The Association Between Cognition of Obstructive Sleep Apnea Patients and Urinary AD7c-NTP Level: Investigation and Application.

BACKGROUND: Obstructive sleep apnea (OSA) is a multi-component disorder, which has many comorbidities, including cognitive impairment. Although its potential risk factors were unknown, they could affect the patient's quality of life and long-term prognosis. OBJECTIVE: The purpose of this study was to investigate the application of urinary Alzheimer's disease-associated neurofilament protein (AD7c-NTP) levels in the assessment of cognitive impairment in OSA patients, and to analyze the predictive value of potential high-risk factors on cognitive impairment in OSA patients. METHODS: 138 young and middle-aged adults were recruited and underwent overnight polysomnographic recording, Montreal Cognitive Assessment (MoCA), and urinary AD7c-NTP test. AD7c-NTP and other factors were further applied as biomarkers to develop a cognition risk prediction model. RESULTS: Compared with the control, OSA patients showed significantly lower MoCA scores and higher urinary AD7c-NTP concentrations, while the severe OSA group appeared more significant. The urinary AD7c-NTP level of the OSA cognitive impairment group was higher than that of the non-cognitive impairment group. The results of regression analysis showed that urinary AD7c-NTP level was an independent predictor of cognitive impairment in OSA patients. Based on urinary AD7c-NTP levels and other selected factors, a multimodal prediction model for assessing the risk of cognitive impairment in OSA patients was initially established. CONCLUSION: The increased urinary AD7c-NTP level could be used as a relevant peripheral biomarker of cognitive impairment in OSA patients. A model using urinary AD7c-NTP combined with other factors was developed and could accurately assess the cognition risk of OSA patients.

Modified technique of closing the port site after multiport thoracoscopic surgery using the shingled suture technique: a single centre experience.

BACKGROUND: Due to improvements in operative techniques and medical equipment, video-assisted thoracoscopic surgery has become a mainstay of thoracic surgery. Nevertheless, in multiport thoracoscopic surgery, there have been no substantial advances related to the improvement of the esthetics of the site of the chest tube kept for postoperative drainage of intrathoracic fluid and decompression of air leak after thoracoscopic surgery. Leakage of fluid and air around the site of the chest tube can be extremely bothersome to patients. METHODS: From March 2019 to April 2020, we used a modified technique of closing the port site in 67 patients and the traditional method in 51 patients undergoing multiport thoracoscopic surgery due to lung disease or mediastinal disease. We recorded patients' age, gender, body mass index, surgical method, postoperative drainage time, and postoperative complications.The NRS pain scale was used to score the pain in each patient on the day of extubation.The PSAS and the OSAS were used for the assessment of scars one month after surgery. RESULTS: In the modified technique group, only one patient (1.49%) had pleural effusion leakage, compared with five patients (9.80%) in the traditional method group (P < 0.05). There were no significant differences in the pain of extubating and wound dehiscence between the two groups. However,the incidence rates of wound dehiscence in the modified technique group were lower than in the traditional method group. There were no post-removal pneumothorax and wound infection in either of the groups. Significant differences in the PSAS and OSAS were observed between the groups,where the modified technique group was superior to the traditional method group. CONCLUSIONS: The modified technique of port site closure is a leak-proof method of fixation of the chest tube after multiport thoracoscopic surgery. Moreover, it is effective and preserves the esthetic appearance of the skin.

Long non-coding RNA KCNQ1 overlapping transcript 1 promotes the progression of esophageal squamous cell carcinoma by adsorbing microRNA-133b.

OBJECTIVE: The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). RESULTS: KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. CONCLUSION: KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.

Long non-coding RNA KCNQ1 overlapping transcript 1 promotes the progression of esophageal squamous cell carcinoma by adsorbing microRNA-133b

OBJECTIVE: The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). RESULTS: KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. CONCLUSION: KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.

Patterns of recurrence in adenocarcinoma of the esophagogastric junction: a retrospective study.

