UNC13D inhibits STING signaling by attenuating its oligomerization on the endoplasmic reticulum.

Stimulator of interferon genes (STING) is an essential signaling protein that is located on the endoplasmic reticulum (ER) and triggers the production of type I interferons (IFN) and proinflammatory cytokines in response to pathogenic DNA. Aberrant activation of STING is linked to autoimmune diseases. The mechanisms underlying homeostatic regulation of STING are unclear. Here, we report that UNC13D, which is associated with familial hemophagocytic lymphohistiocytosis (FHL3), is a negative regulator of the STING-mediated innate immune response. UNC13D colocalizes with STING on the ER and inhibits STING oligomerization. Cellular knockdown and knockout of UNC13D promote the production of interferon-ß (IFN-ß) induced by DNA viruses, but not RNA viruses. Moreover, UNC13D deficiency also increases the basal level of proinflammatory cytokines. These effects are diminished by an inhibitor of STING signaling. Furthermore, the domains involved in the UNC13D/STING interaction on both proteins are mapped. Our findings provide insight into the regulatory mechanism of STING, the previously unknown cellular function of UNC13D and the potential pathogenesis of FHL3.

Candidalysin, a Virulence Factor of Candida albicans, Stimulates Mast Cells by Mediating Cross-Talk Between Signaling Pathways Activated by the Dectin-1 Receptor and MAPKs.

PURPOSE: Although mast cells (MCs) modulate the activity of effector cells during Candida albicans infection, their role in the pathogenesis of candidiasis remains unclear. Candidalysin, a C. albicans-derived peptide toxin, is a crucial factor in fungal infections. We aimed to investigate the effect of candidalysin on MC activation and the underlying molecular mechanism. METHODS: Serum from candidalysin-immunized mice was used to measure candidalysin expression in patients infected with C. albicans. MC degranulation and migration were evaluated by ß-hexosaminidase release assay and chemotaxis assay, respectively. EIA and ELISA were used to evaluate the production of eicosanoids and cytokines/chemokines, respectively. The production of nitric oxide (NO) was measured with a DAF-FM diacetate kit, while reactive oxygen species (ROS) production was analyzed by flow cytometry. MAPK activation was evaluated by Western blotting. RESULTS: We detected high candidalysin expression in the lesions of patients infected with C. albicans, and the MC number was increased in these lesions. LL-37 colocalized with MCs in the lesions of candidiasis patients. Candidalysin-enhanced MC accumulation in mice and treating LAD2 and HMC-1 cells with candidalysin induced their degranulation, migration, and production of pro- and anti-inflammatory cytokines/chemokines, eicosanoids, ROS, NO, and LL-37. Interestingly, C. albicans strains lacking candidalysin failed to induce MC activation. Moreover, candidalysin increased dectin-1 expression, and the inhibition of dectin-1 decreased MC activation. Downstream dectin-1 signaling involved the MAPK pathways. CONCLUSION: The finding that candidalysin causes cutaneous MC activation may improve our understanding of the role of MCs in the pathology of cutaneous C. albicans infection.

Antimicrobial peptide derived from insulin-like growth factor-binding protein 5 improves diabetic wound healing.

Impaired keratinocyte functions are major factors that are responsible for delayed diabetic wound healing. In addition to its antimicrobial activity, the antimicrobial peptide derived from insulin-like growth factor-binding protein 5 (AMP-IBP5) activates mast cells and promotes keratinocyte and fibroblast proliferation and migration. However, its effects on diabetic wound healing remain unclear. Human keratinocytes were cultured in normal or high glucose milieus. The production of angiogenic growth factor and cell proliferation and migration were evaluated. Wounds in normal and streptozotocin-induced diabetic mice were monitored and histologically examined. We found that AMP-IBP5 rescued the high glucose-induced attenuation of proliferation and migration as well as the production of angiogenin and vascular endothelial growth factors in keratinocytes. The AMP-IBP5-induced activity was mediated by the epidermal growth factor receptor, signal transducer and activator of transcription 1 and 3, and mitogen-activated protein kinase pathways, as indicated by the inhibitory effects of pathway-specific inhibitors. In vivo, AMP-IBP5 markedly accelerated wound healing, increased the expression of angiogenic factors and promoted vessel formation in both normal and diabetic mice. Overall, the finding that AMP-IBP5 accelerated diabetic wound healing by protecting against glucotoxicity and promoting angiogenesis suggests that AMP-IBP5 might be a potential therapeutic target for treating chronic diabetic wounds.

