Detection and Tracking of Pedestrians Using Doppler LiDAR

Pedestrian detection and tracking is necessary for autonomous vehicles and traffic manage- ment. This paper presents a novel solution to pedestrian detection and tracking for urban scenarios based on Doppler LiDAR that records both the position and velocity of the targets. The workflow consists of two stages. In the detection stage, the input point cloud is first segmented to form clus- ters, frame by frame. A subsequent multiple pedestrian separation process is introduced to further segment pedestrians close to each other. While a simple speed classifier is capable of extracting most of the moving pedestrians, a supervised machine learning-based classifier is adopted to detect pedestrians with insignificant radial velocity. In the tracking stage, the pedestrian’s state is estimated by a Kalman filter, which uses the speed information to estimate the pedestrian’s dynamics. Based on the similarity between the predicted and detected states of pedestrians, a greedy algorithm is adopted to associate the trajectories with the detection results. The presented detection and tracking methods are tested on two data sets collected in San Francisco, California by a mobile Doppler LiDAR system. The results of the pedestrian detection demonstrate that the proposed two-step classifier can improve the detection performance, particularly for detecting pedestrians far from the sensor. For both data sets, the use of Doppler speed information improves the F1-score and the recall by 15% to 20%. The subsequent tracking from the Kalman filter can achieve 83.9–55.3% for the multiple object tracking accuracy (MOTA), where the contribution of the speed measurements is secondary and insignificant

Discretization of the velocity space in solution of the Boltzmann equation

We point out an equivalence between the discrete velocity method of solving the Boltzmann equation, of which the lattice Boltzmann equation method is a special example, and the approximations to the Boltzmann equation by a Hermite polynomial expansion. Discretizing the Boltzmann equation with a BGK collision term at the velocities that correspond to the nodes of a Hermite quadrature is shown to be equivalent to truncating the Hermite expansion of the distribution function to the corresponding order. The truncated part of the distribution has no contribution to the moments of low orders and is negligible at small Mach numbers. Higher order approximations to the Boltzmann equation can be achieved by using more velocities in the quadrature

Enzyme Replacement Therapy for Mucopolysaccharidosis IIID using Recombinant Human α-N-Acetylglucosamine-6-Sulfatase in Neonatal Mice

There is currently no cure or effective treatment available for mucopolysaccharidosis type IIID (MPS IIID, Sanfilippo syndrome type D), a lysosomal storage disorder (LSD) caused by the deficiency of α-N-acetylglucosamine-6-sulfatase (GNS). The clinical symptoms of MPS IIID, like other subtypes of Sanfilippo syndrome, are largely localized to the central nervous system (CNS), and any treatments aiming to ameliorate or reverse the catastrophic and fatal neurologic decline caused by this disease need to be delivered across the blood–brain barrier. Here, we report a proof-of-concept enzyme replacement therapy (ERT) for MPS IIID using recombinant human α-N-acetylglucosamine-6-sulfatase (rhGNS) via intracerebroventricular (ICV) delivery in a neonatal MPS IIID mouse model. We overexpressed and purified rhGNS from CHO cells with a specific activity of 3.9 × 10⁴ units/mg protein and a maximal enzymatic activity at lysosomal pH (pH 5.6), which was stable for over one month at 4 °C in artificial cerebrospinal fluid (CSF). We demonstrated that rhGNS was taken up by MPS IIID patient fibroblasts via the mannose 6-phosphate (M6P) receptor and reduced intracellular glycosaminoglycans to normal levels. The delivery of 5 μg of rhGNS into the lateral cerebral ventricle of neonatal MPS IIID mice resulted in normalization of the enzymatic activity in brain tissues; rhGNS was found to be enriched in lysosomes in MPS IIID-treated mice relative to the control. Furthermore, a single dose of rhGNS was able to reduce the accumulated heparan sulfate and β-hexosaminidase. Our results demonstrate that rhGNS delivered into CSF is a potential therapeutic option for MPS IIID that is worthy of further development

Conserved L464 in p97 D1–D2 linker is critical for p97 cofactor regulated ATPase activity

p97 protein is a highly conserved, abundant, functionally diverse, structurally dynamic homohexameric AAA enzyme-containing N, D1, and D2 domains. A truncated p97 protein containing the N and D1 domains and the D1–D2 linker (ND1L) exhibits 79% of wild-type (WT) ATPase activity whereas the ND1 domain alone without the linker only has 2% of WT activity. To investigate the relationship between the D1–D2 linker and the D1 domain, we produced p97 ND1L mutants and demonstrated that this 22-residue linker region is essential for D1 ATPase activity. The conserved amino acid leucine 464 (L464) is critical for regulating D1 and D2 ATPase activity by p97 cofactors p37, p47, and Npl4–Ufd1 (NU). Changing leucine to alanine, proline, or glutamate increased the maximum rate of ATP turnover (k_(cat)) of p47-regulated ATPase activities for these mutants, but not for WT. p37 and p47 increased the k_(cat) of the proline substituted linker, suggesting that they induced linker conformations facilitating ATP hydrolysis. NU inhibited D1 ATPase activities of WT and mutant ND1L proteins, but activated D2 ATPase activity of full-length p97. To further understand the mutant mechanism, we used single-particle cryo-EM to visualize the full-length p97^(L464P) and revealed the conformational change of the D1–D2 linker, resulting in a movement of the helix-turn-helix motif (543–569). Taken together with the biochemical and structural results we conclude that the linker helps maintain D1 in a competent conformation and relays the communication to/from the N-domain to the D1 and D2 ATPase domains, which are ∼50 Å away

Survival of infants born with esophageal atresia among 24 international birth defects surveillance programs

Background: Esophageal atresia (EA) affects around 2.3–2.6 per 10,000 births world-wide. Infants born with this condition require surgical correction soon after birth. Most survival studies of infants with EA are locally or regionally based. We aimed to describe survival across multiple world regions. Methods: We included infants diagnosed with EA between 1980 and 2015 from 24 birth defects surveillance programs that are members of the International Clearinghouse for Birth Defects Surveillance and Research. We calculated survival as the proportion of liveborn infants alive at 1 month, 1- and 5-years, among all infants with EA, those with isolated EA, those with EA and additional anomalies or EA and a chromosomal anomaly or genetic syndrome. We also investigated trends in survival over the decades, 1980s–2010s. Results: We included 6,466 liveborn infants with EA. Survival was 89.4% (95% CI 88.1–90.5) at 1-month, 84.5% (95% CI 83.0–85.9) at 1-year and 82.7% (95% CI 81.2–84.2) at 5-years. One-month survival for infants with isolated EA (97.1%) was higher than for infants with additional anomalies (89.7%) or infants with chromosomal or genetic syndrome diagnoses (57.3%) with little change at 1- and 5-years. Survival at 1 month improved from the 1980s to the 2010s, by 6.5% for infants with isolated EA and by 21.5% for infants with EA and additional anomalies. Conclusions: Almost all infants with isolated EA survived to 5 years. Mortality was higher for infants with EA and an additional anomaly, including chromosomal or genetic syndromes. Survival improved from the 1980s, particularly for those with additional anomalies