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| 1 | Hepatic encephalopathy:An approach to its multiple pathophysiological features显示文摘Hepatic encephalopathy(HE)is a neuropsychiatric complex syndrome,ranging from subtle behavioral abnormalities to deep coma and death.Hepatic encephalopathy emerges as the major complication of acute or chronic liver failure.Multiplicity of factors are involved in its pathophysiology,such as central and neuromuscular neurotransmission disorder,alterations in sleep patterns and cognition,changes in energy metabolism leading to cell injury,an oxidative/nitrosative state and a neuroinflammatory condition.Moreover,in acute HE,a condition of imminent threat of death is present due to a deleterious astrocyte swelling.In chronic HE,changes in calcium signaling,mitochondrial membrane potential and long term potential expression,N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations,and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be observed.The main molecule indicated as responsible for all these changes in HE is ammonia.There is no doubt that ammonia,a neurotoxic molecule,triggers or at least facilitates most of these changes.Ammonia plasma levels are increased two-to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite,glutamine(GLN),lead to hyperammonemic conditions.Removal of hepatic ammonia is a differentiated work that includes the hepatocyte,through the urea cycle,converting ammonia into GLN via glutamine synthetase.Under pathological conditions,such as liver damage or liver blood bypass,the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be considered.This editorial will focus on issues where, to the best of our knowledge,more research is needed in order to clarify,at least partially,controversial topics. | Juan Carlos Perazzo Silvina Tallis Amalia Delfante Pablo Andrés Souto Abraham Lemberg Francisco Xavier Eizayaga Salvador Romay | 2012 | World Journal of Hepatology2012，4，3： | 16 |
| 2 | Crohn’s and colitis in children and adolescents显示文摘Crohn's disease and ulcerative colitis can be grouped as the inflammatory bowel diseases(IBD).These conditions have become increasingly common in recent years,including in children and young people.Although much is known about aspects of the pathogenesis of these diseases,the precise aetiology is not yet understood,and there remains no cure.Recent data has illustrated the importance of a number of genes-several of these are important in the onset of IBD in early life,including in infancy.Pain,diarrhoea and weight loss are typical symptoms of paediatric Crohn's disease whereas bloody diarrhoea is more typical of colitis in children.However,atypical symptoms may occur in both conditions:these include isolated impairment of linear growth or presentation with extra-intestinal manifestations such as erythema nodosum.Growth and nutrition are commonly compromised at diagnosis in both Crohn's disease and colitis.Consideration of possible IBD and completion of appropriate investi-gations are essential to ensure prompt diagnosis,thereby avoiding the consequences of diagnostic delay.Patterns of disease including location and progression of IBD in childhood differ substantially from adultonset disease.Various treatment options are available for children and adolescents with IBD.Exclusive enteral nutrition plays a central role in the induction of remission of active Crohn's disease.Medical and surgical therapies need to considered within the context of a growing and developing child.The overall management of these chronic conditions in children should include multi-disciplinary expertise,with focus upon maintaining control of gut inflammation,optimising nutrition,growth and quality of life,whilst preventing disease or treatment-related complications. | Andrew S Day Oren Ledder Steven T Leach Daniel A Lemberg | 2012 | World Journal of Gastroenterology2012，18，41： | 4 |
| 3 | Campylobacter concisus and inflammatory bowel disease显示文摘Investigation of the possible role of Campylobacter concisus(C. concisus) in inflammatory bowel disease(IBD) is an emerging research area. Despite the association found between C. concisus and IBD, it has been difficult to explain how C. concisus, a bacterium that is commonly present in the human oral cavity, may contribute to the development of enteric diseases. The evidence presented in this review shows that some C. concisus strains in the oral cavity acquired zonula occludens toxin(zot) gene from a virus(prophage) and that C. concisus Zot shares conserved motifs with both Vibrio cholerae Zot receptor binding domain and human zonulin receptor binding domain. Both Vibrio cholerae Zot and human zonulin are known to increase intestinal permeability by affecting the tight junctions. Increased intestinal permeability is a feature of IBD. Based on these data, we propose that a primary barrier function defect caused by C. concisus Zot is a mechanism by which zot-positive C. concisus strains may trigger the onset and relapse of IBD. | Li Zhang Hoyul Lee Michael C Grimm Stephen M Riordan Andrew S Day Daniel A Lemberg | 2014 | World Journal of Gastroenterology2014，20，5： | 4 |
