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Ablative fractional laser treatment has been extensively used for resurfacing atrophic acne scars. However, few studies have investigated how the parameters set during laser procedures affect efficacy. In this retrospective study, we examined the relationship between efficacy and Fitzpatrick skin type, gender, age, follow-up duration, energy, and treatment sessions utilizing ablative fractional carbon dioxide (CO

Background. Becker’s nevus (BN) severely affects a patient’s appearance and can lead to depression, especially when it involves the face or neck. Currently, there is no effective treatment. Laser therapy has become popular, but its efficacy has not been confirmed. We evaluated the efficacy and safety of lasers in treating BN. Methods. This retrospective study involved 49 patients exposed to different laser treatments who completed at least one treatment session and follow-up. Results. The patients treated with the 755-nm alexandrite picosecond laser and Q-switched 694-nm ruby laser gained relatively good results: 3.07 ± 1.09 and 2.87 ± 1.14 on the five-point scale and 3.47 ± 0.73 and 3.40 ± 0.85 on the GAIS, respectively. However, the results of the 755-nm alexandrite picosecond laser with a diffractive focus lens array and the fractionated 1064-nm neodymium-doped: yttrium aluminum garnet picosecond laser were poor. Furthermore, there were marked differences between the number of treatment sessions and treatment effects, both for the five-point grading score for pigment clearance (F = 15.246, p < 0.001 ) and GAIS (F = 15.469, p < 0.001 ). Concerning different lasers and efficacy, there were no marked differences between the five-point grading scale and the GAIS ( p > 0.05 ). Conclusions. Although the efficacy of various lasers for BN is not satisfactory and there are no marked differences between picosecond and Q-switched lasers, they can help in selecting an appropriate laser for slight-to -moderate pigment removal. The 755-nm alexandrite picosecond laser is a new option, whereas nonablative fractional picosecond lasers for BN are not recommended. Increasing the number of treatment sessions can improve the curative effect slightly.

IMPORTANCE: The majority of the patients with head and neck cancer (HNC) experience taste dysfunction (TD) during or after radiotherapy (RT). However, prospectively collected data for taste dysfunction have been limited, especially in the era of intensity-modulated RT (IMRT). OBJECTIVE: To evaluate the taste function in patients with HNC receiving IMRT by investigating the association between time course and recovery of TD in both acute and late phases. DESIGN, SETTING, AND PARTICIPANTS: From August 2017 to November 2020, patients treated at the Chang Gung Memorial Hospital with curative or postoperative IMRT for HNC were enrolled in this prospective cohort study. The data analysis was performed from March 2021 to January 2022. EXPOSURES: IMRT with and without concurrent chemotherapy. MAIN OUTCOMES AND MEASURES: Taste function was measured using the whole-mouth solution method for 4 tastes (salt, sweet, sour, and bitter). Subjective evaluations (National Cancer Institute Common Terminology Criteria for Adverse Events [version 4.03] and Subjective Total Taste Acuity scale) were used. Patient self-reported quality of life was evaluated using European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire Head and Neck Module (EORTC QLQ-H&N35). RESULTS: A total of 87 patients (78 [90%] men and 9 [10%] women; mean [range] age, 58 [31-80] years) were enrolled. Overall TD rates were 79 of 86 (91.9%), 63 of 83 (75.9%), 27 of 81 (33.3%), 5 of 56 (8.9%), and 2 of 30 (6.7%) during RT, and 1 week, 3 months, 6 months, and 1 year after RT, respectively. Positive correlation occurred between objectively measured taste loss for the 4 taste qualities and subjective perception of taste loss. Only oral cavity mean dose 4000 cGy or greater predicted TD 3 months after RT. The mean oral cavity doses to the predicted 15% (D(15)), 25% (D(25)), and 50% (D(50)) probabilities were 25, 38, and 60 Gy at 3 months and 57, 60, and 64 Gy at 6 months, respectively. CONCLUSIONS AND RELEVANCE: In this cohort study, most patients still experienced TD during and at 3 months after RT. Only a few patients experienced long-term TD. A high oral cavity dose was associated with TD in patients with HNC receiving IMRT. Reducing oral cavity dose may promote early recovery of taste function after IMRT.

Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous unit, and Propionibacterium acnes (P. acnes) has been implicated in acne inflammation. Numerous studies have shown that non-coding RNAs play important roles in regulating the pathophysiological processes of acne. In addition, the first imprinted long non-coding RNA (lncRNA) identified, H19, plays a critical role in inflammatory disease. However, the expression and role of H19 in AV remain unclear. In this study, we investigated the effects of H19 in keratinocytes and explored the regulatory mechanisms underlying these effects. H19 was upregulated in keratinocytes treated with P. acnes in a concentration-dependent manner. The phosphorylated forms of the nuclear factor (NF)-κB-related proteins IκBα (p-IκBα) and p65 (p-P65) were significantly upregulated after P. acnes treatment. Additionally, secretion of the proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 was upregulated in a concentration-dependent manner. Knockdown of H19 inhibited the expression of p-IκBα and p-P65 as well as the secretion of TNF-α, IL-6, and IL-8 in keratinocytes treated with P. acnes. Moreover, H19 was found to exert its proinflammatory effects by activating NF-κB. H19, which was localized mainly in the cytoplasm of keratinocytes, facilitated Toll-like receptor 2 (TLR2) expression by acting as a miR-196a sponge. H19 thus promoted the activation of NF-κB and the secretion of inflammatory cytokines through the miR-196a/TLR2 axis. These findings provide novel insight into the pathogenesis of AV.

