Automated highway pavement crack recognition under complex environment.

The pavement is vulnerable to damage from natural disasters, accidents and other human factors, resulting in the formation of cracks. Periodic pavement monitoring can facilitate prompt detection and repair the pavement diseases, thereby minimizing casualties and property losses. Due to the presence of numerous interferences, recognizing highway pavement cracks in complex environments poses a significant challenge. Nevertheless, several computer vision approaches have demonstrated notable success in tackling this issue. We have employed a novel approach for crack recognition utilizing the ResNet34 model with a convolutional block attention module (CBAM), which not only saves parameters and computing power but also ensures seamless integration of the module as a plug-in. Initially, ResNet18, ResNet34, and ResNet50 models were trained by employing transfer learning techniques, with the ResNet34 network being selected as a fundamental model. Subsequently, CBAM was integrated into ResBlock and further training was conducted. Finally, we calculated the precision, average recall on the test set, and the recall of each class. The results demonstrate that by integrating CBAM into the ResNet34 network, the model exhibited improved test accuracy and average recall compared to its previous state. Moreover, our proposed model outperformed all other models in terms of performance. The recall rates for transverse crack, longitudinal crack, map crack, repairing, and pavement marking were 88.8%, 86.8%, 88.5%, 98.3%, and 99.9%, respectively. Our model achieves the highest precision of 92.9% and the highest average recall of 92.5%. However, the effectiveness in detecting mesh cracks was found to be unsatisfactory, despite their significant prevalence. In summary, the proposed model exhibits great potential for crack identification and serves as a crucial foundation for highway maintenance.

Apelin-13 deficiency alters cortical bone geometry, organic bone matrix, and inhibits Wnt/ß-catenin signaling.

Adipokines play key roles in the regulation of obesity, type 2 diabetes mellitus, and bone growth. As a newly discovered hormone in the adipokines family, the precise role of Apelin-13 on bone metabolism is not yet clear. Apelin-13 and 25(OH)D3 expression were detected in freshly isolated serum of healthy individuals and osteoporosis patients with ELISA method. Apelin-13 deficient mice were set up and cortical bone geometry was measured with micro-computed tomography (Micro-CT) at 5 months old, then profile of organic bone matrix genes was detected with quantitative Real-Time PCR (qRT-PCR). Wnt/ß-catenin signaling molecules were assayed in primary osteocytes isolated from neonatal calvarias. Apelin-13 and 25(OH)D3 showed decreased expression in osteoporosis patients. Five-month-old Apelin deficient mice exhibited decreased total and bone marrow cavity area and periosteal and endocortical bone surface. Deficiency of Apelin-13 downregulated collagen maturation associated genes (loxl3 and loxl4) and Wnt/ß-catenin signaling, while loxl2 was upregulated, all of which indicated that Apelin-13 could play a role in regulating skeletal homeostasis. The decrease in bone formation in Apelin-13 deficient mice is associated with downregulation of organic bone matrix genes and Wnt/ß-catenin signaling molecules, all of these indicate that association of Apelin-13 with bone mineral density (BMD) could be mediated by Wnt/ß-catenin pathway.

Contrast-induced nephropathy in patients with diabetes mellitus between iso- and low-osmolar contrast media: A meta-analysis of full-text prospective, randomized controlled trials.

PURPOSE: This study was conducted to compare iso-osmolar contrast medium, iodixanol, with low-osmolar contrast media (LOCM) for assessing contrast-induced nephropathy (CIN) incidence, exclusively in the diabetic population. METHOD: A systematic search was conducted for full-text, prospective, randomized controlled trials (RCTs). The primary outcome was incidence of CIN. Medline, Cochrane Central Register of Controlled Trials, and other sources were searched until May 31, 2017. RESULTS: Twelve RCTs finally met the search criteria. Iodixanol did not significantly reduce the risk of CIN (risk ratio [RR]: 0.72, 95% confidence interval (CI): [0.49, 1.04], p = 0.08). However, there was significantly reduced risk of CIN when iodixanol was compared to a LOCM agent iohexol (RR: 0.32, 95% CI [0.12, 0.89]). There were no differences between iodixanol and the other non-iohexol LOCM (RR: 0.92, 95% CI [0.68, 1.25]). CONCLUSION: In diabetic populations, iodixanol is not associated with a significant reduction of CIN risk. Iodixanol is associated with a reduced risk of CIN compared with iohexol, whereas no significant difference between iodixanol and other LOCM could be found.

[JAK2 V617F mutation burden and its clinical implications in 415 patients with myeloproliferative neoplasm].

OBJECTIVE: To detect JAK2 V617F mutation burden and its clinical implications in patients with myeloproliferative neoplasm (MPN). METHODS: JAK2 V617F mutation burden were detected by using MGB Taqman probes and its clinical significance were retrospectively studied in 415 MPN patients. RESULTS: JAK2 V617F was found in 56.9% of all patients [83.5% in polycythemia vera (PV), 55.9% in essential thrombocythemia (ET), 41.9% in primary myelofibrosis (PMF) and 64.7% in MPN-unclassifiable)]. The majority of patients carried heterozygous JAK2 V617F mutation and homozygote was found only in 12 cases (4 in PV, 4 in MPN-U, 2 in PMF, 1 in ET, and 1 in chronic neutrophilic leukemia). Most patients (68.8%) were lower mutation burden (mutation burden<50%), but PV had the highest burden, the moderate burden in PMF and the least in ET. The patient's age and WBC count were significantly correlated with higher mutation burden in PV. WBC count was significantly related to higher mutation burden in ET. WBC count, Hb level and the platelet count were significantly related to higher mutation burden in PMF. CONCLUSION: The mutation burden of JAK2 V617F from high to low was PV, ET and PMF. The majority of JAK2 V617F mutation was heterozygous. JAK2 V617F mutation burden was positively correlated with age, WBC, Hb and platelet counts.

[Expression of liposome-mediated PEDF-GFP gene in the retina of the BN rats through different gene delivery route].

OBJECTIVE: Transducing PEDF-GFP plasmid to the retina of the BN rats with cationic liposome through different gene delivery route, then observe the expression and location of the PEDF-GFP. METHODS: PEDF-GFP plasmid with cationic liposome was delivered to the retina of the BN rat through subretinal injection and intravitreal injection. The expression of GFP was observed under fluorescence microscope, and the mRNA of PEDF gene was detected by RT-PCR. RESULTS: Green fluorescence was emitted from the total retina include RPE cell under fluorescent microscope after 24 h in two gene delivery route, The fluorescence intensity was stronger with time changing. Gradual fluorescence increase in the retina and RPE cells occurred and lasted 4 weeks. The expression of PEDF mRNA was also detected by RT-PCR after 24 h, and maintained stable 4 weeks after infection. CONCLUSIONS: Cationic liposome can mediate PEDF-GFP gene into the retina of the BN rat effectively; subretinal injection and intravitreal injection both are effective gene delivery route; and their stable expression can maintain 4 weeks after transfection.