We evaluated the diagnostic accuracy of teleconsultations for skin diseases common in the army using a smartphone multimedia messaging service (MMS). Images of skin lesions were obtained from 100 army patients using digital cameras built into smartphones. Three remotely located dermatologists received the dermatology images and associated clinical information via the MMS. The teledermatologists' diagnoses were compared with those obtained from face-to-face examinations. The three most common diagnoses made at the dermatology clinics were eczema, viral warts and fungal infections. The mean diagnostic agreement between face-to-face and teledermatology consultations was 71% (SD 2). The mean kappa coefficient was 0.73 (SD 0.06) for the three most common diagnostic categories. The mean values for sensitivity were 78% (SD 0), 88% (SD 21) and 61% (SD 11) for eczema, viral warts and fungal infections, respectively, and the specificity values were above 90% for these skin diseases. Teledermatology consultation using smartphones is simple. Although diagnoses using telemedicine do not perfectly match diagnoses from face-to-face consultations the diagnostic accuracy using smartphones is superior to that of clinicians who are not specialized in dermatology.
which correlates with the improvement in histopathological measures (Puig et al. 2012; submitted for publication).CPI-17 over-expression was associated with normal phenotype recovery. CPI-17 is one of the major Ser/Thr phosphatase isoforms, and its activation suppresses the MYPT1-PP1d activity resulting in muscle contraction (10). CIP-17 expression is detected in multiple cell types (15-17) involved in several processes (16,18). MYTP1 inhibition results in more prominent focal adhesions and absence of cell migration (19). CPI-17 is directly associated with focal adhesion kinases (20) and located at focal adhesions in fibroblasts and keratinocytes (21). MYPT1-PP1d complex can also regulate the dephosphorylation of retinoblastoma protein (pRb) (22) which shows a deregulated activation in AK. We observed that inflammation modulates CPI-17 expression in CFC. Thus, processes such as DNA damage or ROS production may cause CPI-17 down-deregulation, which could lead to uncontrolled MYPT1-PP1d activity. Deregulated phosphatase activity in CFC may affect cell motility, cell adhesion and cell cycle control mediated by pRb.In conclusion, 1-month Eryf-AK treatment improved the field of cancerization and restored normal phenotype in at least a subset of samples, through CPI-17 up-regulation.
Conflict of interestsThe authors state no conflict of interests. The sponsors had no role in the design and conduct of the study and interpretation of data.
Supporting InformationAdditional Supporting Information may be found in the online version of this article: Data S1. Study design. Table S1. Patient demographics and classification based on response to treatment. Table S2. GO's biological processes overrepresented in CFC prior to Eryfotona AK-NMSC treatment. Table S3. GO's biological processes overrepresented in lesional skin post Eryfotona AK-NMSC treatment. Letter to the Editor beneficial effects in chemotherapy-induced alopecia (CIA). We pretreated hair follicles with topical EGF-liposomal solution in the C57BL/6 mouse model of cyclophosphamide-induced alopecia and observed the catagen-inducing property and damage response pathway after CIA. We confirmed that topical EGF application induced a catagen-like stage and found that these catagen-like hairs were protected from chemotherapy-mediated damage. Moreover, our results showed that EGF treatment favoured primary hair recovery via the dystrophic anagen pathway after CIA. Given that hair follicles subjected to less severe chemotherapeutic insult enter the dystrophic anagen pathway followed by primary recovery, the results of this study suggest that catagen inducers could be useful as a new alopecia-protection strategy, especially in the context of CIA.
Alopecia areata (AA) is a common autoimmune disorder mostly presented as round patches of hair loss and subclassified into alopecia totalis/alopecia universalis (AT/AU) based on the area of alopecia. Although AA is relatively common, only 5% of AA patients progress to AT/AU, which affect the whole scalp and whole body respectively. To determine genetic determinants of this orphan disease, we undertook whole-exome sequencing of 6 samples from AU patients, and 26 variants in immune-related genes were selected as candidates. When an additional 14 AU samples were genotyped for these candidates, 6 of them remained at the level of significance in comparison with 155 Asian controls (p<1.92×10−3). Linkage disequilibrium was observed between some of the most significant SNPs, including rs41559420 of HLA-DRB5 (p<0.001, OR 44.57) and rs28362679 of BTNL2 (p<0.001, OR 30.21). While BTNL2 was reported as a general susceptibility gene of AA previously, HLA-DRB5 has not been implicated in AA. In addition, we found several genetic variants in novel genes (HLA-DMB, TLR1, and PMS2) and discovered an additional locus on HLA-A, a known susceptibility gene of AA. This study provides further evidence for the association of previously reported genes with AA and novel findings such as HLA-DRB5, which might represent a hidden culprit gene for AU.
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