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Years and Volumes

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Articles from this Volume

Rodrigo Araújo Fraga-Silva, Sergio Veloso Brant Pinheiro, Andrey Christian Costa Gonçalves, Nathalia Alenina, Michael Bader, and Robson Augusto Souza Santos

Platelets play a critical role in hemostasis and thrombosis.  Platelets become activated, adhere to injured blood vessel walls and aggregate.  This process may result in the formation of an occlusive thrombus leading to heart attacks, stroke and peripheral vascular disease.  Angiotensin-(1-7) is a member of the renin-angiotensin system and exhibits antithrombotic activity.  The mechanism has yet to be elucidated but may involve Mas, a G protein-coupled receptor for angiotensin-(1-7).  Fraga-Silva et al. (28-35) evaluated the participation of platelets and Mas receptor-related mechanisms in antithrombotic activity.  Data show that the antithrombotic effect of angiotensin-(1-7) is Mas-dependent, involves Mas-mediated NO release from platelets and is functionally important in hemostasis.  These results suggest that the angiotensin-(1-7)-Mas axis should be considered as a putative target for development of a new class of drugs used in the treatment of thrombotic diseases.

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Posted by Leah Caracappa on Jan 4, 2008 12:00 AM CST

Imke Bokelmann and Ulrich Mahlknecht

Chronic lymphocytic leukemia (CLL) is one of the most common leukemias in adults in the developed world.  Despite significant advances in cancer treatment, CLL remains incurable.  Accepted treatment regimens are neither curative nor associated with prolonged survival.  CLL cells exhibit impaired apoptosis leading to increased survival of circulating cells.  Valproic acid (VPA) belongs to a relatively new class of agents used for anticancer therapy.  These agents induce apoptosis in malignant cells by upregulation of proapoptotic and repression of antiapoptotic genes.  In this study, Bokelmann and Mahlknecht (20-27) further elucidate the effects of VPA on apoptosis in primary CLL cells.  Their results provide new insights into the pathogenesis of apoptosis mediated by VPA, which in the future may be of use on its own or in combination with other drugs for the treatment of CLL.

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Posted by Leah Caracappa on Jan 3, 2008 12:00 AM CST

Marc G Jeschke, Dagmar Klein, Wolfgang E Thasler, Ulrich Bolder, Hans-Jürgen Schlitt, Karl-Walter Jauch, and Thomas S Weiss

Hepatic homeostasis is essential for survival in critically ill and burned patients.  Insulin administration improves survival and decreases infections in patients; in this study, Jeschke et al. (11-19) investigated whether primary human hepatocytes undergo a stress response and if this response could be altered by insulin administration.  Results indicate that insulin administration decreases hepatic cytokine expression in a dose dependent manner.   There was no difference in glucose concentration or cellular metabolism suggesting insulin’s beneficial effects may be due to a direct anti-inflammatory effect.  The authors conclude that primary hepatocyte cultures may be used as an in vitro model to study hepatocyte stress responses.  This work advances understanding of the molecular mechanisms involved in the protective effect of insulin in critically ill and burned patients.

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Posted by Leah Caracappa on Jan 2, 2008 12:00 AM CST

Gengyun Wen, Gloria M Calaf, Michael A Partridge, Carlos Echiburú-Chau, Yongliang Zhao, Sarah Huang, Yunfei Chai, Bingyan Li, Burong Hu, and Tom K Hei

Arsenic is a trace element found naturally in the environment and has been recognized as a human carcinogen for over 100 years.  Chronic exposure to arsenic results in liver injury, peripheral neuropathy, keratosis and an increased incidence of cancer of the lung, skin, bladder and liver.  In an effort to understand the mechanisms by which arsenic causes cancer, scientists have attempted to develop animal models of arsenic-induced carcinogenesis. However, animals have been remarkably resistant to arsenic-induced cancers and, consequently, in vitro studies have become important as a means of studying arsenic-derived carcinogenic mechanisms.  Many in vitro models have been established using virus and gene incorporation, however, these processes affect genomic stability and intracellular signaling, which may facilitate increased transformation.  In this work, Wen et al. (2-10) established an in vitro arsenic induced transformation model by using H-TERT immortalized human small airway epithelial cells that exhibit characteristics of normal cells.  This work provides the opportunity to study phenotypic and molecular carcinogenic processes induced by arsenic in a more normal cell type.

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Posted by Leah Caracappa on Jan 1, 2008 12:00 AM CST
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