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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 | Hyperammonemia,brain edema and blood-brain barrier alterations in prehepatic portal hypertensive rats and paracetamol intoxication显示文摘AIM: To study the blood-brain barrier integrity, brain edema,animal behavior and ammonia plasma levels in prehepatic portal hypertensive rats with and without acute liver intoxication.METHODS: Adults male Wistar rats were divided into four groups. Group I: sham operation; II: Prehepatic portal hypertension, produced by partial portal vein ligation; III:Acetaminophen intoxication and IV: Prehepatic portal hypertension plus acetaminophen. Acetaminophen was administered to produce acute hepatic injury. Portal pressure, liver serum enzymes and ammonia plasma levels were determined. Brain cortex water content was registered and trypan blue was utilized to study blood brain barrier integrity. Reflexes and behavioral tests were recorded.RESULTS: Portal hypertension was significantly elevated in groups II and IV. Liver enzymes and ammonia plasma levels were increased in groups II, III and IV. Prehepatic portal hypertension (group II), acetaminophen intoxication (group III) and both (group IV) had changes in the blood brain-barrier integrity (trypan blue) and hyperammonemia. Cortical edema was present in rats with acute hepatic injury in groups III and IV. Behavioral test (rota rod) was altered in group IV.CONCLUSION: These results suggest the possibility of another pathway for cortical edema production because blood brain barrier was altered (vasogenic) and hyperammonemia was registered (cytotoxic). Group IV, with behavioral altered test, can be considered as a model for study at an early stage of portal-systemic encephalopathy. | Camila Scorticati Juan P.Prestifilippo Francisco X.Eizayaga Salvador Romay MaríaA Fernández AbrahamLemberg Juan C.Perazzo José L.Castro | 2004 | World Journal of Gastroenterology2004，10，9： | 5 |
| 3 | 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 |
| 4 | C-phycocyanin: a biliprotein with antioxidant, anti-inflammatory and neuroprotective effects 显示文摘 | ROMAY Ch GONZALEZ R LEDON N | 2003 | Curr Protein Pept Sci2003，4，3： | 1 |
| 5 | Anti-inflammatory activity of phycocyanin extract in acetic acid-induced colitis in rats显示文摘 | Gonzalez R Rodriguez S Romay C | 1999 | Pharmacol Res1999，39，： | 1 |
| 6 | Effects of phycocyanin extract on tumor necrosis factor-alpha and nitrite levels in serum of mice treated with endotoxin显示文摘 | Romay C Delgado R Remirez D | 2001 | Arzneimittelforschung2001，51，： | 1 |
| 7 | C-phycocyanin:a biliprotein with antioxidant,anti-inflammatory and neuroprotective effects显示文摘 | Romay CH Gonzalez R Ledon N | 2003 | Curr Protein Pep Sci2003，4，3： | 1 |
| 8 | Thermophoretic deposition of aerosol particles in turbulent pipe flow显示文摘 | Romay Francisco J Takagaki Sho S David Y Pui H and Benjamin Liu Y H | 1998 | Journal of Aerosol Science1998，29，8： | 1 |
| 9 | Particle charge distribution measurement for commonly generated laboratory aerosols显示文摘 | Forsyth B Liu B Romay F | 1998 | Aerosol Science and Technology1998，28，22： | 1 |
| 10 | sLea and sLex expression in colorectal cancer : implications for tumourigene-sis and disease prognosis显示文摘 | PORTELA S V MARTIN C V ROMAY L M | 2011 | Histol Histopathol2011，26，10： | 1 |
