ViNL: Visual Navigation and Locomotion Over Obstacles

We present Visual Navigation and Locomotion over obstacles (ViNL), which enables a quadrupedal robot to navigate unseen apartments while stepping over small obstacles that lie in its path (e.g., shoes, toys, cables), similar to how humans and pets lift their feet over objects as they walk. ViNL consists of: (1) a visual navigation policy that outputs linear and angular velocity commands that guides the robot to a goal coordinate in unfamiliar indoor environments; and (2) a visual locomotion policy that controls the robot's joints to avoid stepping on obstacles while following provided velocity commands. Both the policies are entirely "model-free", i.e. sensors-to-actions neural networks trained end-to-end. The two are trained independently in two entirely different simulators and then seamlessly co-deployed by feeding the velocity commands from the navigator to the locomotor, entirely "zero-shot" (without any co-training). While prior works have developed learning methods for visual navigation or visual locomotion, to the best of our knowledge, this is the first fully learned approach that leverages vision to accomplish both (1) intelligent navigation in new environments, and (2) intelligent visual locomotion that aims to traverse cluttered environments without disrupting obstacles. On the task of navigation to distant goals in unknown environments, ViNL using just egocentric vision significantly outperforms prior work on robust locomotion using privileged terrain maps (+32.8% success and -4.42 collisions per meter). Additionally, we ablate our locomotion policy to show that each aspect of our approach helps reduce obstacle collisions. Videos and code at http://www.joannetruong.com/projects/vinl.htm

Rethinking Sim2Real: Lower Fidelity Simulation Leads to Higher Sim2Real Transfer in Navigation

If we want to train robots in simulation before deploying them in reality, it seems natural and almost self-evident to presume that reducing the sim2real gap involves creating simulators of increasing fidelity (since reality is what it is). We challenge this assumption and present a contrary hypothesis -- sim2real transfer of robots may be improved with lower (not higher) fidelity simulation. We conduct a systematic large-scale evaluation of this hypothesis on the problem of visual navigation -- in the real world, and on 2 different simulators (Habitat and iGibson) using 3 different robots (A1, AlienGo, Spot). Our results show that, contrary to expectation, adding fidelity does not help with learning; performance is poor due to slow simulation speed (preventing large-scale learning) and overfitting to inaccuracies in simulation physics. Instead, building simple models of the robot motion using real-world data can improve learning and generalization

IndoorSim-to-OutdoorReal: Learning to Navigate Outdoors without any Outdoor Experience

We present IndoorSim-to-OutdoorReal (I2O), an end-to-end learned visual navigation approach, trained solely in simulated short-range indoor environments, and demonstrates zero-shot sim-to-real transfer to the outdoors for long-range navigation on the Spot robot. Our method uses zero real-world experience (indoor or outdoor), and requires the simulator to model no predominantly-outdoor phenomenon (sloped grounds, sidewalks, etc). The key to I2O transfer is in providing the robot with additional context of the environment (i.e., a satellite map, a rough sketch of a map by a human, etc.) to guide the robot's navigation in the real-world. The provided context-maps do not need to be accurate or complete -- real-world obstacles (e.g., trees, bushes, pedestrians, etc.) are not drawn on the map, and openings are not aligned with where they are in the real-world. Crucially, these inaccurate context-maps provide a hint to the robot about a route to take to the goal. We find that our method that leverages Context-Maps is able to successfully navigate hundreds of meters in novel environments, avoiding novel obstacles on its path, to a distant goal without a single collision or human intervention. In comparison, policies without the additional context fail completely. Lastly, we test the robustness of the Context-Map policy by adding varying degrees of noise to the map in simulation. We find that the Context-Map policy is surprisingly robust to noise in the provided context-map. In the presence of significantly inaccurate maps (corrupted with 50% noise, or entirely blank maps), the policy gracefully regresses to the behavior of a policy with no context. Videos are available at https://www.joannetruong.com/projects/i2o.htm

Association of β-amyloid level, clinical progression and longitudinal cognitive change in normal older individuals

