Database : MEDLINE Search on : skin [Words] References found : 557797 [refine] Displaying: 1 .. 10   in format [Detailed]

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[PMID]: 23646945 [Au] Autor: Jared SR; Rao JP [Ad] Address: 1 Department of Physiology, Christian Medical College, Vellore - 632002, Tamilnadu, India. [Ti] Title: Effects of Evans Blue and Amiloride on Anti-Diuretic Hormone (ADH)-Induced Sodium Transport Across Frog (Rana hexadactyla) Skin. [So] Source: Zoolog Sci;30(5):402-7, 2013 May. [Is] ISSN: 0289-0003 [Cp] Country of publication: Japan [La] Language: eng [Ab] Abstract: The epithelial sodium channel (ENaC) has four subunits, namely α (alpha), ß (beta), γ (gamma) and δ (delta). The functional ENaC is formed by the combination of either αßγ or δßγ subunits. The aim of the present study is to determine the combination of ENaC subunits predominant on the apical side of the frog skin, and the effect of ADH on sodium transport though these two ENaCs subunit combinations. The ventral abdominal skin of the frog, Rana hexadactyla was mounted in an Ussing-type chamber. The voltage-clamp method was performed to measure the ionic transport across the frog skin with normal Ringer solution (NR) on both sides. Evans blue (300 µM) and amiloride (100 µM) were added to the NR on the apical side and ADH (40 nM) was added on the serosal side. Statistical significance was analyzed by Student's paired t-test and repeated-measures ANOVA, P < 0.05 was considered significant. This study suggests that the ENaC of the frog skin consist of both αßγ and δßγ subunit combinations on the apical side. Though both types of subunit combination are present, the αßγ type was found to be more common than δßγ. ADH increases the sodium transport across the frog skin. The effect of ADH on sodium transport is achieved through the combination of δ-subunits, not through the combination of a-subunits in the skin of Pana hexadactyla. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.2108/zsj.30.402

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[PMID]: 23627672 [Au] Autor: Selig HF; Keck M; Lumenta DB; Mittlböck M; Kamolz LP [Ad] Address: Vienna Burn Center, Division of Plastic and Reconstructive Surgery, Department of Surgery, Medical University of Vienna, Vienna, Austria; Division of Plastic, Aesthetic and Reconstructive Surgery, Department of Surgery, Medical University Graz, Graz, Austria; Department of Hand, Plastic and Reconstructive Surgery with Burn Unit, Eberhard-Karls-University of Tuebingen, BG Trauma Center Tuebingen, Tuebingen, Germany. [Ti] Title: The use of a polylactide-based copolymer as a temporary skin substitute in deep dermal burns: 1-year follow-up results of a prospective clinical noninferiority trial. [So] Source: Wound Repair Regen;21(3):402-9, 2013 May. [Is] ISSN: 1524-475X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Deep dermal burns can be covered with different kind of materials and techniques; one of them is a polylactide-based temporary skin substitute. The aim of this study was to intraindividually compare its 1-year outcome with the results obtained by use of autologous skin grafts in patients suffering from deep dermal burns. A prospective noninferiority trial was designed in order to assess skin quality and scar formation by use of subjective (Vancouver Scar Scale; Patient and Observer Scar Assessment Scale) and objective (noninvasive cutometry) burn scar assessment tools. All items of the Patient and Observer Scar Assessment Scale, except vascularity, were found to be noninferior in the areas covered with the temporary skin substitute vs. autologous skin. Results of objective scar evaluation showed comparable viscoelastic parameters without reaching noninferiority. Overall, the outcome of deep dermal burns covered with a polylactide-based temporary skin substitute revealed satisfactory results in terms of scar formation and skin quality as compared with autologous skin. This paper supports its use in deep dermal burns, where autologous skin donor sites require either to be reserved for coverage of full-thickness skin defects in severe burns or to be saved for reduction of additional morbidity in selected patient collectives. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1111/wrr.12050

