Background Systemic antioxidants, such as oral Polypodium leucotomos extract (PLE), have been found to have photoprotective properties. Objective This study was designed to objectively evaluate the molecular and photobiologic effects of oral administration of PLE. Methods 22 subjects with Fitzpatrick skin phototype I–III were enrolled. On day 1, subjects were irradiated with visible light, ultraviolet A1 (UVA1) and ultraviolet B (UVB; using 308-nm excimer laser). Evaluation was done immediately and 24 hours after irradiation. On days 3 and 4, irradiation and evaluation process was repeated after ingestion of PLE. Results Clinical assessments and colorimetry data showed a decrease in UVB -induced changes in 17 out of 22 subjects post-PLE administration; histology findings demonstrated such a decrease in all 22 subjects. Limitations Only 2 doses of PLE were given. Furthermore, subjects with skin phototypes I–III only were studied. Conclusion This is the first demonstration that PLE has objective measurable suppressive effects on UVB-induced erythema within 2 hours of administration. The results suggest that PLE can potentially be utilized as an adjunctive therapy to lessen the negative photobiologic effects of UVB. In addition, this is the first study to demonstrate the potential correlation between non-invasive colorimetry outcomes and UVB induced molecular damage.
Summary Background Actinic keratoses (AKs) are common premalignant skin lesions triggered by excessive ultraviolet exposure. The majority of AKs regress or persist, but some progress to squamous cell carcinomas. Biomarkers associated with their persistence, progression and regression have not been characterized. Objectives We performed skin biopsies in patients with extensive actinic damage to identify biomarkers that correlate with clinical progression and regression of AKs. Methods This was an observational study of a cohort of patients with extensive actinic damage. AKs were mapped on a clear plastic template in 26 patients at months 3, 6, 9 and 11. Biopsies were taken from randomly selected, predetermined AKs and were evaluated for p53, E‐cadherin, Snail, Slug and Twist. The study is registered at Clinicaltrials.gov: NCT00027976. Results p53 exhibited greater expression in clinically apparent AKs (histological score 2·89 ± 1·45) than in regressed AKs (0·75 ± 0·96); P < 0·01. There was also significantly less membrane E‐cadherin, the lack of which is a marker of epithelial–mesenchymal transition, in clinically apparent AKs (1·89 ± 1·81) than in sun‐exposed skin (3·07 ± 1·75); P < 0·005. The E‐cadherin transcription repressors Snail, Slug and Twist were increased in AKs compared with sun‐exposed skin. A limitation of the study is that measurement of histological biomarkers was not a primary end point. In addition, patients were allowed to apply sunscreens. Conclusions At the molecular level, loss of E‐cadherin and an increase in p53 are linked to the dynamic interplay between the persistence, progression and regression of AKs. What's already known about this topic? Actinic keratoses (AKs) are common dysplastic epidermal lesions that result from chronic and excessive ultraviolet exposure. Biomarkers associated with progression and regression of AK have not been characterized. What does this study add? Decreased E‐cadherin and increased p53, Snail, Slug and Twist (E‐cadherin transcription factors) were associated with progression from AK to nonmelanoma skin cancer. What is the translational message? Strategies targeting these molecules may be effective in reversing rising skin cancer rates. E‐cadherin, p53, Snail, Slug and Twist are potential biomarkers that may be used to assess the efficacy of existing chemopreventive agents.
SummaryThe saliva proteome includes host defense factors and specific bacterial-binding proteins that modulate microbial growth and colonization of tooth surface in the oral cavity. A multidimensional mass spectrometry approach identified the major host-derived salivary proteins which interacted with Streptococcus mutans (strain UA159), the primary microorganism associated with the pathogenesis of dental caries. Two abundant host proteins were found to tightly bind to S. mutans cells, common salivary protein-1 (CSP-1) and deleted in malignant brain tumor 1 (DMBT1, also known as salivary agglutinin or gp340). In contrast to gp340, limited functional information is available on CSP-1. The sequence of CSP-1 shares 38.1% similarity with rat CSP-1. Recombinant CSP-1 (rCSP-1) protein did not cause aggregation of S. mutans cells and was devoid of any significant biocidal activity (2.5 to 10 μg/ml). However, S. mutans cells exposed to rCSP-1 (10 μg/ml) in saliva displayed enhanced adherence to experimental salivary pellicle and to glucans in the pellicle formed on hydroxyapatite surfaces. Thus, our data demonstrate that the host salivary protein CSP-1 binds to S. mutans cells and may influence the initial colonization of this pathogenic bacterium onto tooth surface.
