Advancements in regenerative medicine for aesthetic dermatology. a comprehensive review and future trends

The growing interest in maintaining a youthful appearance has encouraged an accelerated development of innovative, minimally invasive aesthetic treatments for facial rejuvenation and regeneration. The close correlation between tissue repair, regeneration, and aging has paved the way for the application of regenerative medicine principles in cosmetic dermatology. The theoretical substrates of regenerative medicine applications in dermo-aesthetics are plentiful. However, regenerative dermatology is an emerging field and needs more data and in vivo trials to reach a consensus on the standardization of methods. In this review, we summarize the principles of regenerative medicine and techniques as they apply to cosmetic dermatology, suggesting unexplored fields and future directions

Effects of Endogenous Cannabinoid Anandamide on Voltage-Dependent Sodium and Calcium Channels in Rat Ventricular Myocytes

BACKGROUND AND PURPOSE: The endocannabinoid anandamide (N-arachidonoyl ethanolamide; AEA) exerts negative inotropic and antiarrhythmic effects in ventricular myocytes. EXPERIMENTAL APPROACH: Whole-cell patch-clamp technique and radioligand-binding methods were used to analyse the effects of anandamide in rat ventricular myocytes. KEY RESULTS: In the presence of 1-10 μM AEA, suppression of both Na(+) and L-type Ca(2+) channels was observed. Inhibition of Na(+) channels was voltage and Pertussis toxin (PTX) - independent. Radioligand-binding studies indicated that specific binding of [(3) H] batrachotoxin (BTX) to ventricular muscle membranes was also inhibited significantly by 10 μM metAEA, a non-metabolized AEA analogue, with a marked decrease in Bmax values but no change in Kd . Further studies on L-type Ca(2+) channels indicated that AEA potently inhibited these channels (IC50 0.1 μM) in a voltage- and PTX-independent manner. AEA inhibited maximal amplitudes without affecting the kinetics of Ba(2+) currents. MetAEA also inhibited Na(+) and L-type Ca(2+) currents. Radioligand studies indicated that specific binding of [(3) H]isradipine, was inhibited significantly by metAEA. (10 μM), changing Bmax but not Kd . CONCLUSION AND IMPLICATIONS: Results indicate that AEA inhibited the function of voltage-dependent Na(+) and L-type Ca(2+) channels in rat ventricular myocytes, independent of CB1 and CB2 receptor activation

Correlating Optical Coherence Tomography and Other Noninvasive Imaging Features With Atrophic and Hypertrophic Skin Photoaging

Background: According to morphological and clinical differences, atrophic (AP) and hypertrophic (HP) skin photoaging types have been reported. The current study examines the correlation between optical coherence tomography (OCT) and dynamic-OCT (D-OCT) features in subjects with skin photoaging types classified as AP, HP, or controls. Furthermore, we aim to define the correlations between OCT/D-OCT and other noninvasive skin imaging features (standardized clinical photography and reflectance confocal microscopy [RCM]). Methods: We explored the correlations between skin photoaging types, OCT/D-OCT, and noninvasive skin imaging features. A total of 58 patients were clinically classified as AP (n = 17), HP (n = 24), or controls (n = 17). Results: AP subjects showed higher D-OCT vessel assets and vessel densities (p < 0.05) compared to HP and control subjects. A significant correlation was established between standardized clinical evidence of wrinkles and RCM collagen scores. Dermal variations in HP subjects represent the underlying substrate of wrinkles. Conclusions: Despite the limited cohort, these results contribute to the current knowledge of morphologic differences between AP and HP subjects. Treatment should consider morphologic changes according to skin photoaging phenotypes for optimal personalized medicine

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Leukotriene biosynthesis and secondary messengers in rat basophilic leukaemia cells

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