This consensus will introduce the characteristics of fillers used in the surgical cavities of domestic nasal surgery patients based on relevant literature and expert opinions. It will also provide recommendations for the selection of cavity fillers for different nasal diseases, with chronic sinusitis as a representative example.
Humans ; Nasal Cavity/surgery* ; Nasal Surgical Procedures ; China ; Consensus ; Sinusitis/surgery* ; Dermal Fillers

Existing studies have underscored the pivotal role of N-acetyltransferase 10 (NAT10) in various cancers. However, the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma (HNSCC) remain unexplored. In this study, we identified a significant upregulation of RNA-binding protein with serine-rich domain 1 (RNPS1) in HNSCC, where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase, zinc finger SWIM domain-containing protein 6 (ZSWIM6), through direct protein interaction, thereby promoting high NAT10 expression in HNSCC. This upregulated NAT10 stability mediates the enhancement of specific tRNA ac⁴C modifications, subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling, IL-8 signaling, and PTEN signaling that play roles in regulating HNSCC malignant progression, ultimately influencing the survival and prognosis of HNSCC patients. Additionally, we pioneered the development of TRMC-seq, leading to the discovery of novel tRNA-ac⁴C modification sites, thereby providing a potent sequencing tool for tRNA-ac⁴C research. Our findings expand the repertoire of tRNA ac⁴C modifications and identify a role of tRNA ac⁴C in the regulation of mRNA translation in HNSCC.
Humans ; DNA-Binding Proteins ; Head and Neck Neoplasms/genetics* ; N-Terminal Acetyltransferases ; RNA, Transfer ; Serine ; Signal Transduction ; Squamous Cell Carcinoma of Head and Neck

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Objective To explore the relationship between serum high mobility group protein B1(HMGB1)level and anxiety symptoms in patients with cerebral small vessel disease(CSVD).Methods A total of 165 CSVD patients admitted in our department from December 2022 to July 2023 were enrolled as the research subjects.All of them were evaluated by neurologists with Hamilton Anxiety Rating Scale(HAMA),and then those with HAMA score ≥7 were assigned into an anxiety group(70 cases),and the other into a non-anxiety group(95 cases).Non paramet-ric rank sum test was used to compare the serum level of HMGB1 between the two groups of pa-tients.Logistic regression analysis was employed to analyze the risk factors affecting anxiety symptoms in CSVD patients.ROC curve was plotted to evaluate the predictive value of HMGB1 for anxiety symptoms in the patients.Results The serum HMGB1 level was significantly higher in the anxiety group than the non-anxiety group[287.01(188.19,355.54)ng/L vs 260.87(146.48,328.16)ng/L,P＜0.05].Multivariate logistic regression analysis showed that after adjusting for confounding factors,serum HMGB1 level was still a risk factor for anxiety symptoms in CSVD patients(OR=1.004,95％CI:1.000-1.007,P=0.046).Spearman correlation analysis indicated that HMGB1 level was positively correlated with total score of HAMA,insomnia score,and psy-chogenic score(P＜0.05,P＜0.01).The AUC value of HMGB1 in predicting anxiety symptoms in CSVD patients was 0.609(P=0.020).Conclusion Serum HMGB1 level is associated with the oc-currence of anxiety symptoms in CSVD patients,and it has predictive value for the anxiety symp-toms in CSVD patients.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.