Drs Oak and Shafi contributed equally to the manuscript.Funding sources: California Table Grape Commission.IRB approval status: Reviewed and approved by the University of Alabama at Birmingham IRB; approval #F140627004.
Nonmelanoma skin cancers, which include basal cell and squamous cell carcinomas, are among the most common human malignancies. Although they are typically not lethal, they are responsible for tissue deformity and substantial morbidity in humans, particularly in high risk populations such as organ transplant recipients. Solar UVB, which is a major etiologic factor for this kind of malignancy, produces DNA lesions that include cyclobutane pyrimidine dimers (CPD) and 6–4 photoproducts in the skin. Human cells remove these lesions through nucleotide excision repair. Humans lack a DNA glycosylase required to initiate base excision repair of pyrimidine-pyrimidine photoproducts but produce all of the other proteins required for this form of DNA repair process. In this issue of the Journal of Investigative Dermatology, Johnson et al show that a DNA glycosylase derived from Chlorella virus and engineered to enhance tissue penetration and nuclear localization, can effectively remove these UVB-induced DNA lesions in a human skin equivalent model and the protein can be incorporated into a topical formulation for the prevention and treatment of UVB-induced DNA damage. These studies are highly pertinent and suggest that such an enzyme may be eventually incorporated into regimens for the chemoprevention of skin cancers.
Objectives: To determine the correlation of fasting salivary glucose with fasting plasma glucose (FPG) and glycated hemoglobin A1c (HbA1c) for the diagnosis and monitoring of type 2 diabetes mellitus (T2DM). Methods: A case - control study was carried out from 11th March to 30th August 2021, involving 88 participants out of which 44 were healthy controls and 44 participants were known T2DM who had FPG ≥ 126 mg/dl or 7.0 mmol/L. FPG was measured by Glucose oxidase method and HbA1c by National Glycohemoglobin Standardization Program (NGSP) certified chromatography. Results: T2DM group had significantly higher FPG, HbA1c and salivary glucose values. Both diabetics and healthy controls showed a positive correlation of fasting salivary glucose with FPG. The correlation coefficient (r) was 0.689 and 0.477 for cases and control groups respectively. Similarly, a positive correlation of fasting salivary glucose with HbA1c was observed with the value of r 0.433 and 0.498 for diabetic and healthy control groups respectively, when measured separately. For both groups linear regression equations were derived and scatter dot plots were plotted. P value < 0.001 Conclusion: A positive correlation of fasting salivary glucose with FPG and HbA1c was found. As a result, fasting salivary glucose can be utilized instead of plasma glucose for T2DM patients’ screening, diagnosis, and monitoring thereby eliminating the repeated pricks and mental trauma of patients. Keywords: Blood glucose, glycemia, glycated hemoglobin, salivary glucose, Type 2 diabetes mellitus
Cutaneous photoaging is associated with dermal elastic fiber remodeling; daily photoprotection is therefore essential to prevent ultraviolet (UV)-induced skin damage. Green tea (C sinensis), rich in polyphenol catechins (GTC), have been reported to have significant skin benefits in vitro and in vivo. We have performed a double-blind randomised controlled trial to assess whether systemic GTC supplementation can protect dermal elastic fibers from acute UV exposure. Healthy white Caucasians (n¼50; 18-65 years) were randomized (1:1) to 12 weeks daily oral supplement (1080mg GTC with 100mg viatmin C) or placebo (maltodextrin). Biopsies were taken from skin exposed to 3xMED of solar simulated radiation (SSR) and unexposed skin at baseline and post-supplementation; compliance was confirmed by urinary GTC metabolite analysis. Dermal elastic fibers were identified via histology and immunohistochemistry, their distribution assessed in the papillary dermis (from the dermal-epidermal junction to a depth of 100mm) by image analysis. Differences between UV-exposed and unexposed skin were analysed by paired t-test. A total of 44 subjects completed the study, being compliant with supplementation and providing all skin samples. At baseline, SSR induced a significant overall loss of elastic fiber components (P¼ 0.001), and specifically fibulins-2 and-5. Post-supplementation, UV-mediated loss of fibulin-5 remained significant in the placebo group with mean (SD) % fiber area 19.4 (3.8) and 17.7 (4.1) in unexposed and UV-exposed skin resectively (P¼0.01), whilst in the active group fibulin-5 was protected with % fiber area 18.1 (4.0) and 17.1 (2.7) in unexposed and UV-exposed skin respectively (P¼ 0.30). Hence, acute SSR exposure results in elastic fiber remodeling similar to that observed in chronically photoaged skin. Furthermore, in a randomized control trial, dietary GTC protected fibulin-5 microfibrils in the papillary dermis from UV-mediated degradation.
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