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This article discusses the effects of pioglitazone, a medication used to treat chronic inflammatory skin diseases, on vitiligo keratinocytes. Vitiligo is a skin disorder characterized by the loss of melanocytes, and previous research has shown defects in the skin barrier and inflammation in vitiligo-affected skin. The study found that pioglitazone treatment improved keratinocyte differentiation, skin barrier assembly, and reduced inflammation in vitiligo keratinocytes. These findings suggest that pioglitazone may be a potential therapeutic option for vitiligo by preserving and reinforcing the skin barrier and reducing inflammation. [Extracted from the article]

Background: Acne, a disease of the sebaceous gland with multifactorial pathogenesis, affects more than 85% of adolescents. A better deepening of the mechanisms underlying the disease is needed to define effective and mechanism‐targeted treatments. Objective: To understand whether the sebocyte differentiation process could be involved in the pathogenesis of the disease. Methods: Protein expressions were evaluated by Western blot analysis and ELISA; mRNA levels by real‐time RT‐PCR, lipid analysis and lipid peroxidation were performed by gas chromatography, mass spectrometry and spectrophotometric assay. Results: In vitro, low differentiated SZ95 sebocyte expressed an up‐modulation of genes involved in sebogenesis and a higher level of insulin receptor respect to differentiated cells, resulting in an increased response to insulin and in the production of acne‐like sebum. The induction of SZ95 sebocyte differentiation by the peroxisome proliferator‐activated receptor γ (PPARγ) modulator NAC‐GED0507 reduced the response to insulin normalizing the sebum production and decreasing the release of proinflammatory mediators. In vivo treatment of acne patients with NAC‐GED0507 1% gel ameliorated clinical manifestations and induced in sebum the expression of PPARγ, associated with the decrease in mammalian target of rapamycin activation and levels of inflammatory molecules, confirming the results obtained in vitro. Conclusions: The study provides relevant insight into acne pathogenesis, identifying an alteration of sebocyte differentiation as pathogenetic basis of the disease and the induction of the differentiation process as a therapeutic target in acne therapy interfering with all pathogenic mechanisms. Linked Commentary: L. Kemény et al. J Eur Acad Dermatol Venereol 2020; 34: 1637–1638. https://doi.org/10.1111/jdv.16788. [ABSTRACT FROM AUTHOR]

Anionic carbosilane dendrons decorated with sulfonate functions and one thiol moiety at the focal point have been used to synthesize water-soluble gold nanoparticles (AuNPs) through the direct reaction of dendrons, gold precursor, and reducing agent in water, and also through a place-exchange reaction. These nanoparticles have been characterized by NMR spectroscopy, TEM, thermogravimetric analysis, X-ray photoelectron spectroscopy (XPS), UV/Vis spectroscopy, elemental analysis, and zeta-potential measurements. The interacting ability of the anionic sulfonate functions was investigated by EPR spectroscopy with copper(II) as a probe. Different structures and conformations of the AuNPs modulate the availability of sulfonate and thiol groups for complexation by copper(II). Toxicity assays of AuNPs showed that those produced through direct reaction were less toxic than those obtained by ligand exchange. Inhibition of HIV-1 infection was higher in the case of dendronized AuNPs than in dendrons. [ABSTRACT FROM AUTHOR]

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Background Sebum plays a key role in the initiation of the acne lesions. Oxidized sebum lipids cause keratynocytes hyperproliferation and inflammatory cytokines release. Association between sebum oxidation and comedogenesis has been little investigated in comedonal acne. Objectives Evaluation of sebum oxidation parameters and levels of inflammatory cytokines ( IL-1α) in patients with mild comedonal acne ( MCA) before and after the treatment with a mixed RetinSphere®- vitamin E formulation. Methods Sebum excretion rate ( SER), squalene concentration, and oxidation degree of sebum were measured in 18 MCA patients and 10 controls. IL-1α levels in the stratum corneum were measured in both lesional and non-lesional facial areas of MCA patients. Sebum parameters and IL-1α were measured at week 4 of topical treatment. Reflectance confocal microscopy ( RCM) was performed in a subset of four patients at the baseline and at week 4 and all patients were assessed clinically before and following the 8 week-treatment. Results Sebum excretion rate and squalene concentration were comparable between MCA patients and healthy controls. Lipid peroxidation ( LPO) and the percentage of oxidized squalene ( SQOX) were significantly elevated in the sebum of MCA patients. The concentration of the proinflammatory cytokine IL-1α in stratum corneum was significantly higher in the lesional area compared with non-lesional area of the MCA patients at the baseline. At week 4, while SER and squalene concentration did not vary significantly, the LPO levels and the SQOX percentage resulted decreased at a significant extent. Following the treatment, IL-1α concentration in the lesional area reached values comparable to those of unaffected areas. Consistent with the biochemical data, RCM showed the reduction of hyperkeratinization and of inflammatory cells infiltration of the adnexal structures epithelium, significant clinical improvement was recorded at week 8. Conclusion The data further support the involvement of lipid oxidation and particularly by-products of squalene oxidation in comedogenesis. [ABSTRACT FROM AUTHOR]

The accumulation of β-amyloid peptides into senile plaques is one of the hallmarks of Alzheimer's disease (AD). There is mounting evidence that the lipid matrix of neuronal cell membranes plays an important role in the β-sheet oligomerization process of β-amyloid. Aβ(25-35), the sequence of which is GSNKGAIIGLM, is a highly toxic segment of amyloid β (Aβ)-peptides, which forms fibrillary aggregates. In the present work, two spin-labelled Aβ(25-35) analogues containing the nitroxide group of the amino acid TOAC (2,2,6,6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid) as a paramagnetic probe at the N- or the C-terminus of the peptide sequence, respectively, were synthesized in order to investigate the peptide-membrane interaction. The orientation and associated changes of the peptide conformation in the presence of different artificial membrane models (micelles, liposomes) were evaluated by electron paramagnetic resonance and circular dichroism techniques. The results of this study allowed us to propose a model in which the C-terminal portion of the peptide is highly associated to the membrane, while the N-terminal part extends into the aqueous phase with occasional contacts with the lipid head-group region. Interestingly, the interaction of the C-terminal portion of the peptide is particularly enhanced in the presence of sodium dodecyl sulfate (SDS) molecules. Copyright © 2006 European Peptide Society and John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The aim of this study was to compare the degree of occupancy of central nicotinic acetylcholine receptors (nAChR) in isoflurane anaesthetized baboon brain following inhalation of tobacco smoke (one cigarette containing 0.9 mg nicotine) or i.v. nicotine (0.6 mg i.v.). [[sup 18] F]Fluoro-A-85380 and positron emission tomography (PET) were used to assess the distribution volumes (DV) of the radiotracer in selected brain areas using a one-compartment model. Eighty minutes after nicotine i.v., DV was reduced by 50 and 66% in the thalamus and putamen, respectively. Six hours after nicotine, a reduction in DV (27% in the thalamus) was still observed. Eighty minutes after inhalation of tobacco smoke, DV was decreased by 52 and 65% in the thalamus and putamen, respectively. Previous PET experiments have demonstrated a short-lasting interaction of [[sup 11] C]nicotine with nAChRs. Thus, we hypothesized that a metabolite of nicotine with high affinity and long half-live (several hours) could bind at nAChRs. Eighty minutes after a high dose of nornicotine (0.5 mg i.v.), DV was reduced by 53 and 31% in thalamus and putamen, respectively. No significant effect was observed following 0.15 mg nornicotine. Therefore, nornicotine could contribute to the long-lasting occupancy of central nAChRs after smoking. [ABSTRACT FROM AUTHOR]