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| 1 | Role of phosphoinositide 3-kinase in the pathogenesis of acute pancreatitis显示文摘A large body of experimental and clinical data supports the notion that inflammation in acute pancreatitis has a crucial role in the pathogenesis of local and systemic damage and is a major determinant of clinical severity.Thus,research has recently focused on molecules that can regulate the inflammatory processes,such as phosphoinositide 3-kinases(PI3Ks),a family of lipid and protein kinases involved in intracellular signal transduction.Studies using genetic ablation or pharmacologic inhibitors of different PI3 K isoforms,in particular the class I PI3Kδ and PI3Kγ,have contributed to a greater understanding of the roles of these kinases in the modulation of inflammatory and immune responses.Recent data suggest that PI3 Ks are also involved in the pathogenesis of acute pancreatitis.Activation of the PI3K signaling pathway,and in particular of the class IB PI3Kγ isoform,has a significant role in those events which are necessary for the initiation of acute pancreatic injury,namely calcium signaling alteration,trypsinogen activation,and nuclear factor-κB transcription.Moreover,PI3Kγ is instrumental in modulating acinar cell apoptosis,and regulating local neutrophil infiltration and systemic inflammatory responses during the course of experimental acute pancreatitis.The availability of PI3 K inhibitors selective for specific isoforms may provide new valuable therapeutic strategies to improve the clinical course of this disease.This article presents a brief summary of PI3 K structure and function,and highlights recent advances that implicate PI3 Ks in the pathogenesis of acute pancreatitis. | Enrico Lupia Luca Pigozzi Alberto Goffi Emilio Hirsch Giuseppe Montrucchio | 2014 | World Journal of Gastroenterology2014，20，41： | 15 |
| 2 | Microbiome in the setting of burn patients:implications for infections and clinical outcomes显示文摘Burn damage can lead to a state of immune dysregulation that facilitates the development of infections in patients.The most deleterious impact of this dysfunction is the loss of the skin’s natural protective barrier.Furthermore,the risk of infection is exacerbated by protracted hospitalization,urinary catheters,endotracheal intubation,inhalation injury,arterial lines and central venous access,among other mainstays of burn care.Currently,infections comprise the leading cause of mortality after major burn injuries,which highlights the improvements observed over the last 50 years in the care provided to burn victims.The need to implement the empirical selection of antibiotic therapy to treat multidrug-resistant bacteria may concomitantly lead to an overall pervasiveness of difficult-to-treat pathogens in burn centres,as well as the propagation of antimicrobial resistance and the ultimate dysregulation of a healthy microbiome.While preliminary studies are examining the variability and evolution of human and mice microbiota,both during the early and late phase burn injury,one must consider that abnormal microbiome conditions could influence the systemic inflammatory response.A better understanding of the changes in the postburn microbiome might be useful to interpret the provenance and subsequent development of infections,as well as to come up with inferences on the prognosis of burn patients.This review aims to summarise the current findings describing the microbiological changes in different organs and systems of burn patients and how these alterations affect the risks of infections,complications,and,ultimately,healing. | Silvia Corcione Tommaso Lupia Francesco G.De Rosa on behalf of Host and Microbiota Interaction Study Group(ESGHAMI)of the European Society of Clinical Microbiology and Infectious Diseases(ESCMID) | 2020 | Burns & Trauma2020，8，1： | 3 |
