RESUMO
BACKGROUND: Noninvasive skin rejuvenation treatment is growing in recognition to aesthetic medicine. AIM: The objective of the study was to assess the efficacy and the safety of the 675-nm laser source treatment of photodamaged hands. MATERIALS AND METHODS: The study included 21 patients (6 males and 15 females) with a mean age of 63 (± 9) years. Patients were treated with -two to three sessions of the 675-nm laser with a 1-month interval between sessions. Photos of each patient were collected at baseline, and 3 months after the last laser session. The 5-point Global Aesthetic Improvement Scale (GAIS) was recorded with their final assessment session (3 months). RESULTS: The total GAIS scores showed satisfactory results: 15 patients (71%) experienced 4 score (excellent improvement) changes and 6 patients (29%) experienced 3 score (good improvement) changes. Clinical images showed good efficacy and visible aesthetic results for the management of photodamaged skin. No serious adverse effects were recorded. CONCLUSION: This study demonstrates the safety and efficacy of for the aesthetic improvement of skin pigmentation and texture for photodamaged hands.
Assuntos
Hiperpigmentação , Terapia a Laser , Lasers de Estado Sólido , Terapia com Luz de Baixa Intensidade , Envelhecimento da Pele , Masculino , Feminino , Humanos , Pessoa de Meia-Idade , Pele , Terapia a Laser/métodos , Terapia com Luz de Baixa Intensidade/métodos , Hiperpigmentação/etiologia , Hiperpigmentação/cirurgia , Rejuvenescimento , Lasers de Estado Sólido/uso terapêutico , Resultado do TratamentoRESUMO
Unresolved ER stress followed by cell death is recognized as the main cause of a multitude of pathologies including neonatal diabetes. A systematic analysis of the mechanisms of ß-cell loss and dysfunction in Akita mice, in which a mutation in the proinsulin gene causes a severe form of permanent neonatal diabetes, showed no increase in ß-cell apoptosis throughout life. Surprisingly, we found that the main mechanism leading to ß-cell dysfunction is marked impairment of ß-cell growth during the early postnatal life due to transient inhibition of mTORC1, which governs postnatal ß-cell growth and differentiation. Importantly, restoration of mTORC1 activity in neonate ß-cells was sufficient to rescue postnatal ß-cell growth, and to improve diabetes. We propose a scenario for the development of permanent neonatal diabetes, possibly also common forms of diabetes, where early-life events inducing ER stress affect ß-cell mass expansion due to mTOR inhibition.