Nevus of Ota has been successfully treated by lasers. Currently, 1064 nm picosecond Nd:YAG lasers have become available for the treatment of pigmented disorders. However, there are few studies concerning the application of 1064 nm picosecond Nd:YAG laser in nevus of Ota. This study aimed to evaluate the efficacy and safety of a 1064 nm picosecond Nd:YAG laser for the treatment of nevus of Ota. We conducted a retrospective analysis of Chinese patients with nevus of Ota who had been treated with a 1064 nm picosecond Nd:YAG laser. Those who had any other laser treatment during the period of picosecond laser treatment were excluded. Via a visual analog scale for percentage of pigmentary clearance in standard photographs, the treatment efficacy was assessed by three blinded physician evaluators. A total of 16 subjects were included in this retrospective study. The average age at the beginning of treatment was 16.87 years old (range of 4 months to 59 years), and all patients were of Fitzpatrick skin type IV. Total treatment ranged from 1 to 5 sessions. A 1064 nm picosecond Nd:YAG laser with a mean fluence of 1.8-4.3 J/cm2 was used at 3-12 month intervals. The mean efficacy score for all 16 patients was 2.56 after one session, and the mean efficacy score of 13 patients who completed two sessions and nine patients who completed three sessions were 3.15 and 3.51, respectively. Postinflammatory hyperpigmentation after treatment was only observed in 1 (1/16, 6.25%) patient. The 1064 nm picosecond Nd:YAG laser is an effective and safe approach for treating nevus of Ota.

The Cutibacterium acnes (also called Propionibacterium acnes, P. acnes)-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3', 4'-tetrahydroxy-trans-stilbene, PCT) is naturally present in many human diets and plays antioxidant and anti-inflammatory roles that inhibit cell proliferation and migration. We aimed to analyse the functions and underlying mechanisms of PCT in P. acnes-stimulated keratinocytes. First, PCT showed no toxicity against the normal human keratinocyte cell line HaCaT but inhibited P. acnes-induced HaCaT cell proliferation. Next, PCT promoted the nuclear translocation and target gene transcription of the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), thereafter decreasing intracellular reactive oxygen species (ROS) levels. In addition, PCT inhibited the nuclear translocation of p65 [a subunit of nuclear factor kappa B (NF-κB)] and the secretion of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Finally, a transfection assay showed that PCT inhibited P. acnes-induced HaCaT cell proliferation and migration by activating the antioxidant Nrf2 pathway and inhibiting the inflammatory NF-κB pathway. Our data suggested that PCT alleviated P. acnes-induced HaCaT cell proliferation and migration through its antioxidant and anti-inflammatory roles, suggesting the potential of PCT to treat AV.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with complicated genetic inheritance. Programmed death 1 (PD-1), a negative T cell regulator to maintain peripheral tolerance, induces negative signals to T cells during interaction with its ligands and is therefore a candidate gene in the development of SLE. In order to examine whether expression levels of PD-1 contribute to the pathogenesis of SLE, 30 patients with SLE and 30 controls were recruited and their PD-1 expression levels in peripheral blood mononuclear cells (PBMCs) were measured via flow cytometry and quantitative real-time-reverse transcription polymerase chain reaction (RT-PCR). Also, whether PD-1 expression levels are associated with the variant of the SNP rs36084323 and the SLE Disease Activity Index (SLEDAI) was studied in this work. The PD-1 expression levels of SLE patients were significantly increased compared with those of the healthy controls. The upregulated PD-1 expression levels in SLE patients were greatly associated with SLEDAI scores. No significant difference was found between PD-1 expression levels and SNP rs36084323. The results suggest that increased expression of PD-1 may correlate with the pathogenesis of SLE, upregulated PD-1 expression may be a biomarker for SLE diagnosis, and PD-1 inhibitor may be useful to SLE treatment.

Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disease. The T cell immunoglobulin and mucin domain (TIM) family is associated with autoimmune diseases, but its level of expression in the immune cells of patients with SLE is still uncertain. The aim of this study was to examine whether TIM-3 and Galectin-9 (Gal-9) contribute to the pathogenesis of SLE. In total, 30 patients with SLE and 30 healthy controls were recruited, and their levels of TIM-3 expression in peripheral blood mononuclear cells (PBMCs) were examined via flow cytometry. Meanwhile, the levels of Gal-9 expression in serum and in PBMCs were measured via an enzyme-linked immunosorbent assay (ELISA) kit and immunofluorescence staining, respectively. The relation between the level of TIM-3 or Gal-9 expression and the SLE disease activity index (SLEDAI) was also studied. Finally, the function of the TIM-3 and Gal-9 pathway in the pathogenesis of SLE was explored. Our results showed that the levels of expression of TIM-3 and Gal-9 on CD4(+) T cells, CD8(+) T cells, CD56(+) T cells and in serum in patients with SLE were significantly higher than those of healthy controls. We found that the level of Gal-9 expression was significantly higher in both serum and PMBCs of patients with SLE than in healthy controls. The up-regulation of TIM-3 and Gal-9 expression in patients with SLE was closely related to the SLEDAI scores. In addition, Gal-9 blocking antibody significantly inhibited CD3-stimulated PBMC proliferation and Th1-derived cytokines (IL-2, IFN-γ, and TNF-α), Th2-derived cytokines (IL-4, IL-10), a Th17-derived cytokine (IL-17A), and release of a pro-inflammatory factor (IL-6) in patients with SLE. The results suggest that increased expression of TIM-3 and Gal-9 may be a biomarker for SLE diagnosis and that the TIM-3 pathway may be a target for SLE treatment.