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Years and Volumes

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Articles from this Volume

Silvia Bertuglia, Hideo Ichimura, Gianluca Fossati, Kaushik Parthasarathi, Flavio Leoni, Daniela Modena, Piero Cremonesi, Jahar Bhattacharya, and Paolo Mascagni

The ability to inhibit functions of activated endothelial cells represents a promising strategy for pathologies involving abnormal microcirculation activation such as re-occulsion after angioplasty and acute rejection in allo- and zenotransplantation.  Small peptides containing the Lys-Pro motif at the core of their sequence have been shown to stimulate phagocytosis and exhibit antiinflammatory properties.  However, efficacy is uncertain due to limited metabolic stability.  Bertuglia et al. (615-624) synthesized ITF1697, a chemically modified form of these peptides with increased resistance to proteolysis.  Data indicate that ITF1697 can maintain normal arteriolar responses and capillary perfusion during post-ischemic reperfusion by inhibiting calcium-dependent exocytosis of Weibel Palade bodies from endothelial cells, an early hallmark of inflammation.  These results indicate that ITF1697 may be a pharmacological tool for the treatment of pathologies involving abnormal microcirculation activation.

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Posted by Leah Caracappa on Dec 4, 2007 12:00 AM CST
Susanne Rohrbach, Stefan Engelhardt, Martin J Lohse, Karl Werdan, Juergen Holtz, and Ursula Muller-Werdan

Acute activation of a proinflammatory cytokine stress response initially provides the heart with adaptive and protective mechanisms. However, prolonged cytokine activity can lead to overt cardiac decompensation, edema and failure. While several mechanisms of cardiac induction of proinflammatory cytokines have been investigated, the effects of sympathetic overactivity on the proinflammatory stress response are less clear. Beta-adrenoceptor activation contributes to proinflammatory stress responses and in this work, Rohrback et al. (605-614) analyze myocardial cytokine expression under various conditions of B-adrenoceptor activation. Results show that B-adrenoceptor-mediated activation of cAMP-responseive element and activating protein-1 directly contribute to interleukin 6 induction in healthy and failing myocardium. These results advance our understanding of sympathetic activity during cardiac proinflammatory stress.

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Posted by Leah Caracappa on Dec 3, 2007 12:00 AM CST
Tiffany Frey and Antonio De Maio

Sepsis is a systemic response to infection and a major health problem with approximately 750,000 cases per year in the United States.  Adequate therapies do not exist and patient care is mainly supportive.  Statins, which are widely used for the treatment of hypercholesterolemia, also have antiinflammatory effects via mechanisms that are not well understood.  Lipopolysaccharide (LPS) induces an inflammatory response and interacts with CD14, a major LPS binding site on macrophages. Here Frey and De Maio (592-604) investigate the effect of statins on CD14 expression. Their results suggest that statin treatment may modulate macrophage function and have an impact on inflammation and the outcome of sepsis.

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Posted by Leah Caracappa on Dec 2, 2007 12:00 AM CST
Bárbara Macedo, Ana Rita Batista, José Barbas do Amaral, and Maria João Saraiva

Familial amyloidotic polyneuropathy (FAP) is an autosomal dominant hereditary disease characterized by the extracellular deposition of amyloid fibrils in connective tissue.  FAP affects the peripheral nervous system with progressive and severe sensory and autonomic neuropathy.  Early lesion detection using biomarkers may aid in the clinical management of patients.  In order to better define biomarkers for future assessment of prophylactic and therapeutic drugs in the treatment of FAP, Macedo et al. (584-591) extended the search for oxidative stress and apoptotic biomarkers in clincical simples and in animal models.  A robust biomarker profile was identified and may improve future assessment of selected markers in experimental animal studies and in clinical trials.

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Posted by Leah Caracappa on Dec 1, 2007 12:00 AM CST
Oonagh Dowling, Burton Rochelson, Kathleen Way, Yousef Al-Abed, and Christine N Metz

Pregnancy-induced hypertension (PIH), also known as preeclampsia, is one of the major causes of maternal and fetal death.  While the precise cause of PIH is not known, aberrant cytokine production and placenta participation are considered to be important factors.  Gestational cigarette smoking, which is widely accepted to be harmful to both the mother and fetus, is protective against the development of PIH.  Based on the anti-inflammatory activity of nicotine, the major component of cigarettes, Dowling et al. (576-583) examined the effect of nicotine and other cholinergic agonists on placenta inflammatory responses ex vivo. Nicotine and other cholinergic agonists significantly suppress placenta cytokine production following stimulation through the NFkB pathway.  These data suggest that cholinergic agonists, including nicotine, may protect against PIH.

