Impact of One-Lung Ventilation on Oxygenation and Ventilation Time in Thoracoscopic Heart Surgery: A Comparative Analysis with Median Thoracotomy.

BACKGROUND One-lung ventilation is the separation of the lungs by mechanical methods to allow ventilation of only one lung, particularly when there is pathology in the other lung. This retrospective study from a single center aimed to compare 49 patients undergoing thoracoscopic cardiac surgery using one-lung ventilation with 48 patients undergoing thoracoscopic cardiac surgery with median thoracotomy. MATERIAL AND METHODS This single-center retrospective study analyzed patients who underwent thoracoscopic cardiac surgery based on one-lung ventilation (experimental group, n=49). Other patients undergoing a median thoracotomy cardiac operation were defined as the comparison group (n=48). The oxygenation index and the mechanical ventilation time were also recorded. RESULTS There was no significant difference in the immediate oxygenation index between the experimental group and comparison group (P>0.05). There was no significant difference for the oxygenation index between men and women in both groups (P>0.05). The cardiopulmonary bypass time significantly affected the oxygenation index (F=7.200, P=0.009). Operation methods (one-lung ventilation thoracoscopy or median thoracotomy) affected postoperative ventilator use time (F=8.337, P=0.005). Cardiopulmonary bypass time (F=16.002, P<0.001) and age (F=4.384, P=0.039) had significant effects on ventilator use time. There was no significant effect of sex (F=0.75, P=0.389) on ventilator use time. CONCLUSIONS Our results indicated that one-lung ventilation thoracoscopic cardiac surgery did not affect the immediate postoperative oxygenation index; however, cardiopulmonary bypass time did significantly affect the immediate postoperative oxygenation index. Also, one-lung ventilation thoracoscopic cardiac surgery had a shorter postoperative mechanical ventilation use time than did traditional median thoracotomy cardiac surgery.

Convolutional neural network-based artificial intelligence for the diagnosis of early esophageal cancer based on endoscopic images: A meta-analysis.

Background: Early screening and treatment of esophageal cancer (EC) is particularly important for the survival and prognosis of patients. However, early EC is difficult to diagnose by a routine endoscopic examination. Therefore, convolutional neural network (CNN)-based artificial intelligence (AI) has become a very promising method in the diagnosis of early EC using endoscopic images. The aim of this study was to evaluate the diagnostic performance of CNN-based AI for detecting early EC based on endoscopic images. Methods: A comprehensive search was performed to identify relevant English articles concerning CNN-based AI in the diagnosis of early EC based on endoscopic images (from the date of database establishment to April 2022). The pooled sensitivity (SEN), pooled specificity (SPE), positive likelihood ratio (LR+), negative likelihood ratio (LR-), diagnostic odds ratio (DOR) with 95% confidence interval (CI), summary receiver operating characteristic (SROC) curve, and area under the curve (AUC) for the accuracy of CNN-based AI in the diagnosis of early EC based on endoscopic images were calculated. We used the I2 test to assess heterogeneity and investigated the source of heterogeneity by performing meta-regression analysis. Publication bias was assessed using Deeks' funnel plot asymmetry test. Results: Seven studies met the eligibility criteria. The SEN and SPE were 0.90 (95% confidence interval [CI]: 0.82-0.94) and 0.91 (95% CI: 0.79-0.96), respectively. The LR+ of the malignant ultrasonic features was 9.8 (95% CI: 3.8-24.8) and the LR- was 0.11 (95% CI: 0.06-0.21), revealing that CNN-based AI exhibited an excellent ability to confirm or exclude early EC on endoscopic images. Additionally, SROC curves showed that the AUC of the CNN-based AI in the diagnosis of early EC based on endoscopic images was 0.95 (95% CI: 0.93-0.97), demonstrating that CNN-based AI has good diagnostic value for early EC based on endoscopic images. Conclusions: Based on our meta-analysis, CNN-based AI is an excellent diagnostic tool with high sensitivity, specificity, and AUC in the diagnosis of early EC based on endoscopic images.

Exogenous Brain-Derived Neurotrophic Factor at a 50 ng/mL Concentration has a Significant Protective Effect on Bilirubin-Induced Cerebral Cortex Neuronal Injury.

BACKGROUND: Bilirubin encephalopathy is a common disabling disease in neonates. Brain-derived neurotrophic factor (BDNF) plays an important role in the repair and regeneration of nerves following injury, as well as the maintenance of neuronal growth and differentiation. This study aimed to investigate the effect of exogenous BDNF on the apoptosis and survival of in vitro cultured neurons injured by bilirubin as well as determine the optimal BDNF concentration. METHODS: Rat cerebral cortex neurons cultured for 8 days were randomly divided into the control, bilirubin, and BDNF groups. A bilirubin injury model was established. BDNF was added to the BDNF group at a final concentration of 5, 50, and 100 ng/mL 4 hours prior to the addition of bilirubin. The cell morphology was observed via phase contrast microscopy, and the cell viability and apoptotic rate were detected using the methyl thiazolyl tetrazolium method and flow cytometry. RESULTS: The neuronal viability in the bilirubin group was significantly decreased and the apoptotic rate was significantly increased compared with the control group. BDNF significantly improved the impact of bilirubin on neuronal activity; the apoptotic rate was significantly decreased (p < 0.05); however, within 24 - 48 hours, BDNF had no significant effect on the nerve cell viability (p > 0.05). Moreover, the protective effect of different BDNF concentrations also varied (p < 0.05), with the most substantial protective effect at a final concentration of 50 ng/mL. CONCLUSIONS: Bilirubin may damage rat cerebral cortex neurons and induce their apoptosis, whereas BDNF has a protective effect on bilirubin-induced cerebral cortex neuronal injury.

