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Objective: To evaluate the impact of smoking statuses on disease severity and subcutaneous immunotherapy (SCIT) efficacy in allergic rhinitis (AR). Study Design: Open observational cohort study. Setting: Tertiary referral center. Methods: Five hundred and five AR patients undergoing dust mite allergen SCIT were categorized into never smokers, former smokers, and current smokers. AR severity was assessed using widely employed questionnaires. The changes in questionnaire scores pre‐ and post‐SCIT were evaluated for SCIT efficacy. The differences in disease severity and SCIT efficacy were compared for different smoking statuses among AR patients. Results: Compared to never smokers, former and current smokers exhibited higher proportion of male, alcohol, and asthma (P <.05). Current smokers had a greater prevalence of allergic conjunctivitis than former smokers (P <.05). Before SCIT, AR severity was similar across 3 groups, even after adjusting for confounders (P >.05). Current smokers reported lower SCIT efficacy in the first year (P <.05). By the third year, 3 groups showed comparable long‐term efficacy (P >.05). However, current smokers experienced a significant decrease in benefits 2 years post‐SCIT (P <.05) and lower improvement rates at the end of the 3‐years SCIT period and 2 years following SCIT (P <.05). Conclusion: AR patients across different smoking statuses demonstrated similar baseline disease severity and long‐time SCIT efficacy. Active smoking was associated with increased asthma risk, delayed early SCIT efficacy perception, reduced improvement over 3 years, and diminished benefits 2 years after SCIT. Prompt smoking cessation is crucial to mitigate these effects. [ABSTRACT FROM AUTHOR]

This article presents the findings of a large-scale, multi-center study conducted in China on the safety and risk factors associated with subcutaneous immunotherapy (SCIT) using a house dust mite (HDM) formulation. The study included 3,132 patients with allergic rhinitis and/or asthma who underwent SCIT. The results showed a low incidence of systemic reactions (SRs) during SCIT, with the majority of SRs being mild. Risk factors for SRs included asthma, disease duration exceeding five years, and high sensitization. The study emphasizes the importance of personalized therapy, early initiation of immunotherapy, and close monitoring to minimize SR risks. [Extracted from the article]

Histone deacetylases (HDACs) are important in chronic inflammation, and inflammatory responses affect synovium‐derived mesenchymal stem cell (SMSC) function in temporomandibular joint repair. However, the effect of HDACs on SMSC inflammatory activation remains unclear. In this study, temporomandibular joint fibroblast‐like synoviocytes obtained from osteoarthritis patients met the minimal mesenchymal stem cell criteria. Interleukin 1β (IL‐1β) upregulated IL‐6 and IL‐8 expression in SMSCs through nuclear factor‐κB (NF‐κB) pathway activation. IL‐6 and IL‐8 upregulation were blocked by broad‐acting HDAC inhibitors SAHA and LBH589. MC1568 alleviated IL‐1β activation of SMSCs, whereas CI994 and FK228 produced a minimal or opposite effect in vitro. We also found HDAC10 was highly associated with localized IL‐1β expression in vivo and in vitro. HDAC10 knockdown alleviated IL‐1β‐mediated SMSC activation and blocked NF‐κB pathway activation. Conversely, HDAC10 overexpression promoted IL‐6 and IL‐8 expression and IL‐1β‐mediated NF‐κB pathway activation. In conclusion, HDAC10 upregulation contributed to IL‐1β‐mediated inflammatory activation of SMSCs, indicating that HDAC10 may be a novel therapeutic target. [ABSTRACT FROM AUTHOR]

The mechanism of manganism caused by manganese (Mn), an important environmental risk factor for Parkinson's disease, is still unclear. Recent evidence suggested that autophagy participated in neurodegenerative diseases, in which microRNA played a crucial role. However, roles of microRNA in the aberrant autophagy that occurs in neurodegenerative diseases remains controversial. In nervous system, miRNA‐138‐5p is highly expressed and plays a key role in regulating memory and axon regeneration. Importantly, we also found that miR‐138‐5p expression decreased significantly after SH‐SY5Y cells exposed to manganese chloride (MnCl2) in previous study. To explore the role of miR‐138‐5p in Mn‐induced autophagy, autophagy associated indicators were detected. And we found that MnCl2 could induce autophagic dysregulation and inhibit expression of miR‐138‐5p. While the levels of LC3‐II/LC3‐I, Beclin1, and p62, the number of autophagosome formation significantly decreased after miR‐138‐5p over‐expression, which demonstrated that miR‐138‐5p could clearly retard Mn‐induced autophagy. In additional, we found there were classical and evolutionarily conserved miR‐138‐5p binding sites in 3′‐UTR region of SIRT1, which was inhibited when overexpression of miR‐138‐5p. Therefore, it was speculated that elevated expression of SIRT1 may be resulted from inhibition of miR‐138‐5p after cells exposed to MnCl2. Finally, we found that SIRT1 inhibitor EX‐527 suppressed Mn‐induced autophagy as well as miR‐138‐5p, while the suppression was reversed by SIRT1‐specific activator SRT1720. These results indicated that overexpression of miR‐138‐5p suppressed Mn‐induced autophagy by targeting SIRT1. [ABSTRACT FROM AUTHOR]

