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  1. AU="Mendes-Braz, Mariana"
  2. AU="Cone, David C."
  3. AU="Liu, Mingxing"
  4. AU="Ishizaki, Kimihiro"
  5. AU="Sharma, Shuchita"
  6. AU="Mishra, Tanushree"
  7. AU=Chemes H E
  8. AU="Wang, Yuguang"
  9. AU="Wu, Sheng-Hua"
  10. AU="Irwin, Brian"
  11. AU="Vizcaíno-Velázquez, Pilar"
  12. AU="Cairncross, J Gregory"
  13. AU=Small Eusebius
  14. AU="Poppelaars, Marlou"
  15. AU="Hou, Yinmeng"
  16. AU="Tapias, Carlos"
  17. AU=Kojima Shihoko
  18. AU="Alcahut-Rodríguez, Cristian"
  19. AU="Whiteside, Theresa L"
  20. AU="Pappalettere, Carmine"
  21. AU="Bolla, Eleana"
  22. AU="Bajkowski, Jared"
  23. AU="Calleros Basilio, Laura"
  24. AU="Mohamad, Okbah"
  25. AU="Holy, Jon"
  26. AU="Farber, Mark O"
  27. AU="Gal, Adiv"
  28. AU="Badenhorst, Marelise"
  29. AU="Pachner, Andrew R"
  30. AU="Colón-Ramos, Daniel A" AU="Colón-Ramos, Daniel A"
  31. AU="Modzelewska, Dominika"
  32. AU="Boethig, Dietmar"
  33. AU="Jurinović, Luka"
  34. AU="Yashila Patel"
  35. AU="Zheng, Lei" AU="Zheng, Lei"
  36. AU="Seah, Penelope M Y"
  37. AU="Marianna Milano"
  38. AU="London, Kevin"
  39. AU=Pain Debkumar
  40. AU="Snider, Elizabeth"
  41. AU="Klein, J R"
  42. AU="Deslandes, K."
  43. AU="Xie, Dandan"
  44. AU=Ward Helen
  45. AU="Grace Deukmedjian"
  46. AU="Lindeman, Neal"
  47. AU="Okoli, Mary"
  48. AU="Mathew, Philip"
  49. AU=Staros Eric B

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  1. Artikel ; Online: Diabetes Mellitus and Liver Surgery: The Effect of Diabetes on Oxidative Stress and Inflammation.

    Mendes-Braz, Mariana / Martins, Joilson O

    Mediators of inflammation

    2018  Band 2018, Seite(n) 2456579

    Abstract: ... Diabetes ... ...

    Abstract Diabetes mellitus
    Mesh-Begriff(e) Animals ; Diabetes Mellitus, Experimental/immunology ; Diabetes Mellitus, Experimental/metabolism ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Liver/immunology ; Liver/metabolism ; Liver/surgery ; Oxidative Stress/physiology ; Reperfusion Injury/immunology ; Reperfusion Injury/metabolism
    Sprache Englisch
    Erscheinungsdatum 2018-05-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2018/2456579
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  2. Artikel ; Online: Riboflavin (vitamin B-2) reduces hepatocellular injury following liver ischaemia and reperfusion in mice.

    Sanches, Sheila Cristina / Ramalho, Leandra Naira Z / Mendes-Braz, Mariana / Terra, Vânia Aparecida / Cecchini, Rubens / Augusto, Marlei Josiele / Ramalho, Fernando Silva

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2014  Band 67, Seite(n) 65–71

    Abstract: Riboflavin has been shown to exhibit anti-inflammatory and antioxidant properties in the settings of experimental sepsis and ischaemia/reperfusion (I/R) injury. We investigated the effect of riboflavin on normothermic liver I/R injury. Mice were ... ...

