Crack Segmentation Extraction and Parameter Calculation of Asphalt Pavement Based on Image Processing.

Crack disease is one of the most serious and common diseases in road detection. Traditional manual methods for measuring crack detection can no longer meet the needs of road crack detection. In previous work, the authors proposed a crack detection method for asphalt pavements based on an improved YOLOv5s model, which is a better model for detecting various types of cracks in asphalt pavements. However, most of the current research on automatic pavement crack detection is still focused on crack identification and location stages, which contributes little to practical engineering applications. Based on the shortcomings of the above work, and in order to improve its contribution to practical engineering applications, this paper proposes a method for segmenting and analyzing asphalt pavement cracks and identifying parameters based on image processing. The first step is to extract the crack profile through image grayscale, histogram equalization, segmented linear transformation, median filtering, Sauvola binarization, and the connected domain threshold method. Then, the magnification between the pixel area and the actual area of the calibration object is calculated. The second step is to extract the skeleton from the crack profile images of asphalt pavement using the Zhang-Suen thinning algorithm, followed by removing the burrs of the crack skeleton image using the connected domain threshold method. The final step is to calculate physical parameters, such as the actual area, width, segments, and length of the crack with images obtained from the crack profile and skeleton. The results show that (1) the method of local thresholding and connected domain thresholding can completely filter noise regions under the premise of retaining detailed crack region information. (2) The Zhang-Suen iterative refinement algorithm is faster in extracting the crack skeleton of asphalt pavement, retaining the foreground features of the image better, while the connected-domain thresholding method is able to eliminate the missed isolated noise. (3) In comparison to the manual calibration method, the crack parameter calculation method proposed in this paper can better complete the calculation of crack length, width, and area within an allowable margin of error. On the basis of this research, a windowing system for asphalt pavement crack detection, WSPCD1.0, was developed. It integrates the research results from this paper, facilitating automated detection and parameter output for asphalt pavement cracks.

A comparison of non-intubated video-assisted thoracic surgery with spontaneous ventilation and intubated video-assisted thoracic surgery: a meta-analysis based on 14 randomized controlled trials.

BACKGROUND: Video-assisted thoracic surgery (VATS) generally involves endotracheal intubation under general anesthesia. However, inevitably, this may cause intubation-related complications and prolong the postoperative recovery process. Gradually, non-intubated video-assisted thoracic surgery (NIVATS) is increasingly being utilized. However, its safety and efficacy remain controversial. METHODS: Randomized controlled trials (RCTs) published up to August 2020 were selected from the Cochrane Library, Web of Science, PubMed, Embase, and ClinicalTrials.gov databases and included in this study according to the inclusion criteria. Two reviewers screened these RCTs and independently extracted the relevant data. After assessing the risk of bias in these RCTs, a meta-analysis was performed using Review Manager 5.3. Pooled data were meta-analyzed using a random-effects model. RESULTS: Meta-analysis data demonstrated that the mean difference (MD) in the length of hospital stay between non-intubated patients and intubated patients was -1.41 days, with a 95% confidence interval (CI) of -2.47 to -0.34 (P=0.01). The visual analogue scale (VAS) score between the two groups showed a MD of -0.34 (95% CI: -0.58 to -0.10; P=0.006). Patients who underwent NIVATS presented with lower rates of overall complications [odds ratio (OR) 0.41; 95% CI: 0.25 to 0.67; P=0.0004], air leak (OR 0.45; 95% CI: 0.24 to 0.87; P=0.02), pharyngeal discomfort (OR 0.08; 95% CI: 0.04 to 0.17; P<0.00001), hoarseness (OR 0.06; 95% CI: 0.02 to 0.21; P<0.00001), and gastrointestinal reactions (OR 0.23; 95% CI: 0.10 to 0.53; P=0.0005) compared to intubated patients. The anesthesia satisfaction scores in the NIVATS group were significantly higher than those of the VATS group (MD 0.50; 95% CI: 0.12 to 0.88; P=0.009). However, there were no statistically significant differences in the length of operation time (MD 0.90 hours; 95% CI: -0.23 to 2.03; P=0.12) and surgical field satisfaction (1 point) (OR 0.73; 95% CI: 0.34 to 1.59; P=0.43) between the two groups. CONCLUSIONS: NIVATS is a safe and feasible form of intervention that can reduce the postoperative pain and complications of various systems and shorten hospital stay duration without prolonging the operation time.

NRF2 mitigates acute alcohol-induced hepatic and pancreatic injury in mice.

Binge alcohol drinking is an important health concern and well-known risk factor for the development of numerous disorders. Oxidative stress plays a critical role in the pathogenesis of acute alcoholism. Nuclear factor erythroid 2 like 2 (NRF2) is a master regulator of cellular adaptive response to oxidative insults. However, the role of NRF2 in acute alcoholism and associated pathologies remains unclear. We found that Nrf2-knockout (Nrf2-KO) mice had exaggerated hypoglycemia and hypothermia and increased mortality compared to wildtype mice after binge ethanol exposure. This phenotype was partially rescued by providing warm environment and/or glucose administration. Acute high dose of alcohol exposure resulted in substantially worsened liver and pancreatic injuries in Nrf2-KO mice. Importantly, deficiency of Nrf2 allowed severe pancreatitis and pancreatic ß-cell injury with increased insulin secretion and/or leaking during binge ethanol exposure, which contributed to hypoglycemia. In contrast, a clinically used NRF2 activator dimethyl fumarate (DMF) protected against hypoglycemia and lethality induced by acute ethanol exposure. Furthermore, Nrf2-KO mice likely had defective hepatic acetaldehyde metabolism. Taken together, NRF2 plays an important protective role against acute binge alcohol-induced hepatic and pancreatic damage, which may be partially attributable to its primary regulating role in antioxidant response and impact on ethanol metabolism.

Identification of TRAF6 as a ubiquitin ligase engaged in the ubiquitination of SopB, a virulence effector protein secreted by Salmonella typhimurium.

The phosphoinositide phosphatase SopB is one of the effectors injected by Salmonella typhimurium (S.typhimurium) that diversifies its function through a ubiquitin-dependent differential localization. However, it is unclear which E3 ubiquitin ligase is responsible for ubiquitination of SopB. Based on the E1-E2-E3 trio of enzymes responsible for the ubiquitin activation and translocation to substrate proteins, we constructed an in vitro assay of SopB ubiquitination. Using this assay, we purified an E3 ubiquitin ligase, TRAF6, from the Henle-407 S100 extraction that may be responsible for the ubiquitination of SopB. To investigate the functional correlation of TRAF6, we showed that recombinant TRAF6 specifically ubiquitinates SopB in a dose-dependent manner in vitro. Upon infection, the ubiquitination of SopB was absolutely blocked by TRAF6 deletion, as shown in Traf6(-/-) mouse embryonic fibroblasts (MEFs) compared with Traf6(+/+) MEFs. However, the ectopic expression of TRAF6 in Traf6(-/-) MEFs rescued the two species of ubiquitin-conjugated SopB, which strengthens the role of TRAF6 in SopB ubiquitination. The analysis of E2 revealed that UbcH5c and not other E2 conjugating enzymes are required for TRAF6-mediated SopB ubiquitination both in vitro and in vivo. In summary, these results suggest the relevance of UbcH5c/TRAF6 in SopB during S.typhimurium infection and thereby imply that S.typhimurium has evolved a mechanism of utilizing the host's E3 ubiquitin ligase to modify and modulate the function of its effector protein in order to ensure pathogen and host cell survival.