Objective To determine the effect of β-amyloid (Aβ) level on progression risk to mild cognitive impairment (MCI) or dementia and longitudinal cognitive change in cognitively normal (CN) older individuals. Methods All CN from the Australian Imaging Biomarkers and Lifestyle study with Aβ PET and ≥ 3 years follow-up were included (n = 534; age 72 ± 6 years; 27% Aβ positive; follow-up 5.3 ± 1.7 years). Aβ level was divided using the standardized 0–100 Centiloid scale: \u3c 15 CL negative, 15–25 CL uncertain, 26–50 CL moderate, 51–100 CL high, \u3e 100 CL very high, noting \u3e 25 CL approximates a positive scan. Cox proportional hazards analysis and linear mixed effect models were used to assess risk of progression and cognitive decline. Results Aβ levels in 63% were negative, 10% uncertain, 10% moderate, 14% high, and 3% very high. Fifty-seven (11%) progressed to MCI or dementia. Compared to negative Aβ, the hazard ratio for progression for moderate Aβ was 3.2 (95% confidence interval [CI] 1.3–7.6; p \u3c 0.05), for high was 7.0 (95% CI 3.7–13.3; p \u3c 0.001), and for very high was 11.4 (95% CI 5.1–25.8; p \u3c 0.001). Decline in cognitive composite score was minimal in the moderate group (−0.02 SD/year, p = 0.05), while the high and very high declined substantially (high −0.08 SD/year, p \u3c 0.001; very high −0.35 SD/year, p \u3c 0.001). Conclusion The risk of MCI or dementia over 5 years in older CN is related to Aβ level on PET, 5% if negative vs 25% if positive but ranging from 12% if 26–50 CL to 28% if 51–100 CL and 50% if \u3e 100 CL. This information may be useful for dementia risk counseling and aid design of preclinical AD trials

DNA mismatch repair gene MSH6 implicated in determining age at natural menopause

The length of female reproductive lifespan is associated with multiple adverse outcomes, including breast cancer, cardiovascular disease and infertility. The biological processes that govern the timing of the beginning and end of reproductive life are not well understood. Genetic variants are known to contribute to ∼50% of the variation in both age at menarche and menopause, but to date the known genes explain <15% of the genetic component. We have used genome-wide association in a bivariate meta-analysis of both traits to identify genes involved in determining reproductive lifespan. We observed significant genetic correlation between the two traits using genome-wide complex trait analysis. However, we found no robust statistical evidence for individual variants with an effect on both traits. A novel association with age at menopause was detected for a variant rs1800932 in the mismatch repair gene MSH6 (P = 1.9 × 10−9), which was also associated with altered expression levels of MSH6 mRNA in multiple tissues. This study contributes to the growing evidence that DNA repair processes play a key role in ovarian ageing and could be an important therapeutic target for infertilit

DNA mismatch repair gene MSH6 implicated in determining age at natural menopause

notes: PMCID: PMC3976329This is a freely-available open access publication. Please cite the published version which is available via the DOI link in this record.The length of female reproductive lifespan is associated with multiple adverse outcomes, including breast cancer, cardiovascular disease and infertility. The biological processes that govern the timing of the beginning and end of reproductive life are not well understood. Genetic variants are known to contribute to ∼50% of the variation in both age at menarche and menopause, but to date the known genes explain <15% of the genetic component. We have used genome-wide association in a bivariate meta-analysis of both traits to identify genes involved in determining reproductive lifespan. We observed significant genetic correlation between the two traits using genome-wide complex trait analysis. However, we found no robust statistical evidence for individual variants with an effect on both traits. A novel association with age at menopause was detected for a variant rs1800932 in the mismatch repair gene MSH6 (P = 1.9 × 10(-9)), which was also associated with altered expression levels of MSH6 mRNA in multiple tissues. This study contributes to the growing evidence that DNA repair processes play a key role in ovarian ageing and could be an important therapeutic target for infertility.UK Medical Research CouncilWellcome Trus

Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk

The timing of puberty is a highly polygenic childhood trait that is epidemiologically associated with various adult diseases. Using 1000 Genomes Project-imputed genotype data in up to similar to 370,000 women, we identify 389 independent signals (P <5 x 10(-8)) for age at menarche, a milestone in female pubertal development. In Icelandic data, these signals explain similar to 7.4% of the population variance in age at menarche, corresponding to similar to 25% of the estimated heritability. We implicate similar to 250 genes via coding variation or associated expression, demonstrating significant enrichment in neural tissues. Rare variants near the imprinted genes MKRN3 and DLK1 were identified, exhibiting large effects when paternally inherited. Mendelian randomization analyses suggest causal inverse associations, independent of body mass index (BMI), between puberty timing and risks for breast and endometrial cancers in women and prostate cancer in men. In aggregate, our findings highlight the complexity of the genetic regulation of puberty timing and support causal links with cancer susceptibility