Years and Volumes

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Articles from this Volume

Carl Nathan

Over the past few decades more than half of Americans were among the billion people worldwide who had become overweight or obese.  Inflammation has been recognized as a major driver in the pathogenesis of common diseases, such as diabetes and cancer, in which obesity is a major risk factor.  While it is not suggested that obesity’s initial cause is inflammation, it does frequently lead to inflammation that appears to arise first in certain fat deposits.  Nathan (485-492) reviews evidence that reactive oxygen and nitrogen intermediates help drive chronic inflammation in the obese.   

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Posted by Leah Caracappa on Aug 5, 2008 12:00 AM CDT
John R Klune, Rajeev Dhupar, Jon Cardinal, Timothy R Billar, and Allan Tsung

Recent advances in understanding the mechanisms of innate immune system activation have pointed to certain pattern recognition receptors as a common pathway for immune identification of both microbial invasion and tissue injury.  By sensing either pathogens or endogenous danger signals released upon cellular stress or damage, these pattern recognition receptors, or alarmins, are capable of alerting the host to danger by activating the innate immune system.  Klune et al. (476-484) describe the role of an archetypical alarmin, HMGB1, and its potential therapeutic role in various disease states.

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Posted by Leah Caracappa on Aug 4, 2008 12:00 AM CDT
Mario Perl, Joanne Lomas-Neira, Chun-Shiang Chung, and Alfred Ayala

Acute Lung Injury (ALI) is associated with high morbidity and mortality.  ALI is a co-morbid event associated with a diverse family of diseases and the lack of therapeutic options for ALI may result from distinct pathological processes.  Activated neutrophil induced tissue injury and epithelial cell apoptosis-mediated lung damage represent two potentially important candidate pathomechanisms in ALI.  In this review, Perl et al. (465-475) focus on these pathogenic mechanisms as well as the role of small interfering RNA as a potential therapeutic for ALI.

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Posted by Leah Caracappa on Aug 3, 2008 12:00 AM CDT
G Brent Irvine, Omar M El-Agnaf, Ganesh M Shankar, and Dominic M Walsh

Developing effective treatments for neurodegenerative diseases is one of the greatest medical challenges of the 21st century.  Protein aggregation is a common feature of many neurodegenerative diseases and is assumed to play a central role in pathogenesis.  Irvine et al. (451-464) discuss this theme as it relates to Alzheimer’s and Parkinson’s diseases. 

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Posted by Leah Caracappa on Aug 2, 2008 12:00 AM CDT
Xiaoling Qiang, Rongqian Wu, Youxin Ji, Mian Zhou, and Ping Wang

Vascular responsiveness to adrenomedullin (AM), a potent vasoactive peptide, decreases during sepsis and hemorrhage and improves after administration of its binding protein (AMBP-1). While AM/AMBP-1 may be a leading candidate for sepsis and hemorrhage treatment, the high cost of commercial AMBP-1 has limited the development of human AM and AMBP-1 as therapeutic agents.  In this work Qiang et al. (443-450) successfully isolated and purified AMBP-1 from human serum and demonstrated its stability and biological activity in vitro and in vivo. This technique allows further development of human AM/AMBP-1 as a therapy for safe and effective treatment of hemorrhagic shock, sepsis, and ischemic injury.

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Posted by Leah Caracappa on Aug 1, 2008 12:00 AM CDT
Midori Masuda, Katsuya Amano, Shi Yan Hong, Noriko Nishimura, Masayoshi Fukui, Masamichi Yoshika, Yutaka Komiyama, Hiroya Masaki, Toshiji Iwasaka, and Hakuo Takahashi

Atherosclerosis is the buildup of plaque deposits in the arteries. Macrophages play a major role in this vascular lesion development. The FcγRIIIa(CD16) receptor is expressed in a minor subset of peripheral blood monocytes and is present in human atherosclerotic plaques. Soluble FcγRIIIa found in plasma is significantly increased in patients with coronary artery disease. Masuda et al. (436-442) investigated the potential of FcγRIIIa as biomarker for atherosclerosis. Results showed the soluble FcγRIIIa levels were related to the number of risk factors for atherosclerosis including aging, smoking, diabetes, hypertension and cholesterolemia as well as carotid maximum intima-media thickness. This indicates macrophage activation during the incipient stage of atherosclerosis and the potential use of soluble FcγRIIIa as a predictive marker for this disease.

