{"title":"Transforming growth factors and insulin-like growth factors in chronic kidney disease","authors":"R. Mak, W. Cheung","doi":"10.1080/17471060701486225","DOIUrl":"https://doi.org/10.1080/17471060701486225","url":null,"abstract":"Irrespective of its primary etiology, chronic kidney disease (CKD) progresses. Glomerulosclerosis, interstitial fibrosis, and tubular atrophy are key features of CKD. The important roles of the transforming growth factor (TGF) and insulin-like growth factor (IGF) superfamilies have been indicated in recent studies. This review provides an update of the literature on these factors and their interactions in the pathophysiology of the progression of CKD as well as cachexia, which is an important complication. Specifically, the functions of key molecules, such as TGF-β, bone morphogenetic protein-7, myostatin, relaxin, and IGF-I in the pathobiology underlying CKD progression and CKD-associated cachexia are discussed.","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"26 1","pages":"59-64"},"PeriodicalIF":0.0,"publicationDate":"2009-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89267086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"MAP Kinase Phosphatase-1 and Septic Shock.","authors":"Yusen Liu, Thomas P Shanley","doi":"10.1080/17471060701200444","DOIUrl":"10.1080/17471060701200444","url":null,"abstract":"<p><p>Mitogen-activated protein (MAP)(§) kinase cascades are crucial signal transduction pathways in the biosynthesis of proinflammatory cytokines. MAP kinase phosphatase (MKP)-1, an archetypal member of the MKP family, plays a pivotal role in the feedback control of p38 and JNK. In vitro studies using cultured macrophages have provided strong evidence for a critical role of MKP-1 in the restraint of pro-inflammatory cytokine biosynthesis. Recently, a number of studies conducted using MKP-1 knockout mice have verified the importance of MKP-1 in the regulation of p38 and JNK and in the regulation of pro-inflammatory cytokine synthesis. Upon lipopolysaccharide challenge MKP-1 knockout mice produced dramatically greater amounts of inflammatory cytokines, developed severe hypotension, and multi-organ failure, and exhibited a remarkable increase in mortality. These studies demonstrate that MKP-1 is an essential feedback regulator of the innate immune response, and that it plays a critical role in preventing septic shock and multi-organ dysfunction during pathogenic infection.</p>","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"5 2","pages":"68-78"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091010/pdf/nihms-278386.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29877802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of hypothermia in hemorrhagic shock","authors":"F. Shuja, J. P. Almeida, H. Alam","doi":"10.1080/17471060801931245","DOIUrl":"https://doi.org/10.1080/17471060801931245","url":null,"abstract":"Hemorrhagic shock that leads to cardiovascular collapse does not respond well to conventional methods of cardiopulmonary resuscitation. Even when the source of bleeding can be controlled and the circulation restored, cerebral ischemia lasting for >5 min invariably results in severe brain damage. Often the underlying injuries are reparable but the patient dies of irreversible shock. In this setting, strategies to maintain cerebral and cardiac viability long enough to gain control of hemorrhage and restore intravascular volume could be life-saving. This requires an entirely new approach to the problem, with emphasis on rapid total body preservation, repair of injuries during metabolic arrest, and controlled resuscitation, so-called emergency preservation and resuscitation. Currently, hypothermia is the most effective method for preserving cellular viability during prolonged periods of ischemia. Herein, the authors describe the rationale behind the development of this strategy, its impact on various cellular...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"128 1","pages":"151-160"},"PeriodicalIF":0.0,"publicationDate":"2008-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75480340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D. Malinoski, Cristobol Barrios, Hubert D Kim, J. Acosta, G. Schmid-Schönbein, T. Hugli, R. Coimbra, D. Hoyt
