Automatic Internal Stray Light Calibration of AMCW Coaxial Scanning LiDAR Using GMM and PSO

In this paper, an automatic calibration algorithm is proposed to reduce the depth error caused by internal stray light in amplitude-modulated continuous wave (AMCW) coaxial scanning light detection and ranging (LiDAR). Assuming that the internal stray light generated in the process of emitting laser is static, the amplitude and phase delay of internal stray light are estimated using the Gaussian mixture model (GMM) and particle swarm optimization (PSO). Specifically, the pixel positions in a raw signal amplitude map of calibration checkboard are segmented by GMM with two clusters considering the dark and bright image pattern. The loss function is then defined as L1-norm of difference between mean depths of two amplitude-segmented clusters. To avoid overfitting at a specific distance in PSO process, the calibration check board is actually measured at multiple distances and the average of corresponding L1 loss functions is chosen as the actual loss. Such loss is minimized by PSO to find the two optimal target parameters: the amplitude and phase delay of internal stray light. According to the validation of the proposed algorithm, the original loss is reduced from tens of centimeters to 3.2 mm when the measured distances of the calibration checkboard are between 1 m and 4 m. This accurate calibration performance is also maintained in geometrically complex measured scene. The proposed internal stray light calibration algorithm in this paper can be used for any type of AMCW coaxial scanning LiDAR regardless of its optical characteristics

Highly precise AMCW time-of-flight scanning sensor based on digital-parallel demodulation

In this paper, a novel amplitude-modulated continuous wave (AMCW) time-of-flight (ToF) scanning sensor based on digital-parallel demodulation is proposed and demonstrated in the aspect of distance measurement precision. Since digital-parallel demodulation utilizes a high-amplitude demodulation signal with zero-offset, the proposed sensor platform can maintain extremely high demodulation contrast. Meanwhile, as all cross correlated samples are calculated in parallel and in extremely short integration time, the proposed sensor platform can utilize a 2D laser scanning structure with a single photo detector, maintaining a moderate frame rate. This optical structure can increase the received optical SNR and remove the crosstalk of image pixel array. Based on these measurement properties, the proposed AMCW ToF scanning sensor shows highly precise 3D depth measurement performance. In this study, this precise measurement performance is explained in detail. Additionally, the actual measurement performance of the proposed sensor platform is experimentally validated under various conditions

Dexrazoxane for Preventing Anthracycline Cardiotoxicity in Children with Solid Tumors

This study attempted to assess the incidence and outcome of anthracycline cardiotoxicity and the role of dexrazoxane as a cardioprotectant in childhood solid tumors. The dexrazoxane group included 47 patients and the control group of historical cohort included 42. Dexrazoxane was given in the 10:1 ratio to doxorubicin. Fractional shortening and systolic and diastolic left ventricular diameters were used to assess the cardiac function. The median follow-ups were 54 months in the dexrazoxane group and 86 months in the control group. The mean cumulative doses of doxorubicin were 280.8±83.4 mg/m2 in the dexrazoxane group and 266.1±75.0 mg/m2 in the control group. The dexrazoxane group experienced significantly fewer cardiac events (27.7% vs. 52.4%) and less severe congestive heart failure (6.4% vs. 14.3%) than the control group. Thirteen cardiotoxicities including one cardiac death and 2 congestive heart failures occurred in the dexrazoxane group, and 22 cardiotoxicities including 2 cardiac deaths and 4 congestive heart failures, in the control group. Five year cardiac event free survival rates were 69.2% in the dexrazoxane group and 45.8% in the control group (P=0.04). Dexrazoxane reduces the incidence and severity of early and late anthracycline cardiotoxicity in childhood solid tumors

Combined inhibition of Bcl-2 family members and YAP induces synthetic lethality in metastatic gastric cancer with RASA1 and NF2 deficiency

Background Targetable molecular drivers of gastric cancer (GC) metastasis remain largely unidentified, leading to limited targeted therapy options for advanced GC. We aimed to identify molecular drivers for metastasis and devise corresponding therapeutic strategies. Methods We performed an unbiased in vivo genome-wide CRISPR/Cas9 knockout (KO) screening in peritoneal dissemination using genetically engineered GC mouse models. Candidate genes were validated through in vivo transplantation assays using KO cells. We analyzed target expression patterns in GC clinical samples using immunohistochemistry. The functional contributions of target genes were studied through knockdown, KO, and overexpression approaches in tumorsphere and organoid assays. Small chemical inhibitors against Bcl-2 members and YAP were tested in vitro and in vivo. Results We identified Nf2 and Rasa1 as metastasis-suppressing genes through the screening. Clinically, RASA1 mutations along with low NF2 expression define a distinct molecular subtype of metastatic GC exhibiting aggressive traits. NF2 and RASA1 deficiency increased in vivo metastasis and in vitro tumorsphere formation by synergistically amplifying Wnt and YAP signaling in cancer stem cells (CSCs). NF2 deficiency enhanced Bcl-2-mediated Wnt signaling, conferring resistance to YAP inhibition in CSCs. This resistance was counteracted via synthetic lethality achieved by simultaneous inhibition of YAP and Bcl-2. RASA1 deficiency amplified the Wnt pathway via Bcl-xL, contributing to cancer stemness. RASA1 mutation created vulnerability to Bcl-xL inhibition, but the additional NF2 deletion conferred resistance to Bcl-xL inhibition due to YAP activation. The combined inhibition of Bcl-xL and YAP synergistically suppressed cancer stemness and in vivo metastasis in RASA1 and NF2 co-deficiency. Conclusion Our research unveils the intricate interplay between YAP and Bcl-2 family members, which can lead to synthetic lethality, offering a potential strategy to overcome drug resistance. Importantly, our findings support a personalized medicine approach where combined therapy targeting YAP and Bcl-2, tailored to NF2 and RASA1 status, could effectively manage metastatic GC.This research was supported by grants of the National Research Foundation (NRF) funded by the Korean government (NRF-RS-2023–00208984, NRF-2021M3H9A1030260, NRF-2021R1F1A1051220, NRF-2016M3A9D5A01952416)