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Years and Volumes

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Articles from this Volume

Sanah Merchant, Sumekala Nadaraj, Devyani Chowdhury, Vincent A Parnell, Cristina Sison, Edmund J Miller, and Kaie Ojamaa

Cardiopulmonary bypass (CPB) surgery induces a complex inflammatory reaction that may result in multiorgan dysfunction including cardiac contractile depression. Macrophage migration inhibitory factor (MIF) is a central mediator of the innate immune response in patients with autoimmune disorders, severe sepsis, and respiratory distress syndrome. Pediatric cardiac surgery involving CPB induced proinflammatory cytokine production that correlated with postoperative morbidity and cardiopulmonary dysfunction. Merchant et al. (124-130) measured circulating levels of MIF before and after CPB in children and correlated these findings with intra-operative variables and postoperative outcomes. Their data suggest a potential negative effect of high circulating levels of MIF on respiratory and cardiovascular functions in the immediate postoperative period. This supports the development of therapeutic strategies targeting MIF function in this clinical setting.

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Posted by Leah Caracappa on Mar 5, 2008 12:00 AM CST

Alexander Choukèr, Manfred Thiel, Dmitriy Lukashev, Jerrold M Ward, Ines Kaufmann, Sergey Apasov, Michail V Sitkovsky, and Akio Ohta

Acute or chronic hepatitis due to viral infections or autoimmunity affects millions of patients and results in high morbidity. It is important to uncover the mechanisms that regulate immune responses in the liver and those that protect liver tissues from excessive collateral damage. Choukèr et al. (116-123) focused on the relationship between tissue hypoxia and extracellular adenosine-mediated immunosuppression. They tested whether inflammatory tissue damage-associated hypoxia and extracellular adenosine receptor (A2AR) signaling play a role in the physiological anti-inflammatory mechanism that limits liver damage during fulminant hepatitis.  Their data demonstrate that the total body hypoxia-triggered pathway provides protection in acute hepatitis and that hypoxia and A2AR function in the same immunosuppressive and liver tissue-protecting pathway. 

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Posted by Leah Caracappa on Mar 4, 2008 12:00 AM CST

Annette Bruchfeld, Abdul Rashid Qureshi, Bengt Lindholm, Peter Barany, LiHong Yang, Peter Stenvinkel, and Kevin J Tracey

Chronic kidney disease (CKD) is associated with inflammation, malnutrition and an increased risk of cardiovascular disease. High mobility group box 1 (HMGB1), a proinflammatory mediator of tissue injury, is implicated in several inflammatory diseases. Bruchfeld et al. (109-115) completed a post-hoc, cross-sectional study analyzing CKD patients to determine if HMGB1 is elevated. Results reveal that HMGB1 is significantly elevated in CKD patients and correlates with glomerular filtration rate and markers of inflammation and malnutrition. Future studies are needed to determine if HMGB1 may be used as a marker of disease activity, severity and outcome in CKD.

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Posted by Leah Caracappa on Mar 3, 2008 12:00 AM CST

Hani A Jouihan, Paul A Cobine, Robert C Cooksey, Emily A Hoagland, Sihem Boudina, E Dale Abel, Dennis R Winge, and Donald A McClain

Hereditary hemochromatosis is a common autosomal recessive disorder of iron metabolism. Patients with hereditary hemochromatosis accumulate large quantities of iron and often have diabetes, although this pathogenesis is not well understood.  Mitochondria play a crucial role in apoptosis and glucose-stimulated insulin secretion. Jouihan et al. (98-108) used a combination of knockout mice and molecular techniques to test their hypothesis that increased levels of iron may result in mitochondrial dysfunction. Their data suggest that a novel mechanism of iron-induced cellular dysfunction in mitochondria, namely altered uptake of transition metals such as manganese, may play a role in the onset of hereditary hemocromatosis and may represent a therapeutic target for this disease.

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Posted by Leah Caracappa on Mar 2, 2008 12:00 AM CST

Boaz O Owuor, Collins O Odhiambo, Walter O Otieno, Christine Adhiambo, Dominic W Makawiti, and José A Stoute

Plasmodium falciparum is an intracellular human parasite transmitted by the Anopheles mosquito.  P. falciparum malaria causes 1-2 million deaths per year, many occurring as a result of complications such as severe anemia and cerebral malaria. The parasite can directly mediate erythrocyte destruction, but the degree of anemia observed in severe cases cannot be explained solely by this phenomenon. Moreover, the lifespan of uninfected erythrocytes is decreased in infected persons suggesting that soluble factors influence erythrocyte survival. In this work Owuor et al. (89-97) investigated the complement regulatory protein machinery of red cells in children with severe malaria-associated anemia (SMA). The data indicate that deficiencies in complement regulator proteins in erythrocytes of children with SMA translate into declines in the immune complex binding capacity and increases in complement susceptibility. These results in conjunction with differences observed between children with SMA and cerebral anemia suggest that losses in complement receptor 1 and CD55 contribute to increased destruction of erythrocytes in children with SMA. Future investigation into this mechanism of action may lead to additional therapeutic targets for use in malaria-associated anemia.   

