Artificial Neural Network: A Method for Prediction of Surgery-Related Pressure Injury in Cardiovascular Surgical Patients.

PURPOSE: The aim of this study was to build an artificial neural network (ANN) model for predicting surgery-related pressure injury (SRPI) in cardiovascular surgical patients. DESIGN: Prospective cohort study. SUBJECTS AND SETTING: One hundred forty-nine patients who had cardiovascular surgery were included in the study. This study was conducted in a 1000-bed teaching hospital in Eastern China where 250 to 350 cardiac surgeries are performed each year. METHODS: We performed a prospective cohort study among consecutive patients undergoing cardiovascular surgery between January and December 2015. The ANN model was built based on possible SRPI risk factors. The model performance was tested by a receiver operating characteristic curve and the C-index. A C-index from 0.5 to 0.7 is classified as having low accuracy, 0.7 to 0.9 as having moderate accuracy, and 0.9 to 1.0 as having high accuracy. We also compared the actual SRPI incidences based on the ANN stratification. RESULTS: Thirty-seven of 147 patients developed SRPIs, yielding an incidence rate of 24.8% (95% CI, 18.1-32.6). The C-index was 0.815, which showed the ANN model had a moderate prediction value for SRPI. According to the ANN model, the SRPI predicting incidence ranged from 6.4% to 67.7%. Surgery-related pressure injury incidences were significantly different among 3 risk groups stratified by the ANN (P < .05). CONCLUSION: We established an ANN model that provides moderate prediction of SRPI in patients undergoing cardiovascular surgical procedures. Identification and additional associated factors should be incorporated into the ANN model to increase its predictive ability.

Apolipoprotein A-I: Potential Protection Against Intestinal Injury Induced by Dietary Lipid.

The intestinal barrier system protects the human body from harmful factors, by continuously renewing the intestinal epithelium, tight junctions and enteric microbes. However, dietary fat can harm the intestinal epithelial barrier enhancing gut permeability. In recent years, Apolipoprotein A-I has attracted much attention because of its anti-inflammatory properties. Numerous studies have demonstrated that Apolipoprotein A-I can regulate mucosal immune cells, inhibit the progression of inflammation, promote epithelial proliferation and repair, and maintain physical barrier function; it can also regulate angiogenesis, thereby improving local circulation. This article is intended to elucidate the mechanism by which Apolipoprotein A-I improves intestinal barrier damage caused by dietary fat and to review the role of Apolipoprotein A-I in maintaining intestinal homeostasis.

Effect of Impact Velocity and Angle on Impact Wear Behavior of Zr-4 Alloy Cladding Tube.

In the pressurized water reactor nuclear power plant, 316L SS chips were captured by the support grid and continued to affect the Zr-4 cladding tube, causing the fuel rods to wear and perforate. In this work, a 60° acute angle cone of 316L SS was used to simulate the cyclic impact of debris on a Zr-4 alloy tube with different initial impact velocities and impact angles. Results showed that increasing the initial impact velocity will generate a wear debris accumulation layer with a wear-reducing effect, but also promote the extension and expansion of fatigue cracks, resulting in the delamination of Zr-4 alloy tubes. The inclination of the impact angle increases the energy loss. The energy loss rate of the 45° impact is as high as 69.68%, of which 78% is generated by the impact-sliding stage. The normal force is mainly responsible for the wear removal and plastic deformation of Zr-4 alloy tubes. Tangential forces cause severe cutting in Zr-4 alloys and pushes the resulting wear debris away from the contact surfaces.

[Alterations in reactive oxygen species and dimethylarginine dimethylaminohydrolase-asymmetric dimethyl-arginine system in the process of endothelial cell senescence induced by high glucose].

OBJECTIVE: To investigate the changes in reactive oxygen species (ROS) and dimethyl- arginine dimethylaminohydrolase-asymmetric dimethylarginine (DDAH-ADMA) system in the process of endothelial cell senescence after exposure to high glucose. METHODS: The human umbilical vein endothelial cells (HUVECs) were cultured with different concentrations of glucose, e.g. 5.5 mmol/L (normal level), and high levels as 11.0, 22.0 and 33.0 mmol/L, for 48 hours, respectively. Subsequently, SA-ß-gal staining was used to evaluate senescence of cells. Telomerase activity was detected by polymerase chain reaction-enzyme linked immunosorbent assay (PCR-ELISA). The intracellular ROS level was measured by flow cytometry. The ADMA concentration and DDAH activity were determined with high-performance liquid chromatography. RESULTS: Compared with normal glucose concentration group, after the endothelial cells were treated with high glucose concentration (11.0-33.0 mmol/L) for 48 hours, the number of SA-ß-gal positive cells was increased significantly [(7.00±1.73)%, (12.67±2.03)%, (16.00±2.26)% vs. (4.00±1.33)%, P>0.05, P<0.05, P<0.05] and the telomerase activity was inhibited dramatically [(91.32±4.01)%, (78.44±3.78)%, (56.04±3.35)% vs. 100%, all P<0.05]. The ROS level (mfi) was increased in all high glucose groups (159.84±27.52, 188.99±18.77, 244.56±20.96 vs.117.11±18.76, P<0.05 or P<0.01). At the same time, the ADMA (µmol/L) production was increas ed (0.78±0.14, 0.88±0.18, 1.08±0.15 vs. 0.70±0.12, P>0.05, P<0.05, P<0.05), and DDAH activity was decreased [(91.32±4.01)%, (78.44±3.78)%, (56.04±3.35)% vs.100%, all P<0.05]. CONCLUSION: High glucose can accelerate endothelial cells senescence in dose-dependent manner and the underlying mechanism may be related to an increased oxidative stress and change in DDAH-ADMA system.

MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway.

Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury. MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury. However, whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood. In this study, we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo. Our results showed that after ischemia/reperfusion injury, miR-670 expression was obviously increased. After miR-670 expression was inhibited with an miR-670 antagomir, cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced. When miR-670 overexpression was induced by an miR-670 agomir, neuronal apoptosis was increased. In addition, we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits. Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury. These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway, which may be a potential target for treatment of cerebral ischemia/reperfusion injury. The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27, 2017 (IRB No. 2017PS035K).