Bridge displacement is the most basic evaluation index of the health status of a bridge structure. The existing measurement methods for bridge displacement basically fail to realize long-term and real-time dynamic monitoring of bridge structures, because of the low degree of automation and the insufficient precision, causing bottlenecks and restriction. To solve this problem, we proposed a bridge displacement monitoring system based on laser projection-sensing technology. First, the laser spot recognition method was studied. Second, the software for the displacement monitoring system was developed. Finally, a series of experiments using this system were conducted, and the results show that such a system has high measurement accuracy and speed. We aim to develop a low-cost, high-accuracy and long-term monitoring method for bridge displacement based on these preliminary efforts.

PurposeTo detect changes in brain lateralization in patients with mild cognitive impairment (MCI) and Alzheimer’s disease (AD) using resting-state functional magnetic resonance imaging (fMRI).Materials and methodsData from 61 well-matched right-handed subjects were obtained from the Alzheimer’s Disease Neuroimaging Initiative, including 19 healthy controls (HCs), 25 patients with MCI, and 17 patients with AD. First, we divided 256 pairs of seed regions from each hemisphere covering the entire cerebral gray matter. Then, we used the intrinsic laterality index (iLI) approach to quantify the functional laterality using fMRI. One-way ANOVA was employed to estimate the differences in iLI among the three groups. The sum, number and mean value of the iLI were calculated within the thresholds of 0 < |iLI| < 0.2, 0.2 ≤ |iLI| < 0.4, 0.4 ≤ |iLI| < 0.8, and |iLI| ≥ 0.8, to explore the changes in the lateralization of resting-state brain function in patients with MCI and AD.ResultsOne-way ANOVA revealed that the iLIs of the three groups were significantly different. The HCs showed a significant leftward interhemispheric difference within |iLI| ≥ 0.8. Compared with the HCs, the patients with MCI manifested a distinct abnormal rightward interhemispheric asymmetry, mainly within the thresholds of 0.2 ≤ |iLI| < 0.4 and 0.4 ≤ |iLI| < 0.8; in the patients with AD, the normal leftward lateralization that was observed in the HCs disappeared, and an abnormal rightward laterality was expressed within 0.4 ≤ |iLI| < 0.8. By directly comparing the patients with MCI with the patients with AD, an exclusive abnormal rightward laterality was observed in the patients with MCI within the 0.2 ≤ |iLI| < 0.4 threshold, and the normal leftward asymmetry vanished in the patients with AD within the |iLI| ≥ 0.8 threshold.ConclusionGlobal brain lateralization was different among three groups. The abnormal rightward dominance observed in the patients with MCI and AD may indicate that these patients use additional brain resources to compensate for the loss of cognitive function, and the observed disappearance of the leftward laterality in the patients with AD was likely associated with the damage in the left hemisphere. The observed disappearance of the rightward asymmetry in the patients with AD using the 0.2 ≤ |iLI| < 0.4 threshold was likely a sign of decompensation. Our study provides new insights that may improve our understanding of MCI and AD.

Background: Recent studies have indicated that the default mode network (DMN) comprises at least three subsystems: The medial temporal lobe (MTL) and dorsal medial prefrontal cortex (DMPFC) subsystems and a core comprising the anterior MPFC (aMPFC) and posterior cingulate cortex (PCC). Additionally, the disruption of the DMN is related to Alzheimer’s disease (AD). However, little is known regarding the changes in these subsystems in AD, a progressive disease characterized by memory impairment. Here, we performed a resting-state functional connectivity (FC) analysis to test our hypothesis that the memory-related MTL subsystem was predominantly disrupted in AD.Method: To reveal specific subsystem changes, we calculated the strength and number of FCS in the DMN intra- and inter-subsystems across individuals and compared the FC of the two groups. To further examine which pairs of brain regional functional connections contributed to the subsystem alterations, correlation coefficients between any two brain regions in the DMN were compared across groups. Additionally, to identify which regions made the strongest contributions to the subsystem changes, we calculated the regional FC strength (FCS), which was compared across groups.Results: For the intra-subsystem, decreased FC number and strength occurred in the MTL subsystem of AD patients but not in the DMPFC subsystem or core. For the inter-subsystems, the AD group showed decreased FCS and number between the MTL subsystem and PCC and a decreased number between the PCC and DMPFC subsystem. Decreased inter-regional FCS were found within the MTL subsystem in AD patients relative to controls: The posterior inferior parietal lobule (pIPL) showed decreased FC with the hippocampal formation (HF), parahippocampal cortex (PHC) and ventral MPFC (vMPFC). Decreased inter-regional FCS of the inter-subsystems were also found in AD patients: The HF and/or PHC showed decreased FC with dMPFC and TPJ, located in the DMPFC subsystem, and with PCC. AD patients also showed decreased FC between the PCC and TLC of the dMPFC subsystem. Furthermore, the HF and PHC in the MTL subsystem showed decreased regional FCS.Conclusion: Decreased intrinsic FC was mainly associated with the MTL subsystem of the AD group, suggesting that the MTL subsystem is predominantly disrupted.

SUMMARY The spatiotemporal localization and expression of Dll4 are critical for sprouting angiogenesis. However, the related mechanisms are poorly understood. Here we show that G-protein-coupled receptor-kinase interacting protein-1 (GIT1) is a robust endogenous inhibitor of Dll4-Notch1 signaling that specifically controls stalk cell fate. GIT1 is highly expressed in stalk cells but not in tip cells. GIT1 deficiency remarkably enhances Dll4 expression and Notch1 signaling resulting in impaired retinal sprouting angiogenesis, which can be rescued by treatment with the Notch inhibitor, or Dll4 neutralizing antibody. Notch1 regulates Dll4 expression by binding to recombining binding protein suppressor of hairless (RBP-J, a transcriptional regulator of Notch) via a highly conserved ankyrin (ANK) repeat domain. We show that GIT1, which also contains an ANK domain, inhibits the Notch1-Dll4 signaling pathway by competing with Notch1 ANK domain for binding to RBP-J in stalk cells.