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Years and Volumes

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Articles from this Volume

Review Article

Miguel Lopez-Lazaro

 
Cancer kills over six million people worldwide annually. Recently, the mortality rate has begun to decrease, due in part to prevention and early detection of the disease. Unfortunately, many cancers are not detected until tumor cells have metastasized, and the mortality rate in patients with metastatic disease is still high. Much cancer research has been allotted to identifying the genetic alterations of the cancer genome in an effort to personalize cancer therapy and make it more effective. Dr. Lopez-Lazaro discusses an alternative approach, based on the alteration of oxygen metabolism in cancer cells, as a possible, more reliable method of therapy.

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Posted by MolMed Editor on Apr 4, 2010 12:00 AM CDT
Review Article

Asha Jacob, Kavin G Shah, Rongqian Wu, and Ping Wang


There is growing concern worldwide about the threat of nuclear terrorism and subsequently, exposure to radiation. Whole- or partial-body exposure to a high dose of radiation results in acute radiation syndrome (ARS). Little is known about therapeutic approaches for ARS, which is often accompanied by trauma, burn, infection and sepsis—termed radiation combined injury. Jacob et al. review radiation combined therapy and, because of its proven antiinflammatory effects, suggest gherlin as a possible therapy.

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Posted by MolMed Editor on Apr 3, 2010 12:00 AM CDT
Romina Fornes, Paulina Ormazabal, Carlos Rosas, Fernando Gabler, David Vantman, Carmen Romero, and Margarita Vega

Polycystic Ovary Syndrome (PCOS) is a steroid-related disorder that affects between 5–10% of reproductive aged women. PCOS affects endocrine metabolism and is linked with insulin resistance and compensatory hyperinsulinemia. However, little is known about the expression of insulin pathway molecules in endometrial tissue from women diagnosed with PCOS. Fornes et al. examined the levels of several insulin signaling proteins in endometrial from PCOS women with or without hyperinsulinemia. The authors found that the endometrium expresses insulin-sensitive glucose uptake machinery, and that some proteins which belong to insulin signaling pathway show a significantly reduced expression in PCOS patients with hyperinsulinemia. This alteration suggests a disruption in the insulin signaling pathway which may account for impairment in glucose metabolism and homeostasis at the endometrial level.

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Posted by MolMed Editor on Apr 2, 2010 12:00 AM CDT
Riva Brik, Irit Rosen, Dana Savulescu, Iris Borovoi, Moshe Gavish, and Rafael Nagler

Treatment for Juvenile Idiopathic Arthritis (JIA), the most common autoimmune inflammatory disease in children, has drawbacks in terms of costs and side effects, as well as a decrease in efficacy over time. Effective, noninvasive measures of disease status such as salivary testing could help optimize drug dosing regimens. Brik et al. analyzed salivary antioxidant and compositional profiles in JIA patients, and demonstrated that antioxidant status was significantly higher in the saliva of JIA patients. Additionally, the level of matrix metalloproteinases (MMPs), endopeptidases capable of contributing to tissue destruction, was significantly lower in JIA patients undergoing antiTNF treatment as compared with patients not receiving treatment. Thus, antiTNF treatment may modify the degradation process by inhibition of MMP activity.

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Posted by MolMed Editor on Apr 1, 2010 12:00 AM CDT
Michael Bacher, Oliver Deuster, Bayan Aljabari, Rupert Egensperger, Frauke Neff, Frank Jessen, Julius Popp, Carmen Noelker, Jens Peter Reese, Yousef Al-Abed, and Richard Dodel

Inflammatory processes have been implicated in the pathophysiology of Alzheimer’s disease (AD), but the role of macrophage migration inhibitory factor (MIF) had not been thoroughly investigated. MIF is associated with β-amyloid (Aβ) peptide, the main constituent of Alzheimer plaques, demonstrating a proinflammatory etiology in AD. Bacher et al. examined MIF expression and function in vivo and in vitro, confirmed its association with plaques and demonstrated that Aβ-induced toxicity could be mitigated by small molecule inhibition of MIF. Additionally, the authors measured MIF levels in cerebrospinal fluid (CSF) of AD patients, and found an increase of MIF levels as compared with healthy, age-matched controls. These results may implicate MIF in the pathogenesis of AD, and suggest that inhibition of MIF may be a therapeutic strategy in prevention of Alzheimer’s disease onset and progression.