Birth weight is associated with obesity and T2DM in adulthood among Chinese women.

BACKGROUND: Previous studies have indicated an association between birth weight (BW) and type 2 diabetes mellitus (T2DM), but few studies have explored this relationship under different conditions of obesity in adulthood. METHODS: A total of 4,005 individuals from ten provinces of China were randomly selected to participate in this study. We used a questionnaire to collect age, BW, current weight, height, T2DM history, age at T2DM diagnosis, and other variables. The participants were divided into three groups were according to BW trisection (BW ≤ 2500 g for the lower BW group, 2500 g < BW ≤ 3500 g for the normal BW group, and BW > 3500 g for the higher BW group). The cutoff of overweight and obesity were 25 kg/m2 and 28 kg/m2, respectively. RESULTS: The prevalence rates of T2DM among women with lower BW, normal BW and higher BW were 5.2%, 3.6% and 2.0%, respectively. The obesity prevalence rates in the lower BW, normal BW and higher BW groups were 8.1%, 6.7% and 9.0%, respectively. In the obese population, we did not find a relationship between BW and T2DM, but in the nonobese population, we found that with increasing BW, the risk of developing T2DM was reduced. Obese status in adulthood modified the association between BW and the risk of T2DM. CONCLUSION: There is a "U" shape association between BW and risk of adulthood obesity in Chinese women, but this trend is not existed between BW and risk of developing T2DM. In non-overweight females, the risk of developing T2DM decreased with increasing BW, but this trend was not observed in overweight females.

Exogenous factors in the pathogenesis of atopic dermatitis: Irritants and cutaneous infections.

Atopic dermatitis (AD) is a chronic relapsing inflammatory cutaneous disease that is often associated with other atopic symptoms, such as food allergy, allergic rhinitis and asthma, leading to significant morbidity and healthcare costs. The pathogenesis of AD is complicated and multifactorial. Although the aetiology of AD remains incompletely understood, recent studies have provided further insight into AD pathophysiology, demonstrating that the interaction among genetic predisposition, immune dysfunction and environmental provocation factors contributes to its development. However, the increasing prevalence of AD suggests that environmental factors such as irritation and cutaneous infection play a crucial role in triggering and/or aggravating the disease. Of note, AD skin is susceptible to bacterial, fungal and viral infections, and microorganisms may colonize the skin and aggravate AD symptoms. Overall, understanding the mechanisms by which these risk factors affect the cutaneous immunity of patients with AD is of great importance for developing a precision medicine approach for treatment. This review summarizes recent developments in exogenous factors involved in the pathogenesis of AD, with special emphasis on irritants and microbial infections.

Activated NLR family pyrin domain containing 3 (NLRP3) inflammasome in keratinocytes promotes cutaneous T-cell response in patients with vitiligo.