    Abstract Riboflavin has been shown to exhibit anti-inflammatory and antioxidant properties in the settings of experimental sepsis and ischaemia/reperfusion (I/R) injury. We investigated the effect of riboflavin on normothermic liver I/R injury. Mice were submitted to 60 min of ischaemia plus saline or riboflavin treatment (30 μmoles/kg BW) followed by 6 h of reperfusion. Hepatocellular injury was evaluated by aminotransferase levels, reduced glutathione (GSH) content and the histological damage score. Hepatic neutrophil accumulation was assessed using the naphthol method and by measuring myeloperoxidase activity. Hepatic oxidative/nitrosative stress was estimated by immunohistochemistry. Liver endothelial and inducible nitric oxide synthase (eNOS/iNOS) and nitric oxide (NO) amounts were assessed by immunoblotting and a chemiluminescence assay. Riboflavin significantly reduced serum and histological parameters of hepatocellular damage, neutrophil infiltration and oxidative/nitrosative stress. Furthermore, riboflavin infusion partially recovered hepatic GSH reserves and decreased the liver contents of eNOS/iNOS and NO. These data indicate that riboflavin exerts antioxidant and anti-inflammatory effects in the ischaemic liver, protecting hepatocytes against I/R injury. The mechanism of these effects appears to be related to the intrinsic antioxidant potential of riboflavin/dihydroriboflavin and to reduced hepatic expression of eNOS/iNOS and reduced NO levels, culminating in attenuation of oxidative/nitrosative stress and the acute inflammatory response.
    Mesh-Begriff(e) Animals ; Ischemia/pathology ; Liver Diseases/complications ; Liver Diseases/pathology ; Mice ; Reperfusion ; Riboflavin/pharmacology
    Chemische Substanzen Riboflavin (TLM2976OFR)
    Sprache Englisch
    Erscheinungsdatum 2014-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2014.02.013
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  3. Artikel ; Online: The impact of cortisol in steatotic and non-steatotic liver surgery.

    Cornide-Petronio, María Eugenia / Bujaldon, Esther / Mendes-Braz, Mariana / Avalos de León, Cindy G / Jiménez-Castro, Mónica B / Álvarez-Mercado, Ana I / Gracia-Sancho, Jordi / Rodés, Juan / Peralta, Carmen

    Journal of cellular and molecular medicine

    2017  Band 21, Heft 10, Seite(n) 2344–2358

    Abstract: The intent of this study was to examine the effects of regulating cortisol levels on damage and regeneration in livers with and without steatosis subjected to partial hepatectomy under ischaemia-reperfusion. Ultimately, we found that lean animals ... ...

    Abstract The intent of this study was to examine the effects of regulating cortisol levels on damage and regeneration in livers with and without steatosis subjected to partial hepatectomy under ischaemia-reperfusion. Ultimately, we found that lean animals undergoing liver resection displayed no changes in cortisol, whereas cortisol levels in plasma, liver and adipose tissue were elevated in obese animals undergoing such surgery. Such elevations were attributed to enzymatic upregulation, ensuring cortisol production, and downregulation of enzymes controlling cortisol clearance. In the absence of steatosis, exogenous cortisol administration boosted circulating cortisol, while inducing clearance of hepatic cortisol, thus maintaining low cortisol levels and preventing related hepatocellular harm. In the presence of steatosis, cortisol administration was marked by a substantial rise in intrahepatic availability, thereby exacerbating tissue damage and regenerative failure. The injurious effects of cortisol were linked to high hepatic acethylcholine levels. Upon administering an α7 nicotinic acethylcholine receptor antagonist, no changes in terms of tissue damage or regenerative lapse were apparent in steatotic livers. However, exposure to an M3 muscarinic acetylcholine receptor antagonist protected livers against damage, enhancing parenchymal regeneration and survival rate. These outcomes for the first time provide new mechanistic insight into surgically altered steatotic livers, underscoring the compelling therapeutic potential of cortisol-acetylcholine-M3 muscarinic receptors.
    Mesh-Begriff(e) Acetylcholine/metabolism ; Acetylcholine/pharmacology ; Adipose Tissue/metabolism ; Animals ; Cholinergic Agonists/metabolism ; Cholinergic Agonists/pharmacology ; Fatty Liver/blood ; Fatty Liver/metabolism ; Fatty Liver/surgery ; Hepatectomy/methods ; Hydrocortisone/analysis ; Hydrocortisone/blood ; Hydrocortisone/pharmacology ; Liver/metabolism ; Liver/physiopathology ; Liver/surgery ; Liver Regeneration/drug effects ; Obesity/blood ; Obesity/metabolism ; Rats ; Reperfusion Injury/blood ; Reperfusion Injury/metabolism ; Reperfusion Injury/physiopathology
    Chemische Substanzen Cholinergic Agonists ; Acetylcholine (N9YNS0M02X) ; Hydrocortisone (WI4X0X7BPJ)
    Sprache Englisch
    Erscheinungsdatum 2017-04-04
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.13156
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  4. Artikel ; Online: The effect of brain death in rat steatotic and non-steatotic liver transplantation with previous ischemic preconditioning.

