Journal: Archives of dermatological research
Current published estimates of the prevalence of hyperhidrosis in the United States are outdated and underestimate the true prevalence of the condition. The objectives of this study are to provide an updated estimate of the prevalence of hyperhidrosis in the US population and to further assess the severity and impact of sweating on those affected by the condition. For the purposes of obtaining prevalence, a nationally representative sample of 8160 individuals were selected using an online panel, and information as to whether or not they experience hyperhidrosis was obtained. The 393 individuals (210 female, 244 non-Hispanic white, 27 black, mean age 40.3, SE 0.64) who indicated that they have hyperhidrosis were asked further questions, including body areas impacted, severity of symptoms, age of onset, and socioemotional impact of the condition. Current results estimate the prevalence of hyperhidrosis at 4.8 %, which represents approximately 15.3 million people in the United States. Of these, 70 % report severe excessive sweating in at least one body area. In spite of this, only 51 % have discussed their excessive sweating with a healthcare professional. The main reasons are a belief that hyperhidrosis is not a medical condition and that no treatment options exist. The current study’s findings with regard to age of onset and prevalence by body area generally align with the previous research. However, current findings suggest that the severity and prevalence are both higher than previously thought, indicating a need for greater awareness of the condition and its associated treatment options among medical professionals.
Wnt-, Hedgehog- and Notch-signaling cascades are morphogen pathways that play crucial roles in development and tissue homeostasis. While morphogen pathways are tightly regulated at multiple levels, inappropriate activation of Wnt, Hedgehog and Notch signaling has been implicated into the pathogenesis of various diseases. In particular, Wnt, Hedgehog and Notch signaling have emerged as central players in the pathogenesis of fibrotic diseases. Here, we will review the pro-fibrotic effects of Wnt, Hedgehog and Notch signaling in systemic sclerosis (SSc), prototypical systemic fibrotic disease. Wnt, Hedgehog and Notch pathways are activated in SSc. They potently stimulate fibroblasts to differentiate into myofibroblasts and to release collagen and other extracellular matrix components. Genetic or pharmacological inhibition of morphogen pathways effectively prevents experimental fibrosis in different preclinical models and induces regression of pre-established fibrosis. As several inhibitors of Wnt, Hedgehog and Notch have recently been developed with first ones being already approved for clinical trials, morphogen pathways maybe a novel approach for the treatment of fibrosis.
Scarring, tightly associated with fibrosis, is a significant symptomatic clinical problem. Interleukin 10 (IL-10) has been identified as a candidate scar-improving therapy based on preclinical studies. However, the molecular mechanism of IL-10 in scar improvement is still uncertain. In this study, human dermal fibroblasts stimulated with TGF-β1 were treated with IL-10 to analyze the mRNA and some of proteins' expression levels of type I collagen (Col1), type III collagen (Col3), alpha-smooth muscle actin (α-SMA), matrix metalloproteinase-1 (MMP1), MMP2, MMP8 and tissue inhibitor of metalloproteinase 1 (TIMP1), TIMP2 by real-time PCR and Western blot, to observe α-SMA-positive fibroblasts by immunocytochemistry. The contracture and improvement of fibroblast-populated collagen lattice (FPCL) and a murine model of wound healing were used to evaluate the scar-improving effects by histological staining. The results showed that IL-10 can significantly down-regulate the mRNA and protein expression levels of Col1, Col3, α-SMA, and up-regulate the mRNA expression levels of MMP1 and MMP8, and decrease α-SMA-positive fibroblasts. FPCL analysis showed that the IL-10 (20 ng/ml) can significantly inhibit the contracture, improve the architecture of FPCL. Wounds injected with IL-10 demonstrated that the appearance of scar was improved, the wound margin of scarring was narrow, and the deposition of collagens (Col1 and Col3) in regenerated tissue was relieved. These results provide direct evidences that IL-10 has the inhibitory effects on the excessive deposition of extracellular matrix components and fibroblast-to-myofibroblast transition, and show that IL-10 has the potential therapy in prevention and reduction of skin scarring.
