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The main contribution of this paper is the assets of the current and voltage ripples in a buck converter with an LED load. The results indicate that the ripples are different and that it is possible to reduce the passive filter concerning the model of the LED as a simple resistance. The paper presents the design and simulation of a buck converter as a power supply for an LED lamp. Modeling the LED as a resistor and a voltage source (SVRM), the equations to calculate the components of the circuit using the SVRM model are presented, where the Fourier series and phasors are used to calculate the output filter. The equations are validated with SPICE simulations. The results indicate that the SVRM model for the LED load affects the calculation of the output filter of the buck converter as well as the voltage and current ripples, making it a more precise design alternative to the proposed development. [ABSTRACT FROM AUTHOR]

Unsuccessful wound closure in chronic wounds can be linked to altered keratinocyte activation and their inability to re-epithelize. Suggested mechanisms driving this impairment involve unbalanced cytokine signaling. However, the molecular events leading to these aberrant responses are poorly understood. Among cytokines affecting keratinocyte responses, Transforming Growth Factor-β (TFG-β) is thought to have a great impact. In this study, we have used a previously characterized skin epidermal in vitro model, HaCaT cells continuously exposed to TGF-β1, to study the wound recovery capabilities of chronified/senescent keratinocytes. In this setting, chronified keratinocytes show decreased migration and reduced activation in response to injury. Amniotic membrane (AM) has been used successfully to manage unresponsive complicated wounds. In our in vitro setting, AM treatment of chronified keratinocytes re-enabled migration in the early stages of wound healing, also promoting proliferation at later stages. Interestingly, when checking the gene expression of markers known to be altered in TGF-β chronified cells and involved in cell cycle regulation, early migratory responses, senescence, and chronic inflammation, we discovered that AM treatment seemed to reset back to keratinocyte status. The analysis of the evolution of both the levels of keratinocyte activation marker cytokeratin 17 and the spatial-temporal expression pattern of the proliferation marker Ki-67 in human in vivo biopsy samples suggests that responses to AM recorded in TGF-β chronified HaCaT cells would be homologous to those of resident keratinocytes in chronic wounds. All these results provide further evidence that sustained TGF-β might play a key role in wound chronification and postulate the validity of our TGF-β chronified HaCaT in vitro model for the study of chronic wound physiology. [ABSTRACT FROM AUTHOR]