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Posted by MolMed Editor on Mar 4, 2010 12:00 AM CST
Daniela Spano, Roberta Russo, Vittorio Di Maso, Natalia Rosso, Luigi M Terracciano, Massimo Roncalli, Luigi Tornillo, Mario Capasso, Claudio Tiribelli, and Achille Iolascon

Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and ranks third among causes of cancer-related deaths. The severity of the disease, compounded with a lack of good diagnostic markers and treatment strategies, render HCC a major clinical challenge. To garner a better understanding of HCC, Spano et al. performed a systematic functional genomic analysis of human HuH-7 and JHH-6 HCC cells. Of the 11 genes identified, LGALS1 was selected and characterized in the context of HCC patient samples. LGALS1 codes for Galectin-1, a protein involved in various aspects of tumorigenesis. The authors show that Galectin-1 overexpression leads to increased carcinoma cell migration and invasion in vitro. They also show a positive association between increased expression of Galectin-1 and the presence of metastasis, an indicator of cancer aggression. This study clears the way for future investigations to identify markers for the prediction, diagnosis and prognosis of HCC.

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Supplementery Data A1.CEL      B1 .CEL      C1 .CEL      A2 .CEL      B2 .CEL      C2 .CEL 
Posted by MolMed Editor on Mar 3, 2010 12:00 AM CST
Irena Pastar, Olivera Stojadinovic, Agata Krzyzanowska, Stephan Barrientos, Christina Stuelten, Karen Zimmerman, Miroslav Blumenberg, Harold Brem, and Marjana Tomic-Canic

Each year, more than eight million patients develop chronic nonhealing wounds, including venous ulcers (VUs). In normal wound healing, the pleiotropic cytokine TGFβ and its receptors are highly expressed, but not in chronic wounds. Pastar et al. investigated the pathogenesis of VUs by examining TGFβ regulation and found that TGFβ signaling is blocked via the downregulation of its receptors and the attenuation of Smad signaling. This results in the deregulation of TGFβ target genes and consequently a loss of homeostasis and hyperproliferation. The authors suggest that, although exogenously-applied TGFβ may be beneficial for acute wound healing, the disruption of the TGFβ signaling cascade in VUs likely limits the efficacy of this specific treatment strategy.

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Posted by MolMed Editor on Mar 2, 2010 12:00 AM CST
Silvia Deaglio, Semra Aydin, Maurizia Mello Grand, Tiziana Vaisitti, Luciana Bergui, Giovanni D’Arena, Giovanna Chiorino, and Fabio Malavasi

Chronic lymphocytic leukemia (CLL) is the most common type of leukemia, and usually affects the adult population. Like all cancers, an understanding of the specific mechanisms of cell proliferation is crucial for the development of effective CLL treatments. Human CD38, a glycoprotein involved in the catabolism of extracellular nucleotides, is a negative prognostic marker for CLL patients. Malavasi and colleagues characterize the long-term interactions between CD38-positive CLL cells and CD31-positive cells, and thus confirm the role of this protein complex in proliferation, cell migration and homing. These results suggest that the CD31/CD38 axis is part of a network of accessory signals that modify the cellular microenvironment, favoring localization of leukemic cells to growth-permissive sites. Improved understanding of cell–cell interactions could lead to new diagnoses and treatments for CLL.

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Supplementary Data: PDF

Posted by MolMed Editor on Mar 1, 2010 12:00 AM CST