BACKGROUND: The prognosis of adenocarcinoma of the esophagogastric junction (AEG) is poor. Understanding the postoperative recurrence pattern of AEG is helpful to verify the effectiveness of treatment and optimize subsequent treatment, so as to improve prognosis. METHODS: This single-center retrospective study included patients with stage III AEG who underwent surgical treatment between January 2009 and December 2016. According to the different postoperative treatment arm, patients were divided into surgery and surgery plus chemotherapy groups. Recurrence-free survival was used as the outcome to compare the recurrence site and pattern between the groups. RESULTS: In total, were 306 patients enrolled, 123 in the surgery group and 183 in the surgery plus chemotherapy group. During follow-up (median 17.1 months) of 24 months after surgery, 62.0% of patients had tumor recurrence. The overall recurrence rates in the surgery and surgery plus chemotherapy groups were 86.9% and 77.0%, respectively. The recurrence patterns of both groups were mainly distant metastasis. Postoperative chemotherapy reduced the incidence of hematogenous dissemination from 51.2 to 42.0%. Multivariate Cox analysis showed that the pN stage increased the risk of recurrence, while surgery plus chemotherapy reduced the risk. CONCLUSIONS: Patients with AEG have a risk of hematogenous dissemination after surgery. Postoperative treatment arm and pN stage were independent risk factors in patients with AEG. Surgery plus chemotherapy can improve recurrence-free survival and reduce distant metastasis, but they do not have a beneficial role in controlling local recurrence.

Semaphorin 3F Serves as a Tumor Suppressor in Esophageal Squamous Cell Carcinoma and is Associated With Lymph Node Metastasis in Disease Progression.

BACKGROUND: Esophageal squamous cell carcinoma is one of the leading aggressive malignancies with high mortality. Semaphorin 3F has been reported to be involved in lymphangiogenesis by interacting the vascular endothelial growth factor C/neuropilin 2 axis. This study aimed to assess the clinical and functional role of semaphorin 3F and preliminarily evaluate the relationship between semaphorin 3F and lymph node metastasis in esophageal squamous cell carcinoma. METHODS: The messenger RNA expression of semaphorin 3F was analyzed using quantitative real-time polymerase chain reaction. The expression differences of semaphorin 3F between patients having esophageal squamous cell carcinoma with and without lymph node metastasis were assessed, and the correlation of semaphorin 3F with vascular endothelial growth factor C and neuropilin 2 was estimated. The prognostic value of semaphorin 3F was evaluated using Kaplan-Meier survival curves and Cox regression analysis. Gain- and loss-functional cell experiments were performed to explore the biological function of semaphorin 3F, vascular endothelial growth factor C, and neuropilin 2. RESULTS: The messenger RNA expression of semaphorin 3F was reduced in esophageal squamous cell carcinoma tissues compared with normal tissues, and lower semaphorin 3F expression was observed in patients having esophageal squamous cell carcinoma with positive lymph node metastasis. Semaphorin 3F expression was associated with lymph node metastasis and negatively correlated with vascular endothelial growth factor C and neuropilin 2. Lower semaphorin 3F expression was related to a poor overall survival of esophageal squamous cell carcinoma and served as an independent prognostic indicator. In esophageal squamous cell carcinoma cells, semaphorin 3F messenger RNA expression was also decreased compared with normal cells, and the overexpression of semaphorin 3F could significantly inhibit cell proliferation, migration, and invasion. The downregulation of vascular endothelial growth factor C and neuropilin 2 could inhibit cell proliferation, migration, and invasion of esophageal squamous cell carcinoma cells. CONCLUSION: All data indicate that semaphorin 3F serves as a potential prognostic biomarker and tumor suppressor of esophageal squamous cell carcinoma and may be involved in the lymph node metastasis development through regulating neuropilin 2.

MicroRNA­138­5p regulates neural stem cell proliferation and differentiation in vitro by targeting TRIP6 expression.

Research on neural stem cells (NSCs) has recently focused on microRNAs (miRNAs), a class of small non­coding RNAs that have crucial roles in regulating NSC proliferation and differentiation. In the present study, a quantitative­polymerase chain reaction assay revealed that the expression of miRNA (miR)­138­5p was significantly decreased during neural differentiation of NSCs in vitro. Overexpression of miR­138­5p reduced NSC proliferation and increased NSC differentiation. Furthermore, suppression of miR­138­5p via transfection with a miRNA inhibitor enhanced NSC proliferation and attenuated NSC differentiation. Additionally, expression of thyroid hormone receptor interacting protein 6 (TRIP6), a critical regulator of NSCs, was negatively correlated with the miR­138­5p level. A luciferase assay demonstrated that miR­138­5p regulate TRIP6 by directly binding the 3'­untranslated region of the mRNA. Additionally, upregulation of TRIP6 rescued the NSC proliferation deficiency induced by miR­138­5p and abolished miR­138­5p­promoted NSCs differentiation. By contrast, downregulation of TRIP6 produced the opposite effect on proliferation and differentiation of NSCs transfected with anti­miR­138­5p. Taken together, the data suggest that miR­138­5p regulates NSCs proliferation and differentiation, and may be useful in developing novel treatments for neurological disorders via manipulation of miR­138­5p in NSCs.

