Use of a combination of diaphragmatic ultrasound and muscle relaxation monitoring in predicting post-extubation adverse respiratory events among elderly patients in an anesthesia intensive care unit.

OBJECTIVE: The purpose of this study was to examine the feasibility of using a combination of diaphragmatic ultrasound and muscle relaxation monitoring in predicting adverse respiratory events after extubation among elderly patients in an anesthetic intensive care unit (AICU). METHODS: The study participants were 120 elderly patients who were in the AICU after laparoscopic radical resection for colorectal cancer. Based on whether there were critical respiratory events (CREs) after extubation, they were divided into the adverse event group and the non-adverse event group. We used logistic regression to identify factors influencing the occurrence of CREs post-extubation in elderly patients. Using the receiver operating characteristic (ROC) curve, we analyzed the value of each indicator in predicting CREs post-extubation. RESULTS: We included 109 patients in the final analysis. In the adverse event group (n = 19), the age, proportion of females, and proportion of preoperative respiratory diseases were higher than in the non-adverse event group (n = 90). The muscle relaxation value, quiet breathing diaphragmatic excursion during extubation (DE-QB), deep breathing diaphragmatic excursion during extubation (DE-DB), and deep breathing diaphragmatic thickening fraction during extubation (DTF-DB) of patients in the adverse event group were significantly lower than those in the non-adverse event group (P < 0.05). Using binary logistic regression analysis, we identified muscle relaxation value, DE-DB, and DTF-DB during extubation as significant predictors of CREs post-extubation in elderly patients (P < 0.05). The area under the curve (AUC) of the combination of the muscle relaxation value, DE-DB, and DTF-DB during extubation for predicting CREs after extubation in elderly patients was 0.949, which was higher than that of any single indicator. CONCLUSION: The combination of diaphragmatic ultrasound and muscle relaxation monitoring was more accurate in predicting CREs post-extubation among elderly patients in the AICU.

Case report: Malignant vasovagal reflex syndrome during percutaneous transcatheter closure of patent foramen ovale.

Malignant vasovagal reflex syndrome can be induced by pulling of cardiac tissue during percutaneous transcatheter closure of patent foramen ovale. In this case, a patient presented with a malignant vasovagal reflex syndrome characterized by decreased heart rate, cardiac arrest, and ventricular tachycardia. Therefore, it's particularly important to observe patients' heart rate and timely deal with vasovagal reflex syndrome during the operation.

VPS33B interacts with NESG1 to suppress cell growth and cisplatin chemoresistance in ovarian cancer.

The pathogenesis and cisplatin chemoresistance of ovarian cancer (OC) are still unclear. Vacuolar protein sorting-associated 33B (VPS33B) has not been reported in OC to date. In this study, immunohistochemistry was used to detect VPS33B protein expression between OC and ovarian tissues. MTT, EdU, colony formation, cell cycle, in vivo tumorigenesis, western blot, ChIP, EMSA, co-immunoprecipitation (CoIP), qRT-PCR, and microconfocal microscopy were used to explore the function and molecular mechanisms of VPS33B in OC cells. The results of the present study demonstrated that VPS33B protein expression was obviously reduced in OC compared with that in ovarian tissues. Overexpressed VPS33B suppressed cell cycle transition, cell growth, and chemoresistance to cisplatin in vitro and in vivo. Analysis of the mechanism indicated that overexpressed VPS33B regulated the epidermal growth factor receptor (EGFR)/PI3K/AKT/c-Myc/p53/miR-133a-3p feedback loop and reduced the expression of the cell cycle factor CDK4. Nasopharyngeal epithelium-specific protein 1 (NESG1) as a tumor suppressor not only interacted with VPS33B, but was also induced by VPS33B by the attenuation of PI3K/AKT/c-Jun-mediated transcription inhibition. Overexpressed NESG1 further suppressed cell growth by mediating VPS33B-modulated signals in VPS33B-overexpressing OC cells. Finally, NESG1 induced VPS33B expression by reducing the inhibition of PI3K/AKT/c-Jun-mediated transcription. Our study is the first to demonstrate that VPS33B serves as a tumor suppressor, and VPS33B can interact with NESG1 to suppress cell growth and promote cisplatin sensitivity by regulating the EGFR/PI3K/AKT/c-Myc/p53/miR-133a-3p feedback loop in OC cells.

IGFBP2 promotes the EMT of colorectal cancer cells by regulating E-cadherin expression.

This study aimed to investigate the expression of insulin like growth factor binding protein 2 (IGFBP2) in colorectal cancer cells and its effect on the biological characteristics of cancer cells. We first established IGFBP2 knockdown (HCT116-shIGFBP2) and overexpression (HT29-IGFBP2) cell lines. Western blotting was used to evaluate the overexpression and knockdown efficiency. Next, the effect of IGFBP2 on colorectal cancer cell proliferation and migration was evaluated through cell proliferation and wound healing assays, respectively. Cell proliferation experiments showed that the upregulation of IGFBP2 promoted the proliferation of HT29 cells, but the downregulation of IGFBP2 inhibited the proliferation of HCT116 cells. Moreover, a wound healing assay showed that the migration ability of HCT116 cells was significantly reduced after the downregulation of IGFBP2. Also, the level of E-cadherin in HCT116-shIGFBP2 cells was significantly upregulated following IGFBP2 knockdown. Further analyses showed that colorectal cancer cells secreted high levels of IGFBP2 into the extracellular matrix, which inhibited E-cadherin expression as well. Overall, the results of this study showed that IGFBP2 inhibits the expression of E-cadherin and promotes the proliferation and migration of colorectal cancer cells.