Use of Integra and interval brachytherapy in a 2-stage auricular reconstruction after excision of a recurrent keloid.

Keloids present a formidable clinical challenge. Surgical excision in conjunction with radiation therapy may decrease the chance of keloid recurrence. Split-thickness skin grafts, however, are more prone to failure in the setting of radiation.

Therapeutic delivery of hydrogen sulfide for salvage of ischemic skeletal muscle after the onset of critical ischemia.

Background: Recent evidence suggests that hydrogen sulfide is capable of mitigating the degree of cellular damage associated with ischemia-reperfusion injury (IRI).

Methods: This study evaluated the potential utility of hydrogen sulfide in preventing IRI in skeletal muscle by using in vitro (cultured myotubes subjected to sequential hypoxia and normoxia) and in vivo (mouse hind limb ischemia, followed by reperfusion) models to determine whether intravenous hydrogen sulfide delivered after the ischemic event had occurred (pharmacologic postconditioning) conferred protection against IRI. Injury score and apoptotic index were determined by analysis of specimens stained with hematoxylin and eosin and terminal deoxynucleotide transferase-mediated deoxy-uridine triphosphate nick-end labeling, respectively.

Disruption of the mitochondrial thioredoxin system as a cell death mechanism of cationic triphenylmethanes.

Alterations in mitochondrial structure and function are a hallmark of cancer cells compared to normal cells and thus targeting mitochondria has emerged as an novel approach to cancer therapy. The mitochondrial thioredoxin 2 (Trx2) system is critical for cell viability, but its role in cancer biology is not well understood. Recently some cationic triphenylmethanes such as brilliant green (BG) and gentian violet were shown to have antitumor and antiangiogenic activity with unknown mechanisms.

Hydrogen sulfide attenuates intestinal ischemia-reperfusion injury when delivered in the post-ischemic period.

Background And Aim: To investigate whether pharmacologic post-conditioning of intestinal tissue with hydrogen sulfide (HS) protects against ischemia reperfusion injury (IRI).

Methods: In vitro, enterocytes were made hypoxic for 1, 2, or 3 h, treated with media containing between 0 and 100 µM HS 20 min prior to the end of the hypoxic period, then returned to normoxia for 3 h. An apoptotic index (AI) was determined for each time point and (HS).

Development of an acellular bioengineered matrix with a dominant vascular pedicle.

Background: This study assessed the feasibility of creating a tissue engineering platform by decellularization of fasciocutaneous tissue.

Materials And Methods: A fasciocutaneous flap based upon the superficial inferior epigastric artery was harvested from the abdominal wall of 8-wk-old male Sprague-Dawley rats. All cellular components were removed by sequential treatment with sodium azide, DNAse, and sodium deoxycholate.

A portable high-intensity focused ultrasound device for noninvasive venous ablation.

Background: Varicose veins and other vascular abnormalities are common clinical entities. Treatment options include vein stripping, sclerotherapy, and endovenous laser treatment, but all involve some degree of invasive intervention. The purpose of this study was to determine ex vivo the effectiveness of a novel hand-held, battery-operated, high-intensity focused ultrasound (HIFU) device for transcutaneous venous ablation.

Fulvene-5 potently inhibits NADPH oxidase 4 and blocks the growth of endothelial tumors in mice.

Hemangiomas are the most common type of tumor in infants. As they are endothelial cell-derived neoplasias, their growth can be regulated by the autocrine-acting Tie2 ligand angiopoietin 2 (Ang2). Using an experimental model of human hemangiomas, in which polyoma middle T-transformed brain endothelial (bEnd) cells are grafted subcutaneously into nude mice, we compared hemangioma growth originating from bEnd cells derived from wild-type, Ang2+/-, and Ang2-/- mice.

Tris (dibenzylideneacetone) dipalladium, a N-myristoyltransferase-1 inhibitor, is effective against melanoma growth in vitro and in vivo.

Purpose: Melanoma is a solid tumor that is notoriously resistant to chemotherapy, and its incidence is rapidly increasing. Recently, several signaling pathways have been shown to contribute to melanoma tumorigenesis, including constitutive activation of mitogen-activated protein kinase, Akt, and Stat-3. The activation of multiple pathways may account in part for the difficulty in treatment of melanoma.

AKT1 overexpression in endothelial cells leads to the development of cutaneous vascular malformations in vivo.

Background: Vascular malformations are clinical disorders in which endothelial cells fail to remodel and/or undergo programmed cell death, leading to abnormal persistence of blood vessels. The abnormal persistence of vessels makes therapy difficult because these lesions are resistant to interventions that are effective against hemangiomas. Akt1 is a serine-threonine protein kinase, which is a key mediator of resistance to programmed cell death.

Pharmacologic blockade of angiopoietin-2 is efficacious against model hemangiomas in mice.

Hemangioma of infancy is the most common neoplasm of childhood. While hemangiomas are classic examples of angiogenesis, the angiogenic factors responsible for hemangiomas are not fully understood. Previously, we demonstrated that malignant endothelial tumors arise in the setting of autocrine loops involving vascular endothelial growth factor (VEGF) and its major mitogenic receptor vascular endothelial growth factor receptor 2.