Measurements of scar properties by SkinFibroMeter® , SkinGlossMeter® , and Mexameter® and comparison with Vancouver Scar Scale.

BACKGROUND: An objective measurement of scar is important for evaluating treatment outcomes. However, to date, there is no 'gold standard' for quantitative measurement of properties of hypertrophic scar. Existing objective modalities are neither portable nor easy to use. OBJECTIVE: This study aims to validate the correlation between objective measurements with SkinFibrometer® , SkinGlossMeter® , and Mexameter® and subjective assessment with Vancouver Scar Scale (VSS) of keloid and hypertrophic scar. METHODS: A total of 25 patients with keloids and hypertrophic scars were enrolled in this study. Patients were treated with intralesional triamcinolone acetonide at 2-6 week intervals. Scar assessments using VSS, Skinfibrometer, Skinglossmeter, and Mexameter were performed in both scars and contralateral normal skin at each treatment session. Correlations between the measurements by these tools and VSS parameters were examined. RESULTS: We found statistically significant differences between scar and contralateral normal skin using Skinfibrometer, Skinglossmeter, and Mexameter. A strong correlation was found between the VSS pliability scores and the stiffness of skin of Skinfibrometer (r = 0.628, P < 0.001). VSS vascularity scores showed weak correlation with erythema index of Mexameter (r = 0.372, P < 0.001). However, no correlation appeared to exist between any parameters of VSS and Skinglossmeter and between VSS pigmentation scores and the melanin index of Mexameter. CONCLUSION: In our study, Skinfibrometer can be an objective noninvasive evaluation tool for pliability of the scar.

A ß-cyclodextrin, polyethyleneimine and silk fibroin hydrogel containing Centella asiatica extract and hydrocortisone acetate: releasing properties and in vivo efficacy for healing of pressure sores.

BACKGROUND: Pressure sores are lesions caused by impaired blood flow. Conventional dressings can absorb exudates, but do not promote wound healing. A hydrogel composed of ß-cyclodextrin (ß-CD), polyethyleneimine (PEI) and silk fibroin (SF) was assessed for use in healing of pressure sores. METHODS: The hydrogel was prepared by crosslinking ß-CD-grafted PEI and SF using epichlorohydrin. The gel was then immersed in an aqueous solution of Centella asiatica extract (CAE) 0.7 mg/mL and/or hydrocortisone acetate (HCA) 0.5 mg/mL. The in vivo pressure sore-healing efficacy of the dry gel (with or without the drugs) was investigated in terms of the hyperplasia of epidermis and the number of neutrophils in the skin tissue. RESULTS: The specific loading of CAE was 0.0091 g/g of dry gel. The percentage of CAE released at 24 h at pH 3.0, 5.0 and 7.4 was approximately 63.9%, 55.0% and 44.4%, respectively. This pH-dependent release is possibly due to the degree of gel swelling, which decreased with increasing pH. The specific loading of HCA was 0.0050 g/g dry gel, and the percentage release of HCA at 24 h was around 20% at all three pH points. It is likely that HCA release is independent of pH. HCA is a hydrophobic compound, and therefore the release of HCA is affected by the partitioning of HCA between the ß-CD cavity and the bulk water phase, but not by the degree of swelling of the hydrogel. The pressure sores treated with the hydrogel healed in 6 days, compared with 10 days for controls. CONCLUSIONS: In this study, a ß-CD/PEI/SF hydrogel containing CAE and HCA reduced the healing time for pressure sores.

Successful treatment using cyclosporine in a patient with rhupus complicated by aplastic anemia: a case report and review of the literature.

Systemic lupus erythematosus (SLE) co-morbid with rheumatoid arthritis (RA) is known as 'Rhupus syndrome' and is estimated to be present in between 0.01 and 2% of SLE and RA patients. The occurrence of aplastic anaemia in a patient with rhupus is very rare and a treatment for this condition has not been reported. A 52-year-old woman presented complaining of nausea and dizziness during the preceding month. She had been treated for rheumatoid arthritis for 16 years. At the time of presentation, she had a malar rash, multiple arthritis, pancytopenia, pleural effusion, proteinuria, and positive anti-nuclear and anti-dsDNA antibodies. A kidney biopsy revealed ISN/RPS class IV-G (A) lupus nephritis. Bone marrow aspiration and biopsy showed aplastic anaemia with no evidence of viral infection. The patient was successfully treated using cyclosporine and prednisolone and she remained symptom-free at the one-and-a-half-year follow-up. To our knowledge, this is the first report of a successful treatment using cyclosporine in a patient with rhupus complicated by aplastic anaemia.

De novo appearance of primitive neuroectodermal tumor in a patient with systemic lupus erythematosus and moyamoya disease.

Primitive neuroectodermal tumor is a rare brain tumor composed of undifferentiated or poorly differentiated neuroepithelial cells with a high malignant potential that usually occurs in children, and which is only occasionally encountered in adults. A 19-year-old female with systemic lupus erythematosus presented with right hemiparesis and a headache of 10 days duration. Brain magnetic resonance imaging showed a large solid mass with necrotic portions in the left frontoparietal lobe. Primitive neuroectodermal tumor was confirmed by a neuronavigator-guided brain biopsy. This is the first case report of primitive neuroectodermal tumor associated with systemic lupus erythematosus and moyamoya disease. This case demonstrates that brain tumors, such as primitive neuroectodermal tumor, should be included in the differential diagnosis of neurological manifestations in children and adolescent patients with systemic lupus erythematosus.

Zn2+-induced ERK activation mediated by reactive oxygen species causes cell death in differentiated PC12 cells.

Recent studies have provided evidence that Zn2+ plays a crucial role in ischemia- and seizure-induced neuronal death. However, the intracellular signaling pathways involved in Zn2+-induced cell death are largely unknown. In the present study, we investigated the roles of mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinase (JNK), p38 MAPK and extracellular signal-regulated kinase (ERK), and of reactive oxygen species (ROS) in Zn2+-induced cell death using differentiated PC12 cells. Intracellular accumulation of Zn2+ induced by the combined application of pyrithione (5 microM), a Zn2+ ionophore, and Zn2+ (10 microM) caused cell death and activated JNK and ERK, but not p38 MAPK. Preventing JNK activation by the expression of dominant negative SEK1 (SEKAL) did not attenuate Zn2+-induced cell death, whereas the inhibition of ERK with PD98059 and the expression of dominant negative Ras mutant (RasN17) significantly prevented cell death. Inhibition of protein kinase C (PKC) and phosphatidylinositol-3 kinase had little effect on Zn2+-induced ERK activation. Intracellular Zn2+ accumulation resulted in the generation of ROS, and antioxidants prevented both the ERK activation and the cell death induced by Zn2+. Therefore, we conclude that although Zn2+ activates JNK and ERK, only ERK contributes to Zn2+-induced cell death, and that ERK activation is mediated by ROS via the Ras/Raf/MEK/ERK signaling pathway.