[Early treatment with hepatocyte growth factor improves pulmonary artery and right ventricular remodeling in rats with pulmonary artery hypertension by modulating cytokines expression].

OBJECTIVE: To investigate the effect of early treatment with hepatocyte growth factor (HGF) on the cytokine expression and pulmonary artery, right ventricular (RV) remodeling in the rat model of pulmonary artery hypertension (PAH). METHODS: The rat model of PAH was produced by injecting monocrotaline, and the model rats were randomly divided into empty adenovirus transfection group (MCT group, n = 10) and HGF gene transfection group(HGF group, n = 10). Another group of rats served as the Sham operation group (Sham group n = 10). After 4 weeks of HGF gene transfection, the histological sections of the lungs and right ventricular (RV) were stained with hematoxylin-eosin (HE) and the pulmonary artery and RV remodeling were examined. The rat lung sections were also immunostained with antibodies against factor VIII, and the capillary density were calculated. Meanwhile, the mRNA expression of TNF-α, IL-6, IL-1ß and TGF-ß1 in pulmonary arteries and RV were detected by RT-PCR. RESULTS: HGF gene treatment significantly decreased the ratio of vessel wall thickness to pulmonary artery diameter and the ratio of vessel wall area to total area, and increased the capillary density of lung in PAH rats. HGF gene treatment also significantly decreased cross-sectional area of cardiomyocytes and collagen deposited in RV. Moreover, HGF gene treatment significantly decreased the expression of cytokines in pulmonary artery (TNF-α: 0.82 ± 0.07 vs 0.49 ± 0.09, IL-6: 1.13 ± 0.19 vs 0.68 ± 0.09, IL-1ß: 0.86 ± 0.11 vs 0.51 ± 0.07, TGF-ß1: 1.18 ± 0.12 vs 0.59 ± 0.10) and RV (TNF-α: 0.79 ± 0.11 vs 0.48 ± 0.08, IL-6: 1.03 ± 0.11 vs 0.63 ± 0.09, IL-1ß: 0.81 ± 0.11 vs 0.52 ± 0.07, TGF-ß1: 0.94 ± 0.12 vs 0.53 ± 0.10) in MCT induced PAH rats (P < 0.05) . CONCLUSION: Early treatment with HGF improves pulmonary artery and RV remodeling, possibly by decreasing the expression of TNF-α, IL-6, IL-1ß and TGF-ß1 in pulmonary arteries and RV.

Hepatocyte growth factor improves right ventricular remodeling in pulmonary arterial hypertensive rats via decreasing neurohormonal activation and inhibiting apoptosis.

BACKGROUND: Hepatocyte growth factor (HGF) inhibits the development of pulmonary artery hypertension (PAH) by reducing pulmonary artery pressure and right ventricle (RV) hypertrophy. However, whether HGF can prevent RV remodeling via inhibiting apoptosis in RV cardiomyocytes and decreasing neurohormonal activation remains unknown. METHODS: The PAH and subsequent RV remodeling in rats were induced by subcutaneous injection of monocrotaline (MCT). The PAH rats were transfected with adenovirus carrying HGF (Ad-HGF) via intratracheal instillation. Three weeks after transfection, the hemodynamics indexes were measured, serum levels for angiotonin II (ANG II) and brain natriuretic peptide (BNP) were determined by ELISA. Histological analysis was used to assess the RV hypertrophy and fibrosis. The cardiomyocyte apoptosis in RV was assayed by TUNEL staining. The mRNA expression of BNP, angiotensin-converting enzyme (ACE), Bax and Bcl-2 in RV was determined by reverse transcriptase polymerase chain reaction (RT-PCR), the protein expression of transforming growth factor (TGF)-ß1 and tumor necrosis factor (TNF)-α in RV was determined by Western blotting. RESULTS: HGF treatment significantly decreased the mean PAH, RV systolic pressure, serum ANG II and BNP levels. HGF treatment also significantly decreased the RV hypertrophy, collagen deposition, and the number of apoptotic cardiomyocytes. Moreover, HGF treatmemt significantly decreased the expression of BNP, ACE, Bax, TGF-ß1, and TNF-α, while it significantly increased the expression of Bcl-2. CONCLUSIONS: Gene transfer of HGF decreases MCT-induced PAH and improves RV remodeling. This effect is mediated not only by improving the hemodynamics but also by decreasing neurohormonal activation and inhibiting cardiomyocytes apoptosis. HGF gene treatment may be an effective strategy for improving RV remodeling in MCT-induced PAH.