Non-intubated deep paralysis: a new anaesthesia strategy for vocal cord polypectomy.

BACKGROUND: Vocal cord polyp is common otorhinolaryngological disease, traditionally treated by vocal cord polypectomy under a supporting laryngoscope with general anaesthesia. Although it is safe and controllable, it would cause some anaesthesia complications. Moreover, the complex process of general anaesthesia may significantly reduce surgical efficiency. Avoiding these problems remains an important issue. METHODS: All patients were subjected to the standard non-intubated deep paralysis (NIDP) protocol consisting of four phases. An emergency plan was launched when NIDP cannot be implemented successfully. Patient characteristics, blood gas and monitoring data were collected during NIDP. Data concerning satisfaction, complications and duration of anaesthesia and recovery were collected to assess its effectiveness. RESULT: Among 20 enrolled patients, the success rate of NIDP was 95%. Only one patient failed in completing NIDP. Blood gas analysis revealed that the partial pressure of oxygen and carbon dioxide was maintained at safe levels. Monitoring during NIDP revealed fluctuations in mean arterial pressure between 110 and 70 mmHg, and the heart rate was stable at 60-100 beats per minute. The duration of anaesthesia and postoperative recovery were 13.0 ± 2.84 and 5.47 ± 1.97 min, respectively. All patients and surgeons were satisfied with NIDP, and no complications were detected before discharge. CONCLUSION: NIDP can be safely applied to patients and can replace general anaesthesia in vocal cord polypectomy. It can significantly reduce the duration of anaesthesia and postoperative recovery. No anaesthesia complications occurred without intubation, and patients and surgeons were satisfied with NIDP. TRIAL REGISTRATIONS: This single-centre, prospective study was registered on clinicaltrial.gov (NCT04247412) on 30th July 2020.

A Bibliometric Analysis of Endoscopic Sedation Research: 2001-2020.

Background and Aims: To evaluate endoscopic sedation research and predict research hot spots both quantitatively and qualitatively using bibliometric analysis. Methods: We extracted relevant publications from the Web of Science Core Collection (WoSCC) on 13 December 2020. We examined the retrieved data by bibliometric analysis (e.g., co-cited and cluster analysis, keyword co-occurrence) using the software CiteSpace and VOSviewer and the website of bibliometrics, the Online Analysis Platform of Literature Metrology (http://bibliometric.com/), to analyse and predict the trends and hot spots in this field. Main Results: We identified 2,879 articles and reviews on endoscopic sedation published between 2001 and 2020. Although the overall trend is increasing, with slight fluctuation in some years, there were significant increases in 2007 and 2012. In respect of the contributions on endoscopic sedation research, the United States (US) had the greatest number of publications, and it was followed by Japan and China. In addition, collaboration network analysis revealed that the most frequent collaboration was between the US and China. Six of the top ten most prolific research institutions were located in the US. The most publications on endoscopic sedation research in the past two decades were found primarily in journals on gastroenterology and hepatology. Keyword co-occurrence and co-citation cluster analysis revealed the most popular terms relating to endoscopic sedation in the manner of cluster labels; these included patient anxiety, tolerance, ketamine, propofol, hypoxia, nursing shortage, endoscopic ultrasonography, colorectal cancer, carbon dioxide insufflation, and water exchange (WE). Keyword burst detection suggested that propofol sedation, adverse event, adenoma detection rate (ADR), hypoxemia, and obesity were newly-emergent research hot spots. Conclusions: Our findings showed that hypoxia, adverse event, and ADR, along with conscious sedation and propofol sedation, have been foci of endoscopic sedation research over the past 20 years. The research focus has shifted from sedative drugs to sedative complications and endoscopy quality control, which means that there will be higher requirements and standards for sedative quality and endoscopy quality in the future.

Neuropeptide Y1 receptor antagonist promotes osteoporosis and microdamage repair and enhances osteogenic differentiation of bone marrow stem cells via cAMP/PKA/CREB pathway.

Osteoporosis is a common metabolic bone disorder in the elderly population. The accumulation of bone microdamage is a critical factor of osteoporotic fracture. Neuropeptide Y (NPY) has been reported to regulated bone metabolism through Y1 receptor (Y1R). In this study the effects and mechanisms of Y1R antagonist on prevention for osteoporosis were characterized. In the clinical experiment, compared with osteoarthritis (OA), osteoporosis (OP) showed significant osteoporotic bone microstructure and accumulation of bone microdamage. NPY and Y1R immunoreactivity in bone were stronger in OP group, and were both correlated with bone volume fraction (BV/TV). In vivo experiment, Y1R antagonist significantly improved osteoporotic microstructure in the ovariectomized (OVX) rats. And Y1R antagonist promoted RUNX2, OPG and inhibit RANKL, MMP9 in bone marrow. In vitro cell culture experiment, NPY inhibited osteogenesis, elevated RANKL/OPG ratio and downregulated the expression of cAMP, p-PKAs and p-CREB in BMSCs, treated with Y1R antagonist or 8-Bromo-cAMP could inhibit the effects of NPY. Together, Y1R antagonist improved the bone microstructure and reduced bone microdamage in OVX rats. NPY-Y1R could inhibit osteoblast differentiation of BMSCs via cAMP/PKA/CREB pathway. Our findings highlight the regulation of NPY-Y1R in bone metabolism as a potential therapy strategy for the prevention of osteoporosis and osteoporotic fracture.

Overexpression of hSNF2H in glioma promotes cell proliferation, invasion, and chemoresistance through its interaction with Rsf-1.

hSNF2H partners with Rsf-1 to compose the Rsf complex to regulate gene expression. Recent studies indicated that hSNF2H was overexpressed in several human cancers. However, its expression pattern and biological mechanism in glioma remain unexplored. In this study, we found that hSNF2H was overexpressed in 32 % of glioma specimens. hSNF2H overexpression correlated with advanced tumor grade (p = 0.0338) and Rsf-1 positivity in glioma tissues (p = 0.016). Small interfering RNA (siRNA) knockdown was performed in A172 and U87 cell lines. MTT, colony formation assay, and cell cycle analysis showed that knockdown of hSNF2H inhibited cell proliferation, colony formation ability, and cell cycle transition. Matrigel invasion assay showed that hSNF2H depletion inhibited invasive ability of glioma cells. In addition, we demonstrated that hSNF2H depletion decreased temozolomide resistance of A172 and U87 cell lines and increased temozolomide induced apoptosis. Furthermore, hSNF2H depletion decreased cyclin D1, cyclin E, p-Rb, MMP2, cIAP1, Bcl-2 expression, and phosphorylation of IκBα and p65, suggesting hSNF2H regulates apoptosis through NF-κB pathway. Immunoprecipitation showed that hSNF2H could interact with Rsf-1 in both cell lines. To validate the involvement of Rsf-1, we checked the change of its downstream targets in Rsf-1 depleted cells. In Rsf-1 depleted cells, changes of cyclin E, Bcl-2, and p-IκBα were not significant using hSNF2H siRNA treatment. In conclusion, our study demonstrated that hSNF2H was overexpressed in human gliomas and contributed to glioma proliferation, invasion, and chemoresistance through regulation of cyclin E and NF-κB pathway, which is dependent on its interaction with Rsf-1.