{"title":"Role of pancreatic enzymes in the development of multiple organ failure after shock","authors":"D. Malinoski, Cristobol Barrios, Hubert D Kim, J. Acosta, G. Schmid-Schönbein, T. Hugli, R. Coimbra, D. Hoyt","doi":"10.1080/17471060801925288","DOIUrl":"https://doi.org/10.1080/17471060801925288","url":null,"abstract":"The gastrointestinal tract has been implicated as one of the main organ systems involved in the initiation of the acute inflammatory response that often follows shock. The exocrine functions of the pancreas include the secretion of digestive enzymes into the duodenal lumen. These intraluminal pancreatic enzymes may play a pivotal role in the pathogenesis of multiorgan failure after shock. This article reviews the literature surrounding the hypothesis that digestive enzymes produced by the pancreas are involved in the initiation of the systemic inflammatory response after shock and, ultimately, contribute to multiorgan failure and death.","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"36 1","pages":"161-167"},"PeriodicalIF":0.0,"publicationDate":"2008-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82642431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Moreno‐Vinasco, J. Jacobson, P. Bonde, S. Sammani, T. Mirzapoiazova, W. Vigneswaran, Joe G. N. Garcia
{"title":"Attenuation of Rodent Lung Ischemia Reperfusion Injury by Sphingosine 1 Phosphate","authors":"L. Moreno‐Vinasco, J. Jacobson, P. Bonde, S. Sammani, T. Mirzapoiazova, W. Vigneswaran, Joe G. N. Garcia","doi":"10.1080/17471060701505289","DOIUrl":"https://doi.org/10.1080/17471060701505289","url":null,"abstract":"Objective. Lung ischemia–reperfusion (IR) injury, a sequela of transplantation characterized by alveolar damage, edema and inflammation in donor lungs, remains a significant cause of transplant failure despite improvements in lung preservation techniques. We investigated the effects of sphingosine 1-phosphate (S1P), a potent vascular barrier-protective agent, in a rat model of IR injury. Material and methods. S1P (26.5 mg/kg, i.v.) or vehicle was administered 15 min prior to ischemia via pulmonary artery ligation (1 h) and subsequent reperfusion (2 h). Lung vascular permeability and inflammation were assessed. Results. Animals pretreated with S1P exhibited reduced bronchoalveolar lavage (BAL) inflammatory cells (32% decrease; p<0.05), BAL neutrophils (63% decrease; p<0.04), and BAL albumin content (57% decrease; p<0.04) compared to controls. Lung myeloperoxidase activity, an index of parenchymal leukocyte infiltration, was also attenuated in S1P-treated animals (63% decrease; p<0.05). Finally, consistent ...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"36 1","pages":"106-114"},"PeriodicalIF":0.0,"publicationDate":"2008-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75817813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hyponatremia in critical illness","authors":"O. Kozak, A. Rabinstein","doi":"10.1080/17471060701272393","DOIUrl":"https://doi.org/10.1080/17471060701272393","url":null,"abstract":"Hyponatremia is the commonest electrolyte disorder in hospitalized patients and is associated with increased morbidity and mortality. Although most patients are asymptomatic at presentation, many present neurological symptoms which can easily be overlooked and have the potential to progress and produce neurological sequelae, and even death, if not diagnosed and treated promptly. The classification of hyponatremia is based on serum osmolality and the volume status of the patient. When iatrogenic causes are excluded, inadequate secretion of antidiuretic hormone and cerebral salt wasting are the commonest mechanisms of hyponatremia in neurological and critically ill patients and their differentiation is crucial because they require drastically different management. The risks of overly rapid correction (which mostly comprise osmotic demyelination) must be borne in mind when treating hyponatremia. Management mainly depends on the speed of onset of hyponatremia and the presence of symptoms. Vasopressin antagoni...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"13 1","pages":"9-14"},"PeriodicalIF":0.0,"publicationDate":"2008-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72828441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Disruption of the innate immune system by mifepristone and lethal toxin of Clostridium sordellii","authors":"R. Miech","doi":"10.1080/17471060701200402","DOIUrl":"https://doi.org/10.1080/17471060701200402","url":null,"abstract":"The innate immune system is an immediate host response system for combating invading bacteria by initiating a protective local tissue inflammatory response. Pattern recognition molecules that are uniquely expressed in bacteria activate the host's Toll-like receptors to produce cytokines in the form of the pro-inflammatory chemokines and interleukins. If the synthesis of pro-inflammatory cytokines is not properly controlled by cortisol, pro-inflammatory cytokines gain access to the systemic circulation and result in a systemic cytokine storm that is responsible for initiating septic shock and multiple organ dysfunctions. Cortisol-activated glucocorticoid receptors result in the synthesis and release of the anti-inflammatory cytokine interleukin-10, which prevents the further synthesis of pro-inflammatory cytokines. During a mifepristone-induced abortion, the blockade of glucocorticoid receptors by mifepristone results in the disruption of the innate immune system. The combination of ischemic decidua, necro...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"83 1","pages":"122-126"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83804204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Axelsson, E. Andersson, R. Andersson, Å. Lasson