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[PMID]: 23627585 [Au] Autor: Ding J; Ma Z; Shankowsky HA; Medina A; Tredget EE [Ad] Address: Wound Healing Research Group, Division of Plastic and Reconstructive Surgery. [Ti] Title: Deep dermal fibroblast profibrotic characteristics are enhanced by bone marrow-derived mesenchymal stem cells. [So] Source: Wound Repair Regen;21(3):448-55, 2013 May. [Is] ISSN: 1524-475X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Hypertrophic scars are a significant fibroproliferative disorder complicating deep injuries to the skin. We hypothesize that activated deep dermal fibroblasts are subject to regulation by bone marrow-derived mesenchymal stem cells (BM-MSCs), which leads to the development of excessive fibrosis following deep dermal injury. We found that the expression of fibrotic factors was higher in deep burn wounds compared with superficial burn wounds collected from burn patients with varying depth of skin injury. We characterized deep and superficial dermal fibroblasts, which were cultured from the deep and superficial dermal layers of normal uninjured skin obtained from abdominoplasty patients, and examined the paracrine effects of BM-MSCs on the fibrotic activities of the cells. In vitro, deep dermal fibroblasts were found higher in the messenger RNA (mRNA) levels of type 1 collagen, alpha smooth muscle actin, transforming growth factor beta, stromal cell-derived factor 1, and tissue inhibitor of metalloproteinase 1, an inhibitor of collagenase (matrix metalloproteinase 1). As well, deep dermal fibroblasts had low matrix metalloproteinase 1 mRNA, produced more collagen, and contracted collagen lattices significantly greater than superficial fibroblasts. By co-culturing layered fibroblasts with BM-MSCs in a transwell insert system, BM-MSCs enhanced the fibrotic behavior of deep dermal fibroblasts, which suggests a possible involvement of BM-MSCs in the pathogenesis of hypertrophic scarring. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1111/wrr.12046

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[PMID]: 23627548 [Au] Autor: Musyoka JN; Liu MC; Pouniotis DS; Wong CS; Bowtell DD; Little PJ; Getachew R; Möller A; Darby IA [Ad] Address: Health Innovations Research Institute, School of Medical Sciences, RMIT University, Bundoora. [Ti] Title: Siah2-deficient mice show impaired skin wound repair. [So] Source: Wound Repair Regen;21(3):437-47, 2013 May. [Is] ISSN: 1524-475X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Hypoxia is associated with the dermal wound healing process and hypoxia signaling is presumed to be crucial for normal wound repair. The Siah2 ubiquitin ligase controls the abundance of hypoxia-inducible factor-1 alpha, and loss of Siah2 results in destabilization of hypoxia-inducible factor-1 alpha under hypoxia. Utilizing Siah2(-/-) mice we demonstrate that cutaneous wound healing is impaired in these mice. Wounds in Siah2(-/-) mice heal slower and are associated with delayed induction of myofibroblast infiltration and reduced collagen deposition. This coincides with delayed angiogenesis and reduced macrophage infiltration into the wounds of Siah2(-/-) mice. We furthermore demonstrate that primary Siah2(-/-) dermal fibroblasts have reduced migratory capacities and produce less collagen than wild-type fibroblasts. Additionally, Siah2(-/-) fibroblasts showed conserved responses to transforming growth factor-ß at the receptor level (pSmad 2C activation) but reduced responses downstream. Together, our data show, for the first time, that Siah2 is involved as a positive regulator in the wound healing response. Understanding the role of hypoxia signaling in tissue repair and fibrosis and interference with the hypoxia signaling pathway via regulation of Siah2 may provide new targets for clinical regulation of fibrosis and scarring. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1111/wrr.12045

