiesterase inhibitors and histone deacetylase inhibitors is discussed. | Javier Escobar Javier Pereda Alessandro Arduini Juan Sastre Juan Sandoval Luis Aparisi Gerardo López-Rodas Luis Sabater | 2010 | World Journal of Gastrointestinal Pharmacology and Therapeutics2010，1，3： | 2 |
| 3 | Antibodies to carbonic anhydrase and IgG4 levels in idiopathic chronic pancreatitis:relevance for diagnosis of autoimmune pancreatitis显示文摘 | APARISI L FARRE A GOMEZ-CAMBRONERO L et s | 2005 | Gut2005，54，5： | 1 |
| 4 | Autoantibodies to GABA- ergic neurons and pancreatic beta cells in stiff-man syndrome显示文摘 | Solimena M Folli F Aparisi R | 1990 | N Engl J Med1990，322，22： | 1 |
| 5 | Efficacy and safety of ethanol injections in 18 cases of vertebral hemangioma: A mean fullow-up of 2 years 显示文摘 | Bas T Aparisi F Bas JL | 2001 | Spine2001，26，14： | 1 |
| 6 | Eficacy and safety of ethanol injections in 18 cases of vertebral hemangioma显示文摘 | Bas T Aparisi F Bas JL | 2001 | Spine2001，26，14： | 1 |
| 7 | Interaction between cytokines and oxidative stress in acute pancreatitis显示文摘 | Pereda J Sabater L Aparisi L | 2006 | Curr Med Chem2006，13，23： | 1 |
| 8 | Interaction between cytokines and oxidative stress in acute pancreatitis显示文摘 | Pereda J Sabater L Aparisi L | 2006 | Curr Med Chem2006，13，23： | 1 |
| 9 | Prognostic radiographic aspects of spondylolisthesis显示文摘 | Saraste H Brostrom LA Aparisi T | 1984 | Acta Radiol Diagn (Stockh)1984，25，： | 1 |
| 10 | Antibodies to car- bonic anhydrase and IgG4 levels in idiopathic chronic pancreatitis: relevance for diagnosis of autoimmune pancreatitis显示文摘 | Aparisi L Farre A Gomez-Cambronero L | 2005 | Gut2005，54，5： | 1 |
| 11 | Eosinophilic granuloma:MRI manifestations 显示文摘 | Behran J Aparisi F Bonmati LM | 1993 | Skeletal Radiol1993，22，： | 1 |
| 12 | Pancreatic function af- ter severe acute biliary pancreatitis: the role of necrosectomy 显示文摘 | Sabater L Pareja E Aparisi L | 2004 | Pancreas2004，28，1： | 1 |
| 13 | Interaction between cytokines and oxidative stress in acute pancreatitis 显示文摘 | Pereda J Sabater L Aparisi L | 2006 | Curr Med Chem2006，13，23： | 1 |
| 14 | Rapid identifica- tion of Candida glabrata using a new commercial kit 显示文摘 | Pem6n J Aparisi N Garcfa-Esteban C | 2004 | Rev Ibe- roam Micol2004，21，2： | 1 |
| 15 | A comparison of T control charts with variable sampling schemes as opposed to MEWMA chart显示文摘 | Aparisi F Haro C L | 2003 | International Journal of Production Research2003，41，10： | 1 |
| 16 | Pancreatic function after severe acute biliary pancreatitis: the role of necrosectomy 显示文摘 | Sabater L Pareja E Aparisi L | 2004 | Pancreas2004，28，1： | 1 |
| 17 | Autoantibodies to GABA-ergic neurons and pancreatic beta cells in stiff-man syndrome显示文摘 | Solimena M Folli F Aparisi R | 1990 | N Engl J Med1990，322，22： | 1 |
| 18 | 显示文摘 | Aparisi L Farre A Gomez-Cambronero L | 2005 | Gut2005，54，5： | 1 |
| 19 | Pancreatic Function after Acute Biliary Pancreatitis: Does It Change?显示文摘 | Eugenia Pareja Ibars Enrique Artigues Sánchez de Rojas Luis Aparisi Quereda Ricardo Fabra Ramis Vicente Martínez Sanjuan Ramón Trullenque Peris | 2002 | World Journal of Surgery2002，，4： | 1 |
| 20 | The Spanish Pancreatic Club recommendations for the diagnosis and treatment of chronic pancreatitis: Part 1 (diagnosis)显示文摘 | J. Martínez A. Abad-González J.R. Aparicio L. Aparisi J. Boadas E. Boix G. de las Heras E. Domínguez-Mu?oz A. Farré L. Fernández-Cruz L. Gómez J. Iglesias-García K. García-Malpartida L. Guarner J. Lari?o-Noia F. Lluís A. López X. Molero O. Moreno-Pérez S. | 2013 | Pancreatology2013，，1： | 1 |
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