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Articles from this Volume

Review Article

Carla Jennewein, Nguyen Tran, Patrick Paulus, Peter Ellinghaus, Johannes Andreas Eble, and Kai Zacharowski

 
Coagulation is a process of blood clot formation that is initiated not only by a complex cascade upon injury to a blood vessel, but also in response to inflammation. Uncontrolled activation of the coagulation system contributes to inflammation. Coagulation is initiated by the activation of thrombin that triggers fibrin formation, while fibrin is cleaved by plasmin resulting in the lysis of clots that is accompanied by the generation of fibrin D and E fragments. Coagulation is not only affected by inflammation, but various coagulation factors including fibrin(ogen) and fibrin degradation products modulate the inflammatory response by affecting leukocyte migration and cytokine production. In this review article, Jennewein et al. discuss the interaction between inflammation and coagulation and the modulation of inflammation by fibrin(ogen) and fibrin fragments.
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Posted by MolMed Editor on Jun 14, 2011 12:00 AM CDT
Li-Fong Seet, Wing Sum Lee, Roseline Su, Sharon N Finger, Jonathan G Crowston, and Tina T Wong
 
Glaucoma is a disease of the eye resulting in optic nerve damage, leading to progressive, irreversible loss of vision. Elevated intraocular pressure (IOP) is the most common risk factor in glaucoma which can be surgically managed by glaucoma filtration surgery (GFS). However, the major obstacle to achieving long-term surgical success is the post-operative subconjunctival scarring response. Several experimental models for studying the scarring response after GFS have been described but they all have limitations. In this study, Seet et al. have developed a murine model of GFS and discussed the validity of their model and its similarity to human glaucoma filtration surgery. The authors also demonstrated the key mechanisms whereby mitomycin c treatment modulates the antiscarring response in this model.

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Posted by MolMed Editor on Jun 13, 2011 12:00 AM CDT
Soo-Young Choi, Kyu Yup Lee, Hyun-Jin Kim, Hyo-Kyeong Kim, Qing Chang, Hong-Joon Park, Chang-Jin Jeon, Xi Lin, Jinwoong Bok, and Un-Kyung Kim
 
Hearing loss (HL) is one of the most common sensory disorders, affecting about 2 out of 1000 newborns. Mutations in the gap junction beta 2 (GJB2) gene are responsible for approximately 50% of autosomal recessive nonsyndromic HL and more than 150 different variants have been reported in the GJB2 gene. In this study, Choi et al. performed functional analyses and population study for two variants of GJB2 to clarify the possible roles of these variants in HL. Results indicate the variants affect the rate of intracellular substrate transfer and calcium ion transfer along with hemichannel permeability. Based upon these findings, the authors suggest HL may be associated with these variants and additional research is needed to extend the findings.

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Posted by MolMed Editor on Jun 12, 2011 12:00 AM CDT
Bixi Jian, Shaolong Yang, Dongquan Chen, Luyun Zou, John C Chatham, Irshad Chaudry, and Raghavan Raju
 
Cardiac dysfunction and mortality associated with trauma and sepsis increase with age. Mitochondria play a critical role in the energy demand of cardiac muscles, and thereby on the function of the heart. Specific molecular pathways responsible for mitochondrial functional alterations after injury in relation to aging are largely unknown. To further investigate this, 6- and 22-monthold rats were subjected to trauma-hemorrhage (T-H) or sham operation and euthanized following resuscitation. Left ventricular tissue was profiled using our custom rodent mitochondrial gene chip (RoMitochip). Our experiments demonstrated a declined left ventricular performance and decreased alteration in mitochondrial gene expression with age following T-H and we have identified c-Myc, a pleotropic transcription factor, to be the most upregulated gene in 6- and 22-month-old rats after T-H. Following T-H, while 142 probe sets were altered significantly (39 up and 103 down) in 6-month-old rats, only 66 were altered (30 up and 36 down) in 22-month-old rats; 36 probe sets (11 up and 25 down) showed the same trend in both groups. The expression of c-Myc and cardiac death promoting gene Bnip3 were increased, and Pgc1-α and Ppar-α a decreased following T-H. Eleven tRNA transcripts on mtDNA were upregulated following T-H in the aged animals, compared with the sham group. Our observations suggest a cmyc–regulated mitochondrial dysfunction following T-H injury and marked decrease in age-dependent changes in the transcriptional profile of mitochondrial genes following T-H, possibly indicating cellular senescence. To our knowledge, this is the first report on mitochondrial gene expression profile following T-H in relation to aging.

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Posted by MolMed Editor on Jun 11, 2011 12:00 AM CDT
Zhong-Wei Zhang, Jian Cheng, Fei Xu, Ming Yuan, Jun-Bo Du, Jing Shang, Yong Wang, Lei Du, Zi-Lin Li, and Shu Yuan
 
While total cellular RNA may increase or decrease gradually during growth or as a result of stress, overall levels usually remain stable. However, in this work Zhang et al. observed mammalian cell RNAs double within 24 hours in response to free heme accumulation (ischemia reperfusion and malaria infection) or a high level of sugar treatment (diabetes). Pretreatment with either glucose or heme for 24 hours subsequently alleviated oxidative damage caused by diabetes, ischemia reperfusion or malarial infection. The authors postulate the rapid RNA amplification may play an important role in mammalian response to diabetes, ischemia reperfusion and malaria infection-derived oxidative stress and manipulation of RNA may offer a new direction for treatment.