Abstract: Tertiary butyl alcohol (TBA) is a principal metabolite of methyl tertiary‐butyl ether (MTBE), a common pollutant worldwide in the ground or underground water, which is found to produce nervous system damage. Nevertheless, few data regarding the effects of TBA has been reported. Studies indicated that oxidative stress plays a pivotal role in MTBE neurotoxic mechanism. Sirtuin 1 (SIRT1) has been reported to exert a neuroprotective effect on various neurologic diseases via resistance to oxidative stress by deacetylating its substrates. In this study, we examined levels of oxidative stress after exposure to TBA for 6 h in HT22 cells and HT22 cells with SIRT1 silencing (transfected with SIRT1 siRNA) or high expression (preconditioned with agonists SRT1720). We found that TBA activated oxidative stress by increasing generation of intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and Oxidized glutathione (GSSG), and decreasing contents of superoxide dismutase (SOD) and glutathione reductase (GSH). In additional, levels of TBA‐induced oxidative stress were aggravated when SIRT1 silenced but alleviated when SIRT1 enhanced. Our study indicated that SIRT1 mitigated oxidative stress induced by TBA. [ABSTRACT FROM AUTHOR]

Objective: To investigate the clinical effect of retroauricular hairline approach in submandibular gland resection assisted by endoscope. Methods: A total of 18 patients with submandibular gland benign tumors treated in our hospital from September 2022 to September 2023 were selected. A 5 cm incision was designed in the retroauricular hairline, and the flap was turned over directly to the anterior edge of sternocleidomastoid muscle, then the flap was turned over to build the cavity through endoscopic surgery, and submandibular gland resection was completed with the assistance of endoscope. After operation, a negative pressure drainage was placed into the hairline, and the wound was closed by continuous intracutaneous suture. The clinical effect was evaluated after 3-6 months follow-up. Results: All patients underwent submandibular gland resection with endoscopic assistance as planned, and none of them converted to submaxillary incision during operation. The operation time was 65-97 min, with an average of 75 min. Intraoperative bleeding was 10-20 mL, with an average of 14 mL.No tongue numbness, wound infection, or tumor recurrence occurred after operation. However, there were 10 patients with ear numbness and discomfort of auricle after surgery, which gradually recovered after 6-9 months of follow-up. Two patients had crooked mouth after surgery, and the symptoms were gradually relieved after follow-up. All incisions healed in stage I and were concealed. Conclusion: Endoscopic retroauricular hairline approach is a choice for submandibular gland resection with good cosmetic effect, less trauma and fewer complications., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Nasal epithelium provides a physical barrier to potentially harmful stimuli. Cilia, which is on the apical side of the human nasal epithelial cells (HNEpCs), plays a critical role in removing inhaled harmful matter. Ciliary beat frequency (CBF) and ciliary beat pattern (CBP) are the two important indicators for ciliary beat function. However, impacts of the fine particulate matter (PM 2.5 ) on CBF and CBP are still unknown. We aimed to evaluate the impact of PM 2.5 on the ciliary beat function of the HNEpCs and its potential mechanisms. After exposed to PM 2.5 for 12 h, cilia of HNEpCs were in disordered arrangement. The ciliary coverage rate was decreased after PM 2.5 exposure of a series of concentration, while the proportion of basal cells was continuously increased and could be observed on the apical side of the HNEpCs which is hardly be observed without PM 2.5 exposure. PM 2.5 increased the CBF after 12 h exposure, while 24 h exposure increased the CBF at the relative lower dosage groups and then made a decrease at relative higher dosage groups. CBF were classified into two different types, which had different changes following PM 2.5 exposure. CBP showed significant changes characterized as the increased dyskinesia index. Total levels of cellular ATP and the mitochondrial membrane potential were decreased following 12 h exposure of PM 2.5 , while no change was found in O 2 consumption. In conclusion, PM 2.5 impact the ciliary beat function of HNEpCs, and the mitochondrial dysfunction might play an important role in it., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

The mechanism of manganism caused by manganese (Mn), an important environmental risk factor for Parkinson's disease, is still unclear. Recent evidence suggested that autophagy participated in neurodegenerative diseases, in which microRNA played a crucial role. However, roles of microRNA in the aberrant autophagy that occurs in neurodegenerative diseases remains controversial. In nervous system, miRNA-138-5p is highly expressed and plays a key role in regulating memory and axon regeneration. Importantly, we also found that miR-138-5p expression decreased significantly after SH-SY5Y cells exposed to manganese chloride (MnCl 2 ) in previous study. To explore the role of miR-138-5p in Mn-induced autophagy, autophagy associated indicators were detected. And we found that MnCl 2 could induce autophagic dysregulation and inhibit expression of miR-138-5p. While the levels of LC3-II/LC3-I, Beclin1, and p62, the number of autophagosome formation significantly decreased after miR-138-5p over-expression, which demonstrated that miR-138-5p could clearly retard Mn-induced autophagy. In additional, we found there were classical and evolutionarily conserved miR-138-5p binding sites in 3'-UTR region of SIRT1, which was inhibited when overexpression of miR-138-5p. Therefore, it was speculated that elevated expression of SIRT1 may be resulted from inhibition of miR-138-5p after cells exposed to MnCl 2 . Finally, we found that SIRT1 inhibitor EX-527 suppressed Mn-induced autophagy as well as miR-138-5p, while the suppression was reversed by SIRT1-specific activator SRT1720. These results indicated that overexpression of miR-138-5p suppressed Mn-induced autophagy by targeting SIRT1., (© 2019 Wiley Periodicals, Inc.)