RESUMEN

IMPORTANCE: The use of social media by dermatology journals and professional and patient-centered dermatology organizations remains largely unknown and, to our knowledge, has yet to be fully evaluated. OBJECTIVE: To evaluate and quantify the extent of involvement of dermatology journals, professional dermatology organizations, and dermatology-related patient advocate groups on social networking sites. DESIGN, SETTING, AND PARTICIPANTS: We obtained an archived list of 102 current dermatology journals from SCImago on the World Wide Web and used the list to investigate Facebook, Twitter, and individual journal websites for the presence of social media accounts. We identified professional and patient-centered dermatology organization activity on social networks through queries of predetermined search terms on Google, Facebook, Twitter, and LinkedIn. The activity of each entity was documented by recording the following metrics of popularity: the numbers of Facebook "likes," Twitter "followers," and LinkedIn "members." MAIN OUTCOMES AND MEASURES: The numbers of Facebook likes, Twitter followers, and LinkedIn members corresponding to each dermatology journal and each professional and patient-related dermatology organization. RESULTS: On July 17, 2012, of the 102 dermatology journals ranked by SCImago, 12.7% were present on Facebook and 13.7% on Twitter. We identified popular dermatology journals based on Facebook likes and Twitter followers, led by the Journal of the American Academy of Dermatology and Dermatology Times, respectively. Popular professional dermatology organizations included dermRounds Dermatology Network (11 251 likes on Facebook and 2900 followers on Twitter). The most popular dermatology patient-centered organizations were the Skin Cancer Foundation (20 119 likes on Facebook), DermaTalk (21 542 followers on Twitter), and the National Psoriasis Foundation (200 members on LinkedIn). CONCLUSIONS AND RELEVANCE: Patient-centered and professional dermatology organizations use social networking sites; however, academic journals tend to lag behind significantly. Although some journals are active in social media, most have yet to recognize the potential benefits of fully embracing popular social networks.

Asunto(s)

Dermatología , Publicaciones Periódicas como Asunto/estadística & datos numéricos , Medios de Comunicación Sociales/estadística & datos numéricos , Sociedades Médicas/estadística & datos numéricos , Comunicación en Salud/métodos , Humanos , Internet/estadística & datos numéricos , Defensa del Paciente/estadística & datos numéricos , Atención Dirigida al Paciente/organización & administración

RESUMEN

The Physician Quality Reporting System (PQRS) was established in 2006 by the Centers for Medicare and Medicaid Services (CMS) as part of an incentive process to improve healthcare preventive practices. As of 2011, there were 235 PQRS measures but only three specific to skin diseases, specifically melanoma. To measure current usage of the PQRS among dermatologists in Colorado, a survey was distributed at the 2011 Colorado Dermatological Society Meeting. Of the 120 physician attendees, 60 responded, yielding a response rate of 50%. Compared with responses from a similar 2010 survey, a significantly higher number of physicians are using PQRS, as well as E-prescribing and EHR systems. This is likely owing to the fact that CMS will require mandatory reporting of these measures in 2015. Respondents from the current survey commented that a major hurdle to PQRS reporting is the inability to submit data through existing EHR or billing systems. Currently, CMS requires PQRS reporting through a designated registry such as that provided by the AAD. Some practices have opted to report metrics such as tobacco and alcohol screening, since these can be reported through their billing systems. The results suggest structural improvements in the PQRS reporting system could improve compliance.

Asunto(s)

Dermatología/estadística & datos numéricos , Registros Electrónicos de Salud/estadística & datos numéricos , Prescripción Electrónica/estadística & datos numéricos , Pautas de la Práctica en Medicina , Centers for Medicare and Medicaid Services, U.S. , Colorado , Calidad de la Atención de Salud/tendencias , Estados Unidos

RESUMEN

The link between psychological stress and aging is intuitive although the underlying mechanisms are not well defined. Evidence suggests that chronic psychological stress stimulates the autonomic nervous system, renin-angiotensin system, and the hypothalamic-pituitary-adrenal axis when the body attempts to resolve perceived threats to homeostasis. Prolonged activation of these pathways can result in chronic immune dysfunction, increased production of reactive oxygen species, and DNA damage, which are known to contribute to the again of skin and other tissues. Despite the lack of conclusive evidence directly linking psychological stress to skin aging, mechanisms by which stress leads to immune dysfunction, oxidative radicals, and ultimately DNA damage via neuronal, endocrine, and immune modulation may present a possible intervention for skin aging. In addition to the wide array of anti-oxidant therapies being developed to combat aging, the topical use of beta-blockers such as timolol, angiotensin receptor blockers such as valsartan, glucocorticoid blockers such as mifepristone, and cholinergic modulators including botulinum toxin, might be potential therapeutic strategies to prevent skin aging. Given the current understanding of these pathways, it would be premature to utilize such modalities for prevention of skin aging at this time, but future research into this type of topical pharmacologic anti-aging intervention may be promising.

