Imaging of annulus-formation interface using reverse time migration based on ultrasonic pitch-catch measurements: Case studies from an experimental well and a field well.

Cased-hole logging using ultrasonic pitch-catch modality is a proven technique for cement bond evaluation in cased holes. However, complex measuring environments such as tool and casing eccentering makes it difficult to precisely separate and pick the third interface echoes from full ultrasonic Lamb waves, leading to ambiguous identification of annulus-formation interface. To overcome this problem, we propose an improved cased-hole reverse time migration approach for ultrasonic pitch-catch measurements to image the annulus-formation interface. The missing ultrasonic Lamb waveforms between far and near receivers due to insufficient spatial sampling are reconstructed based on the optimized theoretical phase velocity of zero-order anti-symmetric Lamb mode waves. Additionally, we apply the hybrid illumination imaging condition to mitigate the imaging noises around the true reflectors and sources. Data examples from a physical experimental well and a field well demonstrate that the proposed approach is an effective method for characterizing the annulus-formation interface without requiring precise knowledge of the velocity distribution in the region behind the casing. Furthermore, test on an experimental well has indicated that the method has the potential to detect the absence of cement in the annulus medium.

Circ_0062166 aggravates cerebral ischemia-reperfusion injury through targeting miR-526b-5p/BCL2L13 axis.

BACKGROUND: Cerebral ischemia-reperfusion (CIR) injury is a severe disease, which may cause serious dysfunction of the brain. Most circular RNAs (circRNAs) have been demonstrated to play a significant role in CIR injury. However, a novel circRNA, circ_0062166 (circ_BCL2L13) has not been investigated for CIR injury. Hence, we aim to disclose the role of circ_0062166 in CIR injury in this study. METHODS: Firstly, RT-qPCR was applied to examine the expression of circ_0062166 in oxygen-glucose deprivation and reoxygenation (OGD/R) cell model. Functional assays were conducted to detect the role of circ_0062166 in CIR injury. RNA pull down, RIP and luciferase reporter assays were implemented to probe into the regulatory mechanism of circ_0062166. RESULTS: Circ_0062166 was significantly up-regulated in neuro-2A (N2A) neuroblastoma cells following OGD/R. Functionally, the silencing of circ_0062166 inhibited cell proliferation and promoted cell apoptosis under OGD/R condition. From the perspective of mechanism, circ_0062166 functioned as a competing endogenous RNA (ceRNA) for microRNA-526b-5p (miR-526b-5p) and regulated BCL2 like 13 (BCL2L13). Eventually, the promoting role of the circ_0062166/miR-526b-5p/BCL2L13 axis in the CIR injury was verified. CONCLUSION: To sum up, the present study has demonstrated that circ_0062166/miR-526b-5p/BCL2L13 axis accelerated the progression of CIR injury, which might provide effective strategies for CIR injury therapy.