    Jiménez-Castro, Mónica B / Meroño, Noelia / Mendes-Braz, Mariana / Gracia-Sancho, Jordi / Martínez-Carreres, Laia / Cornide-Petronio, Maria Eugenia / Casillas-Ramirez, Araní / Rodés, Juan / Peralta, Carmen

    Journal of hepatology

    2015  Band 62, Heft 1, Seite(n) 83–91

    Abstract: Background & aims: Most liver grafts undergoing transplantation derive from brain dead donors, which may also show hepatic steatosis, being both characteristic risk factors in liver transplantation. Ischemic preconditioning shows benefits when applied ... ...

    Abstract Background & aims: Most liver grafts undergoing transplantation derive from brain dead donors, which may also show hepatic steatosis, being both characteristic risk factors in liver transplantation. Ischemic preconditioning shows benefits when applied in non-brain dead clinical situations like hepatectomies, whereas it has been less promising in the transplantation from brain dead patients. This study examined how brain death affects preconditioned steatotic and non-steatotic liver grafts undergoing transplantation.
    Methods: Steatotic and non-steatotic grafts from non-brain dead and brain dead-donors were cold stored for 6h and then transplanted. After 2, 4, and 16 h of reperfusion, hepatic damage was analysed. In addition, two therapeutic strategies, ischemic preconditioning and/or acetylcholine pre-treatment, and their underlying mechanisms were characterized.
    Results: Preconditioning benefits in non-brain dead donors were associated with nitric oxide and acetylcholine generation. In brain dead donors, preconditioning generated nitric oxide but did not promote acetylcholine upregulation, and this resulted in inflammation and damage. Acetylcholine treatment in brain dead donors, through PKC, increased antioxidants and reduced lipid peroxidation, nitrotyrosines and neutrophil accumulation, altogether protecting against damage. The combination of acetylcholine and preconditioning conferred stronger protection against damage, oxidative stress and neutrophil accumulation than acetylcholine treatment alone. These superior beneficial effects were due to a selective preconditioning-mediated generation of nitric oxide and regulation of PPAR and TLR4 pathways, which were not observed when acetylcholine was administered alone.
    Conclusions: Our findings propose the combination of acetylcholine+preconditioning as a feasible and highly protective strategy to reduce the adverse effects of brain death and to ultimately improve liver graft quality.
    Mesh-Begriff(e) Animals ; Brain Death ; Disease Models, Animal ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Fatty Liver/surgery ; Ischemic Preconditioning/methods ; Liver Transplantation ; Oxidative Stress ; Rats ; Rats, Zucker
    Sprache Englisch
    Erscheinungsdatum 2015-01
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2014.07.031
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  5. Artikel ; Online: Resistin and visfatin in steatotic and non-steatotic livers in the setting of partial hepatectomy under ischemia-reperfusion.

    Elias-Miró, Maria / Mendes-Braz, Mariana / Cereijo, Ruben / Villarroya, Francesc / Jiménez-Castro, Mónica B / Gracia-Sancho, Jordi / Guixé-Muntet, Sergi / Massip-Salcedo, Marta / Domingo, Joan Carles / Bermudo, Raquel / Rodés, Juan / Peralta, Carmen

    Journal of hepatology

    2014  Band 60, Heft 1, Seite(n) 87–95

    Abstract: Background & aims: This study examined whether the regulation of resistin and visfatin could reduce damage and improve regeneration in both steatotic and non-steatotic livers undergoing partial hepatectomy under ischemia-reperfusion, a procedure ... ...