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[PMID]: 23627460 [Au] Autor: Kieran I; Knock A; Bush J; So K; Metcalfe A; Hobson R; Mason T; O'Kane S; Ferguson M [Ad] Address: Clinical Trials Unit, Renovo Ltd, Manchester, UK. [Ti] Title: Interleukin-10 reduces scar formation in both animal and human cutaneous wounds: Results of two preclinical and phase II randomized control studies. [So] Source: Wound Repair Regen;21(3):428-36, 2013 May. [Is] ISSN: 1524-475X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Cutaneous scarring affects up to 100 million people per annum. There is no effective scar reducing/preventing therapeutic developed to date. Interleukin (IL)-10 is an anti-inflammatory and antifibrotic cytokine. In the embryo it is important for scarless wound repair. We investigated the effect on wound healing and scarring of a double deletion of the IL-10 and IL-4 genes in a knockout (KO) mouse model, and also the effect of exogenous addition of recombinant human (rh) IL-10 into rat and human cutaneous incisions. Mouse study: Two incisions were made on the dorsal skin of 20 double IL-4/IL-10 KO mice and 20 wild-type (WT) controls. Rat study: Three concentrations of rhIL-10 were investigated. Four incisions were made on the dorsal skin of 30 rats. Each rat received two concentrations. Each incision receiving a concentration of rhIL-10 was matched with a control incision, which received either placebo or standard care. Human study: Eight concentrations of rhIL-10 were investigated. Four incisions were made on each arm of 175 healthy volunteers. Four incisions received four different concentrations, which were matched with four control incisions that received either standard care or placebo. KO mice healed with poor scar histology and increased inflammation. rhIL-10-treated rat incisions healed with decreased inflammation, better scar histology, and better macroscopic scar appearance. rhIL-10-treated human incisions at low concentrations healed with better macroscopic scar appearance and less red scars. IL-10 is an important cytokine in wound healing and its suppression of inflammation and scarring is demonstrated in mice and rats with a translational effect in humans. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1111/wrr.12043

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[PMID]: 23627416 [Au] Autor: Otranto M; Nascimento AP; Monte-Alto-Costa A [Ad] Address: Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. [Ti] Title: Insulin resistance impairs cutaneous wound healing in mice. [So] Source: Wound Repair Regen;21(3):464-72, 2013 May. [Is] ISSN: 1524-475X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Obesity is associated with significant changes in skin combined with metabolic alterations such as insulin resistance. Our aim was to investigate the effects of insulin resistance induced by a high-fat diet on cutaneous wound healing. Male C57BL/6 mice were fed standard chow (SC group) or high-fat chow (HFC group) for 30 weeks. On day 0 (28th week), an excisional wound was performed. After 14 days (30th week), the mice were euthanized. Starting from the 8th week, the HFC group had a higher body weight. The HFC group became intolerant to glucose, resistant to insulin, and presented increased plasma cholesterol and triglyceride levels. The wound area was greater in the HFC group. The inflammatory infiltrate and the amount of "fibroblast-like" cells increased in superficial regions of the lesions in the HFC group. The collagen fibers were more organized and denser in the SC group. Hydroxyproline levels were lower in the HFC group. The nitric oxide synthase-2-positive cells were higher in the HFC group. Lipid peroxidation and protein carbonyl levels were higher in the HFC group. The expression levels of alpha-smooth muscle actin and transforming growth factor-ß were higher in the HFC group. These findings support the hypothesis that insulin resistance leads to delayed cutaneous wound healing. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1111/wrr.12042

