ABSTRACT: Data from skin swabs. Swabs collected from volunteers armpits, chests, upper and lower back. Study aims to reveal an impact of clothing onto the human body and microbiome
Project description:Obesity and associated metabolic outcomes define the metabolic syndrome. Interestingly, an under-appreciated fact is that body fat distribution, rather than total body fat amount, is a key determinant of metabolic disease. Indeed, in contrast to upper-body obesity, lower-body fat accumulation inversely correlates with metabolic risks. Understanding processes regulating upper- vs. lower-body fat expansion is paramount to predict (and prevent) these risks. We combine functional, proteomics, transcriptomics and epigenomics analyses to identify chromatin-associated mechanisms of adipose depot-specific fat expansion. Here, we analyze by RNA-seq the transcriptome of adipocytes differentiated in vitro from human gluteal (lower-body) and abdominal subcutaneous (upper-body) depots-derived adipose stem cells. We aim to identify adipose depot-specific and temporal differences in the up- or down-regulation of gene expression, and relate these differences to changes in chromatin states.
Project description:Obesity and associated metabolic outcomes define the metabolic syndrome. Interestingly, an under-appreciated fact is that body fat distribution, rather than total body fat amount, is a key determinant of metabolic disease. Indeed, in contrast to upper-body obesity, lower-body fat accumulation inversely correlates with metabolic risks. Understanding processes regulating upper- vs. lower-body fat expansion is paramount to predict (and prevent) these risks. We combine functional, proteomics, transcriptomics and epigenomics analyses to identify chromatin-associated mechanisms of adipose depot-specific fat expansion. Here, we analyze by RNA-seq the transcriptome of adipose stem cells (ASCs) from gluteal (lower-body) and abdominal subcutaneous (upper-body) depots induced to differentiate in vitro towards the adipogenic lineage. We aim to identify adipose depot-specific and temporal differences in the up- or down-regulation of gene expression, and a later stage relate these differences to changes in chromatin states.
Project description:For analyzing the exploratory nasal commensal viruses, we performed the metatranscriptomic analysis of the nose swabs from the enrolled AR patients both before and after treatments, as well as sequenced the nose swabs from a set of healthy volunteers without AR history.Simultaneously, to assess the expression of interferon-stimulated genes in patients with allergic rhinitis, we analyzed the gene expression of host reads.
Project description:LC-MS/MS data were collected from skin swabs of 11 volunteers over a period of 9 weeks and for one volunteer during one week. Volunteers were asked to follow instructions required over our 9 weeks study: - We provided the same head to toe shampoo to all volunteers, that was used during shower for the first 6 weeks. - Week 1 to week 3: no other beauty products was used. - Week 4 to week 6: we provided 5 selected commercial beauty products that all volunteers applied daily on specific body part (deodorant for armpits, soothing foot powder for feet, sunscreen for face and moisturizer for arm back). - Week 7 to week 9: back to normal routine. - Samples were collected every week, before during and after application of beauty products.
Project description:Psoriasis is a common chronic inflammatory skin disease. Treatments lead to substantial improvement of most psoriasis plaques. However, it can be challenging to reach disease resolution in certain hard to treat areas such as scalp, and lower extremity. Here we map histologic and spatial transcriptomic differences between psoriasis lesions across different anatomical locations, to understand if differences can be linked to plaque-site specific treatment resistance. Quantitative immunohistochemical analysis and transcriptomic digital spatial profiling were performed on skin punch biopsies obtained from unaffected areas on the trunk, lesional (LS) areas of the scalp, upper extremity and lower extremity of 12 patients with psoriasis. Histological analysis showed no significant differences in epidermal thickness among LS skin from different body locations. Immunohistochemical markers (CD3, CD4, CD8, CD103, CD207, IL-12RB1, IL-17A, IL-23R, RORγt, FOXP3, and MPO) did not differ significantly between LS sites. Whole transcriptome spatial RNA profiling identified several differentially expressed genes that revealed site-specific transcriptomic differences. Notably, IL-23 signaling was significantly enriched in the lower extremity epidermis, and IL-17 signaling was more pronounced in the epidermis of LS samples. These findings highlight minimal histological and immunohistochemical variation, yet significant transcriptomic and pathway differences between psoriasis body locations, suggesting potential targets for site-specific therapeutic strategies.
Project description:Fgf18 gene is strongly expressed in hair follicles of mouse dorsal skin during regressing (catagen) and resting (telogen) phases of hair cycle, but not in growth (anagen) phase. This study aims at identifying the effects of FGF18 local delivery on the anagen phase of hair cycle. To define genes affected by local delivery of FGF18 during anagen phase of hair cycle, we injected FGF18 protein subcutaneously into back skin of C3H/HeN mice on day 4 of depilation-induced anagen. As control PBS was injected in place of FGF18. After 24 h (61-d-old), total RNA was isolated from the back skin and purified to poly A RNA. The RNA samples were pooled for each group. Gene expression was analyzed by one-color analysis using single array for each group.
Project description:Gene expression changes were assessed from the non sun-exposed skin of the lower back of 98 healthy males aged 19-86. We show that contrary to previous thought, genome wide transcriptional activity does not display an exclusively linear correlation with ageing, but rather, in human skin, undergoes a period of significant transient change between 30 and 45 years of age. The identified transient transcriptional changes suggest a period of heightened metabolic activity and cellular damage mediated primarily through the actions of TP53 (tumour protein 53) and TNF (tumour necrosis factor). We also identified a subgroup of the population characterised by increased expression of a large group of hair follicle genes that correlates strongly with a younger age of onset and increasing severity of androgenetic alopecia. Skin was collected from the lower back at the level of the belt, aproximately 5cm lateral to midline from healthy males, (defined as; non-smoking, no hospital admissions in the previous 5 years, no significant medical conditions or medications). Each sample was individually hybridised to an exon 1.0 ST array.
Project description:Hypertrophic scars arise from dysregulated wound healing under prolonged mechanical tension, causing disfiguring fibrosis. However, limited preclinical models replicate key features of human tension-induced scarring. We developed an innovative murine model utilizing suture anchoring to impose persistent transverse-axial stretch across healing incisions, mimicking excessive wound tension that leads to hypertrophy clinically. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage while leaving wound edges on the lower back relaxed. This localized anchoring restrained wound contraction, maintaining high tension throughout remodeling analogous to scars widening under stress. Stretched upper wounds developed profound fibrotic changes compared to relaxed controls. Scars induced by suture-anchored tension displayed macroscopic hypertrophy, hardness, erythema, and pruritis up to 3 months. Histologically, scars induced by suture-anchored tension were hypercellular, hypervascular, hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. MiRNA sequencing revealed the different signature in suture-anchored tension induced hypertrophic scars compared to control normal scars.
Project description:The risk of getting non-melanoma skin cancer varies over 40-fold across the body. Here we map mutations in normal skin in high and low risk sites in normal donors and those with an increased risk of skin cancer. The density of mutations varied widely, with evidence of positive and negative genetic selection. Regional differences in mutational signatures in high and low cancer risk sites and preferential selection of mutants of TP53 in high risk skin and FAT1 in lower risk skin were observed. 10% of clones had copy number changes in cancer associated genes and the largest had multiple driver mutations with loss of heterozygosity. In hair follicles, a proposed site of origin of skin cancers, mutations in the upper follicle resembled adjacent skin, but the lower follicle was sparsely mutated. We conclude cancer risk reflects the efficiency of transformation of oncogenic mutants rather than the density of mutant clones.