Prognostic value of circulating tumor cells in esophageal cancer.

AIM: To perform a meta-analysis of the related studies to assess whether circulating tumor cells (CTCs) can be used as a prognostic marker of esophageal cancer. METHODS: PubMed, Embase, Cochrane Library and references in relevant studies were searched to assess the prognostic relevance of CTCs in patients with esophageal cancer. The primary outcome assessed was overall survival (OS). The meta-analysis was performed using the random effects model, with hazard ratio (HR), risk ratio (RR) and 95% confidence intervals (95%CIs) as effect measures. RESULTS: Nine eligible studies were included involving a total of 911 esophageal cancer patients. Overall analyses revealed that CTCs-positivity predicted disease progression (HR = 2.77, 95%CI: 1.75-4.40, P < 0.0001) and reduced OS (HR = 2.67, 95%CI: 1.99-3.58, P < 0.00001). Further subgroup analyses demonstrated that CTCs-positive patients also had poor OS in different subsets. Moreover, CTCs-positivity was also significantly associated with TNM stage (RR = 1.48, 95%CI: 1.07-2.06, P = 0.02) and T stage (RR = 1.44, 95%CI: 1.13-1.84, P = 0.003) in esophageal cancer. CONCLUSION: Detection of CTCs at baseline indicates poor prognosis in patients with esophageal cancer. However, this finding relies on data from observational studies and is potentially subject to selection bias. Prospective trials are warranted.

[Construction of a lentivirus vector expressing wheat germ agglutinin and its infection in human adipose-derived stem cells].

OBJECTIVE: To construct a lentivirus vector carrying wheat germ agglutinin (WGA) and evaluate its ability of tracing WGA in the brain of mice with ischemic brain injury. METHODS: WGA gene was inserted into the lentiviral vector Plvx IRES-ZsGreen1 using genetic engineering methods. 293T cells were transfected with the vector and 3 packaging plasmids (RPEV, PRRE, and VSVG) to obtain the recombinant lentivirus for infection of human adipose-derived stem cells (hADSCs). The infected hADSCs were injected into the damaged brain area by in situ injection in a mouse model of middle cerebral artery occlusion (MCAO) and the expression of GFP was traced. RESULTS: Immunofluorescence identification detected WGA protein expression in the infected hADSCs, which survived in the infarct area of mice with MCAO. CONCLUSION: Packaging WGA gene in lentivirus is a reliable approach to allow efficient neuroanatomical tracing of various cells.

[Evaluation of noninvasive positive pressure ventilation in treatment for patients with severe acute respiratory syndrome].

OBJECTIVE: To analyze the effects of noninvasive positive pressure ventilation (NIPPV) on oxygenation of severe acute respiratory syndrome (SARS) patients, and to discuss the timing point for mechanical ventilation. METHODS: Twenty-five SARS patients with respiratory dysfunction treated with NIPPV were studied retrospectively in order to evaluate the influences within 24 hours after initiation of ventilatory support on their physiological indices and oxygenation. Patients with SARS were divided into two groups: survivor group (n=13) and non-survivor group (n=12). We compared the acute physiology and chronic health evaluation (APACHEII) score, respiratory rate (RR),saturation of oxygen (SpO(2)) and modificative respiratory index (MRI) for the survivors and non-survivors before NIPPV and after NIPPV for twenty-four hours, respectively. RESULTS: Although NIPPV administered via full-face masks might be an effective treatment for rapidly improving vital signs and gas exchange and sense of dyspnea in both groups during the initial 24 hours of ventilatory support, the patients in non-survivor group had higher APACHEII score, respiratory rates and lower SpO(2), MRI than the patients in survivor group (P<0.05) at the same intervals after initiation of support. CONCLUSION: Noninvasive ventilation should be used as a substitutive tool for endotracheal intubation an alternative treatment for acute respiratory failure related to SARS. Therefore, we should make efforts to avoid missing the time point for NIPPV or intubation, and we should not be restricted to the available indications for NIPPV or IPPV.