BACKGROUND: Keratinocytes can function as innate immune cells under oxidative stress and aggravate the cutaneous T-cell response that undermines melanocytes in the setting of vitiligo. The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a regulator of innate immunity that exists in keratinocytes. However, the role of the NLRP3 inflammasome in the pathogenesis of vitiligo has not been investigated. OBJECTIVE: We sought to explicate the contribution of the activated NLRP3 inflammasome in keratinocytes to the autoimmune response in patients with vitiligo. METHODS: Perilesional and serum samples from patients with vitiligo were collected to examine the status of the NLRP3 inflammasome in the setting of vitiligo. Cultured keratinocytes were treated with H2O2 to investigate the mechanism for NLRP3 inflammasome activation under oxidative stress. Peripheral blood T cells were extracted from patients with vitiligo to explore the influence of the NLRP3 inflammasome on the T-cell response in patients with vitiligo. RESULTS: Expressions of NLRP3 and downstream cytokine IL-1ß were consistently increased in perilesional keratinocytes of patients with vitiligo. Notably, serum IL-1ß levels were increased in patients with vitiligo, correlated with disease activity and severity, and decreased after effective therapy. Furthermore, oxidative stress promoted NLRP3 inflammasome activation in keratinocytes through transient receptor potential cation channel subfamily M member 2 (TRPM2), a redox-sensitive cation channel, which was dependent on TRPM2-mediated calcium influx. More importantly, blocking TRPM2-induced NLRP3 inflammasome activation in keratinocytes impaired chemotaxis for CD8+ T cells and inhibited the production of cytokines in T cells in patients with vitiligo. CONCLUSION: Oxidative stress-induced NLRP3 inflammasome activation in keratinocytes promotes the cutaneous T-cell response, which could be targeted for the treatment of vitiligo.

Homocysteine induces melanocytes apoptosis via PERK-eIF2α-CHOP pathway in vitiligo.

Vitiligo is a depigmentation disorder that develops as a result of the progressive disappearance of epidermal melanocytes. The elevated level of amino acid metabolite homocysteine (Hcy) has been identified as circulating marker of oxidative stress and known as a risk factor for vitiligo. However, the mechanism underlying Hcy-regulated melanocytic destruction is currently unknown. The present study aims to elucidate the effect of Hcy on melanocytic destruction and its involvement in the pathogenesis of vitiligo. Our results showed that Hcy level was significantly elevated in the serum of progressive vitiligo patients. Notably, Hcy induced cell apoptosis in melanocytes via activating reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress protein kinase RNA-like ER kinase (PERK)-eukaryotic translation initiation factor 2α (eIF2α)-C/EBP homologous protein (CHOP) pathway. More importantly, folic acid, functioning in the transformation of Hcy, could lower the intracellular Hcy level and further reverse the apoptotic effect of Hcy on melanocytes. Additionally, Hcy disrupted melanogenesis whereas folic acid supplementation could reverse the melanogenesis defect induced by Hcy in melanocytes. Taken together, Hcy is highly increased in vitiligo patients at progressive stage, and our in vitro studies revealed that folic acid could protect melanocytes from Hcy-induced apoptosis and melanin synthesis inhibition, indicating folic acid as a potential benefit agent for patients with progressive vitiligo.

Decreased Serum Exosomal miR-152-3p Contributes to the Progression of Acute Ischemic Stroke.

BACKGROUND: The current study aims to investigate the expression and potential role of exosome-derived miR-152-3p in acute ischemic stroke (AIS) patients. METHODS: Exosomes were isolated from AIS patients and healthy controls. The level of exosome miR-152-3p was examined using RT-PCR. Receiver operating characteristic (ROC) curves were used to assess exosome miR-152-3p as a biomarker, and the area under the curve (AUC) was reported. RESULTS: Our data showed that the expression of serum exosome miR-152-3p in patients with AIS was significantly lower than in healthy controls. In contrast to those with NIHSS score < 7, the level of exosome miR-152-3p was significantly reduced in AIS patients with NIHSS score ≥ 7, indicating that the decrease of exosome miR-152-3p level is significantly related to the severity of endothelial injury. Moreover, the lowest level of exosome miR-152-3p was found in large-artery atherosclerosis (LAA) patients compared to that in small-vessel occlusion (SAA), cardioembolism (CE) and stroke of undetermined etiology (SUE) group. In addition, exosome miR-152-3p level was significantly lower in acute phase than in chronic phase. ROC curve showed that the AUC of exosome miR-152-3p level was 0.935, which indicated that exosome miR-152-3p level could distinguish AIS patients from non-healthy controls. CONCLUSIONS: In summary, exosome miR-152-3p is a risk factor of cerebral infarction. Enhancing the expression of exosome miR-152-3p in the circulating system may be a promising strategy for the prevention and treatment of AIS.