| 11 | IRAK4 inhibition: a promising strategy for treating RA joint inflammation and bone erosion显示文摘Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis(RA)patients could reflect activation of innate immune mechanisms.Herein,we show that a TLR7 GU-rich endogenous ligand,miR-Let7b,potentiates synovitis by amplifying RA monocyte and fibroblast(FLS)trafficking.miR-Let7b ligation to TLR7 in macrophages(MΦs)and FLSs expanded the synovial inflammatory response.Moreover,secretion of M1 monokines triggered by miR-Let7b enhanced Th1/Th17 cell differentiation.We showed that IRAK4 inhibitor(i)therapy attenuated RA disease activity by blocking TLR7-induced M1 MΦor FLS activation,as well as monokine-modulated Th1/Th17 cell polarization.IRAK4i therapy also disrupted RA osteoclastogenesis,which was amplified by miR-Let7b ligation to joint myeloid TLR7.Hence,the effectiveness of IRAK4i was compared with that of a TNF inhibitor(i)or anti-IL-6R treatment in collagen-induced arthritis(CIA)and miR-Let7b-mediated arthritis.We found that TNF or IL-6R blocking therapies mitigated CIA by reducing the infiltration of joint F480+iNOS+MΦs,the expression of certain monokines,and Th1 cell differentiation.Unexpectedly,these biologic therapies were unable to alleviate miR-Let7b-induced arthritis.The superior efficacy of IRAK4i over anti-TNF or anti-IL-6R therapy in miR-Let7b-induced arthritis or CIA was due to the ability of IRAK4i therapy to restrain the migration of joint F480+iNOS+MΦs,vimentin+fibroblasts,and CD3+T cells,in addition to negating the expression of a wide range of monokines,including IL-12,MIP2,and IRF5 and Th1/Th17 lymphokines.In conclusion,IRAK4i therapy may provide a promising strategy for RA therapy by disconnecting critical links between inflammatory joint cells. | Sadiq Umar Karol Palasiewicz Katrien Van Raemdonck Michael V.Volin Bianca Romay MAsif Amin Ryan K.Zomorrodi Shiva Arami Mark Gonzalez Vikram Rao Brian Zanotti David A.Fox Nadera Sweiss Shiva Shahrara | 2021 | Cellular & Molecular Immunology2021，18，9： | 1 |
| 12 | Antioxidant and anti-inflammatory properties of C-phycocyanin from blue- green algae显示文摘 | Romay C H Armesto J Remirez D | 1998 | Inflamm Res1998，47，1： | 1 |
| 13 | C-phycocyanin:a biliprotein with antioxidant,anti-inflammatory and neuroprotective effects显示文摘 | ROMAY C GONZALEZ R LEDON N | 2003 | Current Protein and Peptide Science2003，4，3： | 1 |
| 14 | In vivo effects of an inhibitor of nuclear factorkappa B on thrombogenic properties of antiphospholipid antibodies显示文摘 | MontielManzano G RomayPenabad Z Papalardo de martinez E | 2007 | Ann N Y Acad Sci2007，1108，： | 1 |
| 15 | Second generation micro-orifice uniform deposit impactor, 120 moudi-ii: design, evaluation, and application to long-term ambient sampling显示文摘 | Marple V Olson B Romay F | 2014 | Aerosol Science and Technology2014，48，4： | 1 |
| 16 | C-phycocyanin: a biliprotein with antioxidant, anti-inflammatory and neu- roprotective effects显示文摘 | Romay C Gonzalez R Ledon N | 2003 | Current Protein & Peptide Science2003，4，3： | 1 |
| 17 | Thermophoretic Deposition of Aerosol Particles in Turbulent Pipe Flow 显示文摘 | Francisco j Romay Sho S Takagaki David Y H Pui | 1998 | Journal of Aerosol Science1998，29，： | 1 |
| 18 | C-phycocyanin: a biliprotein with antioxidant, anti-inflammatory and neuroprotective effects 显示文摘 | Romay C Delgado R Ledon N | 2003 | Curr Protein Pept Sci2003，4，： | 1 |
| 19 | Experimental Study of Particle Deposition in Bends of Circular Cross Section显示文摘 | PUIDY H ROMAY N F LIU BY H | 1987 | Aerosol Science and Technology1987，7，3： | 1 |
| 20 | Effects of phycocyanin extract on tumor necrosis factor-alpha and nitrite levels in serum of mice treated with endotoxin显示文摘 | Romay C Delgado R Remirez D | 2001 | Arzneimittelforsch2001，51，： | 1 |
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