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Posted by Leah Caracappa on Mar 1, 2008 12:00 AM CST

Review Article

Husnain K Haider, Ibrahim Elmadbouh, Michel Jean-Baptiste, and Muhammad Ashraf

Myocardial infarction is the most common cause of congestive heart failure.  In the US alone, it affects approximately 5 million patients over the age of 65 with staggering economic costs.  Heart transplantation is the gold standard therapeutic intervention, but this approach is hampered by the paucity of donor organs and high risk surgery.  Therapeutic angiogenesis and myogenesis could restore perfusion of ischemic myocardium and improve contractility.  These therapeutic modalities must be considered as complementary rather than competing in order to exploit their advantages for optimal beneficial effects.  The resistant nature of cardiomyocytes to gene transfection can be overcome by ex vivo delivery of therapeutic genes to the heart using genetically modified stem cells. This article (79-86) rovides a critical appreciation of the ex vivo gene delivery approach using genetically modified stem cells to achieve angiomyogenesis for the treatment of infarcted heart.

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Posted by Leah Caracappa on Feb 5, 2008 12:00 AM CST

Review Article

Guillaume Monneret, Fabienne Venet, Alexandre Pachot, and Alain Lepape

Septic syndromes represent a major although largely under-recognized healthcare problem worldwide accounting for hundreds of thousands of deaths every year.  Sepsis deeply perturbs immune homeostasis by inducing an initial systemic inflammatory response; an ensuing anti-inflammatory process acts initially as a negative feedback regulator of the inflammatory response, but ultimately becomes deleterious as nearly all immune functions are compromised.  This review (64-78) focuses on immune dysfunctions described in septic patients and on their potential use as markers on a routine standardized basis for prediction of adverse outcome or of occurrence of secondary nosocomial infections.

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Posted by Leah Caracappa on Feb 4, 2008 12:00 AM CST

Elena Westphal, Susanne Rohrbach, Michael Buerke, Hagen Behr, Dorothea Darmer, Rolf-Edgar Silber, Karl Werdan, and Harald Loppnow

Proinflammatory cytokines are potent modulators of cardiovascular diseases such as acute myocardial infarction, atherosclerosis and chronic heart failure.  Previous studies have investigated the expression of single members of the interleukin 1 and caspase families; however, expression has not been compared in patients suffering from ischemic or dilated cardiomyopathy.  Westphal et al. (55-63) analyzed the mRNA expression of the IL-1 family members and caspases-1 and -3 in nonfailing human donor heart tissue and in myocardium of patients with ischemic or dilated cardiomyopathy.  Their data provide evidence for an altered ratio of IL-1/IL-1ra in dilated cardiomyopathy patients.  This dysregulation may contribute to pathogenesis and/or progression of heart disease by modulating the otherwise balanced IL-1-mediated functions in cardiovascular cells.

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Posted by Leah Caracappa on Feb 3, 2008 12:00 AM CST

Inna L Botchkina, David E Rivadeneira, Kevin Watkins, Martin S Karpeh, and Galina I Botchkina

Gastrointestinal cancers have the highest incidence of all cancers worldwide with over 3 million cases per year and 2.2 million deaths.  The generally asymptomatic onset makes early detection and accurate staging of gastrointestinal cancers difficult.  Despite the multitude of oncogenic pathways and tumor suppressor mechanisms, telomerase has emerged as a valuable cancer marker.  In this work, Botchkina et al. (45-54) evaluated whether telomerase activity could be used as a reliable marker for gastrointestinal cancers in exfoliated/disseminated human epithelial cells.  Results show that real-time quantitative telomeric repeat amplificaton protocol (RTQ-TRAP) assessment of telomerase activity in immunomagnetically sorted peritoneal epithelial cells has both 100% sensitivity and negative predictive value for gastrointestinal cancers.  This method may be considered as a valuable tool and useful addition to current standard diagnostic methods.

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Posted by Leah Caracappa on Feb 2, 2008 12:00 AM CST

Minou Adib-Conquy, Thierry Pedron, Anne-France Petit-Bertron, Olivier Tabary, Harriet Corvol, Jacky Jacquot, Annick Clément, and Jean-Marc Cavaillon

Circulating neutrophils from cystic fibrosis patients differ from those of healthy subjects and may reflect mutations or deletions of the cystic fibrosis transmembrane regulator.  This may lead to the disturbance of neutrophils either directly or as a consequence of on-going inflammation or infection.  To investigate the genetic differences between normal and cystic fibrosis neutrophils, Adib-Conquy et al. (36-44) compared gene expression profiles from cystic fibrosis patients with those from healthy subjects.  Analysis showed an upregulation of 62 genes and downregulation of 27 genes in CF patient neutrophils.  These results demonstrate that neutrophils from cystic fibrosis patients display a modified gene expression profile associated with disease.  G-CSF spontaneously released by neutrophils could activate these cells within an autocrine loop.

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Posted by Leah Caracappa on Feb 1, 2008 12:00 AM CST
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