Aflatoxins are carcinogenic secondary metabolites of fungi that contaminate many staple crops and foods. Aflatoxin contamination is a worldwide problem, especially in developing countries, posing health hazards, e.g., causing aflatoxicosis and hepatocellular carcinoma, and even death. Biological solutions for aflatoxin detoxification are environmentally friendly and a cheaper alternative than chemical methods. The aims of the current study were to investigate: (1) the ability of MSMEG_5998, an aflatoxin-degrading F420H2-dependent reductase from Mycobacterium smegmatis, to degrade aflatoxin B1 (AFB1) and reduce AFB1-caused damage in HepG2 cell culture model; and (2) whether a thioredoxin (Trx) linkage of MSMEG_5998 enhanced the enzyme activity. We show that Trx-linked MSMEG_5998 degraded 63% AFB1 and native MSMEG_5998 degraded 31% after 4 h at 22 °C, indicating that the Trx-linked enzyme had a better AFB1-degrading ability. In a HepG2 cell culture model, Trx-linked MSMEG_5998 reduced DNA damage and p53-mediated apoptosis caused by AFB1 to a greater extent than the native enzyme. These findings suggest that Trx-linked MSMEG_5998 could potentially be developed to protect the liver from AFB1 damage, or as a candidate protein to reduce AFB1-related toxicity in animals.

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Background/Aim: Sinonasal rhabdomyosarcoma (RMS) is a rare soft tissue malignancy. Due to the limited cases, the clinicopathological features and prognostic factors are still not well understood. Patients and Methods: This retrospective review included eight patients with sinonasal RMS at our institution between 2004 and 2020. Patient demographics, tumor features, Intergroup Rhabdomyosarcoma Study Group (IRSG) stage and clinical group, treatment strategy, and survival rates were evaluated. Kaplan-Meier analysis and log-rank tests were performed to analyze the possible prognostic factors. Results: We observed a predominance of male sex and alveolar-type tumor in sinonasal RMS. Nasal obstructions and neck masses were the most common symptoms. Patients with pretreatment lactate dehydrogenase (LDH) levels >400 U/l and negative immunohistochemical staining for desmin or MyoD1 had lower survival rates. Conclusion: In patients with sinonasal RMS, pretreatment LDH levels >400 U/l and negative immunohistochemical staining for desmin or MyoD1 may suggest a poor prognosis. These factors can not only contribute to the prediction of prognosis in patients with sinonasal RMS but also facilitate the design of more appropriate treatment strategies.Rhabdomyosarcoma (RMS) is a malignant tumor with a propensity for skeletal muscle differentiation. It is the most common soft tissue sarcoma in children, accounting for approximately 50% of all pediatric soft tissue sarcomas (1-3). However, it is rare in adults, accounting for <1% of all adult malignancies. RMS can be classified into four histological subtypes: embryonal (ERMS), alveolar (ARMS), pleomorphic (PRMS), and spindle cell/sclerotic. ERMS is the most common type, followed by ARMS (4, 5). ARMS is more aggressive than the other subtypes and is often associated with a worse prognosis. ARMS can be further classified according to the presence or absence of the paired box (Pax) proteins 3 and 7/forkhead box O1 (PAX3/7-FOXO1) fusion gene. The outcome in patients with fusionnegative ARMS is indistinguishable from that in ERMS and differs significantly from that in ARMS with fusion genes (6).Approximately 35% of RMS cases arise in the head and neck region, including the orbital, parameningeal, and nonparameningeal areas (3). Tumors in the parameningeal areas have the worst outcome among those in the head and neck region, especially the paranasal sinuses, owing to the structural complexity and tendency for central nervous system (CNS) and skull base invasion (3,7,8). As the tumor location affects the disease prognosis, it appears alongside the usual TNM in the Intergroup Rhabdomyosarcoma Staging Group (IRSG) staging of RMS (9). In addition, the IRSG clinical group for RMS is based on the extent of residual disease after resection and evidence of regional lymph node (LN) or distal metastasis, which is one of the most important prognostic factors in RMS. The treatment strategy for RMS, which includes surgery, chemotherapy, and radiotherapy, is risk-based. The main treatment strategy for si...

Background Olfactory dysfunction is a common disease and it may be caused by sinonasal inflammation, toxin inhalation, or neurological disorders. After sinonasal inflammation, if both olfactory neuroinflammation and olfactory dysfunction occur still under investigation. Objective This study aimed to investigate whether neuroinflammation and olfactory dysfunction occur after lipopolysaccharide (LPS)-initiated rhinosinusitis. Methods Adult C57BL/6 mice were intranasally administered with LPS for 3 weeks. The olfactory function was evaluated with a buried food test. The inflammatory status of sinonasal cavity and olfactory bulb was evaluated with histology and biochemistry. Results After 3-week LPS treatment, mice developed olfactory dysfunction, sinonasal cavity, and olfactory bulb inflammation. LPS-treated mice had greater sinonasal mucosal thickness. Besides, pro-inflammatory interleukin-6, the number of goblet cells and neutrophils in the sinonasal cavity was increased after LPS administration. The olfactory sensory neurons in the olfactory epithelium and the olfactory bulb were decreased, and the olfactory function was impaired by LPS administration. Inflammatory cytokines such as interferon-γ and tumor necrosis factor-α were increased in the olfactory bulb. Conclusion This study showed that LPS-initiated rhinosinusitis caused olfactory neuroinflammation and olfactory dysfunction in mice.

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