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Years and Volumes

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Articles from this Volume

Review Article

Raghavan Raju, Kirby I Bland, and Irshad H Chaudry

Trauma-hemorrhage leads to prolonged immune suppression, sepsis and multiple organ failure. The immunological events following trauma-hemorrhage have been elucidated and may be gender dependent. The hormone estrogen protects women from complications associated with injury, trauma and sepsis. In this review, Raju et al. (213-221) summarize current knowledge regarding estrogen modulation of immunity and its promise as a therapeutic for the treatment of adverse conditions following trauma-hemorrhage.

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Posted by Leah Caracappa on Apr 7, 2008 12:00 AM CDT

Review Article

Tobias A Rupprecht, Uwe Koedel, Volker Fingerle, and Hans-Walter Pfister


Lyme borreliosis is the most common human tick-borne disease in the Northern hemisphere. It is caused by the spirochete Borrelia burgdorferi which enters the host through a tick bite on the skin. In this review, Rupprecht et al. (205-212) describe current knowledge regarding the pathogenesis of acute Lyme neuroborreliosis (LNB), from invasion to inflammation of the central system.

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

Review Article

Michael A Flierl, Daniel Rittirsch, Markus Huber-Lang, J Vidya Sarma, and Peter A Ward


Catecholamines, which regulate immune and inflammatory responses, derive from the adrenal medulla and presynaptic neurons. Recent studies reveal that T cells also can synthesize and release catecholamines which then can regulate T cell function. Macrophages and neutrophils, when stimulated, can generate and release catecholamines de novo which, in an autocrine/paracrine manner, regulate mediator release via engagement of adrenergic receptors. Here, Flierl et al. (195-204) review the roles of catecholamines and their receptors in immunity and inflammation. 

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Posted by Leah Caracappa on Apr 5, 2008 12:00 AM CDT

Gregory D Van Vickle, Chera L Esh, Tyler A Kokjohn, R Lyle Patton, Walter M Kalback, Dean C Luehrs, Thomas G Beach, Amanda J Newel, Francisco Lopera, Bernardino Ghetti, Ruben Vidal, Eduardo M Castaño, and Alex E Roher 

Alzheimer’s disease (AD) increasingly affects the elderly population and now represents the third most common cause of death among aged adults. As the average life expectancy increases, the number of subjects with AD is expected to rise almost exponentially, quadrupling by the year 2050. A complete understanding of the deleterious effects of amyloid is needed to understand the pathophysiology of AD.  Van Vickle et al. (184-194) used a combination of histological, immunohistochemical, biochemical and mass spectrometric methods to examine the structure and morphology of the amyloid species produced in a patient with a presenilin mutation. Their results show increased amounts of CT99 and Aβ42 peptides as well as substantially longer Aβ peptides. These findings may lead to the design of therapeutic interventions for Alzheimer’s disease.


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Posted by Leah Caracappa on Apr 4, 2008 12:00 AM CDT

Renata Alleva, Marco Tomasetti, Davide Sartini, Monica Emanuelli, Emanuele Nasole, Ferruccio Di Donato, Battista Borghi, Lory Santarelli, and Jiri Neuzil

Non-healing ulceration is a serious complication of diabetes mellitus, conditions such as paralysis that inhibit movement, and aging. Wound healing is a complex process and chronic wounds arise from recurrent or chronic injuries and/or low levels of bacterial contamination. These injuries often fail to heal because persistently elevated levels of proinflammatory cytokines lead to high concentrations of proteases, which degrade growth factors and matrix metalloproteinase proteins (MMPs) essential to normal wound healing. Hyperbaric oxygen (HBO) therapy in conjunction with α-lipoic acid (LA) administration has been used for the successful treatment of non-healing wounds by inhibiting reactive oxygen species and inflammatory mediators, and accelerating ulcer regression. Alleva et al. (175-183) evaluated the effect of LA on gene expression in chronic wound patients treated with HBO. Results show that LA supplementation in combination with HBO therapy downregulated inflammatory cytokines and growth factors, in turn affecting expression of MMPs and promoting the healing process.

