Picosecond-Domain Fractional Laser Treatment Over Hyaluronic Acid Fillers: In Vivo and Clinical Studies.

BACKGROUND AND OBJECTIVES: Combined sequential treatments with multiple modalities such as lasers and soft-tissue fillers are commonly required for the treatment of atrophic acne scars. Recently, fractional treatment with picosecond-domain lasers has proven to be effective for skin rejuvenation and scar treatment. However, little is known about the effects of picosecond-domain fractional laser treatment over hyaluronic acid fillers (HAFs). We aimed to evaluate the in vivo tissue responses to 1064 nm picosecond-domain fractional neodymium:yttrium-aluminum-garnet (Nd:YAG) laser treatments using microlens array (MLA) applied over pre-injected HAF in rats. In addition, we evaluated the efficacy and safety of this combined same-day treatment for atrophic acne scars in patients. STUDY DESIGN/MATERIALS AND METHODS: Sprague-Dawley rats were subjected to 1064 nm picosecond-domain fractional Nd:YAG laser treatment immediately after HAF dermal injection. Skin specimens were histologically evaluated on days 0, 7, and 21. In a clinical study, 36 patients with acne scars were treated concurrently with 1064 nm MLA-type picosecond lasers and HAFs. The patients were scheduled to receive two consecutive treatments at 4-week intervals, with a follow-up visit at 12 weeks after the final treatment. Acne scar photographs were graded using the Goodman and Baron's qualitative and quantitative scales at baseline and 12 weeks post-procedure. RESULTS: Picosecond-domain fractional laser treatment immediately after the dermal injection of HAF into rats did not cause any histological changes in the filler or surrounding skin. In a clinical study, treated subjects (n = 36) achieved significant improvement in acne scars and patient satisfaction. No serious adverse events were observed. CONCLUSIONS: Combined picosecond laser and HAF treatment were proven to be safe and effective based on in vivo and clinical study results. Facial rejuvenation and scar treatment using a picosecond-domain fractional laser may be performed immediately after HAF injection. Lasers Surg. Med. © 2020 Wiley Periodicals, Inc.

Wnt/ß-catenin and ERK pathway activation: A possible mechanism of photobiomodulation therapy with light-emitting diodes that regulate the proliferation of human outer root sheath cells.

BACKGROUND: Outer root sheath cells (ORSCs) play important roles in maintaining hair follicle structure and provide support for the bulge area. The hair growth promoting effects of photobiomodulation therapy (PBMT) have been reported, but the mechanisms for this in human ORCs (hORSCs) have rarely been studied. OBJECTIVE: The aim of this study was to investigate the effect of various wavelengths of light-emitting diode (LED) irradiation on human ORSCs (hORSCs). METHODS: LED irradiation effects on hORSC proliferation and migration were examined with MTT assay, BrdU incorporation assay and migration assays. hORSCs were irradiated using four LED wavelengths (415, 525, 660, and 830 nm) with different low energy levels. LED irradiation effects on the expression of molecules associated with the Wnt/ß-catenin signaling and ERK pathway, hair stem cell markers, and various growth factors and cytokines in hORSCs were examined with real-time PCR and Western blot assay. The effect of the LED-irradiated hORSCs on cell proliferation of human dermal papilla cells (hDPCs) was examined with co-culture and MTT assay. RESULTS: PBMT with LED light variably promoted hORSC proliferation and suppressed cell apoptosis depending on energy level. LED irradiation induced Wnt5a, Axin2, and Lef1 mRNA expression and ß-catenin protein expression in hORSCs. Phosphorylation of ERK, c-Jun, and p38 in hORSCs was observed after LED light irradiation, and ERK inhibitor treatment before irradiation reduced ERK and c-Jun phosphorylation. Red light-treated hORSCs showed substantial increase in IL-6, IL-8, TNF-a, IGF-1, TGF-ß1, and VEGF mRNA. Light irradiation at 660 and 830 nm projected onto hORSCs accelerated in vitro migration. LED-irradiated hORSCs increased hDPCs proliferation when they were co-cultured. The conditioned medium from LED-irradiated hORSCs was sufficient to stimulate hDPCs proliferation. CONCLUSION: These results demonstrate that LED light irradiation induced hORSC proliferation and migration and inhibited apoptosis in vitro. The growth-promoting effects of LEDs on hORSCs appear to be associated with direct stimulation of the Wnt5a/ß-catenin and ERK signaling pathway. Lasers Surg. Med. 49:940-947, 2017. © 2017 Wiley Periodicals, Inc.