    Abstract Background & aims: This study examined whether the regulation of resistin and visfatin could reduce damage and improve regeneration in both steatotic and non-steatotic livers undergoing partial hepatectomy under ischemia-reperfusion, a procedure commonly applied in clinical practice to reduce bleeding.
    Methods: Resistin and visfatin were pharmacologically modulated in lean and obese animals undergoing partial hepatectomy under ischemia-reperfusion.
    Results: No evident role for these adipocytokines was observed in non-steatotic livers. However, obese animals undergoing liver surgery showed increased resistin in liver and plasma, without changes in adipose tissue, together with visfatin downregulation in liver and increment in plasma and adipose tissue. Endogenous resistin maintains low levels of visfatin in the liver by blocking its hepatic uptake from the circulation, thus regulating the visfatin detrimental effects on hepatic damage and regenerative failure. Indeed, the administration of anti-resistin antibodies increased hepatic accumulation of adipocyte-derived visfatin, exacerbating damage and regenerative failure. Interestingly, treatment with anti-visfatin antibodies protected steatotic livers, and similar results were obtained with the concomitant inhibition of resistin and visfatin. Thus, when visfatin was inhibited, the injurious effects of anti-resistin antibodies disappeared. Herein we show that upregulation of visfatin increased NAD levels in the remnant steatotic liver, whereas visfatin inhibition decreased them. These later observations suggest that visfatin may favour synthesis of NAD instead of DNA and induces alterations in amino acid metabolism-urea cycle and NO production, overall negatively affecting liver viability.
    Conclusions: Our results indicate the clinical potential of visfatin blocking-based therapies in steatotic livers undergoing partial hepatectomy with ischemia-reperfusion.
    Mesh-Begriff(e) Animals ; Cytokines/antagonists & inhibitors ; Cytokines/physiology ; Fatty Liver/physiopathology ; Hepatectomy ; Liver/metabolism ; Liver Regeneration/physiology ; Male ; NAD/metabolism ; Nicotinamide Phosphoribosyltransferase/antagonists & inhibitors ; Nicotinamide Phosphoribosyltransferase/physiology ; Rats ; Rats, Wistar ; Rats, Zucker ; Reperfusion ; Resistin/antagonists & inhibitors ; Resistin/physiology
    Chemische Substanzen Cytokines ; Resistin ; Retn protein, rat ; NAD (0U46U6E8UK) ; Nicotinamide Phosphoribosyltransferase (EC 2.4.2.12) ; nicotinamide phosphoribosyltransferase, rat (EC 2.4.2.12)
    Sprache Englisch
    Erscheinungsdatum 2014-01
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2013.07.041
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  6. Artikel ; Online: The effects of glucose and lipids in steatotic and non-steatotic livers in conditions of partial hepatectomy under ischaemia-reperfusion.

    Mendes-Braz, Mariana / Elias-Miró, Maria / Kleuser, Burkhard / Fayyaz, Susann / Jiménez-Castro, Mónica B / Massip-Salcedo, Marta / Gracia-Sancho, Jordi / Ramalho, Fernando S / Rodes, Juan / Peralta, Carmen

    Liver international : official journal of the International Association for the Study of the Liver

    2014  Band 34, Heft 7, Seite(n) e271–89

    Abstract: Background: Steatosis is a risk factor in partial hepatectomy (PH) under ischaemia-reperfusion (I/R), which is commonly applied in clinical practice to reduce bleeding. Nutritional support strategies, as well as the role of peripheral adipose tissue as ... ...