{"title":"Nuclear factor-κB activation in response to active site-inhibited factor VIIa pretreatment during acute pancreatitis in the rat","authors":"J. Axelsson, E. Andersson, R. Andersson, Å. Lasson","doi":"10.1080/17471060801886167","DOIUrl":"https://doi.org/10.1080/17471060801886167","url":null,"abstract":"Objective. Active site-inhibited factor VII (fVIIai) has previously been reported to reduce remote organ inflammation during acute pancreatitis. The aim of this study was to investigate whether the anti-inflammatory properties of fVIIai in remote organs are mediated through nuclear factor (NF)-κB. Material and methods. Acute pancreatitis in the rat was induced using retrograde intraductal infusion of sodium taurodeoxycholate. Upregulation of NF-κB activity was evaluated using an enzyme-linked immunosorbent assay. Results. An increase in NF-κB activity could be seen in the lungs, which was reduced to normal levels at both 1 and 6 h following pretreatment with fVIIai. In the liver, the greatest treatment effects were seen at 1 h, but were still notable at 6 h. In the ileum, treatment effects were seen only at 6 h. Simultaneous fVIIai and N-acetylcysteine treatment ameliorated many of the treatment effects of fVIIai. In the pancreas, no differences could be seen. Conclusion. fVII inhibition reduces NF-κB act...","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"39 1","pages":"85-92"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88185055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Scarpelini, S. Rhind, H. Tien, K. Leung, S. Rizoli
{"title":"Effects of hypertonic saline on the development of acute lung injury following traumatic shock","authors":"S. Scarpelini, S. Rhind, H. Tien, K. Leung, S. Rizoli","doi":"10.1080/17471060801931260","DOIUrl":"https://doi.org/10.1080/17471060801931260","url":null,"abstract":"Hypertonic saline (HS) is a promising fluid resuscitation therapy with the potential to reduce lung injury caused by severe trauma. The experimental evidence that HS has hemodynamic, anti-inflammatory, immunological, and neuroprotective properties and that it attenuates post-traumatic lung injury and multiple organ dysfunction syndrome (MODS) is undeniable. Laboratory evidence continues to accumulate to suggest that administration of HS affects cells, organs, and the neuro-humoral response to trauma, which affects both the innate and adaptive immunity. In contrast to the experimental findings, no clinical study to date has demonstrated that resuscitation of trauma patients with HS significantly reduces lung injury and MODS. Two recent clinical trials have confirmed that HS exerts similar hemodynamic, anti-inflammatory, and immunological effects as in experimental models. While it is possible that in humans such effects do not result in attenuation of post-traumatic lung injury and MODS, another explanation could be that no clinical study to date was powered to identify such clinical outcomes. An ongoing large, multicenter, randomized clinical trial across the USA and Canada is the first that is powered to determine whether resuscitation with a single dose of HS reduces post-traumatic lung dysfunction and consequently should become part of the resuscitation of severely traumatized patients.","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"15 1","pages":"99-105"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89762259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of the neutrophil in myocardial ischemia–reperfusion injury","authors":"J. Paśnik, K. Zeman","doi":"10.3109/17471060802227122","DOIUrl":"https://doi.org/10.3109/17471060802227122","url":null,"abstract":"This article reviews the role of neutrophils in myocardial ischemia–reperfusion injury. A number of studies have demonstrated that myocardial ischemia–reperfusion injury is an acute inflammatory process in which neutrophils are involved by accumulating at the site of ischemia injury. This process requires signals and pro-inflammatory molecules to direct neutrophils to the site of ischemia, and cell adhesion molecules to connect them with the endothelium.","PeriodicalId":89424,"journal":{"name":"Journal of organ dysfunction","volume":"1 1","pages":"193-207"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89056081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}