Morphological Fabrication of Rubber Cutaneous Receptors Embedded in a Stretchable Skin-Mimicking Human Tissue by the Utilization of Hybrid Fluid

Sensors are essential in the haptic technology of soft robotics, which includes the technology of humanoids. Haptic sensors can be simulated by the mimetic organ of perceptual cells in the human body. However, there has been little research on the morphological fabrication of cutaneous receptors embedded in a human skin tissue utilizing artificial materials. In the present study, we fabricated artificial, cell-like cutaneous receptors embedded in skin tissue mimicking human skin structure by utilizing rubber. We addressed the fabrication of five cutaneous receptors (free nerve endings, Krause and bulbs, Meissner corpuscles, Pacinian corpuscles and Ruffini endings). In addition, we investigated the effectiveness of the fabricated tissue for mechanical and thermal sensing. At first, in the production of integrated artificial skin tissue, we proposed a novel magnetic, responsive, intelligent, hybrid fluid (HF), which is suitable for developing the hybrid rubber skin. Secondly, we presented the fabrication by utilizing not only the HF rubber but our previously proposed rubber vulcanization and adhesion techniques with electrolytic polymerization. Thirdly, we conducted a mechanical and thermal sensing touch experiment with the finger. As a result, it demonstrated that intelligence as a mechanoreceptor or thermoreceptor depends on its fabric: the HF rubber sensor mimicked Krause and bulbs has the thermal and pressing sensibility, and the one mimicked Ruffini endings the shearing sensibility.

Two-dimensional thermo-mechanical fractional responses to biological tissue with rheological properties

Purpose The system of equations for fractional thermo-viscoelasticity is used to investigate two-dimensional bioheat transfer and heat-induced mechanical response in human skin tissue with rheological properties. Design/methodology/approach Laplace and Fourier’s transformations are used. The resulting formulation is applied to human skin tissue subjected to regional hyperthermia therapy for cancer treatment. The inversion process for Fourier and Laplace transforms is carried out using a numerical method based on Fourier series expansions. Findings Comparisons are made with the results anticipated through the coupled and generalized theories. The influences of volume materials properties and fractional order parameters for all the regarded fields are examined. The results indicate that volume relaxation parameters, as well as fractional order parameters, play a major role in all considered distributions. Originality/value Bio-thermo-mechanics includes bioheat transfer, biomechanics, burn injury and physiology. In clinical applications, knowledge of bio-thermo-mechanics in living tissues is very important. One can infer from the numerical results that, with a finite distance, the thermo-mechanical waves spread to skin tissue, removing the unrealistic predictions of the Pennes’ model.

Correction to: Single-cell transcriptome conservation in a comparative analysis of fresh and cryopreserved human skin tissue: pilot in localized scleroderma

An amendment to this paper has been published and can be accessed via the original article.

Rapid Isolation of Functional ex vivo Human Skin Tissue-Resident Memory T Lymphocytes

Studies in animal models have shown that skin tissue-resident memory T (TRM) cells provide enhanced and immediate effector function at the site of infection. However, analyses of skin TRM cells in humans have been hindered by the lack of an optimized isolation protocol. Here, we present a combinatorial strategy-the 6-h collagenase IV digestion and gentle tissue dissociation – for rapid and efficient isolation of skin TRM cells with skin tissue-specific immune features. In comparison with paired blood circulating memory T cells, these ex vivo isolated skin T cells express typical TRM cell markers and display higher polyfunctional properties. Moreover, these isolated cells can also be assessed for longer periods of time in ex vivo cultures. Thus, the optimized isolation protocol provides a valuable tool for further understanding of human skin TRM cells, especially for direct comparison with peripheral blood T cells at the same sample collection time.

Elucidating the cellular mechanism for E2-induced dermal fibrosis

Background Both TGFβ and estradiol (E2), a form of estrogen, are pro-fibrotic in the skin. In the connective tissue disease, systemic sclerosis (SSc), both TGFβ and E2 are likely pathogenic. Yet the regulation of TGFβ in E2-induced dermal fibrosis remains ill-defined. Elucidating those regulatory mechanisms will improve the understanding of fibrotic disease pathogenesis and set the stage for developing potential therapeutics. Using E2-stimulated primary human dermal fibroblasts in vitro and human skin tissue ex vivo, we identified the important regulatory proteins for TGFβ and investigated the extracellular matrix (ECM) components that are directly stimulated by E2-induced TGFβ signaling. Methods We used primary human dermal fibroblasts in vitro and human skin tissue ex vivo stimulated with E2 or vehicle (ethanol) to measure TGFβ1 and TGFβ2 levels using quantitative PCR (qPCR). To identify the necessary cell signaling proteins in E2-induced TGFβ1 and TGFβ2 transcription, human dermal fibroblasts were pre-treated with an inhibitor of the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathway, U0126. Finally, human skin tissue ex vivo was pre-treated with SB-431542, a TGFβ receptor inhibitor, and ICI 182,780, an estrogen receptor α (ERα) inhibitor, to establish the effects of TGFβ and ERα signaling on E2-induced collagen 22A1 (Col22A1) transcription. Results We found that expression of TGFβ1, TGFβ2, and Col22A1, a TGFβ-responsive gene, is induced in response to E2 stimulation. Mechanistically, Col22A1 induction was blocked by SB-431542 and ICI 182,780 despite E2 stimulation. Additionally, inhibiting E2-induced ERK/MAPK activation and early growth response 1 (EGR1) transcription prevents the E2-induced increase in TGFβ1 and TGFβ2 transcription and translation. Conclusions We conclude that E2-induced dermal fibrosis occurs in part through induction of TGFβ1, 2, and Col22A1, which is regulated through EGR1 and the MAPK pathway. Thus, blocking estrogen signaling and/or production may be a novel therapeutic option in pro-fibrotic diseases.