Resveratrol and oxyresveratrol are naturally occurring phenolic compounds with various bioactivities, but their uses in cosmetics have been partly limited by their chemical instabilities. This study was performed to examine the anti-melanogenic effects of the acetylated derivatives from resveratrol and oxyresveratrol. Resveratrol and oxyresveratrol were chemically modified to triacetyl resveratrol and tetraacetyl oxyresveratrol, respectively. The acetylated compounds were less susceptible than the parent compounds to oxidative discoloration. The acetylated compounds inhibited the activities of tyrosinases less than parent compounds in vitro, but they were as effective at cellular melanogenesis inhibition, indicating bioconversion to parent compounds inside cells. Supporting this notion, the parent compounds were regenerated when the acetylated compounds were digested with cell lysates. Although resveratrol and triacetyl resveratrol inhibited tyrosinase activity less effectively than oxyresveratrol and tetraacetyl oxyresveratrol in vitro, they inhibited cellular melanogenesis more effectively. This discrepancy was explained by strong inhibition of tyrosinase expression by resveratrol and triacetyl resveratrol. Experiments using a reconstituted skin model indicated that resveratrol derivatives can affect melanin synthesis and cell viability to different extents. Collectively, this study suggests that acetylated derivatives of resveratrol have great potential as anti-melanogenic agents for cosmetic use in terms of efficacy, safety, and stability.
The global population of bed bugs (Cimex lectularius and Cimex hemipterus, family Cimicidae) has undergone a significant resurgence since the late 1990s. This is likely due to an increase in global travel, trade, and the number of insecticide-resistant bed bugs. The global bed bug population is estimated to be increasing by 100-500 % annually. The worldwide spread of bed bugs is concerning, because they are a significant socioeconomic burden and a major concern to public health. According to the United States Environmental Protection Agency, bed bugs are “a pest of significant health importance.” Additionally, 68 % of U.S. pest professionals reported that bed bugs are the most challenging pest to treat. Upwards of 45 disease pathogens have been reported in bed bugs. Recent studies report that bed bugs may be competent vectors for pathogens, such as Bartonella quintana and Trypanosoma cruzi. However, public health reports have thus far failed to produce evidence that major infectious disease outbreaks have been associated with bed bugs. Since many disease pathogens have previously been reported in bed bugs and the worldwide bed bug population is now drastically increasing, it stands to reason to wonder if bed bugs might transmit human pathogens. This review includes a literature search on recently published clinical and laboratory studies (1990-2016) investigating bed bugs as potential vectors of infectious disease, and reports the significant findings and limitations of the reviewed studies. To date, no published study has demonstrated a causal relationship between bed bugs and infectious disease transmission in humans. Also, we present and propose to expand on previous hypotheses as to why bed bugs do not transmit human pathogens. Bed bugs may contain “neutralizing factors” that attenuate pathogen virulence and, thereby, decrease the ability of bed bugs to transmit infectious disease.
The use of underarm cosmetics is common practice in the Western society to obtain better body odor and/or to prevent excessive sweating. A survey indicated that 95 % of the young adult Belgians generally use an underarm deodorant or antiperspirant. The effect of deodorants and antiperspirants on the axillary bacterial community was examined on nine healthy subjects, who were restrained from using deodorant/antiperspirant for 1 month. Denaturing gradient gel electrophoresis was used to investigate the individual microbial dynamics. The microbial profiles were unique for every person. A stable bacterial community was seen when underarm cosmetics were applied on a daily basis and when no underarm cosmetics were applied. A distinct community difference was seen when the habits were changed from daily use to no use of deodorant/antiperspirant and vice versa. The richness was higher when deodorants and antiperspirants were applied. Especially when antiperspirants were applied, the microbiome showed an increase in diversity. Antiperspirant usage led toward an increase of Actinobacteria, which is an unfavorable situation with respect to body odor development. These initial results show that axillary cosmetics modify the microbial community and can stimulate odor-producing bacteria.
