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Vector search has drawn a rapid increase of interest in the research community due to its application in novel AI applications. Maximizing its performance is essential for many tasks but remains preliminary understood. In this work, we investigate the root causes of the scalability bottleneck of using intra-query parallelism to speedup the state-of-the-art graph-based vector search systems on multi-core architectures. Our in-depth analysis reveals several scalability challenges from both system and algorithm perspectives. Based on the insights, we propose iQAN, a parallel search algorithm with a set of optimizations that boost convergence, avoid redundant computations, and mitigate synchronization overhead. Our evaluation results on a wide range of real-world datasets show that iQAN achieves up to 37.7× and 76.6× lower latency than state-of-the-art sequential baselines on datasets ranging from a million to a hundred million datasets. We also show that iQAN achieves outstanding scalability as the graph size or the accuracy target increases, allowing it to outperform the state-of-the-art baseline on two billion-scale datasets by up to 16.0× with up to 64 cores. 

Multi-band photometric observations of 11 totally eclipsing contact binaries were carried out. Applying the Wilson–Devinney program, photometric solutions were obtained. There are two W-subtype systems, which are CRTS J133031.1+161202 and CRTS J154254.0+324652, and the rest of the systems are A-subtype systems. CRTS J154254.0 + 324652 has the highest fill-out factor with 94.3 per cent, and the lowest object is CRTS J155009.2 + 493639 with only 18.9 per cent. The mass ratios of the 11 systems are all less than 0.1, which means that they are extremely low-mass ratio binary systems. We performed period variation investigation and found that the orbital periods of three systems decrease slowly, which may be caused by the materials may transfer from the primary component to the secondary component, and those of six systems increase slowly, which indicates that the materials may transfer from the secondary component to the primary component. LAMOST low-resolution spectra of four objects were analysed, and using the spectral subtraction technique, Hα emission line was detected, which means that the four objects exhibit chromospheric activity. In order to understand their evolutionary status, the mass–luminosity and mass–radius diagrams were plotted. The two diagrams indicate that the primary component is in the main sequence evolution stage, and the secondary component is above TAMS, indicating that they are over-luminous. To determine whether the 11 systems are in a stable state, the ratio of spin angular momentum to orbital angular momentum (Js/Jo) and the instability parameters were calculated, and we argued that CRTS J234634.7 + 222824 is on the verge of a merger.

 

Abstract During October 2019 and March 2020, the luminous red supergiant Betelgeuse demonstrated an unusually deep minimum of its brightness. It became fainter by more than one magnitude and this is the most significant dimming observed in the recent decades. While the reason for the dimming is debated, pre-phase of supernova explosion, obscuring dust, or changes in the photosphere of the star were suggested scenarios. Here, we present spectroscopic studies of Betelgeuse using high-resolution and high signal-to-noise ratio near-infrared spectra obtained at Weihai Observatory on four epochs in 2020 covering the phases of during and after dimming. We show that the dimming episode is caused by the dropping of its effective temperature by at least 170 K on 2020 January 31, that can be attributed to the emergence of a large dark spot on the surface of the star. 

Abstract Background α-Synuclein (aSyn) aggregation is thought to play a central role in neurodegenerative disorders termed synucleinopathies, including Parkinson’s disease (PD). Mouse aSyn contains a threonine residue at position 53 that mimics the human familial PD substitution A53T, yet in contrast to A53T patients, mice show no evidence of aSyn neuropathology even after aging. Here, we studied the neurotoxicity of human A53T, mouse aSyn, and various human-mouse chimeras in cellular and in vivo models, as well as their biochemical properties relevant to aSyn pathobiology. Methods Primary midbrain cultures transduced with aSyn-encoding adenoviruses were analyzed immunocytochemically to determine relative dopaminergic neuron viability. Brain sections prepared from rats injected intranigrally with aSyn-encoding adeno-associated viruses were analyzed immunohistochemically to determine nigral dopaminergic neuron viability and striatal dopaminergic terminal density. Recombinant aSyn variants were characterized in terms of fibrillization rates by measuring thioflavin T fluorescence, fibril morphologies via electron microscopy and atomic force microscopy, and protein-lipid interactions by monitoring membrane-induced aSyn aggregation and aSyn-mediated vesicle disruption. Statistical tests consisted of ANOVA followed by Tukey’s multiple comparisons post hoc test and the Kruskal-Wallis test followed by a Dunn’s multiple comparisons test or a two-tailed Mann-Whitney test. Results Mouse aSyn was less neurotoxic than human aSyn A53T in cell culture and in rat midbrain, and data obtained for the chimeric variants indicated that the human-to-mouse substitutions D121G and N122S were at least partially responsible for this decrease in neurotoxicity. Human aSyn A53T and a chimeric variant with the human residues D and N at positions 121 and 122 (respectively) showed a greater propensity to undergo membrane-induced aggregation and to elicit vesicle disruption. Differences in neurotoxicity among the human, mouse, and chimeric aSyn variants correlated weakly with differences in fibrillization rate or fibril morphology. Conclusions Mouse aSyn is less neurotoxic than the human A53T variant as a result of inhibitory effects of two C-terminal amino acid substitutions on membrane-induced aSyn aggregation and aSyn-mediated vesicle permeabilization. Our findings highlight the importance of membrane-induced self-assembly in aSyn neurotoxicity and suggest that inhibiting this process by targeting the C-terminal domain could slow neurodegeneration in PD and other synucleinopathy disorders.