Objective:To explore the clinical efficacy of the coblation resection of lingual thyroglossal duct cysts under self-retaining laryngoscopy. Methods:A retrospective analysis was conducted on the clinical data of 22 patients with lingual thyroglossal duct cysts admitted to our hospital from December 2016 to December 2023. There were 16 males and 6 females, aged 2 years to 12 years and 3 months（mean: 4 years 1 month; median: 3 years 3 months）. The lingual thyroglossal duct cysts were removed by coblation under self-retaining laryngoscopy. If the cysts could not be removed completely, the epithelial cells of the remaining cysts would be ablated. Results:There were 22 cases of lingual thyroglossal duct cysts，13 cases （59.1%） of lingual thyroglossal duct cysts had laryngeal stridor and dyspnea. The postoperative follow-up period is 3 months to 7 years. 11 cases （50.0%） underwent secondary laryngoscopic evaluation.There were 4 cases of recurrence （18.2%）, with no laryngeal obstruction,bleeding, or nerve damage. Conclusion:Laryngeal stridor and dyspnea are the main clinical symptoms of lingual thyroglossal duct cysts in children. The coblation resection of lingual thyroglossal duct cysts under self-retaining laryngoscopy is safe and effective. Cyst recurrence correlates strongly with residual cyst walls, emphasizing the need for enhanced intraoperative visualization and refined surgical precision.
Humans ; Thyroglossal Cyst/surgery* ; Male ; Female ; Child ; Retrospective Studies ; Child, Preschool ; Laryngoscopy/methods* ; Treatment Outcome ; Catheter Ablation/methods*

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

Parkinson's disease (PD) is one of the hotspots in the research field of neurodegenerative diseases, and its pathogenesis is still controversial. Trace metal elements play an important role in normal growth and development of the human body. Metal ions can cross the blood-brain barrier and enter the brain, leading to α-synapnuclein aggregation, mitochondrial dysfunction, and degeneration of dopaminergic neurons, and then inducing the occurrence of PD. This article mainly reviewed the potential mechanisms of metal elements in PD, discussed the role of metabolic imbalance of common trace metals (copper, iron, manganese, and zinc) in PD, and put forward new insights into the treatment of PD.

Objective: To establish a method for in vitro expansion of regulatory T cells (Tregs) for clinical study and immunotherapy. Methods: CD4⁺ T cells were isolated from BALB/c spleens by magnetic activated cell sorting (MACS), then cultured in 24-well plates coated with anti-CD3/CD28 microbeads in the presence of 100 U/ml interleukin-2 (IL-2) and 5 ng/ml recombinant human transforming growth factor-β (rhTGF-β). The purity of the expanded Tregs were tested by flow cytometry. In vitro inhibition of CD4⁺ CD25^-T cells response by expanded Tregs was measured by mixed lymphocyte reaction test. The number and the viability of the expanded Tregs were detemined by trypan blue staining. Results: Tregs were expanded up to 20 folds after 5 days in culture, and the activity was (93±4)%. The purity of expanded Tregs were (79.1±1.5)%, and maintained suppressive ability. Conclusions We can obtain large numbers of Tregs with highly purity and suppressive ability, thereby providing a solution to the availability of sufficient Tregs in clinical study and immunotherapy.

Objective:To observe the clinical efficacy of interaction acupuncture combining with routine acupuncture for intractable facial palsy.
Methods:A total of 60 eligible cases were randomly allocated into a treatment group (n=30) and a control group (n=30). Cases in the treatment group received interaction and routine acupuncture, whereas cases in the control group received routine acupuncture alone. The treatment was done once a day and 10 times made up a course of treatment. The patients were treated for a total of 3 courses and there were no intervals between two courses.
Results:The total effective rate was 93.3% in the treatment group (including 17 recovery cases, 11 improvement cases and 2 failure cases), versus 76.7% in the control group (including 8 recovery cases, 15 improvement cases and 7 failure cases), showing a statistical difference (P<0.05).
Conclusion:Combining interaction and routine acupuncture can obtain better effect than routine acupuncture alone for intractable facial palsy.

Objective To construct an Apoptin prokaryotic vector,aiming to produce antigenic fusion protein Apoptin. Methods The Apoptin gene was amplified from the template of plasmid pSSCHG/NT4-Apoptin-HA2-TAT by PCR.The Apoptin was sub-cloned into the multiple clone sites of plasmid pET-28a(+) to get the prokaryotic vector of pET-28a(+)-Apoptin,which was transformed into E.coli BL21(DE3).Expression of E.coli BL21(DE3) was induced by IPTG.The specific protein expression was detected by SDS-PAGE. Results The fusion protein was expressed with high efficiency in E.coli BL21(DE3) transformed by pET-28a(+)-Apoptin after induction with IPTG.The specific fusion protein had an apparent related molecular weight of about 17 000 ku as indicated by SDA-PAGE analysis. Conclusion The Apoptin prokaryotic expression vector with pET-28a(+)-Apoptin can effectively express Apoptin fusion protein,laying a foundation for further study of Apoptin and preparation of antibodies against Apoptin.