Wound healing after dermal injury is an imperfect process, inevitably leading to scar formation as the skin re-establishes its integrity. The resulting scars have different characteristics to normal skin, ranging from fine-line asymptomatic scars to problematic scarring including hypertrophic and keloid scars. Scars appear as a different colour to the surrounding skin and can be flat, stretched, depressed or raised, manifesting a range of symptoms including inflammation, erythema, dryness and pruritus, which can result in significant psychosocial impact on patients and their quality of life. In this paper, a comprehensive literature review coupled with an analysis of levels of evidence (LOE) for each published treatment type was conducted. Topical treatments identified include imiquimod, mitomycin C and plant extracts such as onion extract, green tea, Aloe vera, vitamin E and D, applied to healing wounds, mature scar tissue or fibrotic scars following revision surgery, or in combination with other more established treatments such as steroid injections and silicone. In total, 39 articles were included, involving 1703 patients. There was limited clinical evidence to support their efficacy; the majority of articles (n = 23) were ranked as category 4 LOE, being of limited quality with individual flaws, including low patient numbers, poor randomisation, blinding, and short follow-up periods. As trials were performed in different settings, they were difficult to compare. In conclusion, there is an unmet clinical need for effective solutions to skin scarring, more robust long-term randomised trials and a consensus on a standardised treatment regime to address all aspects of scarring.
When determined in vitro, the SPF of certain commercial sunscreen products can be lower than the SPF indicated on the label. The study of the composition of this type of product enabled us to note that the majority contained substances reputed to have anti-inflammatory properties. This effect is shown by inhibiting the erythema, without protecting the skin, which constitutes a serious public health problem. The anti-inflammatory effects of αbisabolol-, allantoin- and 18-β-glycyrrhetinic acid-based emulsions, as well as commercial sun products containing any one of these molecules, have been tested with phorbol myristate acetate on mice. The effectiveness of these sunscreens products is quantified using two indicators: SPF (sun protection factor) and PF-UVA (protection factor-UVA) by in vitro method. We were thus able to show that certain sun products have an anti-inflammatory effect, which in turn causes the SPF value shown on the product to be overestimated, indeed sometimes by considerably large margins.
Recently, VEGFR-2 has been detected not only in vascular and lymphatic endothelial cells but also in some non-vascular endothelial cells, particularly human hair follicles, sebaceous glands, and sweat glands. In addition, VEGFR-2 has been confirmed to play direct roles in hair follicle keratinocyte regulation beyond simply angiogenesis. To elucidate whether VEGFR-2 activation plays a role in hair follicle cycling regulation, immunofluorescence of VEGFR-2 expression was performed during hair cycling of the dorsum of the mouse induced by hair plucking. We observed that staining for VEGFR-2 in hair follicles during anagen II and IV was much stronger than during anagen VI, catagen and telogen. During anagen II, intense staining for VEGFR-2 was observed on the keratinocyte strands of the hair follicle. Subsequently, we detected intense staining for VEGFR-2 in the ORS, IRS and hair bulb during anagen IV. Moderate staining for VEGFR-2 was detected in the ORS and hair bulb, but staining was most intense in IRS during anagen VI. During catagen, staining for VEGFR-2 in the IRS remained intense, while staining in the ORS and hair bulb was significantly weakened and was negative in the dermal papilla. During telogen, we detected VEGFR-2 in germ cells, cap, and club hair adjoining the epidermis. In conclusion, VEGFR-2 was expressed on the hair follicles of the dorsum of the mouse and varied in expression on the mouse hair follicles during hair cycling, suggesting that VEGFR-2 may exert roles in hair cycle regulation in hair follicles on the dorsum of mice.
Adult wild-type mice are not supposed to be proper models for ultraviolet radiation (UVR)-induced melanoma since melanocytes are confined to hair follicles and cannot be sufficiently reached by UVR. On the other hand, in mutated mouse models used for melanoma research limitations, including an altered immune system and selection of affected pathways, lead to tumors phenotypically quite different from naturally occurring melanomas. We compared the distribution of epidermal melanocytes in UVR and not-UVR-exposed wild-type C57BL/6 mice. Starting at the age of 8 weeks, mice were exposed to physiologic doses of UVR three times weekly over 16 weeks. Back skin biopsies were taken 4, 8, 12 and 16 weeks after initiation of exposure, and stained for Melan-A, representing a highly selective marker for melanocytes. Surprisingly, after exposure to UVR, Melan-A positive cells were detected also in the interfollicular epidermis of C57BL/6 mice. We conclude that UVR is capable of inducing interfollicular epidermal melanocytes in wild-type mice.