Selective photothermolysis in acne treatment: The impact of laser power.

BACKGROUND: Selective photothermolysis (SPT) using a 1726 nm laser has emerged as a safe and effective treatment option for acne vulgaris by targeting sebaceous glands (SG). Power output plays a crucial role in determining treatment selectivity and efficacy. AIMS: This work highlights the advantages of a higher-power laser source and outlines the limitations of lower-power laser sources and the subsequent impact on treatment. METHODS: Light transport and bioheat transfer simulations were performed to demonstrate photothermal impact on the SG and the surrounding dermis when irradiated by a high- or lower-power laser source. RESULTS: The simulations showed that a single higher-power-shorter-pulse (HPSP) selectively increases SG temperature well beyond bulk temperatures, which is desirable for SPT. Selectivity decreases linearly with power for the single lower-power-longer-pulses (LPLP) exposure. A multiple-LPLP approach elevates bulk temperatures significantly more than a single-pulse strategy, compromising selectivity. CONCLUSION: The goal of SPT is to damage SG safely and effectively by creating an intense temperature rise localized to the SG while moderately increasing the dermis temperature. This goal is mostly achieved with higher-power lasers that deliver a single HPSP. Lower-power lasers, longer pulse widths, and multi-pulse strategies result in higher bulk temperatures and lower SG selectivity, making such treatment challenging to execute while adding a higher risk of discomfort and downtime.

A novel 1726-nm laser system for safe and effective treatment of acne vulgaris.

Selective photothermolysis of the sebaceous glands has the potential to be an effective alternative for treating acne vulgaris. However, the translation of this technique to clinical settings has been hindered by a lack of appropriate energy sources to target sebaceous glands, concerns surrounding safety, and treatment-related discomfort and downtime. In this work, we introduce the first FDA-approved system that combines a 1726-nm laser and efficient contact cooling to treat mild, moderate, and severe acne effectively while ensuring safety and minimal patient discomfort without adjunct pain mitigation techniques. Light transport and bioheat transfer simulations were performed to demonstrate the system's efficacy and selectivity. The resulting thermal damage to the skin and sebaceous glands was modeled using the Arrhenius kinetic model. Numerical simulations demonstrated that combining laser energy and optimal contact cooling could induce a significant temperature increase spatially limited to the sebaceous gland; this results in highly selective targeting and maximum damage to the sebaceous gland while preserving other skin structures. In vivo human facial skin histology results corroborated the simulation results. The studies reported here demonstrate that the presented 1726-nm laser system induces selective photothermolysis of the sebaceous gland, providing a safe and effective method for the treatment of acne vulgaris.

Vibrational dissipation and dephasing of I2 (v = 1-19) in solid Kr.

Time- and frequency-resolved coherent anti-Stokes Raman scattering is used to carry out systematic measurements of vibrational dephasing on I2 (v = 1-19) isolated in solid Kr, as a function of temperature, T = 7-45 K. The observed quantum beats, omega(v', v") allow an accurate reconstruction of the solvated molecular potential, which is well represented by the Morse form: omega(e) = 211.56 +/- 0.14, omega(e)chi(e) = 0.658 +/- 0.006. Near T = 7 K, the coherence decay rates gamma(v,0) become independent of temperature and show a linear v-dependence, indicative of dissipation, which must be accompanied by the simultaneous creation of at least four phonons. At higher temperatures, the T-dependence is exponential and the v-dependence is quadratic, characteristic of pure dephasing via pseudo-local phonons. A normal mode analysis suggests librations as the principle modes responsible for pure dephasing.

Introduction of a new regulatory mechanism into human hemoglobin.

Previous studies on bovine hemoglobin (HbBv) have suggested amino acid substitutions, which might introduce into human hemoglobin (HbA) functional characteristics of HbBv, namely a low intrinsic oxygen affinity regulated by Cl(-). Accordingly, we have constructed and characterized a multiple mutant, PB5, [beta(V1M + H2 Delta + T4I + P5A + A76K)] replacing four amino acid residues of HbA with those present at structurally analogous positions in HbBv, plus an additional substitution, beta T4I, which does not occur in either HbBv or HbA. This 'pseudobovine' hemoglobin has oxygen binding properties very similar to those of HbBv: the P(50) of HbA, PB5 and HbBv in the absence of Cl(-) are 1.6, 4.6 and 4.8 torr, respectively, and in 100 mM Cl(-) are 3.7, 10.5 and 12 torr, respectively. Moreover, PB5 has 3-fold slower autoxidation rate compared to HbA and HbBv. These are desirable characteristics for a human hemoglobin to be considered for use as a clinical artificial oxygen carrier. Although the functional properties of PB5 and HbBv are similar, van't Hoff plots indicate that the two hemoglobins interact differently with water, suggesting that factors regulating the R to T equilibrium are not the same in the two proteins. A further indication that PB5 is not a functional mimic of HbBv derives from PB5(control), a human hemoglobin with the same substitutions as PB5, except the beta T4I replacement. PB5(control) has a high oxygen affinity (P(50)=2.3 torr) in the absence of Cl(-), but retains the Cl(-) effect of PB5. The Cl(-) regulation of oxygen affinity in PB5 involves lysine residues at beta 8 and beta 76. PB4, which has the same substitutions as PB5 except beta A76K, and PB6, which has all the substitutions of PB5 plus beta K8Q, both have a low intrinsic oxygen affinity, like HbBv and PB5, but exhibit a decreased sensitivity to Cl(-). Since HbBv has lysine residues at both beta 8 and beta 76, these results imply that Cl(-) regulation in HbBv likewise involves these two residues. The mechanism responsible for the low intrinsic oxygen affinity of HbBv remains unclear. It is suggested that residues peculiar to HbBv at the alpha(1)beta(1) interface may play a role.