Asunto(s)

Envejecimiento de la Piel/fisiología , Estrés Psicológico/fisiopatología , Acetilcolina/fisiología , Envejecimiento/fisiología , Sistema Nervioso Autónomo/fisiopatología , Catecolaminas/fisiología , Enfermedad Crónica , Citocinas/fisiología , Daño del ADN , Hormonas/fisiología , Humanos , Sistema Hipotálamo-Hipofisario/fisiopatología , Inflamación , Neuroinmunomodulación/fisiología , Estrés Oxidativo , Sistema Hipófiso-Suprarrenal/fisiopatología , Sistema Renina-Angiotensina/fisiología , Piel/inmunología , Piel/patología , Piel/fisiopatología , Envejecimiento de la Piel/patología , Envejecimiento de la Piel/efectos de la radiación , Luz Solar/efectos adversos

Asunto(s)

Antivirales/uso terapéutico , Retinitis por Citomegalovirus/tratamiento farmacológico , Farmacorresistencia Viral Múltiple/efectos de los fármacos , Inmunosupresores/uso terapéutico , Isoxazoles/uso terapéutico , Viremia/tratamiento farmacológico , Administración Oral , Adulto , Antivirales/administración & dosificación , Antivirales/farmacocinética , Citomegalovirus/genética , Retinitis por Citomegalovirus/virología , Farmacorresistencia Viral Múltiple/genética , Femenino , Estudios de Seguimiento , Humanos , Inmunosupresores/administración & dosificación , Inmunosupresores/farmacocinética , Isoxazoles/farmacocinética , Trasplante de Riñón , Leflunamida , Viremia/virología

RESUMEN

Apoptosis-associated Speck-like protein containing a CARD (caspase recruitment domain) (ASC) was originally named because it triggered apoptosis in certain tumors. More recently, however, ASC was found to be a central adaptor protein of inflammasome, which mediates the secretion of protumorigenic inflammation. Here we examined the role of ASC in tumorigenesis of human melanoma. Compared with primary melanoma, ASC protein expression was generally downregulated in metastatic melanoma. Although overexpressing ASC in metastatic melanoma showed no effects on cell viability, silencing ASC with short hairpin RNA induced G1 cell cycle arrest, reduced cell viability, and suppressed tumorigenesis in metastatic melanoma. On the other hand, silencing ASC in primary melanoma reduced cell death, increased cell viability, and enhanced tumorigenesis. In primary and metastatic melanoma cells, ASC knockdown inhibited inflammasome-mediated caspase-1 activity and IL-1ß secretion. However, phosphorylated IκB kinase (IKK)α/ß expression and NF-κB activity were suppressed in metastatic melanoma and enhanced in primary melanoma after ASC knockdown. These findings suggest stage-dependent dual roles of ASC in tumorigenesis. ASC expression in primary melanoma inhibits tumorigenesis by reducing IKKα/ß phosphorylation and inhibiting NF-κB activity. In metastatic melanoma, on the other hand, this inhibitory effect is diminished, and ASC induces tumorigenic pathways through enhanced NF-κB activity and inflammasome-mediated IL-1ß secretion.

Asunto(s)

Proteínas del Citoesqueleto/metabolismo , Inflamasomas/genética , Inflamasomas/metabolismo , Melanoma/secundario , Neoplasias Cutáneas/patología , Animales , Proteínas Adaptadoras de Señalización CARD , Caspasas/metabolismo , Caspasas Iniciadoras , Línea Celular Tumoral , Supervivencia Celular/inmunología , Proteínas del Citoesqueleto/genética , Femenino , Regulación Neoplásica de la Expresión Génica/inmunología , Humanos , Inflamasomas/inmunología , Interleucina-1beta/metabolismo , Melanoma/inmunología , Melanoma/metabolismo , Ratones , Ratones Desnudos , FN-kappa B/metabolismo , Estadificación de Neoplasias , ARN Interferente Pequeño/genética , Transducción de Señal/inmunología , Neoplasias Cutáneas/inmunología , Neoplasias Cutáneas/metabolismo , Células Tumorales Cultivadas

RESUMEN

The inflammasome is a multi-protein complex that mediates immune responses to microbial, host, and environmental signals. When active, inflammasomes regulate caspase-1 activation and IL-1ß secretion. There is a strong link between inflammation and cancer, and IL-1ß is one of the major molecules involved in both of these disease processes. Here we review the role of inflammasomes in regulating IL-1ß secretion, and the impact of this pathway on cancer pathogenesis, with a focus on melanoma. This represents an exciting new area of research, and could potentially result in new targets for melanoma therapeutics in the future.

