Acne Scars

Plast Reconstr Surg. 2009 Jul; 124(1): 102-13Chin MS, Lancerotto L, Helm DL, Dastouri P, Prsa MJ, Ottensmeyer M, Akaishi S, Orgill DP, Ogawa RBACKGROUND: Mechanical forces modulate wound healing and scar formation through mechanotransduction. In response to mechanical stimulation, neuropeptides are released from peripheral terminals of primary afferent sensory neurons, influencing skin and immune cell functions and increasing vascular permeability, causing neurogenic inflammation. METHODS: A computer-controlled device was used to stretch murine skin. C57Bl6 mice (n = 26) were assigned to a cyclical square-wave tensile stimulation for 4 hours or continuous stimulation for 4 hours. Stretched skin was analyzed for expression of the neuropeptides, substance P and calcitonin gene-related peptide, their receptors (NK1R and calcitonin gene-related peptide receptor component protein), and growth factors (nerve growth factor, transforming growth factor beta1, vascular endothelial growth factor, and epidermal growth factor) using immunohistochemistry and real-time reverse-transcriptase polymerase chain reaction. RESULTS: Cyclical stimulation resulted in a significant increase in expression of neuropeptides and growth factors, whereas the corresponding peptide receptors were down-regulated. Transcription of neuropeptide mRNA was elevated in stretched skin, which proves that neuropeptides are released from not only peripheral terminals of nerve fibers but also resident skin cells. CONCLUSIONS: The authors' results suggest that skin stretching may alter cell physiology by stimulating neuropeptide expression, and that cyclical mechanical force may be more effectively stimulating mechanosensitive nociceptors or mechanoreceptors (mechanosensors) on cells.

Fibrogenesis Tissue Repair. 2009 Jun 26; 2(1): 3Romagnani P, Kalluri RABSTRACT: In most adult epithelia the process of replacing damaged or dead cells is maintained through the presence of stem/progenitor cells, which allow epithelial tissues to be repaired following injury. Existing evidence strongly supports the presence of stem cells in the adult kidney. Indeed, recent findings provide evidence in favour of a role for intrinsic renal stem cells and against a physiological role for bone marrow-derived stem cells in the regeneration of renal epithelial cells. In addition, recent studies have identified a subset of CD24+CD133+ renal progenitors within the Bowman's capsule of adult human kidney, which provides regenerative potential for injured renal epithelial cells. Intriguingly, CD24+CD133+ renal progenitors also represent common progenitors of tubular cells and podocytes during renal development. Chronic injury causes dysfunction of the tubular epithelial cells, which triggers the release of fibrogenic cytokines and recruitment of inflammatory cells to injured kidneys. The rapid interposition of scar tissue probably confers a survival advantage by preventing infectious microorganisms from invading the wound, but prevents subsequent tissue regeneration. However, the existence of renal epithelial progenitors in the kidney suggests a possible explanation for the regression of renal lesions which has been observed in experimental animals and even in humans. Thus, manipulation of the wound repair process in order to shift it towards regeneration will probably require the ability to slow the rapid fibrotic response so that renal progenitor cells can allow tissue regeneration rather than scar formation.

J Cardiovasc Electrophysiol. 2009 Jun 26; Wijnmaalen AP, Schalij MJ, Bootsma M, Kies P, DE Roos A, Putter H, Bax JJ, Zeppenfeld KOutcome in Scar-Related RV Tachycardia. Introduction: Patients with established arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) based on task force (TF) criteria and ventricular tachycardia (VT) are at risk of VT recurrence and sudden death. Data on patients with VT due to right ventricular (RV) scar not fulfilling TF criteria are lacking. The purpose of this study was to assess the long-term arrhythmia recurrence rate and outcome in patients with scar-related right VT with and without a diagnosis of ARVC/D. Methods: Sixty-four patients (age 43.5 +/- 15 years, 49 males) presenting with nonischemic scar-related VT of RV origin were studied. Scar was identified by electroanatomical mapping, contrast echocardiography, and/or magnetic resonance imaging (MRI). Patients were evaluated and treated according to a standard institute protocol. Results: Twenty-nine (45%) patients were diagnosed with ARVC/D according to TF criteria (TF+) and 35 (55%) with RV scar of undetermined origin (TF-) at the end of follow-up (64 +/- 42 months). Patients were treated with antiarrhythmic drugs, radiofrequency catheter ablation, and/or implantable cardioverter-defibrillator (ICD) implantation. VT recurrence-free survival for TF+ and TF- was 76% versus 74% at 1 year and 45% versus 50% at 4 years (P = ns). Patients with fast index VT (cycle length [CL] 250 ms, n = 33) (61% vs 3%, P < 0.001). Conclusions: Scar-related RV VTs have a high recurrence rate in TF+ and TF- patients. Patients presenting with a fast index VT are at high risk for fast VT recurrence and may benefit most from ICD therapy.