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Posted by MolMed Editor on Jun 10, 2011 12:00 AM CDT
Pei Wang, Feng-Jiao Yang, Hui Du, Yun-Feng Guan, Tian-Ying Xu, Xue-Wen Xu, Ding-Feng Su, and Chao-Yu Miao
 
Obesity has reached epidemic proportions worldwide, and accumulating evidence indicates that obesity is a heterogeneous disorder affected by both genetic and non-genetic factors. The fat mass– and obesity-associated (FTO) gene is tightly associated with the pathophysiology of obesity, however, the exact role of FTO remains poorly understood. Here, Wang et al. used a model of energy restriction to investigate expression levels of FTO mRNA and protein in peripheral metabolic tissues and in the brain, and to explore the involvement of the leptin signaling pathway in FTO regulation. Their results provide evidence that the LepRb-STAT3 signaling pathway is involved in the brain FTO downregulation during energy restriction. This work further extends our understanding of FTO's role in obesity.

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Posted by MolMed Editor on Jun 9, 2011 12:00 AM CDT
Marc G Jeschke, Robert Kraft, Juquan Song, Gerd G Gauglitz, Robert A Cox, Natasha C Brooks, Celeste C Finnerty, Gabriela A Kulp, David N Herndon, and Darren Boehning
 
As one of the most severe forms of trauma occurring in over two million people in the United States of America per year, burn injury causes hepatic dysfunction associated with endoplasmic reticulum (ER) stress and induction of the unfolded protein response (UPR). Insulin has been shown to attenuate hepatic damage and to improve liver function, however, the underlying mechanisms by which insulin exerts its effects on liver structure and function are not understood. In this study, Jeschke et al. investigated the molecular mechanisms by which insulin administration improves hepatic structure and function post-burn. Results indicate Insulin significantly alleviates burn induced ER stress, hepatocyte apoptosis, mitochondrial abnormalities, and inflammation, leading to improved hepatic structure and function. Their results support the use of insulin therapy after traumatic injury to improve patient outcomes.

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Posted by MolMed Editor on Jun 8, 2011 12:00 AM CDT
Jennifer M Peterson, William Kline, Benjamin D Canan, Daniel J Ricca, Brian Kaspar, Dawn A Delfín, Kelly DiRienzo, Paula R Clemens, Paul D Robbins, Albert S Baldwin, Pat Flood, Pravin Kaumaya, Michael Freitas, Joe N Kornegay, Jerry R Mendell, Jill A Rafael-Fortney, Denis C Guttridge, and Paul ML Janssen
 
Duchenne Muscular Dystrophy (DMD) is a deadly genetic disease mainly characterized by progressive weakness of the skeletal musculature. In one specific manifestation, the deterioration of diaphragm muscles leads to infection and respiratory failure. The nuclear factor kappa β (NF-Κβ) signaling pathway has been implicated as a contributing factor in this process. Here, Peterson et al. explore the clinical potential of various formulations of an NF-Κβ inhibitor, the NEMO Binding Domain (NBD) peptide. Results indicate a water-soluble NBD peptide significantly restored diaphragm contractile function and improved histopathological indices of disease in experimental models. Current treatment options for DMD are limited and this effort may provide a needed treatment strategy for these patients.

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Posted by MolMed Editor on Jun 7, 2011 12:00 AM CDT
Ashish Chogle, Heng-Fu Bu, Xiao Wang, Jeffrey B Brown, Pauline M Chou, and Xiao-Di Tan
 
Inflammatory bowel disease (IBD) describes the inflammatory conditions of the large and small intestine including Crohn's disease and Ulcerative colitis. The pathogenesis of IBD is gradually being unraveled and may be the result of a combination of genetic, environmental, and immunological factors. Milk fat globule–EGF factor 8 (MFG-E8) plays an important role in maintaining the integrity of the intestinal mucosa and accelerates its healing in experimental models of sepsis. In the present study, Chogle et al. examined the role of MFG-E8/lactadherin in a model of IBD pathogenesis, tested its protective effects, and explored the therapeutic roles of MFG-E8 in experimental colitis. Their data suggest that MFG-E8 is an essential protective factor for gut epithelial homeostasis and exogenous administration of MFG-E8 may represent a novel therapeutic target in inflammatory bowel disease.

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Posted by MolMed Editor on Jun 6, 2011 12:00 AM CDT
Matthew M Burg, Aaron Soufer, Rachel Lampert, Dorothea Collins, and Robert Soufer
 
Coronary artery disease (CAD) is a disease of chronic inflammation characterized in part by macrophage infiltration of atherosclerotic plaques. Macrophages continuously release inflammatory cytokines that provoke endothelial cell dysfunction. Endothelin-1 (ET-1) is a potent endogenous vasoconstrictor that can be rapidly released by activated macrophages and the vascular endothelium in response to stimuli of short duration, including those triggered by emotional stress. This may lead to coronary plaque rupture and triggered cardiac events.  Here, Burg et al. examine the contribution of changes in autonomic activity provoked by a laboratory stressor to changes in circulating ET-1 among patients with CAD.  The recall of a previously anger-provoking incident by CAD patients induced sympathetic arousal and parasympathetic withdrawal, the latter of which predicted an associated increase in circulating ET-1. These results suggest future examination of autonomic influences on atherosclerotic leukocytes, endothelial cell function, and the dynamics of ET-1 are warranted.

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Posted by MolMed Editor on Jun 5, 2011 12:00 AM CDT
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