    Abstract Background: Steatosis is a risk factor in partial hepatectomy (PH) under ischaemia-reperfusion (I/R), which is commonly applied in clinical practice to reduce bleeding. Nutritional support strategies, as well as the role of peripheral adipose tissue as energy source for liver regeneration, remain poorly investigated.
    Aims: To investigate whether the administration of either glucose or a lipid emulsion could protect steatotic and non-steatotic livers against damage and regenerative failure in an experimental model of PH under I/R. The relevance of peripheral adipose tissue in liver regeneration following surgery is studied.
    Methods: Steatotic and non-steatotic rat livers were subjected to surgery and the effects of either glucose or lipid treatment on damage and regeneration, and part of the underlying mechanisms, were investigated.
    Results: In non-steatotic livers, treatment with lipids or glucose provided the same protection against damage, regeneration failure and ATP drop. Adipose tissue was not required to regenerate non-steatotic livers. In the presence of hepatic steatosis, lipid treatment, but not glucose, protected against damage and regenerative failure by induction of cell cycle, maintenance of ATP levels and elevation of sphingosine-1-phosphate/ceramide ratio and phospholipid levels. Peripheral adipose tissue was required for regenerating the steatotic liver but it was not used as an energy source.
    Conclusion: Lipid treatment in non-steatotic livers provides the same protection as that afforded by glucose in conditions of PH under I/R, whereas the treatment with lipids is preferable to reduce the injurious effects of liver surgery in the presence of steatosis.
    Mesh-Begriff(e) Adenosine Triphosphate/metabolism ; Analysis of Variance ; Animals ; Ceramides ; Fatty Liver/drug therapy ; Fatty Liver/metabolism ; Fatty Liver/surgery ; Glucose/metabolism ; Glucose/pharmacology ; Hepatectomy/adverse effects ; Ischemia/etiology ; Ischemia/metabolism ; Lipids/pharmacology ; Liver/drug effects ; Liver/physiology ; Lysophospholipids ; Rats ; Regeneration/drug effects ; Regeneration/physiology ; Reperfusion ; Sphingosine/analogs & derivatives
    Chemische Substanzen Ceramides ; Lipids ; Lysophospholipids ; sphingosine 1-phosphate (26993-30-6) ; Adenosine Triphosphate (8L70Q75FXE) ; Glucose (IY9XDZ35W2) ; Sphingosine (NGZ37HRE42)
    Sprache Englisch
    Erscheinungsdatum 2014-08
    Erscheinungsland United States
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2102783-3
    ISSN 1478-3231 ; 1478-3223
    ISSN (online) 1478-3231
    ISSN 1478-3223
    DOI 10.1111/liv.12348
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  7. Artikel ; Online: Adiponectin and resistin protect steatotic livers undergoing transplantation.

    Jiménez-Castro, Mónica B / Casillas-Ramírez, Araní / Mendes-Braz, Mariana / Massip-Salcedo, Marta / Gracia-Sancho, Jordi / Elias-Miró, María / Rodés, Juan / Peralta, Carmen

    Journal of hepatology

    2013  Band 59, Heft 6, Seite(n) 1208–1214

    Abstract: Background & aims: Numerous steatotic livers are discarded for transplantation because of their poor tolerance to ischemia-reperfusion. Controversial roles for adiponectin and related adipocytokines visfatin and resistin have been described in different ...

    Abstract Background & aims: Numerous steatotic livers are discarded for transplantation because of their poor tolerance to ischemia-reperfusion. Controversial roles for adiponectin and related adipocytokines visfatin and resistin have been described in different liver pathologies, nevertheless it is unknown their possible implication in ischemia-reperfusion injury associated with liver transplantation. Our study aimed at characterizing the role of the adiponectin-derived molecular pathway in transplantation with steatotic and non-steatotic liver grafts.
    Methods: Steatotic and non-steatotic liver transplantation was carried out and the hepatic levels of adiponectin, visfatin and resistin were measured and modulated either pharmacologically or surgically.
    Results: Steatotic liver grafts exhibited downregulation of both adiponectin and resistin when subjected to transplantation. Adiponectin pre-treatment only protected steatotic grafts and did it so through a visfatin-independent and resistin-dependent mechanism. Adiponectin-derived resistin accumulation activated the PI3K/Akt pathway, unravelling AMPK as an upstream mediator of adiponectin's actions in steatotic grafts. Strategies aimed at increasing adiponectin including either AMPK activators or the induction of ischemic preconditioning (which activates AMPK) increased resistin accumulation, prevented the downregulation of PI3K/Akt pathway and protected steatotic liver grafts. Conversely, PI3K/Akt pathway upregulation and hepatic protection induced by adiponectin were abolished when resistin action was inhibited.
    Conclusions: Our findings reveal a new protective pathway in steatotic liver transplantation, namely AMPK-adiponectin-resistin-PI3K/Akt, which may help develop new strategies aimed at increasing either adiponectin or resistin in the steatotic liver undergoing transplant to ultimately increase organ donor pool and reduce waiting list.
    Mesh-Begriff(e) AMP-Activated Protein Kinases/physiology ; Adiponectin/physiology ; Animals ; Cytokines/physiology ; Fatty Liver/surgery ; Liver Transplantation ; Nicotinamide Phosphoribosyltransferase/physiology ; Phosphatidylinositol 3-Kinases/physiology ; Proto-Oncogene Proteins c-akt/physiology ; Rats ; Rats, Zucker ; Resistin/physiology ; Signal Transduction
    Chemische Substanzen Adiponectin ; Cytokines ; Resistin ; Retn protein, mouse ; Nicotinamide Phosphoribosyltransferase (EC 2.4.2.12) ; nicotinamide phosphoribosyltransferase, mouse (EC 2.4.2.12) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Sprache Englisch
    Erscheinungsdatum 2013-12
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2013.07.015
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  8. Artikel ; Online: Retinol binding protein 4 and retinol in steatotic and nonsteatotic rat livers in the setting of partial hepatectomy under ischemia/reperfusion.