Symptomatic aggravation after corticosteroid pulse therapy in definite sporadic Creutzfeldt-Jakob disease with the feature of Hashimoto's encephalopathy.

BACKGROUND: Creutzfeldt-Jakob disease and Hashimoto's encephalopathy often show similar clinical presentation. Among Creutzfeldt-Jakob disease mimics, Hashimoto's encephalopathy is particularly important as it is treatable with corticosteroids. Thus, in cases of middle-aged woman diagnosed with probable Creutzfeldt-Jakob disease and who exhibit high titers of antithyroid antibodies, corticosteroid pulse therapy is typically performed with expectations of near complete recovery from Hashimoto's encephalopathy. Herein, we provide the first case report that exhibited a negative effect of corticosteroid pulse therapy for a patient with Creutzfeldt-Jakob disease with features of Hashimoto's encephalopathy. CASE PRESENTATION: We report a case of 59-year-old Asian woman with blurred vision, dysarthria, myoclonus, and rapidly progressive dementia. Cerebrospinal fluid showed 14-3-3 protein positive. Electroencephalogram showed periodic sharp waves (1.5 Hz) at the bilateral frontal or occipital areas. Magnetic resonance imaging showed high signal intensities at the bilateral cerebral cortex, caudate nucleus, and putamen. The patient was diagnosed with probable Creutzfeldt-Jakob disease. However, serum analysis showed a high titer of antithyroid antibodies. We started corticosteroid pulse therapy with subsequent aggravation of seizure activity including generalized myoclonus, epilepsia parialis continua, and ballistic dyskinesia, which was effectively treated with clonazepam. CONCLUSION: We provide evidence of a case of Creutzfeldt-Jakob disease that exhibited clinical deterioration after corticosteroid therapy. Although histopathological confirmation with brain biopsy is not easily available in Creutzfeldt-Jakob disease patients, selective initiation of corticosteroid pulse therapy should be considered in cases of uncertain diagnosis for differentiation with Hashimoto's encephalopathy.

Different risk factor profiles between transient global amnesia and transient ischemic attack: a large case-control study.

BACKGROUND: The pathophysiology of transient global amnesia (TGA) is not fully understood. This study was conducted to identify the cardiovascular risk factors of TGA compared to those of transient ischemic attack (TIA) and normal controls, using a large number of subjects. In addition to the comparison of risk factors, an association between the observed cardiovascular risk factors in the current study and a pathophysiological mechanism recently investigated was speculated upon. MATERIALS AND METHODS: We performed a retrospective case-control study that compared 293 TGA patients to 632 TIA patients and 293 age- and sex-matched normal controls. Demographic details and cardiovascular risk factors were carefully recorded. RESULTS: TGA patients had a significantly higher prevalence of ischemic heart disease and hyperlipidemia; however, they had a lower prevalence of hypertension, diabetes mellitus, ischemic stroke and atrial fibrillation when compared to TIA patients. When compared to age- and sex-matched normal controls, TGA patients also had a significantly higher prevalence of hyperlipidemia, previous ischemic stroke and ischemic heart disease. CONCLUSION: The cardiovascular risk factors identified in TGA patients in this study were different from those of previously reported studies. This disproportionate prevalence of cardiovascular risk factors may constitute possible evidence that TGA and TIA differ in their pathophysiological mechanism. In addition, some cardiovascular risk factors, such as hyperlipidemia and ischemic heart disease, should be regarded as possible risk factors of TGA.