| 3 | Diagnostic accuracy and reproducibility of pleural and lung ultrasound in discriminating cardiogenic causes of acute dyspnea in the Emergency Department显示文摘 | Gian Alfonso Cibinel Giovanna Casoli Fabrizio Elia Monica Padoan Emanuele Pivetta Enrico Lupia Alberto Goffi | 2012 | Internal and Emergency Medicine2012，，1： | 2 |
| 4 | Ablation of phosphoinositide 3 - kinase gamma reduces the severity of acute panereatitis 显示文摘 | Lupia E Goffi A De Giuli P | 2004 | Am J Pathol2004，165，6： | 1 |
| 5 | Nephrin expression is reduced in human diabetic nephropathy:Evidence for a distinct role for glycated albumin and angiotensin Ⅱ显示文摘 | Doublier S Salvidio G Lupia E | 2003 | Diabeties2003，52，4： | 1 |
| 6 | Platelet-activating factor enhances vascular endothelial growth factor-induced endothelial cell motility and neoangiogenesis in murine matrigel model 显示文摘 | Montrucchi G Lupia E Battaglia E | 2000 | Arterioscler Thromb Vasc Biol2000，20，1： | 1 |
| 7 | IGF-1 decreases collagen degradation in diabetic NOD mesangial cells:implications for diabetic nephropathy显示文摘 | Lupia E Elliot SJ Lenz O | 1999 | Diabetes1999，48，8： | 1 |
| 8 | CD63 tetraspanin is a negative driver of epithelial-to-mesenchymal transition in human melanoma cells 显示文摘 | Lupia A Peppicelli S Witort E | 2014 | J Invest Dermatol2014，134，12： | 1 |
| 9 | Ablation of phosphoinositide 3-kinase-y reduces the severity of acute pancrea/i/is显示文摘 | Lupia E Goffi A Azzolino O | 2004 | Am J Pathol2004，165，6： | 1 |
| 10 | 17 beta-estradiol and tamoxifen upregulate estrogen receptor beta expression and control podocyte signaling pathways in a model of type 2 diabetes显示文摘 | Catanuto P Doublier S Lupia E | 2009 | Kidney Int2009，75，11： | 1 |
| 11 | Nephrin expression is re- duced in human diabetic nephropathy: evidence for a distinct role for glycated albumin and angiotensin H 显示文摘 | Doublier S Salvidio G Lupia E | 2003 | Diabetes2003，52，4： | 1 |
| 12 | Nephrin expression isreduced in human diabetic nephropathy:evidence for a distinct rolefor glycated albumin and angiotensin II显示文摘 | Doublier S Salvidio G Lupia E | 2003 | Diabetes2003，52，4： | 1 |
| 13 | Ablation of phosphoinositide 3-kinase-γ reduces the severity of acute pancreatitis显示文摘 | Lupia E Goffi A De Giuli P | 2004 | Am J Pathol2004，165，6： | 1 |
| 14 | Nephrin expression is reduced in human diabetic nephropathy:evidence for a dis- tinct role for glycated albumin and angiotensin 11显示文摘 | Doublier S Salvidio G Lupia E | 2003 | Diabe- tes2003，52，4： | 1 |
| 15 | Pentosan polysulfate in- hibits atherosclerosis in Watanabe heritable hyperlipidemic rabbits: differential modulation of metalloproteinase-2 and-9 显示文摘 | Lupia E Zheng F Grosjean F | 2012 | Laboratory Investigation a Journal of Technical Meth- ods and Pathology2012，92，23： | 1 |
| 16 | Increased blood levels of platelet-activating factor in insulin-dependent diabetic patients with microalbuminuria显示文摘 | Cavallo-Perin P Lupia E Gruden G | 2000 | Nephrol Dial Transplant2000，15，7： | 1 |
| 17 | Elevated thrombopoietin in plasma of burned patients without and with sepsis enhances platelet activation显示文摘 | Lupia E Bosco O Mariano F | | 0，，06： | 1 |
| 18 | Ablation nase-gamma reduces the severity of acute pancreatitis 显示文摘 | Lupia E Goffi A De Giuli P | 2004 | Am J Patho12004，165，6： | 1 |
| 19 | Testosterone and17β-estradiol have opposite effects on podocyte apoptosisthat precedes glomerulosclerosis in female estrogenreceptor knockout mice显示文摘 | Doublier S Lupia E Catanuto P | 2011 | Kidney Int2011，79，4： | 1 |
| 20 | Nitric oxide mediates angiogenesis induced in vivo by plateletactivating factor and tumor necrosis factor-alpha显示文摘 | Montrucchio G Lupia E de Martino A | 1997 | Am J Pathol1997，151，2： | 1 |
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