Target intensity correction method based on incidence angle and distance for a pulsed Lidar system.

Pulsed light detecting and ranging (Lidar) is capable of acquiring comprehensive target information within a single pulse, including distance and intensity data. Intensity data reflects the target's backscattered intensity and is commonly regarded as a crucial observational parameter associated with target reflectivity information. Multiple studies have indicated the potential of intensity data in various applications within pulsed Lidar contexts. However, the intensity data is influenced by the incident angle and distance; hence it cannot directly manifest target characteristics. Consequently, a prerequisite for its usage is the implementation of intensity calibration. This paper presents a target intensity correction method based on an improved tail model, designed for preprocessing intensity data. First, the pulse echo signal equation is derived by incorporating the improved tail model with the detected target. On this foundation, a target echo intensity correction model is established to correct the intensities at various incident angles to those at the normal direction. Lastly, the derived approach is validated through simulation analysis, and practical experiments are conducted on a constructed pulsed Lidar system. These experiments meticulously investigate the influences of incident angle and distance, two prominent factors, on echo intensity. In the context of incident angle correction experiments, the mean absolute errors (MAEs) in calibrated values for diverse targets all remain within 0.04 V. Prior to correction, the maximum MAE for the cystosepiment is 0.505 V; after the correction it is reduced to merely 0.02 V, indicating a 96% reduction in error. Furthermore, all discrepancies exhibit an error standard deviation (ESD) of 0.03 V or less, showcasing favorable stability. For distance correction, under normal incidence conditions, a diverse set of targets is measured at different distances to achieve corrected MAE and ESD within 0.05 V. Consequently, the proposed method effectively achieves intensity correction concerning incident angles and distances. To achieve this, a reflectivity lookup table for the relevant targets was established. Combining this with the corrected intensity information enabled target identification in the three-dimensional imaging of pulsed Lidar.

Quantitative Profiling of Serum Carnitines Facilitates the Etiology Diagnosis and Prognosis Prediction in Heart Failure.

BACKGROUND: The perturbation of fatty acid metabolism in heart failure (HF) has been a critical issue. It is unclear whether the amounts of circulating carnitines will benefit primary etiology diagnosis and prognostic prediction in HF. This study was designed to assess the diagnostic and prognostic values of serum carnitine profiles between ischemic and non-ischemic derived heart failure. METHODS: HF patients (non-ischemic dilated cardiomyopathy: DCM-HF, n = 98; ischemic heart disease: IHD-HF, n = 63) and control individuals (n = 48) were enrolled consecutively. The serum carnitines were quantitatively measured using the UHPLC-MS/MS method. All patients underwent a median follow-up of 28.3 months. Multivariate Cox regression analysis was performed during the prognosis evaluation. RESULTS: Amongst 25 carnitines measured, all of them were increased in HF patients, and 20 acylcarnitines were associated with HF diagnosis independently. Seven acylcarnitines were confirmed to increase the probability of DCM diagnosis independently. The addition of isobutyryl-L-carnitine and stearoyl-L-carnitine to conventional clinical factors significantly improved the area under the receiver operating characteristic curve (ROC) from 0.771 to 0.832 (p = 0.023) for DCM-HF diagnosis (calibration test for the composite model: Hosmer-Lemeshow χ2 = 7.376, p = 0.497 > 0.05). Using a multivariate COX survival analysis adjusted with clinical factors simultaneously, oleoyl L-carnitine >300 nmol/L (HR = 2.364, 95% CI = 1.122-4.976, p = 0.024) and isovaleryl-L-carnitine <100 nmol/L (HR = 2.108, 95% CI = 1.091-4.074, p = 0.026) increased the prediction of all-cause mortality independently, while linoleoyl-L-carnitine >420 nmol/L, succinyl carnitine >60 nmol/L and isovaleryl-L-carnitine <100 nmol/L increased the risk of HF rehospitalization independently. CONCLUSIONS: Serum carnitines could not only serve as diagnostic and predictive biomarkers in HF but also benefit the identification of HF primary etiology and prognosis.