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Posted by Leah Caracappa on Nov 4, 2007 12:00 AM CDT
Catia Bellucci, Cinzia Lilli, Tiziano Baroni, Lucilla Parnetti, Sandro Sorbi, Carla Emiliani, Eleonora Lumare, Paolo Calabresi, Stefania Balloni, and Maria Bodo

Alzheimer’s disease (AD) accounts for over 50 percent of dementia disorders and extracellular matrix (ECM) molecules and growth factors, such as fibroblast growth factor (FGF), play a crucial role in this disease.  While AD is characterized by amyloid deposits, it has been suggested that amyloid accumulation is only partly responsible for the neurodegeneration observed in this disease.  Here, Bellucci et al. (542-550) examined skin fibroblasts from familial and sporadic AD patients to determine if phenotypic alterations in ECM production were present in non-neuronal AD cells associated with the expression and response of FGF.  Their results show different ECM synthesis and mRNA levels in the two populations of AD patients.  These data suggests that in addition to being characterized by the known pathologies affecting the nervous system, AD may also be associated with abnormalities in somatic peripheral cells.

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Posted by Leah Caracappa on Oct 5, 2007 12:00 AM CDT
Victor Trevino, Francesco Falciani, and Hugo A Barrera-Saldaña

Among the many benefits of the Human Genome Project are new and powerful tools such as the genome-wide hybridization devices referred to as microarrays.  Initially designed to measure gene transcriptional levels, microarray technologies are now used for comparing other genome features among individuals and their tissues and cells.  Results provide valuable information on disease subcategories, disease prognosis and treatment outcome.  This review by Trevino et al. (527-541) describes the technology and applications that reveal our genetic inheritance. 

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Posted by Leah Caracappa on Oct 4, 2007 12:00 AM CDT
Bhupesh K Prusty, Suresh Hedau, Ajay Singh, Premashis Kar, and Bhudev C Das

Viral hepatitis constitutes a major public health problem in developing countries. In addition to parentally transmitted hepatitis B and C viruses, enterically transmitted hepatitis E virus (HEV) infection is mainly responsible for epidemics related to poor hygiene and sanitation. In several countries, fulminant hepatic failure (FHF) leads to high mortality rates in HEV-infected pregnant women.  While decreased cell-mediated immunity is a major cause of death, the exact mechanisms remain unknown.  Here, Prusty et al. (518-526) investigated the role of NF-kB in hepatitis virus-infected pregnant women manifesting severe liver damage.  Results indicate that suppression of p65 expression may be associated with the breakdown of immunity and severe liver degeneration leading to patient death.  These findings provide a molecular basis for developing therapeutic approaches to target HEV-infected pregnant women.

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Posted by Leah Caracappa on Oct 3, 2007 12:00 AM CDT
Ensari Guneli, Zahide Cavdar, Huray Islekel, Sulen Sarioglu, Serhat Erbayraktar, Muge Kiray, Selman Sokmen, Osman Yilmaz, and Necati Gokmen

Ischemia reperfusion (I/R) injury occurs in a variety of clinical conditions and is associated with high morbidity and mortality.  Reperfusion injury occurs as a result of blood flow restoration to an ischemic, or blood-restricted, region.  The resulting tissue injury may be more damaging than the original ischemic injury.  While the exact mechanisms have not been elucidated, oxidative stress mediators are believed to play an important role.  Erythropoietin (EPO) produced by the kidney in the regulation of red blood cells also acts as a tissue-protecting factor.  Though the favorable effects of EPO are not fully understood, Guneli et al. (509-517) examined the effect of recombinant human EPO on I/R intestinal injury.  Their results indicate that EPO protects against intestinal I/R injury in rats by reducing oxidative stress and apoptosis, which the authors attribute to the antioxidative properties of EPO.  Knowledge regarding EPO signaling pathways in the intestine may lead to its use in clinical practice in the future.

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Posted by Leah Caracappa on Oct 2, 2007 12:00 AM CDT
Thomas P Shanley, Natalie Cvijanovich, Richard Lin, Geoffrey L Allen, Neal J Thomas, Allen Doctor, Meena Kalyanaraman, Nancy M Tofil, Scott Penfil, Marie Monaco, Kelli Odoms, Michael Barnes, Bhuvaneswari Sakthivel, Bruce J Aronow, and Hector R Wong

Septic shock affects a large number of children worldwide.  Morbidity and mortality associated with pediatric septic shock remain high and current therapy is limited to prevention and supportive care.  Translational research at the genomic level may represent a powerful approach to more comprehensively understand the biological complexity of pediatric septic shock.  In this work, Shanley et al. (495-508) generated genome-level expression profiles from children with septic shock. Gene expression and functional analyses demonstrated time-dependent, differential regulation of genes involved in multiple signaling pathways and gene networks, primarily related to immunity and inflammation.  The data represent the largest reported cohort of patients with septic shock subjected to longitudinal genome-level expression profiling.  The data further advance our genome-level understanding of pediatric septic shock and support novel hypotheses.

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Posted by Leah Caracappa on Oct 1, 2007 12:00 AM CDT
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