OBJECTIVE: To investigate the short-term effectiveness of uni-portal non-coaxial spinal endoscopic surgery (UNSES) via crossing midline approach (CMA) in the treatment of free lumbar disc herniation (FLDH). METHODS: Between March 2024 and June 2024, 16 patients with FLDH were admitted and treated with UNSES via CMA. There were 9 males and 7 females with an average age of 55.1 years (range, 47-62 years). The disease duration was 8-30 months (mean, 15.6 months). The pathological segments was L _{3, 4} in 4 cases, L _{4, 5} in 5 cases, and L ₅, S ₁ in 7 cases. The preoperative pain visual analogue scale (VAS) score was 6.9±0.9 and the Oswestry disability index (ODI) was 57.22%±4.16%. The operation time, intraoperative bleeding volume, postoperative hospital stay, and incidence of complications were recorded. The spinal pain and functional status were evaluated by VAS score and ODI, and effectiveness was evaluated according to the modified MacNab criteria. CT and MRI were used to evaluate the effect of nerve decompression. RESULTS: All 16 patients underwent operation successfully without any complications. The operation time was 63-81 minutes (mean, 71.0 minutes). The intraoperative bleeding volume was 47.3-59.0 mL (mean, 55.0 mL). The length of hospital stay after operation was 3-4 days (mean, 3.5 days). All patients were followed up 1-3 months, with 15 cases followed up for 2 months and 14 cases for 3 months. The VAS score and ODI gradually decreased over time after operation, and there were significant differences between different time points ( P<0.05). At 3 months after operation, the effectiveness was rated as excellent in 12 cases and good in 2 cases according to the modified MacNab criteria, with an excellent and good rate of 100%. CT and MRI during follow-up showed a significant increase in the diameter and cross-sectional area of the spinal canal, indicating effective decompression of the canal. CONCLUSION When using UNSES to treat FLDH, choosing CMA for nerve decompression has the advantages of wide decompression range, large operating space, and freedom of operation. It can maximize the preservation of the articular process, avoid fracture and breakage of the isthmus, clearly display the exiting and traversing nerve root, and achieve good short-term effectiveness.
Humans ; Male ; Intervertebral Disc Displacement/diagnostic imaging* ; Middle Aged ; Female ; Lumbar Vertebrae/surgery* ; Endoscopy/methods* ; Treatment Outcome ; Operative Time ; Pain Measurement ; Length of Stay

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.

Osteoporosis is a systemic metabolic bone disease characterized by decreased bone mass, damage to bone tissue microstructure, increased bone fragility, and susceptibility to fractures, while sarcopenia is a syndrome characterized by progressive reduction in overall muscle mass and functional decline. Based on the common pathophysiological mechanism and close correlation between the two, the concept of "osteosarcopenia" has gradually emerged to describe the simultaneous attenuation of muscles and bones. Signaling pathways serve as important signal transmission channels between muscles and bones, and if abnormal, they can lead to osteosarcopenia. The aim of this article, therefore, is to review the signaling pathways related to osteogenesis and myogenesis, such as Hedgehog, Hippo, mTOR, MAPK, in order to provide new ideas for targeted treatment of osteosarcopenia.

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.