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[PMID]: 23531093 [Au] Autor: Serra R; Buffone G; Falcone D; Molinari V; Scaramuzzino M; Gallelli L; de Franciscis S [Ad] Address: Department of Medical and Surgical Science, School of Medicine, University Magna Gracia of Catanzaro, Catanzaro, Italy. [Ti] Title: Chronic venous leg ulcers are associated with high levels of metalloproteinases-9 and neutrophil gelatinase-associated lipocalin. [So] Source: Wound Repair Regen;21(3):395-401, 2013 May. [Is] ISSN: 1524-475X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Venous ulcers are related to dysfunctions in extracellular matrix. Both matrix metalloproteinases (MMP) and neutrophil gelatinase-associated lipocalin (NGAL) could play a role in the healing process in patients with chronic venous ulcers. We evaluated the role of MMP-9 and NGAL in the healing process in venous ulceration. We performed an open-label, parallel groups, single clinical center study. Patients with chronic venous leg ulcers represented the test group (Group I), whereas patients without chronic ulcers represented the control group (Group II). In Group I plasma and wound fluid samples were collected at the time of admission, at the time of the surgery, and at the follow-up, while ulcer tissues were taken at the time of the surgery. In Group II, plasma and wound fluid were collected at admission and at the time of the surgery, whereas skin tissues were collected at the time of the surgery. Enzyme-linked immunosorbent assay test was used to evaluate the levels of MMP-9 and NGAL in plasma and wound fluid, whereas Western blot analysis was performed to estimate the expression of MMP-9 and NGAL in tissues. Enzyme-linked immunosorbent assay tests revealed significantly higher levels of MMP-9 and NGAL in both plasma and wound fluid of patients with ulcers compared to patients without ulcers (p < 0.01). Moreover, Western blot analysis documented an increased expression of MMP-9 and NGAL in biopsy tissue of patients with ulcers compared to patients without ulcers (p < 0.01). In conclusion MMP-9 and NGAL may correlate with the clinical course of venous ulcers. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1111/wrr.12035

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[PMID]: 23264185 [Au] Autor: Lin CL; Fu YS; Hsiao TH; Hsieh YL [Ad] Address: Department of Neurosurgery, Kaohsiung Medical University Hospital, Kaohsiung, 80708, Taiwan. [Ti] Title: Enhancement of purinergic signalling by excessive endogenous ATP in resiniferatoxin (RTX) neuropathy. [So] Source: Purinergic Signal;9(2):249-57, 2013 Jun. [Is] ISSN: 1573-9546 [Cp] Country of publication: Netherlands [La] Language: eng [Ab] Abstract: ATP is a ligand of P2X family purinoceptors, and exogenous ATP administration evokes pain behaviors. To date, there is a lack of systematic studies to address relationships between endogenous ATP and neuropathic pain. In this report, we took advantage of a mouse model of resiniferatoxin (RTX)-induced neuropathic pain to address the role of endogenous ATP in neuropathic pain. After RTX administration, endogenous ATP markedly increased in dorsal root ganglia (DRGs) (p < 0.01) and skin tissues (p < 0.001). The excessive endogenous ATP was removed by apyrase, an ATP hydrolyzing enzyme, administration via either a lumbar puncture route (p < 0.001) or an intraplantar injection (p < 0.001), which led to the normalization of neuropathic pain. In addition, intraplantar treatment with apyrase caused mechanical analgesia. Linear analyses showed that the densities of P2X3(+) neurons (r = -0.72, p < 0.0001) and P2X3(+) dermal nerves (r = -0.72, p < 0.0001) were inversely correlated with mechanical thresholds. Moreover, the contents of endogenous ATP in skin tissues were linearly correlated with P2X3(+) dermal nerves (r = 0.80, p < 0.0001) and mechanical thresholds (r = -0.80, p < 0.0001). In summary, this study demonstrated that enhanced purinergic signalling due to an increase in endogenous ATP after RTX-induced nerve injury contributed to the development of neuropathic pain. The data in this report provide a new therapeutic strategy for pain control by targeting the endogenous ligand of purinergic signalling. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1007/s11302-012-9347-y

