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Present Therapies (present + therapy)
Selected AbstractsROLE OF MACROPHAGES IN COMPLICATIONS OF TYPE 2 DIABETESCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2007GH TeschArticle first published online: 15 AUG 200 SUMMARY 1Macrophage accumulation is a feature of Type 2 diabetes and is associated with the development of diabetic complications (nephropathy, atherosclerosis, neuropathy and retinopathy). The present article reviews the current evidence that macrophages contribute to the complications of Type 2 diabetes. 2Macrophage-depletion studies in rodent models have demonstrated a causal role for macrophages in the development of diabetic complications. 3Components of the diabetic milieu (high glucose, advanced glycation end-products and oxidized low-density lipoprotein) promote macrophage accumulation (via induction of chemokines and adhesion molecules) and macrophage activation within diabetic tissues. 4Macrophages mediate diabetic injury through a variety of mechanisms, including production of reactive oxygen species, cytokines and proteases, which result in tissue damage leading to sclerosis. 5A number of existing and experimental therapies can indirectly reduce macrophage-mediated injury in diabetic complications. The present article discusses the use of these therapies, given alone and in combination, in suppressing macrophage accumulation and activity. 6In conclusion, current evidence supports a critical role for macrophages in the evolution of diabetic complications. Present therapies are limited in slowing the progression of macrophage-mediated injury. Novel strategies that are more specific at targeting macrophages may provide better protection against the development of Type 2 diabetic complications. [source] The theoretical basis of cancer-stem-cell-based therapeutics of cancer: can it be put into practice?BIOESSAYS, Issue 12 2007Isidro Sánchez-García In spite of the advances in our knowledge of cancer biology, most cancers remain not curable with present therapies. Current treatments consider cancer as resulting from uncontrolled proliferation and are non-specific. Although they can reduce tumour burden, relapse occurs in most cases. This was long attributed to incomplete tumour elimination, but recent developments indicate that different types of cells contribute to the tumour structure, and that the tumour's cellular organization would be analogous to that of a normal tissue, with a main mass of differentiating cells sensitive to anti proliferative agents, together with a small percentage of quiescent, resistant stem cells responsible for replenishing the tumour: the Cancer Stem Cells (CSCs). Anti-CSCs targeted therapeutic agents would prevent tumour regeneration. New mouse models tailored to exploit this novel concept will be critical to develop CSC-based anti-cancer therapies. Here we review the biological basis and the therapeutic implications of the stem-cell model of cancer. BioEssays 29:1269,1280, 2007. © 2007 Wiley Periodicals, Inc. [source] Cancer stem cells and chemoradiation resistanceCANCER SCIENCE, Issue 10 2008Hideshi Ishii Cancer is a disease of genetic and epigenetic alterations, which are emphasized as the central mechanisms of tumor progression in the multistepwise model. Discovery of rare subpopulations of cancer stem cells (CSCs) has created a new focus in cancer research. The heterogeneity of tumors can be explained with the help of CSCs supported by antiapoptotic signaling. CSCs mimic normal adult stem cells by demonstrating resistance to toxic injuries and chemoradiation therapy. Moreover, they might be responsible for tumor relapse following apparent beneficial treatments. Compared with hematopoietic malignancies, conventional therapy regimes in solid tumors have improved the overall survival marginally, illustrating the profound impact of treatment resistance. This implies that the present therapies, which follow total elimination of rapidly dividing and differentiated tumor cells, need to be modified to target CSCs that repopulate the tumor. In this review article, we report on recent findings regarding the involvement of CSCs in chemoradiation resistance and provide new insights into their therapeutic implications in cancer. (Cancer Sci 2008; 99: 1871,1877) [source] Fenestration of the superior medullary velum as treatment for a trapped fourth ventricle: A feasibility studyCLINICAL ANATOMY, Issue 2 2004R. Shane Tubbs Abstract We developed a novel approach for fenestration of the trapped fourth ventricle utilizing the superior medullary velum (valve of Vieussens). Trapped fourth ventricles, which are seen often in the pediatric hydrocephalic population, are troublesome entities surgically. A right burr hole was carried out in 10 adult cadavers with no gross intracranial pathology and the superior medullary velum was fenestrated to the quadrigeminal cistern with the aid of an endoscope. This technique was carried out easily in all cadaveric specimens. With endoscopy, no vascular insult was appreciated either before or after fenestration of the superior medullary velum. These preliminary findings demonstrate that fenestration of the superior medullary velum may provide a good alternative to the present therapy of shunting trapped fourth ventricles, a therapy wrought with complications. Clin. Anat. 17:82,87, 2004. © 2004 Wiley-Liss, Inc. [source] | |||||||||||||