Imaging of Port Wine Stain Lesions Using a Multi-Sensor Photoacoustic Probe

2004 ◽  
Author(s):  
John S. Viator ◽  
Steven L. Jacques ◽  
Guillermo Aguilar
Keyword(s):  
Human Skin ◽  
Acoustic Waves ◽  
Basal Layer ◽  
Depth Profiling ◽  
Spatial Relationship ◽  
Skin Surface ◽  
Port Wine Stain ◽  
Port Wine ◽  
Nanosecond Pulses ◽  
Visible Reflectance

Successful treatment of port wine stain (PWS) birthmarks in human skin utilizes cryogen spray cooling (CSC) in conjunction with laser treatment. CSC pre-cools the epidermis to protect it from subsequent laser irradiation which raises the temperature of both the epidermis and the deeper PWS. As the epidermal temperature is depressed by cryogen, damage to the skin surface is minimized while the PWS reaches temperatures sufficient to permanently damage the lesion. In order to optimize cooling and laser heating dosages and to properly guide laser therapy, the spatial relationship of epidermal melanin and PWS must be known. Photoacoustic depth profiling of human skin uses low energy, nanosecond pulses of laser light to induce acoustic waves in optically absorbing media, such as blood and melanin. We used a 532 nm Nd:YAG laser to measure total epidermal melanin content in human skin, comparing the results with visible reflectance spectroscopy. Furthermore, we performed numerical simulations of photoacoustic generation in skin, showing that a hemisperical acoustic sensor array could be used to reconstruct the rete pattern of epidermal melanin in the basal layer. Finally, we built a hemispherical probe for use in future experiments for imaging of human skin.

scholarly journals Performance evaluation of pulsed photothermal profiling of port wine stain in human skin

2004 ◽  
Vol 75 (6) ◽  
pp. 2048-2055 ◽  
Author(s):  
Bincheng Li ◽  
Boris Majaron ◽  
John A. Viator ◽  
Thomas E. Milner ◽  
J. Stuart Nelson
Keyword(s):  
Performance Evaluation ◽  
Human Skin ◽  
Port Wine Stain ◽  
Port Wine

scholarly journals The Pathogenesis of Port Wine Stain and Sturge Weber Syndrome: Complex Interactions between Genetic Alterations and Aberrant MAPK and PI3K Activation

2019 ◽  
Vol 20 (9) ◽  
pp. 2243 ◽  
Author(s):  
Vi Nguyen ◽  
Marcelo Hochman ◽  
Martin C. Mihm ◽  
J. Stuart Nelson ◽  
Wenbin Tan
Keyword(s):  
Endothelial Cells ◽  
Human Skin ◽  
Current Knowledge ◽  
Vascular Malformations ◽  
Genetic Alterations ◽  
Future Research ◽  
Port Wine Stain ◽  
Port Wine ◽  
Weber Syndrome ◽  
Sturge Weber Syndrome

Port wine stain (PWS) is a congenital vascular malformation involving human skin. Approximately 15–20% of children a facial PWS involving the ophthalmic (V1) trigeminal dermatome are at risk for Sturge Weber syndrome (SWS), a neurocutaneous disorder with vascular malformations in the cerebral cortex on the same side of the facial PWS lesions. Recently, evidence has surfaced that advanced our understanding of the pathogenesis of PWS/SWS, including discoveries of somatic genetic mutations (GNAQ, PI3K), MAPK and PI3K aberrant activations, and molecular phenotypes of PWS endothelial cells. In this review, we summarize current knowledge on the etiology and pathology of PWS/SWS based on evidence that the activation of MAPK and/or PI3K contributes to the malformations, as well as potential futuristic treatment approaches targeting these aberrantly dysregulated signaling pathways. Current data support that: (1) PWS is a multifactorial malformation involving the entire physiological structure of human skin; (2) PWS should be pathoanatomically re-defined as “a malformation resulting from differentiation-impaired endothelial cells with a progressive dilatation of immature venule-like vasculatures”; (3) dysregulation of vascular MAPK and/or PI3K signaling during human embryonic development plays a part in the pathogenesis and progression of PWS/SWS; and (4) sporadic low frequency somatic mutations, such as GNAQ, PI3K, work as team players but not as a lone wolf, contributing to the development of vascular phenotypes. We also address many crucial questions yet to be answered in the future research investigations.

scholarly journals In vivo, high-resolution, three-dimensional imaging of port wine stain microvasculature in human skin

2013 ◽  
Vol 45 (10) ◽  
pp. 628-632 ◽  
Author(s):  
Gangjun Liu ◽  
Wangcun Jia ◽  
J. Stuart Nelson ◽  
Zhongping Chen
Keyword(s):  
High Resolution ◽  
Human Skin ◽  
Three Dimensional ◽  
Port Wine Stain ◽  
Port Wine ◽  
Three Dimensional Imaging

Effects of hypobaric pressure on human skin: Feasibility study for port wine stain laser therapy (Part I)

2005 ◽  
Vol 36 (2) ◽  
pp. 124-129 ◽  
Author(s):  
Guillermo Aguilar ◽  
Lars O. Svaasand ◽  
J. Stuart Nelson
Keyword(s):  
Laser Therapy ◽  
Human Skin ◽  
Feasibility Study ◽  
Port Wine Stain ◽  
Port Wine

scholarly journals Ex vivo infection of human skin with herpes simplex virus 1 reveals mechanical wounds as insufficient entry portals via the skin surface

2021 ◽  
Author(s):  
nydia De La Cruz ◽  
Maureen Moeckel ◽  
Lisa Wirtz ◽  
Katharina Sunaoglu ◽  
Wolfram Malter ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Human Skin ◽  
Ex Vivo ◽  
Basal Layer ◽  
Skin Surface ◽  
Herpes Simplex Virus 1 ◽  
Infected Cells ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus 1 (HSV-1) enters its human host via the skin or mucosa. The open question is how the virus invades this highly protective tissue in vivo to approach its receptors in the epidermis and initiate infection. Here, we performed ex vivo infection studies in human skin to investigate how susceptible the epidermis and dermis are to HSV-1 and whether wounding facilitates viral invasion. Upon ex vivo infection of complete skin, only sample edges demonstrated infected cells. After removal of the dermis, HSV 1 efficiently invaded the basal layer, and from there, gained access to suprabasal layers supporting a high susceptibility of the epidermis. In contrast, only single infected cells were detected in the papillary layer of the separated dermis. Interestingly, after wounding, nearly no infection of the epidermis was observed via the skin surface. However, if the wounding of the skin samples led to breaks through the dermis, HSV-1 infected mainly keratinocytes via the wounded dermis. The application of latex beads revealed only occasional entry via the wounded dermis, however, facilitated penetration via the wounded skin surface. Thus, we suggest that the wounded human skin surface allows particle penetration but still provides barriers that prevent HSV 1 invasion.

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