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[PMID]: 23474133 [Au] Autor: Anders D; Gompper B; Kräuchi K [Ad] Address: Thermophysiological Chronobiology, Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Switzerland. [Ti] Title: A two-night comparison in the sleep laboratory as a tool to challenge the relationship between sleep initiation, cardiophysiological and thermoregulatory changes in women with difficulties initiating sleep and thermal discomfort. [So] Source: Physiol Behav;114-115:77-82, 2013 Apr 10. [Is] ISSN: 1873-507X [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: Cardiovascular and thermophysiological changes accompany the decision to fall asleep. A relationship between core body temperature and heart rate variability (HRV) especially during the sleep onset episode is suggested, but only few data are available, investigating a relationship between skin temperature and HRV at this time span. This study was aimed to elucidate the pattern of body temperature (i.e. distal and proximal skin temperature), heart rate and its variability in a specific population of ten healthy women having both, thermal discomfort from cold extremities and difficulties initiating sleep for two subsequent nights in the laboratory. Furthermore, changes in sleep, temperature or cardiac regulation were examined after 16-h of constant posture conditions. Due to a faster decline of arousals, the build-up of sleep stage 2, slow wave sleep and hence delta power is promoted in the second night compared to the first. Both, proximal and distal skin temperatures show an increase after lights out. Distal skin temperature around lights out is already higher during the second night. Proximal skin temperature starts at the same temperature level for both nights but was significantly reduced in the second hour after lights out during the second night. The distal-proximal skin temperature gradient (DPG), as a measure for distal dilatation of the skin vasculature, starts with a lower level after lights out in the first night, compared to the second. Different dynamics and differences between the two nights in skin temperature or sleep variables, but not in heart rate and HRV variables were found during the sleep initiation episode. Thus, a direct causality between these functions seems rather unlikely in the present study sample. The described differences between both nights might occur from delayed relaxation, reflected in a slower decrease of arousals, prolonged sleep onset latency and a lower DPG at the first night. Especially the latter finding confirms nicely the statement that warm extremities promote a rapid onset of sleep. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review

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[PMID]: 23650524 [Au] Autor: Seppanen E; Roy E; Ellis R; Bou-Gharios G; Fisk NM; Khosrotehrani K [Ad] Address: The University of Queensland, UQ Centre for Clinical Research, Herston Campus, Brisbane, Australia. [Ti] Title: Distant mesenchymal progenitors contribute to skin wound healing and produce collagen: evidence from a murine fetal microchimerism model. [So] Source: PLoS One;8(5):e62662, 2013. [Is] ISSN: 1932-6203 [Cp] Country of publication: United States [La] Language: eng [Ab] Abstract: The contribution of distant and/or bone marrow-derived endogenous mesenchymal stem cells (MSC) to skin wounds is controversial. Bone marrow transplantation experiments employed to address this have been largely confounded by radiation-resistant host-derived MSC populations. Gestationally-acquired fetal MSC are known to engraft in maternal bone marrow in all pregnancies and persist for decades. These fetal cells home to damaged maternal tissues, mirroring endogenous stem cell behavior. We used fetal microchimerism as a tool to investigate the natural homing and engraftment of distant MSC to skin wounds. Post-partum wild-type mothers that had delivered transgenic pups expressing luciferase under the collagen type I-promoter were wounded. In vivo bioluminescence imaging (BLI) was then used to track recruitment of fetal cells expressing this mesenchymal marker over 14 days of healing. Fetal cells were detected in 9/43 animals using BLI (Fisher exact p = 0.01 versus 1/43 controls). These collagen type I-expressing fetal cells were specifically recruited to maternal wounds in the initial phases of healing, peaking on day 1 (n = 43, p<0.01). This was confirmed by detection of Y-chromosome+ve fetal cells that displayed fibroblast-like morphology. Histological analyses of day 7 wounds revealed vimentin-expressing fetal cells in dermal tissue. Our results demonstrate the participation of distant mesenchymal cells in skin wounds. These data imply that endogenous MSC populations are likely recruited from bone marrow to wounds to participate in healing. [Pt] Publication type: JOURNAL ARTICLE [Em] Entry month: 1305 [Js] Journal subset: IM [St] Status: In-Data-Review [do] DOI: 10.1371/journal.pone.0062662

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