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Posted by Leah Caracappa on Jul 10, 2008 12:00 AM CDT
Fernanda B Fernandes, Frida L Plavnik, Andressa MS Teixeira, Dejaldo M deJesus Christofalo, Sergio A Ajzen, Elisa MS Higa, Fernanda A Ronchi, Ricardo de Castro Cintra Sesso, and Dulce E Casarini

Hypertension, or high blood pressure, is a critical public health problem. Hypertensive patients often do not exhibit symptoms, leaving them unaware of their risk. Development of early biomarkers for hypertension may help identify those at risk before an adverse outcome such as heart attack or stroke may occur. Fernandes et al. (429-435) examined the association between urinary angiotension I-converting enzyme (ACE), a vascular regulator, and other hypertensive elements including C-reactive protein, homocysteine plasma levels, urinary nitric oxide and endothelial function. Findings suggest that healthy subjects with the 90kDa isoform of ACE and a family history of hypertension exhibited endothelial dysfunction. This data may lead to the development of a biomarker to assess future hypertension risks.

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Posted by Leah Caracappa on Jul 9, 2008 12:00 AM CDT
Hongkuan Fan, Basilia Zingarelli, Vashaunta Harris, George E Tempel, Perry V Halushka, and James A Cook

Overactivity of the innate immune system results in systemic inflammatory response syndrome (SIRS) and septic shock. Lack of the Gi protein results in augmented inflammatory responses to lipopolysaccharide (LPS).  Since lysophosphatidic acid (LPA) activates Gi proteins, Fan et al. (422-428) hypothesized that LPA could inhibit LPS-induced inflammatory responses through activation of Gi-coupled anti-inflammatory signaling pathways.  Results demonstrate LPA has an anti-inflammatory effect on LPS-induced systemic inflammation through ERK1/2, serine/threonine phosphatases and P13 kinase signaling pathways. Targeting LPA and the corresponding signaling pathways may result in potential therapeutic treatments for sepsis.

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Posted by Leah Caracappa on Jul 8, 2008 12:00 AM CDT
Yvonne Wettergren, Elisabeth Odin, Staffan Nilsson, Göran Carlsson, and Bengt Gustavsson

Colorectal cancer (CRC) is the third leading cause of cancer deaths in Western countries. Development of distant metastases by tumor cells spread from the primary tumor site is a major cause of death. Using biomarkers to identify CRC patients who would benefit from adjuvant treatment may decrease the risk of recurrence. Low folate levels are seen in CRC patients with poor survival. Folate levels affect gene-specific hypermethylation, and in this work Wettergren et al. (412-421) investigated whether hypermethylation of the p16 promoter in mucosa could be detected and related to survival of CRC patients.  Patients with p16 hypermethylation in the mucosa had an increased risk of cancer-related death and shorter disease-free survival. Hypermethylation of p16 was identified as an independent prognostic parameter for cancer-specific survival and an independent predictor of disease free survival.  

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Posted by Leah Caracappa on Jul 7, 2008 12:00 AM CDT
Efstathia Papageorgiou, Nea Pitulis, Menelaos Manoussakis, Peter Lembessis, and Michael Koutsilieris

Prostate cancer is the most common malignancy in men over 60 and is associated with significant cancer-related mortality in its advanced stage.  PPARγ is overexpressed in prostate cancer and PPARγ ligands promote cell cycle arrest and apoptosis in prostate cancer cells.  Papageorgiou et al. (403-411) analyzed the ability of two PPARγ ligands to increase cytotoxicity and suppress survival in PC-3 prostate cancer cells. While both ligands induced cytostasis, only the synthetic ligand inhibited the survival factor action of IGF-1 on chemotherapy-induced apoptosis of PC-3 cells via a non-genomic action.  This attenuation of IGF-1-dependent signaling in PC-3 cells could have clinical implications for the management of androgen ablation-refractory and chemotherapy-resistant advanced prostate cancer patients with bone metastasis.

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Posted by Leah Caracappa on Jul 6, 2008 12:00 AM CDT
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