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Years and Volumes

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Articles from this Volume

Harold Brem, Olivera Stojadinovic, Robert F Diegelmann, Hyacinth Entero, Brian Lee, Irena Pastar, Michael Golinko, Harvey Rosenberg, and Marjana Tomic-Canic

Chronic wounds are reaching epidemic proportions in elderly, those with diabetes, and disabled persons. Costs exceed 25 Billion Dollars per year in the US alone. They impair quality of life and increase healthcare spending around the world. Removing devitalized tissue from chronic wounds, termed surgical debridement, is a treatment mainstay done in part to stimulate healing. However, objectively identifying the borders for surgical debridement cannot be done because the integument is physiologically impaired. Limitations are due to a knowledge deficit regarding the molecular mechanisms involved in wound healing. In this study, Brem et al. (30-39) assessed the histology, biological responses, and gene expression profiles of wound tissue in patients before and after debridement. Analyses showed that biopsies from non-healing edges exhibit a distinct pathogenic morphology when compared with adjacent non-ulcerated skin. The authors also conclude that each of this regions in chronic ulcers contain distinct cell sub-populations with varying healing capacities. These sub-populations can be identified by gene expression profiling that can be used to guide surgical debridement. In the future, molecular markers may be developed to identify the tissue with best healing capacity, making surgical debridement more accurate and therapy more efficacious.

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Posted by Leah Caracappa on Jan 4, 2007 12:00 AM CST
Rainer Mittermayr, Anatoly Osipov, Christina Piskernik, Susanne Haindl, Peter Dungel, Carina Weber, Yuri A Vladimirov, Heinz Redl, and Andrey V Kozlov

Decreased peripheral blood flow related to impaired microcirculatory vasodilation has been shown to occur in certain disease states including peripheral vascular disease, diabetes mellitus, hypercholesterolemia, hypertension, chronic renal failure, abdominal aortic aneurysmal disease and venous insufficiency, as well as in menopause, advanced age and obesity.  Impaired peripheral blood flow appears also as a serious complication of transplantation and plastic surgery often resulting in transplant loss.  Nitric Oxide (NO) is one of the most important physiological regulators of the microcirculation, which activates vasodilation.  It has recently been shown that nitrosyl complexes of hemoglobin (NO-Hb) are sensitive to low level blue laser irradiation, suggesting that laser irradiation can facilitate the release of biologically active NO, which can a(e)ffect tissue perfusion.  Here, Mittermayr et al. (22-29) evaluate the therapeutic value of blue laser irradiation for local tissue perfusion after surgical intervention.  Blue laser irradiation of NO-Hb in blood caused the decomposition of NO-Hb complexes and the release of free NO.  The data demonstrate that blue laser irradiation improves local tissue perfusion in a controlled manner and stimulates NO release from NO-Hb complexes.  This study provides a new approach to improve local blood supply applicable to flap surgery, non-surgical delay strategies or impaired blood supply in problematic superficial regions. 

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Posted by Leah Caracappa on Jan 3, 2007 12:00 AM CST
Zhi Yao, Xu-chun Che, Rong Lu, Min-na Zheng, Zhi-feng Zhu, Jin-ping Li, Xu Jian, Lin-xi Shi, Jun-yan Liu, and Wen-yuan Gao

Tyroserleutide (YSL) is an active, low-molecular-weight polypeptide, comprised of three amino acids, that has shown antitumoreffects on human hepatocarcinoma BEL-7402 in vitro and in vivo. In this study, we evaluated the inhibition of YSL on invasion andadhesion of the mouse B16-F10 melanoma cell line by injecting B16-F10 cells into the tail veins of C57BL/6 mice to establish an ex-perimental lung metastasis model. YSL inhibited B16-F10 cell metastasis to lung, reducing the number and area of metastasis le-sions. When we treated B16-F10 cells with YSL (0.01, 0.1, 1, 10,or 100 μg/mL) in vitro, we found that YSL inhibited the proliferationof B16-F10 cells with a 28.11% rate of inhibition. YSL significantly decreased the adhesiveness of B16-F10 cells to Matrigel with a29.15% inhibition rate; YSL also significantly inhibited the invasion of B16-F10 cells, producing an inhibition of 35.31%. By analyseswith Western blot and real-time RT-PCR, we found that YSL markedly inhibited the expression of ICAM-1 in B16-F10 cells. These datasuggest that YSL inhibits the growth, invasion, and adhesion of B16-F10 cells.

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Posted by Leah Caracappa on Jan 2, 2007 12:00 AM CST
Tih-Shih Lee, Shrikant Mane, Tore Eid, Hongyu Zhao, Aiping Lin, Zhong Guan, Jung H Kim, Jeffrey Schweitzer, David King-Stevens, Peter Weber, Susan S Spencer, Dennis D Spencer, and Nihal C de Lanerolle

Patients with temporal lobe epilepsy (TLE) often exhibit a neuropathological condition referred to as “hippocampal sclerosis” or “Ammon’s horn sclerosis” which is characterized by hippocampal atrophy, induration, distinctive neuronal loss and astroglial proliferation.  Despite extensive neuropathological investigations, the precise role of the sclerotic hippocampus in the causation and maintenance of seizures in TLE has yet to be defined.  In order to gain new insight on the role of sclerosis in the pathophysiology of TLE, Lee et al. (1-13) examined the gene expression profile of sclerotic and non-sclerotic hippocampi surgically removed from TLE patients.  The differentially expressed gene set in sclerotic hippocampi revealed an increased expression of genes associated with molecular signaling pathways, in particular those associated with astrocytes.  The results from this study provide an integrative framework and form the basis for future experimental exploration of the pathophysiolgoy of TLE. 

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Posted by Leah Caracappa on Jan 1, 2007 12:00 AM CST
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