Biological Characteristics and Molecular Mechanism of Fludioxonil Resistance in Botrytis cinerea From Henan Province of China.

The gray mold caused by Botrytis cinerea has a significant impact on tomato production throughout the world. Although the synthetic fungicide fludioxonil can effectively control B. cinerea, there have been several reports of resistance to this fungicide. This study indicated that all of the fludioxonil-resistant strains tested, including one field-resistant isolate and four laboratory strains, had reduced fitness relative to sensitive isolates. In addition to having reduced growth, sporulation, and pathogenicity, the resistant strains were more sensitive to osmotic stress and had significantly (P < 0.05) higher peroxidase activity. BOs1, a kinase in the high-osmolarity glycerol stress response signal transduction pathway, is believed to harbor mutations related to fludioxonil resistance. Sequence analysis of their BOs1 sequences indicated that the fludioxonil-resistant field isolate, XXtom1806, had four point mutations resulting in four amino acid changes (I365S, S531G, T565N, and T1267A) and three amino acids (I365S, S531G, and T565N) in the histidine kinases, adenylyl cyclases, methyl-accepting chemotaxis receptors, and phosphatases domain, which associated with fludioxonil binding. Similarly, two of the laboratory strains, XXtom-Lab1 and XXtom-Lab4, had three (Q846S, I1126S, and G415D) and two (P1051S and V1241M) point mutations, respectively. A third strain, XXtom-lab3, had a 52-bp insertion that included a stop codon at amino acid 256. Interestingly, the BOs1 sequence of the fourth laboratory strain, XXtom-lab5, was identical to those of the sensitive isolates, indicating that an alternative resistance mechanism exists. The study also found evidence of positive cross-resistance between fludioxonil and the dicarboximide fungicides procymidone and iprodione, but no cross-resistance was detected with any other fungicides tested, including boscalid, carbendazim, tebuconazole, and fluazinam.

Role of Antimicrobial Peptides in Skin Barrier Repair in Individuals with Atopic Dermatitis.

Atopic dermatitis (AD) is a common chronic inflammatory skin disease that exhibits a complex interplay of skin barrier disruption and immune dysregulation. Patients with AD are susceptible to cutaneous infections that may progress to complications, including staphylococcal septicemia. Although most studies have focused on filaggrin mutations, the physical barrier and antimicrobial barrier also play critical roles in the pathogenesis of AD. Within the physical barrier, the stratum corneum and tight junctions play the most important roles. The tight junction barrier is involved in the pathogenesis of AD, as structural and functional defects in tight junctions not only disrupt the physical barrier but also contribute to immunological impairments. Furthermore, antimicrobial peptides, such as LL-37, human b-defensins, and S100A7, improve tight junction barrier function. Recent studies elucidating the pathogenesis of AD have led to the development of barrier repair therapy for skin barrier defects in patients with this disease. This review analyzes the association between skin barrier disruption in patients with AD and antimicrobial peptides to determine the effect of these peptides on skin barrier repair and to consider employing antimicrobial peptides in barrier repair strategies as an additional approach for AD management.

Genetic polymorphism of the Nrf2 promoter region is associated with vitiligo risk in Han Chinese populations.