EMD and VMD-GWO parallel optimization algorithm to overcome Lidar ranging limitations.

Pulsed Lidar can obtain rich target information in one pulse, but the echo pulse signal is extremely susceptible to low laser transmitting power and complex target environments, resulting in an amplitude that is too low, which affects detection efficiency and ranging accuracy. In this paper, a variational modal decomposition based on gray wolf optimizer (VMD-GWO) and an empirical mode decomposition (EMD) parallel for denoising and signal enhancement in pulse Lidar is proposed and demonstrated completely. First, the adaptive strategy EMD is used for denoising the signal to obtain effective information. The combination of optimal VMD parameters of quadratic penalty αv and decomposition mode k was obtained by using the GWO to select the modal component with the smallest center frequency as effective information. Second, EMD and VMD-GWO parallel optimization algorithms are used to reconstruct the signal to obtain denoising and enhanced signals. Finally, a real experiment was carried out with the pulse Lidar ranging equipment. Our method compared with EMD-soft, EMD-VMD,WL-db4//EMD-DT and WL-db4//VMD has achieved greater improvement. When the target distance and the reflectivity of the reflectivity plate are 30 m and 10%, respectively, the peak signal-to-noise ratio (PSNR) of the weak echo signal calculated by our method can reach 11.5284 dB. And when in the dead zone of the system ranging, it is effectively denoising and enhancing the signal.

Competition between H4PteGlu and H2PtePAS Confers para-Aminosalicylic Acid Resistance in Mycobacterium tuberculosis.

Tuberculosis remains a serious challenge to human health worldwide. para-Aminosalicylic acid (PAS) is an important anti-tuberculosis drug, which requires sequential activation by Mycobacterium tuberculosis (M. tuberculosis) dihydropteroate synthase and dihydrofolate synthase (DHFS, FolC). Previous studies showed that loss of function mutations of a thymidylate synthase coding gene thyA caused PAS resistance in M. tuberculosis, but the mechanism is unclear. Here we showed that deleting thyA in M. tuberculosis resulted in increased content of tetrahydrofolate (H4PteGlu) in bacterial cells as they rely on the other thymidylate synthase ThyX to synthesize thymidylate, which produces H4PteGlu during the process. Subsequently, data of in vitro enzymatic activity experiments showed that H4PteGlu hinders PAS activation by competing with hydroxy dihydropteroate (H2PtePAS) for FolC catalysis. Meanwhile, over-expressing folC in ΔthyA strain and a PAS resistant clinical isolate with known thyA mutation partially restored PAS sensitivity, which relieved the competition between H4PteGlu and H2PtePAS. Thus, loss of function mutations in thyA led to increased H4PteGlu content in bacterial cells, which competed with H2PtePAS for catalysis by FolC and hence hindered the activation of PAS, leading to decreased production of hydroxyl dihydrofolate (H2PtePAS-Glu) and finally caused PAS resistance. On the other hand, functional deficiency of thyA in M. tuberculosis pushes the bacterium switch to an unidentified dihydrofolate reductase for H4PteGlu biosynthesis, which might also contribute to the PAS resistance phenotype. Our study revealed how thyA mutations confer PAS resistance in M. tuberculosis and provided new insights into studies on the folate metabolism of the bacterium.

The existence of 5-hydroxymethylcytosine and 5-formylcytosine in both DNA and RNA in mammals.

We developed a novel strategy by oxidation-derivatization combined mass spectrometry analysis for the determination of 5-hydroxymethylcytosine and 5-formylcytosine in both DNA and RNA. We reported the presence of 5-formylcytosine in RNA of mammals and found that ascorbic acid and hydroquinone can increase the oxidation of 5-methylcytosine to 5-hydroxymethylcytosine in DNA and RNA.