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
Author(s):  
John S. Viator ◽  
Steven L. Jacques ◽  
Guillermo Aguilar

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.


2019 ◽  
Vol 20 (9) ◽  
pp. 2243 ◽  
Author(s):  
Vi Nguyen ◽  
Marcelo Hochman ◽  
Martin C. Mihm ◽  
J. Stuart Nelson ◽  
Wenbin Tan

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.


2013 ◽  
Vol 45 (10) ◽  
pp. 628-632 ◽  
Author(s):  
Gangjun Liu ◽  
Wangcun Jia ◽  
J. Stuart Nelson ◽  
Zhongping Chen

2005 ◽  
Vol 36 (2) ◽  
pp. 124-129 ◽  
Author(s):  
Guillermo Aguilar ◽  
Lars O. Svaasand ◽  
J. Stuart Nelson

1996 ◽  
Vol 11 (3) ◽  
pp. 199-204 ◽  
Author(s):  
J. S. Nelson ◽  
T. E. Milner ◽  
B. S. Tanenbaum ◽  
D. M. Goodman ◽  
M. J. C. Van Gemert

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