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Articles from this Volume

Mary Leung, David Rosen, Scott Fields, Alessandra Cesano, and Daniel R Budman

The BRCA genes are commonly linked with hereditary breast and ovarian cancers with a potential lifetime risk as high as 50% and 40% respectively. Hereditary breast cancers linked to these genes exhibit defective homologous DNA repair (HR) and patients with either BRCA-1 or BRCA-2 defective genes have genomic instability. As a result, the cell depends on alternate DNA repair processes, such as base excision repair (BER), which requires Poly(ADP-ribose) polymerase 1 (PARP-1). In this review, Leung et al. discuss the current state of PARP-1 understanding and suggest ways in which inhibition of this gene may contribute to enhanced efficacy of a wide range of chemotherapeutics.

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Posted by Leah Caracappa on Aug 16, 2011 12:00 AM CDT

Review Article

Nerea Subirán, Luis Casis, and Jon Irazusta

Endogenous opioid peptides are substances involved in cell communication. They are present in various organs and tissues of the male and female reproductive tract. Recent studies suggest the opioid system can participate in the regulation of reproductive physiology at multiple levels. A better understanding of the implications of the opioid system in reproductive processes may contribute to clarifying the etiology of many cases of infertility, and the effect of opiate abuse on fertility. Subiran et al. reviewed current knowledge regarding the role of the opioid system in male fertility. Additionally, the authors suggest that novel biochemical tool for the diagnosis and treatment of male infertility could be based on components of the opioid system.

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Posted by Leah Caracappa on Aug 15, 2011 12:00 AM CDT

Alexander R Moschen, Clemens Molnar, Barbara Enrich, Sabine Geiger, Christoph F Ebenbichler, and Herbert Tilg

Morbid obesity is associated with a state of chronic inflammation. Members of the Interleukin-1 cytokine family (IL-1F) are produced by human adipose tissue in obesity and many IL-1F members act in an antiinflammatory manner. Moschen et al. investigate over 20 severely obese patients undergoing laparoscopic adjustable gastric banding to understand the effect excessive weight loss may have on subcutaneous adipose tissue and liver expression of cytokines. Results suggest excessive weight loss significantly affects expression of IL-1F members in adipose and liver tissue, thereby potentially contributing to the improvement of insulin resistance and inflammation in our patients. Targeting proinflammatory cytokines might reveal an attractive treatment concept in obesity related inflammatory disorders.

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Supplementary Data  PDF

Posted by Leah Caracappa on Aug 14, 2011 12:00 AM CDT

Monica Colombo, Giovanna Cutrona, Daniele Reverberi, Sonia Fabris, Antonino Neri, Marina Fabbi, Giovanni Quintana, Giovanni Quarta, Fabio Ghiotto, Franco Fais, and Manlio Ferrarini

Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world and is characterized by monoclonal accumulation in the blood and peripheral lymphoid organs. Evidence indicates that antigens may play a fundamental role in expanding B cells prior to transformation and in sustaining survival/expansion of cells in the early steps of leukemogenesis, when they are not capable of independent growth. However, whether antigenic stimulation or selection contributes to the expansion of fully transformed CLL clones is unknown. In this work, Colombo et al. provide evidence of fully transformed CLL cells utilizing the process of antigenic stimulation that may lead to clonal expansion. The special features of this CLL case support the notion that antigenic stimulation continues after the process of leukemogenesis is completed and leads to the selective expansion of subclones. Further understanding this mechanism may lead to future treatment options for CLL.

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Posted by Leah Caracappa on Aug 13, 2011 12:00 AM CDT

Ricardo Gehrau, Daniel Maluf, Kellie Archer, Richard Stravitz, Jihee Suh, Ngoc Le, and Valeria Mas

Liver transplantation (LT) is the chosen treatment for patients with advanced liver disease and cirrhosis. Acute cellular rejection (ACR) and hepatitis C virus (HCV) infection recurrence (HCVrec) are common complications post-liver transplantation (LT) in HCV patients. ACT and HCVrec both share common clinical and histological features, increasing difficulty in the differential diagnosis. ACR rate after LT is especially controversial in HCV positive recipients because of the overlapping clinical and histological features with HCVrec. Despite some promising results, reliable diagnostic biomarkers are still lacking. Gehrau et al. investigated differential gene expression, using microarrays in liver samples from HCV transplant recipients with HCVrec disease, and ACR in the setting of HCV infection. The study identified and validated four differentially expressed genes as potential biomarkers for differential diagnosis of both complications, HCVrec and ACR.