Asunto(s)

Inflamasomas/fisiología , Inflamación/etiología , Melanoma/etiología , Humanos , Interleucina-1/antagonistas & inhibidores , Interleucina-1/fisiología , Melanoma/tratamiento farmacológico , Transducción de Señal/fisiología , Microambiente Tumoral

RESUMEN

Epigallocatechin-3-gallate (EGCG), the major polyphenolic component of green tea, has been demonstrated to possess anti-inflammatory, antioxidant, anti-mutagenic and anti-carcinogenic properties. The anti-melanoma effect of EGCG has been previously suggested, but no clear mechanism of action has been established. In this study, we demonstrated that EGCG inhibits melanoma cell growth at physiological doses (0.1-1 µM). In the search for mechanisms of EGCG-mediated melanoma cell suppression, we found that NF-κB was inhibited, and that reduced NF-κB activity was associated with decreased IL-1ß secretion from melanoma cells. Since inflammasomes are involved in IL-1ß secretion, we investigated whether IL-1ß suppression was mediated by inflammasomes, and found that EGCG treatment led to downregulation of the inflammasome component, NLRP1, and reduced caspase-1 activation. Furthermore, silencing the expression of NLRP1 abolished EGCG-induced inhibition of tumor cell proliferation both in vitro and in vivo, suggesting a key role of inflammasomes in EGCG efficacy. This paper provides a novel mechanism for EGCG-induced melanoma inhibition: inflammasome downregulation→decreased IL-1ß secretion→decreased NF-κB activities→decreased cell growth. In addition, it suggests inflammasomes and IL-1ß could be potential targets for future melanoma therapeutics.

Asunto(s)

Antineoplásicos/uso terapéutico , Camellia sinensis/química , Catequina/análogos & derivados , Melanoma/tratamiento farmacológico , Polifenoles/uso terapéutico , Neoplasias Cutáneas/tratamiento farmacológico , Animales , Catequina/uso terapéutico , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Femenino , Humanos , Inflamación/tratamiento farmacológico , Inflamación/metabolismo , Interleucina-1beta/metabolismo , Melanoma/patología , Ratones , Ratones Desnudos

RESUMEN

Physicians wearing white coats are perceived as having more authority, being more friendly and being more attractive than those not wearing white coats, and patients report that they prefer their dermatologist to wear a white coat. The aim of the study was to determine the prevalence of dermatologists wearing white coats on practice websites. We searched Google for dermatology practice websites in six states representing distinct geographic regions in the United States. The first one hundred search results were evaluated, and photographs of dermatologists on these websites were examined for the presence or absence of white coats. Most (77%) of dermatologists did not wear white coats. The highest prevalence was in the eastern states of Massachusetts and South Carolina, with 29% and 39%, respectively. Colorado had the lowest rate at 13%. Rates were essentially equal when segmented by gender. Although patients report that they prefer their dermatologist to wear a white coat, dermatologists often do not wear a white coat on their practice websites.

RESUMEN

Ellagic is a polyphenolic compound with anti-fibrotic and antioxidant properties, and exhibits antitumor properties against various cancer cells in vitro. There are few studies, however, which examine the effects of ellagic acid on melanoma. In the present study, we observe effects of ellagic acid on melanoma cells in vitro. Three metastatic melanoma cell lines (1205Lu, WM852c and A375) were examined to determine the effects of ellagic acid on melanoma cell viability, cell-cycle, apoptosis, NF-κß activity, and IL-1ß & IL-8 secretion. Cell viability assays demonstrated that ellagic acid possesses an inhibitory effect on cell proliferation at concentrations between 25 and 100 µM. In addition, ellagic acid promoted G1 cell cycle arrest, increased levels of apoptosis and decreased synthesis of IL-1ß and IL-8 in melanoma cells. Ellagic acid also decreased NF-κß activity, suggesting at least one potential mechanism by which ellagic acid may exert its effects in melanoma cells. Our findings support further investigation into prospective roles for ellagic acid as a therapeutic, adjuvant, or preventive agent for melanoma.