| 4 | Altered blood-brain barrier permeability in rats with prehepatic portal hypertension turns to normal when portal pressure is lowered显示文摘AIM: To study the blood-brain barrier integrity in prehe-patic portal hypertensive rats induced by partial portal vein ligation, at 14 and 40 d after ligation when portal pressure is spontaneously normalized. METHODS: Adult male Wistar rats were divided into four groups: GroupⅠ: Sham14d, sham operated; GroupⅡ: PH14d, portal vein stenosis; (both groups were used 14 days after surgery); GroupⅢ: Sham40d, Sham operated and GroupⅣ: PH40d Portal vein stenosis (GroupsⅡandⅣused 40 d after surgery). Plasma ammonia, plasma and cerebrospinal fluid protein and liver enzymes concentrations were determined. Trypan and Evans blue dyes, systemically injected, were investigated in hippocampus to study blood-brain barrier integrity. Portal pressure was periodically recorded. RESULTS: Forty days after stricture, portal pressure was normalized, plasma ammonia was moderately high, and both dyes were absent in central nervous system parenchyma. All other parameters were reestablished. When portal pressure was normalized and ammonia level was lowered, but not normal, the altered integrity of blood-brain barrier becomes reestablished. CONCLUSION: The impairment of blood-brain barrier and subsequent normalization could be a mechanism involved in hepatic encephalopathy reversibility, Hemo-dynamic changes and ammonia could trigger blood-brain barrier alterations and its reestablishment. | Francisco Eizayaga Camila Scorticati Juan P Prestifilippo Salvador Romay Maria A Fernandez José L Castro Abraham Lemberg Juan C Perazzo | 2006 | World Journal of Gastroenterology2006，12，9： | 3 |
| 5 | Obesity and the metabolic syndrome 显示文摘 | Keller KB Lemberg C | 2003 | Am J Crit Care2003，12，2： | 1 |
| 6 | Obesity and the metabolic syndrome 显示文摘 | Keller KB Lemberg L | 2003 | Am J Crit Care2003，12，2： | 1 |
| 7 | Pupillography as an objective indicator of fatigue显示文摘 | Morad Y Lemberg H Yofe N | 2000 | Curr Eye Res2000，21，1： | 1 |
| 8 | Novel markers in the acute coronary syndrome: BNP, IL-6, PAPP-A显示文摘 | Futterman LG Lemberg L | 2002 | Am J Crit Care2002，11，2： | 1 |
| 9 | On the mechanism of SPP-catalysed intramembrane proteolysis: conformational control of peptide bond hydrolysis in the plane of the membrane显示文摘 | Lemberg M K Martoglio B | 2004 | FEBS Lett2004，564，： | 1 |
| 10 | Fifty percent of patinets with coro- nary artery disease Do not have any of the conventional factors 显示文摘 | Futtennnan LG Lemberg L | 1998 | Am J Crit Care1998，7，3： | 1 |
| 11 | Pharmacology oxycodone:does it explain why oxycodone has become a bestselling strong opioid显示文摘 | Lemberg KK Heiskanen TE Kontinen VK | 2009 | Scand J Pain2009，1，5： | 1 |
| 12 | Cardiovascular Autonomic Dysfunction and hemodynamic response to anesthetic Iinduction in patients with coronary artery disease and diabetes mellitus显示文摘 | Keyl C Lemberger P Palitzsch KD | 1999 | Anesth Analg1999，88，5： | 1 |
| 13 | Prinzmetal's angina显示文摘 | Lemberg L | 2004 | Am J Crit Care2004，13，4： | 1 |
| 14 | A comparison of the use of transoesophageal Doppler and thermodilution techniques for cardiac output determination显示文摘 | Keyl G Roding P Lemberger P | 1996 | Eur J Anaesthesiol1996，13，2： | 1 |
| 15 | Peroxisome proliferator-activated receptors: a nuclear receptor signaling pathway in lipid physiology显示文摘 | Lemberger T Desvergne B Wahli W | 1996 | Annu Rev Cell Dev Biol1996，12，： | 1 |
| 16 | Diffuse axonal injury:analysis of 100 patients wish radiological signs显示文摘 | Guiburd J N Lemberger A | 1990 | Neurosurgery1990，27，3： | 1 |
| 17 | Gender differences in acute cordnary events显示文摘 | Keller K B Lemberg L | 2000 | Am J Crit Care2000，9，3： | 1 |
| 18 | Intramembrane proteolysis promotes trafficking of hepatitis C virus core protein to lipid droplets 显示文摘 | McLauchlan J Lemberg M K Hope G | 2002 | Embo J2002，21，： | 1 |
| 19 | Novel markers in the acute coronary syndrome:BNP,IL-6,PAPP-A-Cardiology Casebook显示文摘 | Futterman LG Lemberg L | 2002 | Am J Crit Care2002，11，2： | 1 |
| 20 | Novel makers in acute coronary syndrome: BNP, IL-6, PAPP-A显示文摘 | Futtermann LG Lemberg L | 2002 | Am J Crit Car2002，11，： | 1 |
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