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Supplementary Data  PDF
 

Posted by Leah Caracappa on Aug 12, 2011 12:00 AM CDT
Elise Duval, Nicolas Bigot, Magalie Hervieu, Ikuyo Kou, Sylvain Leclercq, Philippe Galéra, Karim Boumediene, and Catherine Baugé

Osteoarthritis (OA), the most prevalent form of skeletal disease, is characterized by joint cartilage degeneration. Despite its frequency, the details of OA etiology and pathogenesis remain unclear. A genetic association between the cartilage extracellular matrix protein asporin (ASPN) and OA has been reported. In order to further understand the role of ASPN in OA, Duval et al. investigated ASPN expression in human articular chondrocytes (HAC). Results show proinflammatory cytokines downregulated ASPN, while TGFβ1 upregulated it. Additionally, the authors propose a role for the transcription factor Sp1 in the regulation of ASPN expression. These results indicate ASPN is finely regulated in cartilage and suggest a key role for Sp1 in chondrocytes.

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Posted by Leah Caracappa on Aug 11, 2011 12:00 AM CDT

Changchun Hou, Haijin Zhao, Laiyu Liu, Wenjun Li, Xiaoting Zhou, Yanhua Lv, Xiangbo Shen, Zhenyu Liang, Shaoxi Cai, and Fei Zou

Asthma and chronic obstructive pulmonary disease (COPD) are obstructive airway diseases characterized by chronic inflammation of the respiratory tract. High mobility group protein B1 (HMGB1) has been implicated as an important mediator in the pathogenesis of both of these conditions. However, HMGB1 expression in asthma and COPD patient serum and sputum have not been characterized. In this study, Hou et al. examined sputum and plasma concentrations of HMGB1 in COPD and asthmatic patients with varying disease severity. HMGB1 sputum and plasma concentrations in asthma and COPD were significantly higher compared with control subjects, and were negatively correlated with forced expiratory volume 1 s (FEV1), FEV1 (% predicted). HMGB1 sputum level in COPD patients was significantly higher than those of asthma patients. HMGB1 levels in asthmatic and COPD patients were positively correlated with neutrophil counts and percentage of neutrophils. These data support a potential role for HMGB1 as a biomarker and diagnostic tool for the differential diagnosis of asthma and COPD.

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Posted by Leah Caracappa on Aug 10, 2011 12:00 AM CDT

Mathias Riebold, David Mankuta, Elad Lerer, Salomon Israel, Songfa Zhong, Luba Nemanov, Mikhail V Monakhov, Shlomit Levi, Nurit Yirmiya, Maya Yaari, Fabio Malavasi, and Richard P Ebstein

Deficits in social behavior associated with autistic spectrum disorder (ASD) have been connected to specific variants of CD38. CD38 transcription is highly sensitive to several cytokines and vitamins such as ATRA, and here Riebold et al. demonstrate that retinoids may play a beneficial role in the treatment of ASD. The authors explore an in vitro model in which ATRA is applied to lymphoblastoid cell (LBC) lines from ASD patients, which show reduced CD38 mRNA levels, and their parents. They showed that the addition of this retinoid increases CD38 transcription to normal levels in these cells, suggesting a novel approach for ASD treatment. In light of this work, CD38 may prove important in the diagnosis and therapy of ASD.

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Posted by Leah Caracappa on Aug 9, 2011 12:00 AM CDT

Gwenny Manel Fuhler, Sander Henricus Diks, Maikel Petrus Peppelenbosch, and William Garrow Kerr

Multiple myeloma (MM) is a malignancy of plasma cell origin that is largely confined to the bone marrow (BM). MM leads to renal failure, hypercalcemia and skeletal destruction resulting in a median length of survival at diagnosis of only 3-5 years. Research indicates that phosphorylation of proteins plays a pivotal role in cell growth and survival. Therefore, knowing the status of phosphorylation based signaling pathways in MM cells could provide critical information for understanding MM cell survival. Here, Fuhler et al. developed a strategy to detect enzymatic activities for the phosphorylation of different kinase substrates and applied it to primary MM isolates. The MM phosphoproteome and their normal plasma cell counterparts proved to be significantly different. Fuhler et al. used these differences to propose two therapeutic applications that target specific proteins and deregulated kinases. Such therapies may increase the survival rate for patients suffering from this deadly blood cancer.

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Supplementary Data PDF

Posted by Leah Caracappa on Aug 8, 2011 12:00 AM CDT

Yinzhong Zhang, Xinchun Lin, Kiyokazu Koga, Koichiro Takahashi, Helena M Linge, Adriana Mello, Teresina Laragione, Percio S Gulko, and Edmund J Miller

Pulmonary infection is a major cause of mortality and morbidity, and the magnitude of lung inflammation correlates with patient survival. Neutrophils are critical to the pathogenesis of acute lung injury and their migration into joints is regulated by arthritis severity quantitative trait loci (QTLs). However, it is unclear whether these QTLs contribute to the regulation of lung inflammation in pneumonias. Zhang et al. examined two experimental models, which differ in these QTLs and susceptibility to joint inflammation, and found there are significant differences in the regulation of pulmonary inflammation induced by bacterial products. These differences are associated with different alveolar macrophage phenotypes, specifically differences in MAPK signaling pathways. Their data may lead to understanding of the compartmentalization of the lung inflammatory response and tissue-specific regulation of the immune responses.

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Posted by Leah Caracappa on Aug 7, 2011 12:00 AM CDT
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