The nuclear factor erythroid-derived two-like 2-antioxidant response element (Nrf2-ARE) pathway and its downstream antioxidant enzyme heme oxygenase-1 (HMOX1 or HO-1) play essential roles in H2 O2 -induced oxidative damage in human melanocytes. However, the link between Nrf2 promoter polymorphisms and susceptibility to oxidative stress-related diseases such as vitiligo is unknown. This study evaluated the association of the Nrf2 and HO-1 genes polymorphisms with vitiligo susceptibility. In this case-control study of 1136 Han Chinese vitiligo patients and 1200 controls, Nrf2 (rs35652124 and rs6721961) and HO-1 (rs2071746) genes were genotyped by PCR-restriction fragment length polymorphism analysis. Overall, a significantly decreased risk of vitiligo was found to be associated with Nrf2 rs35652124 CC and combined (CT+CC) genotypes [odds ratio (OR) 0.64, 95% confidence interval (CI) 0.50-0.83 and OR, 0.84, 95% CI 0.71-0.99, respectively], as well as among subgroups: female, onset age ≤20 and never smoker. We subsequently found that Nrf2 rs35652124 C allele had higher transcriptional activity in the luciferase reporter assay compared with Nrf2 rs35652124 T allele. Furthermore, we investigated serum HO-1 activity was associated with the rs35652124 CT+CC genotype and lower in patients than in controls (P = 0.024). Logistic regression analysis showed a dose-response relationship between lower vitiligo risk and increased HO-1 activity in rs35652124 CT+CC genotype carriers (Ptrend < 0.05). These findings indicate that the C allele of rs35652124 located in the promoter region of Nrf2 gene is associated with protective effect on vitiligo in a Han Chinese population.

[Study on lignans of Gentianella acuta].

OBJECTIVE: To study the lignans from the whole plant of Gentianella acuta. METHODS: The compounds were isolated by various chromatographic techniques and indentified by spectroscopic methods. RESULTS: Nine compounds were isolated and identified as (7R,8S) -dehydrodiconiferyl alcohol-4,9'-O-beta-D-glucopyranoside (1), alaschanisoside A (2), citrusin A (3), olivil-4'-O-beta-D-glucopyranoside (4), leptolepisol D (5), acanthoside D (6), (+) pinoresinol-4-O-beta-D-glucopyranoside (7), (+) 8-hydroxypinoresinol-4-O-beta-D-glucopyranoside (8), and (+) pinoresinol-8-O-beta-D-glucopyranoside (9). CONCLUSION: Compounds 1 - 9 are isolated from this plant for the first time, compounds 1 and 9 are isolated from Gentianella genus for the first time,and compounds 2, 3 and 5 - 8 are isolated from Gentianaceae family for the first time.

High Temperature Oxidation Behavior of Additive Manufactured Ti6Al4V Alloy with the Addition of Yttrium Oxide Nanoparticles.

Titanium alloys face challenges of high temperature oxidation during the service period when used as aircraft engine components. In this paper, the effect of Y2O3 addition on the oxidation behavior and the microstructural change of the Ti6Al4V alloy fabricated by selective laser melting (SLM) was comprehensively studied. The results show that the surface of the Ti6Al4V alloy is a dense oxide layer composed of TiO2 and Al2O3 compounds. The thickness of the oxide layer of the Ti6Al4V increased from 59.55 µm to 139.15 µm. In contrast, with the addition of Y2O3, the thickness of the oxide layer increased from 35.73 µm to 80.34 µm. This indicates that the thickness of the oxide layer formation was a diffusion-controlled process and, therefore, the thickness of the oxide layer increased with an increase in temperature. The Ti6Al4V-1.0 wt.% Y2O3 alloy exhibits excellent oxidation resistance, and the thickness is significantly lower than that of the Ti6Al4V alloy. The oxidation kinetics of the Ti6Al4V and Ti6Al4V-1.0 wt.% Y2O3 alloys at 600 °C and 800 °C follows a parabolic rule, whereas the oxidation of the Ti6Al4V and Ti6Al4V-1.0 wt.% Y2O3 alloys at 1000 °C follows the linear law. The average microhardness values of Ti6Al4V samples after oxidation increased to 818.9 ± 20 HV0.5 with increasing temperature, and the average microhardness values of the Ti6Al4V-1.0 wt.% Y2O3 alloy increases until 800 °C and then decreases at 1000 °C. The addition of Y2O3 shows a significant improvement in the microhardness during the different temperatures after oxidation.

Membranal Expression of Calreticulin Induced by Unfolded Protein Response in Melanocytes: A Mechanism Underlying Oxidative Stress-Induced Autoimmunity in Vitiligo.

