Smell and taste dysfunction in patients infected with the Omicron variant of severe acute respiratory syndrome coronavirus-2.

BACKGROUND: Smell and taste dysfunctions (STD) are frequently observed in patients with coronavirus disease (COVID-19). OBJECTIVES: To investigate the clinical characteristics of STD in COVID-19 patients. MATERIAL AND METHODS: One-hundred six COVID-19 adult patients with the Omicron variant were enrolled. The clinical features of patients with and without STD were compared using questionnaires, laboratory tests, and imaging examinations. RESULTS: Of the 76 patients with smell and/or taste dysfunction, age (p = .002), vaccination time (p = .024), history of systemic diseases (p = .032), and smoking status (p = .044) were significantly different from those of the controls (n = 34). Fatigue (p = .001), headache (p = .004), myalgia (p = .047), and gastrointestinal discomfort (p = .001) were observed more frequently in these patients than in controls. The Hospital Anxiety and Depression Scale score of these patients was significantly higher than that of controls (p < .001). The taste visual assessment scale score of the STD group was significantly lower than that of the taste dysfunction group (p = .001), and perceptions of sour, sweet, and salty tastes were worse in the STD group than in the taste dysfunction group (p < .001). CONCLUSIONS AND SIGNIFICANCE: COVID-19 patients had similar changes in smell and/or taste dysfunctions and worse emotional states, possibly correlated with some factors, including age and vaccination time.

Role and Function of Regulatory T Cell in Chronic Rhinosinusitis with Nasal Polyposis.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a subtype of chronic rhinosinusitis characterized by high edema in the stroma, albumin deposition, and formation of pseudocysts. The pathogenesis of CRSwNP is not yet fully understood. Regulatory T (Treg) cells are a subset of CD4+ T cells that play a suppressive immunoregulatory role in the process of CRSwNP. Recent studies have found that there was a significant reduction in Treg cells in polyp tissues, which leads to the onset of CRSwNP. An imbalance between Th17 and Treg cells can also aggravate inflammation toward the Th2 type. This review focuses on our understanding of the function and role of Treg cells and their regulatory factors and clinical significance in CRSwNP. We also summarize the current drug treatments for CRSwNP with Tregs as the potential therapeutic target, which will provide new ideas for the treatment of CRSwNP in the future.

SLC3A2 inhibits ferroptosis in laryngeal carcinoma via mTOR pathway.

OBJECTIVE: This study aimed to explore the mRNA and protein expression of SLC3A2 in laryngeal carcinoma cells and tissues, and functional regulatory mechanism of SLC3A2 in cell ferroptosis of laryngeal carcinoma. METHODS: We chose the key gene-SLC3A2 of DEGs from TCGA by bioinformatics analysis, and then we constructed stable knockdown of SLC3A2 in laryngeal carcinoma cells. MTT assay and clonogenic assay were used to determine cell viability and cell growth, respectively. The mRNA and protein expression were determined by RT-qPCR and western blotting, respectively. Xenograft tumor model was used to determine the role of SLC3A2 in tumor growth. RESULTS: The results of limma analysis recovered that 92 genes were involved in both upregulated DEGs and high risk of poor prognosis, whereas 36 genes were involved in both downregulated DEGs and low risk of poor prognosis. Pathway enrichment analysis indicated that mTOR signaling pathway and ferroptosis exerted a role in regulating these intersection genes. Moreover, SLC3A2 is a key gene in ferroptosis in laryngeal carcinoma. SLC3A2 is highly expressed in laryngeal carcinoma tissues and cells. Patients with high SLC3A2 expression exerted poor survival. SLC3A2 deficiency inhibited cell proliferation and foci formation. Furthermore, knockdown of SLC3A2 expression induced the efficacy of ferroptosis and suppressed ferroptosis related proteins expression. Mechanically, SLC3A2 deficiency facilitated ferroptosis through upregulating the expression of mTOR and P70S6K, whereas inhibited p-mTOR and p-P70S6K expression in laryngeal carcinoma cells. SLC3A2 deficiency inhibited tumorigenesis in nude mice. CONCLUSION: Our study suggests that SLC3A2 negatively regulates ferroptosis through mTOR pathway in laryngeal carcinoma.

Decellularized tracheal scaffolds in tracheal reconstruction: An evaluation of different techniques.

In humans, the trachea is a conduit for ventilation connecting the throat and lungs. However, certain congenital or acquired diseases may cause long-term tracheal defects that require replacement. Tissue engineering is considered a promising method to reconstruct long-segment tracheal lesions and restore the structure and function of the trachea. Decellularization technology retains the natural structure of the trachea, has good biocompatibility and mechanical properties, and is currently a hotspot in tissue engineering studies. This article lists various recent representative protocols for the generation of decellularized tracheal scaffolds (DTSs), as well as their validity and limitations. Based on the advancements in decellularization methods, we discussed the impact and importance of mechanical properties, revascularization, recellularization, and biocompatibility in the production and implantation of DTS. This review provides a basis for future research on DTS and its application in clinical therapy.

Photo-crosslinked HAMA hydrogel with cordycepin encapsulated chitosan microspheres for osteoarthritis treatment.

Autophagy is a protective mechanism in normal cartilage. The present study aimed to investigate the synergistic therapeutic effect of promotion of chondrocyte autophagy via exposure to cordycepin encapsulated by chitosan microspheres (CM-cordycepin) and photo-crosslinked hyaluronic acid methacrylate (HAMA) hydrogel, with the goal of evaluating CM-cordycepin as a treatment for patients with osteoarthritis. First, we developed and evaluated the characteristics of HAMA hydrogels and chitosan microspheres. Next, we measured the effect of cordycepin on cartilage matrix degradation induced by IL1-ß in chondrocytes and an ex vivo model. Cordycepin protects cartilage from degradation partly by activation of autophagy. Moreover, we surgically induced osteoarthritis in mice, which were injected intra-articularly with CM-cordycepin and HAMA. The combination of CM-cordycepin and HAMA hydrogel retarded the progression of surgically induced OA. Cordycepin ameliorated cartilage matrix degradation at least partially by inducing autophagy in vivo. Our results demonstrate that the combination of cordycepin encapsulated by CMs and photo-crosslinked HAMA hydrogel could be a promising strategy for treating patients with osteoarthritis.