    Elias-Miró, Maria / Massip-Salcedo, Marta / Raila, Jens / Schweigert, Florian / Mendes-Braz, Mariana / Ramalho, Fernando / Jiménez-Castro, Mónica B / Casillas-Ramírez, Araní / Bermudo, Raquel / Rimola, Antoni / Rodes, Juan / Peralta, Carmen

    Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society

    2012  Band 18, Heft 10, Seite(n) 1198–1208

    Abstract: Steatotic livers show increased hepatic damage and impaired regeneration after partial hepatectomy (PH) under ischemia/reperfusion (I/R), which is commonly applied in clinical practice to reduce bleeding. The known function of retinol-binding protein 4 ( ... ...

    Abstract Steatotic livers show increased hepatic damage and impaired regeneration after partial hepatectomy (PH) under ischemia/reperfusion (I/R), which is commonly applied in clinical practice to reduce bleeding. The known function of retinol-binding protein 4 (RBP4) is to transport retinol in the circulation. We examined whether modulating RBP4 and/or retinol could protect steatotic and nonsteatotic livers in the setting of PH under I/R. Steatotic and nonsteatotic livers from Zucker rats were subjected to PH (70%) with 60 minutes of ischemia. RBP4 and retinol levels were measured and altered pharmacologically, and their effects on hepatic damage and regeneration were studied after reperfusion. Decreased RBP4 levels were observed in both liver types, whereas retinol levels were reduced only in steatotic livers. RBP4 administration exacerbated the negative consequences of liver surgery with respect to damage and liver regeneration in both liver types. RBP4 affected the mobilization of retinol from steatotic livers, and this revealed actions of RBP4 independent of simple retinol transport. The injurious effects of RBP4 were not due to changes in retinol levels. Treatment with retinol was effective only for steatotic livers. Indeed, retinol increased hepatic injury and impaired liver regeneration in nonsteatotic livers. In steatotic livers, retinol reduced damage and improved regeneration after surgery. These benefits of retinol were associated with a reduced accumulation of hepatocellular fat. Thus, strategies based on modulating RBP4 could be ineffective and possibly even harmful in both liver types in the setting of PH under I/R. In terms of clinical applications, a retinol pretreatment might open new avenues for liver surgery that specifically benefit the steatotic liver.
    Mesh-Begriff(e) Animals ; Disease Models, Animal ; Fatty Liver/metabolism ; Fatty Liver/surgery ; Hepatectomy/methods ; Ischemia/complications ; Liver/blood supply ; Liver/metabolism ; Liver/surgery ; Liver Regeneration/drug effects ; Male ; Rats ; Rats, Zucker ; Reperfusion/adverse effects ; Reperfusion Injury/etiology ; Reperfusion Injury/prevention & control ; Retinol-Binding Proteins, Plasma/metabolism ; Retinol-Binding Proteins, Plasma/pharmacology ; Time Factors ; Vitamin A/metabolism ; Vitamin A/pharmacology ; Vitamin A/therapeutic use
    Chemische Substanzen Rbp4 protein, rat ; Retinol-Binding Proteins, Plasma ; Vitamin A (11103-57-4)
    Sprache Englisch
    Erscheinungsdatum 2012-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2006866-9
    ISSN 1527-6473 ; 1527-6465
    ISSN (online) 1527-6473
    ISSN 1527-6465
    DOI 10.1002/lt.23489
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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