Calreticulin (CRT), a damage-associated molecular pattern molecule, is reported to translocate from the endoplasmic reticulum to the membrane in melanocytes under oxidative stress. To investigate the potential role of CRT in the pathogenesis of vitiligo, we analyzed the correlation between CRT and ROS in serum and lesions of vitiligo, detected CRT and protein kinase RNA-like endoplasmic reticulum kinase (PERK) expression in vitiligo lesions, and studied the production of CRT and mediators of unfolded protein response (UPR) pathway and then tested the chemotactic migration of CD8+ T cells or CD11c+ CD86+ cells. Initially, we verified the overexpression of CRT in perilesional epidermis that was positively correlated with the disease severity of vitiligo. Furthermore, the PERK branch of UPR was confirmed to be responsible for the overexpression and membranal translocation of CRT in melanocytes under oxidative stress. We also found that oxidative stress-induced membranal translocation of CRT promoted the activation and migration of CD8+ T cells in vitiligo. In addition, dendritic cells from patients with vitiligo were also prone to maturation with the coincubation of melanocytes harboring membranal CRT. CRT could be induced on the membrane of melanocytes through UPR and might play a role in oxidative stress-triggered CD8+ T-cell response in vitiligo.

Enhancing Acetate Utilization in Phaeodactylum tricornutum through the Introduction of Acetate Transport Protein.

The diatom Phaeodactylum tricornutum, known for its high triacylglycerol (TAG) content and significant levels of n-3 long chain polyunsaturated fatty acids (LC-PUFAs), such as eicosapentaenoic acid (EPA), has a limited ability to utilize exogenous organic matter. This study investigates the enhancement of acetate utilization in P. tricornutum by introducing an exogenous acetate transport protein. The acetate transporter gene ADY2 from Saccharomyces cerevisiae endowed the organism with the capability to assimilate acetate and accelerating its growth. The transformants exhibited superior growth rates at an optimal NaAc concentration of 0.01 M, with a 1.7- to 2.0-fold increase compared to the wild-type. The analysis of pigments and photosynthetic activities demonstrated a decline in photosynthetic efficiency and maximum electron transport rate. This decline is speculated to result from the over-reduction of the electron transport components between photosystems due to acetate utilization. Furthermore, the study assessed the impact of acetate on the crude lipid content and fatty acid composition, revealing an increase in the crude lipid content and alterations in fatty acid profiles, particularly an increase in C16:1n-7 at the expense of EPA and a decrease in the unsaturation index. The findings provide insights into guiding the biomass and biologically active products production of P. tricornutum through metabolic engineering.

Experimental Study on Liquid Metal Embrittlement of Al-Zn-Mg Aluminum Alloy (7075): From Macromechanical Property Experiment to Microscopic Characterization.

This study is a multiscale experimental investigation into the embrittlement of Al-Zn-Mg aluminum alloy (7075-T6) caused by liquid metal gallium. The results of the experiment demonstrate that the tensile strength of the 7075-T6 aluminum alloy significantly weakens with an increase in the embrittlement temperature and a prolonged embrittlement time, whereas it improves with an increase in the strain rate. On the basis of the analysis of the experimental data, the sensitivity of the embrittlement of 7075-T6 aluminum alloy by liquid gallium to the loading strain rate is significantly higher compared to other environmental factors. In addition, this study also includes several experiments for microscopic observation, such as Scanning Electron Microscope (SEM) observation, Energy-Dispersive Spectrometer (EDS) spectroscopy, and Electron Back Scatter Diffraction (EBSD) analysis. The experimental observations confirmed the following: (1) gallium is enriched in the intergranular space of aluminum; (2) the fracture mode of 7075-T6 aluminum alloy changes from ductile to brittle fracture; and (3) the infiltration of liquid gallium into aluminum alloys and its enrichment in the intergranular space result in the formation of new dislocation nucleation sites, in addition to the original dislocations cutting and entanglement. This reduces the material's ability to undergo plastic deformation, intensifies stress concentration at the dislocation nucleation point, and, ultimately, leads to the evolution of dislocations into cracks.