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Posted by Leah Caracappa on Apr 3, 2008 12:00 AM CDT

Kazuhiko Yamamoto, Abdallah Nihrane, Jason Aglipay, Juan Sironi, Steven Arkin, Jeffrey M Lipton, Toru Ouchi, and Johnson M Liu

Fanconi anemia is a genetic disorder that predisposes affected individuals to hematopoietic failure, birth defects, leukemia and squamous cell carcinoma of the head, neck and cervix. Pre-cancerous legions are believed to trigger the DNA damage response (DDR). Yamamoto et al. (167-174) focused on the DDR in Fanconi anemia and its putative role as a checkpoint barrier to cancer. They describe a processing defect that leads to general DDR upregulation and suggest that cancer in Fanconi anemia may arise from selection for cells that escape from a chronically activated DDR checkpoint.

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Posted by Leah Caracappa on Apr 2, 2008 12:00 AM CDT

Dionysios J Papachristou, Eugenia Papadakou, Efthimia K Basdra, Panagiotis Baltopoulos, Elias Panagiotopoulos, and Athanasios G Papavassiliou

Menisci, located in the knee, are wedge-shaped half moon structures made of cartilage. Menisci can fail due to biomechanical or biochemical cues, the latter often attributed to osteoarthritis of the knee. The molecular events underpinning the pathogenesis of meniscal degeneration remain elusive.  Papachristou et al. (160-166) immunohistochemically examined the expression of p38 MAPK, its phosphorylated/activated form (p-p38), its target NF-kB, and COX-2 in ruptured menisci. Further, they also investigated their involvement in meniscal degeneration development. Their findings demonstrate increased expression of elements of the p38-NF-kB pathway and COX-2 in disintegrated fibrocartilage, suggesting a role for these molecules in the pathobiochemistry of meniscal degeneration and consequential rupture.

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Posted by Leah Caracappa on Apr 1, 2008 12:00 AM CDT

Helga Joos, Wolfgang Albrecht, Stefan Laufer, Heiko Reichel, and Rolf E Brenner

Osteoarthritis is one of the most common joint diseases and severely restricts patient mobility. The cartilage destruction that takes place is not only associated with an imbalance of anabolic and catabolic processes, but also with poorly understood alterations in the cytoskeletal organization of chondrocytes.
In this work, Joos et al. (150-158) investigated the effects of IL-1β on components of the chondrocyte cytoskeleton on different expression levels. Results show that IL-1β is involved in the regulation of various cytoskletal components in human chondrocytes and may be relevant in osteoarthritis pathogenesis. A deeper knowledge of these molecular processes may set the pathogenetic mechanisms of degenerative joint diseases in a novel context.

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Posted by Leah Caracappa on Mar 8, 2008 12:00 AM CST

Peter Krasnov, Tatyana Michurina, Michael A Packer, Yuri Stasiv, Naoki Nakaya, Kateri A Moore, Kenneth E Drazan, and Grigori Enikolopov

Nitric oxide (NO), a crucial regulator of vasodilation, immunity and neurotransmission, is also involved in regulating the balance between proliferation and differentiation in several developmental and differentiation settings. In the hematopoietic system, NO contributes to the regulation of hematopoietic stem and progenitor cells in the bone marrow.  While action of NO in the hematopoietic system can be readily demonstrated, neither the contribution of individual NO synthase (NOS) isoforms nor their mode of action are understood. In this work, Krasnov et al. (141-149) investigated these mechanisms and their results suggest that nNOS-produced NO acts as a paracrine regulator of hematopoietic stem cells and that nNOS-selective inhibitors may have therapeutic potential for hematopoiesis-related disorders.

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Posted by Leah Caracappa on Mar 7, 2008 12:00 AM CST

Lilong Tang, Chunyu Deng, Ming Long, Anli Tang, Shulin Wu, Yugang Dong, Louis D Saravolatz, and Julius M Gardin

Acute myocardial infarction (AMI) has been a major public health problem for decades. Nearly 1 million patients in the U.S. suffer from AMI annually. While AMI mortality has decreased with the advent of new procedures, it still reaches twenty percent.  The mechanism mediating ventricular arrhythmia after AMI remains ambiguous. Tang et al. (131-140) tested the role of thrombin receptor activation in the generation of post-AMI ventricular arrhythmia. Results indicate that increased thrombin receptor activation and expression in the infarcted left ventricle after AMI may contribute to ventricular arrhythmia through a mechanism involving glibenclamide-sensitive potassium channels. These findings open the door for new therapeutic targets in acute myocardial infarction.

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Posted by Leah Caracappa on Mar 6, 2008 12:00 AM CST
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