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Previously considered a skin disease exclusively affecting adolescents, characterized by inflammatory and non-inflammatory skin lesions, acne vulgaris is now increasingly observed in adult life, including post-menopause. Today, adult female acne (AFA) is a common chronic inflammatory disease of the pilosebaceous unit, with polymorphic lesions presenting as open or closed comedones, papules, pustules, and even nodules or cysts, often with the presence of sequelae. AFA may persist from adolescence or manifest de novo in adulthood. Its etiology is multifactorial, involving genetic, hormonal, dietary, and environmental factors, yet still incompletely understood. Increased sebum production, keratinocyte hyper-proliferation, inflammation, and reduced diversity of Cutibacterium acnes strains are the underlying disease mechanisms. During menopausal transition, a relative increase in androgen levels occurs, just as estrogens begin to decline, which can manifest itself as acne. Whereas most AFA exhibit few acne lesions with normo-androgenic serum levels, baseline investigations including androgen testing panel enable associated comorbidities to be eliminated, such as polycystic ovarian syndrome, congenital adrenal hyperplasia, or tumors. Another interesting feature is AFA's impact on quality of life, which is greater than in adolescents, being similar to other chronic diseases like asthma. The therapeutic approach to AFA depends on its severity and associated features. This review investigates the intricate facets of AFA, with a specific focus on incidence rates, treatment modalities, and the curious impact of menopause. Utilizing insights from contemporary literature and scientific discussions, this article seeks to advance our understanding of AFA, offering new perspectives to shape clinical practices and improve patient outcomes. [ABSTRACT FROM AUTHOR]

Previously considered a skin disease exclusively affecting adolescents, characterized by inflammatory and non-inflammatory skin lesions, acne vulgaris is now increasingly observed in adult life, including post-menopause. Today, adult female acne (AFA) is a common chronic inflammatory disease of the pilosebaceous unit, with polymorphic lesions presenting as open or closed comedones, papules, pustules, and even nodules or cysts, often with the presence of sequelae. AFA may persist from adolescence or manifest de novo in adulthood. Its etiology is multifactorial, involving genetic, hormonal, dietary, and environmental factors, yet still incompletely understood. Increased sebum production, keratinocyte hyper-proliferation, inflammation, and reduced diversity of Cutibacterium acnes strains are the underlying disease mechanisms. During menopausal transition, a relative increase in androgen levels occurs, just as estrogens begin to decline, which can manifest itself as acne. Whereas most AFA exhibit few acne lesions with normo-androgenic serum levels, baseline investigations including androgen testing panel enable associated comorbidities to be eliminated, such as polycystic ovarian syndrome, congenital adrenal hyperplasia, or tumors. Another interesting feature is AFA's impact on quality of life, which is greater than in adolescents, being similar to other chronic diseases like asthma. The therapeutic approach to AFA depends on its severity and associated features. This review investigates the intricate facets of AFA, with a specific focus on incidence rates, treatment modalities, and the curious impact of menopause. Utilizing insights from contemporary literature and scientific discussions, this article seeks to advance our understanding of AFA, offering new perspectives to shape clinical practices and improve patient outcomes. [ABSTRACT FROM AUTHOR]

Pine pitch canker (PPC), caused by Fusarium circinatum, affects Pinus species worldwide. Although no effective solutions have yet been found to control it, there is a growing interest in using biological control agents (BCA) such as Trichoderma to avoid the application of chemical‐based products. Using species with an increasing level of susceptibility to PPC (Pinus pinea, Pinus pinaster and Pinus radiata), this study aimed to evaluate the effect of Trichoderma viride pre‐inoculation on disease development, assessing several physiological and hormonal parameters. A 2‐week period elapsed between T. viride and F. circinatum inoculation. Sampling for each species was performed independently when at least 50% of the plants of one of the inoculated groups developed disease symptoms. Fusarium circinatum infection reduced water status and photosynthesis, but increased proline, abscisic acid and jasmonic acid concentrations in plants of P. radiata and P. pinaster with symptoms; while in P. pinea water relations were maintained and anthocyanin accumulation occurred in the presence of F. circinatum. In P. radiata, T. viride pre‐inoculation accelerated disease progression, with some PPC‐induced responses augmented (decreased water potential and photosynthesis; increased substomatal CO2 concentration) and novel changes not found in seedlings inoculated exclusively with F. circinatum (increased electrolyte leakage and salicylic acid; decreased relative water content). This suggests that T. viride may be initially recognized as an invading organism, subverting the plant defence mechanisms for successful root colonization. If seedlings are not allowed to recover from this state, pathogen infection may thus be facilitated, highlighting the importance of application timing in BCA strategies. [ABSTRACT FROM AUTHOR]

A 3-year follow-up study was performed of bone metabolism and bone changes induced by surgical menopause as a consequence of hysterectomy and oophorectomy (OVX) is 52 nonmenopausal women. We investigated 22 bone parameters and determined seven bone indices as indicators of bone mineral content by dual energy X-ray absorptiometry (DXA), quantitative computed tomography (QCT), and microdensitometry (MD). The significant correlations between levels of sex hormones and/or bone parameters and bone indices demonstrated that marked sex-steroid deficiency after surgical menopause induced bone uncoupling during high bone turnover and subsequent rapid bone loss on the early period after OVX. Principal component analysis using correlation coefficients suggested a seven-loading-factor matrix composed of bone parameters and a two-loading-factor matrix composed of bone indices. Two groups of parameters--estradiol and estriol, and androstenedione together, and luteinizing hormone and follicle stimulating hormone together--indicated that the rate of bone loss was greater in the trabecular bone than in the cortical bone. Three other groups of parameters--urine calcium, urine hydroxyproline, and serum bone Gla-protein together; serum alkaline phosphatase, serum calcium, and 1,25-dihydroxycholecalciferol [1,25(OH)2D] together; and plasma tartrate-resistant acid phosphatase--indicated that bone uncoupling, with a prevalence of resorption over formation of bone, was greater in trabecular bone than is cortical bone and also that magnitude and rate of bone loss in the axial vertebrae surpassed those in the appendicular metacarpals after OVX. Two other groups of parameters, namely, trabecular bone mineral density (Dd) and bone mineral content (Dc), both measured by DXA, and bone mineral density (L2, L3), measured by QCT, together; and the cortical thickness index (MCI), cortical bone mineral density (sigmaGS/D), and the ratio of GSmin/max, measured by MD, indicated that the relative rates of bone reduction at the 3-year follow-up were greater in the axial vertebrae than in the appendicular metacarpals. Thus, bone change in the trabecular bone was associated with rapid loss during the early phase after OVX, whereas that in the cortical bone was slow during the late phase. [ABSTRACT FROM AUTHOR]