Analyzing psychological resilience in college students: A decision tree model.

In the evolving landscape of higher education, particularly in the post-pandemic era, it is crucial for college students to face societal challenges and achieve success by understanding and predicting psychological resilience. To deepen our understanding of psychological resilience, this study used a decision tree model to explore influencing factors. We surveyed 776 college students and collected data on demographic information, self-esteem, sense of school belonging, pro-environmental behavior, subjective well-being, internet game addiction, life autonomy, and academic procrastination using several scales. The decision tree model identified eight key predictors of psychological resilience, which are as follows in order of importance: self-esteem, sense of school belonging, pro-environmental behavior, subjective well-being, academic procrastination, life autonomy, internet game addiction, and academic achievement. This model's accuracy reached 73.985 %, emphasizing its potential utility in educational settings. The findings not only provide a novel and data-driven perspective to understand psychological resilience in college students compared to existing research but also provide practical guidance for educational practitioners and policymakers on how to develop psychological resilience in college students.

Preschool teachers' knowledge, beliefs, and self-efficacy concerning autism: A parallel mixed-methods study of an intervention to improve autism identification.

LAY ABSTRACT: Preschool teachers can play a critical role in early detection of autism. Equipping preschool teachers with prerequisite knowledge and skills would allow them to identify children with probable autism and referral to diagnostic services. This study aimed to investigate the impact of an educational module (EMiASD) that prepared preschool teachers to identify autism symptoms. The sample included 144 preschool teachers, of which 120 were stratified and randomly assigned to an intervention arm receiving training in EMiASD (n = 60) or a comparison arm receiving standard training (n = 60) using a parallel mixed-methods design. Responses to open-ended questions about video case studies revealed improvement in the identification of autism symptoms in preschool teachers in the intervention arm, in contrast to preschool teachers in the comparison arm. Moreover, significant changes in knowledge, belief, and self-efficacy about autism favoured EMiASD. Overall, these results demonstrate the influence of EMiASD in the Yemeni cultural context.

Dezocine as preemptive analgesia alleviates ultrapulse CO2 fractional laser treatment induced pain in patients with acne scars.

BACKGROUND: Ultrapluse CO2 fractional laser technology has emerged as an effective treatment for scar management. However, one drawback of this modality is the pain caused during the procedure. This study aims to explore the efficacy and safety of dezocine (DZC) as preemptive analgesia for reduction of pain induced by ultrapulse CO2 fractional laser treatment for acne scars. METHODS: The study cohort included 78 outpatients with acne scars between February and April 2023. Patients were randomly assigned into three groups with intravenous injection (iv) of DZC prior to laser treatment: (1) control, iv of saline; (2) DZC group 1 (DZC_1), iv of DZC at 0.15 mg/kg; and (3) DZC_2, iv of DZC at 0.20 mg/kg. After 30 min, one session of ultrapulse CO2 fractional laser treatment on acne scars was performed. Hemodynamics, visual analogue scale (VAS), and anxiety visual analog test (AVAT) were monitored prior to, during, and after the procedure. RESULTS: Operative success rates for patients in the control, DZC_1, and DZC_2 groups were 34.6%, 84.6%, and 100%, respectively. DZC administered with either dosage significantly reduced the VAS and AVAT scores of patients in treatment groups as compared with the subjects in the control group during the course of ultrapulse CO2 fractional laser treatment. Patients in DZC_1 and DZC_2 groups did not show any significant difference in hemodynamic parameters, VAS, and AVAT scores. Temporary adverse effects such as nausea and dizziness were observed in some subjects after treatment; the symptoms were quickly dissolved after a rest in supine position. CONCLUSIONS: DZC as preemptive analgesia could effectively reduce pain and anxiety induced by ultrapulse CO2 fractional laser treatment in patients. This study provided an option of preemptive anesthesia to minimize the pain and discomforts associated with laser treatments in clinical practices.