Shepherding Slots to Objects: Towards Stable and Robust Object-Centric Learning

Object-centric learning (OCL) aspires general and compositional understanding of scenes by representing a scene as a collection of object-centric representations. OCL has also been extended to multi-view image and video datasets to apply various data-driven inductive biases by utilizing geometric or temporal information in the multi-image data. Single-view images carry less information about how to disentangle a given scene than videos or multi-view images do. Hence, owing to the difficulty of applying inductive biases, OCL for single-view images remains challenging, resulting in inconsistent learning of object-centric representation. To this end, we introduce a novel OCL framework for single-view images, SLot Attention via SHepherding (SLASH), which consists of two simple-yet-effective modules on top of Slot Attention. The new modules, Attention Refining Kernel (ARK) and Intermediate Point Predictor and Encoder (IPPE), respectively, prevent slots from being distracted by the background noise and indicate locations for slots to focus on to facilitate learning of object-centric representation. We also propose a weak semi-supervision approach for OCL, whilst our proposed framework can be used without any assistant annotation during the inference. Experiments show that our proposed method enables consistent learning of object-centric representation and achieves strong performance across four datasets. Code is available at \url{https://github.com/object-understanding/SLASH}

Impact of Vegetation on Land-Atmosphere Coupling Strength and Its Implication for Desertification Mitigation over East Asia

Desertification of the East Asian drylands and the consequent dust transport have been serious concerns for adjacent Asian countries as well as the western United States. Tree planting has been considered one applicable strategy to mitigate the desertification. However, the desired effect of the tree planting would not be brought to fruition unless the newly planted trees change the coupling characteristics between the land and the atmosphere. Based on this perception, we attempt to clarify the effects of vegetation on the coupling strength between the atmosphere and land surface, and we suggest the most efficient areas of tree planting for desertification mitigation in East Asia. Using regional vegetation-atmosphere coupled model simulations, coupling strength with and without vegetation was computed and compared with each other. An increased vegetation fraction reduces the coupling strength in June, July, and August (JJA), primarily due to decreased evapotranspiration variability. This effect is pronounced over the Manchurian Plains and the highly populated areas of Beijing and Tianjin. The reduced coupling strength tends to weaken feedback between soil moisture and precipitation as a maintenance mechanism of warm season droughts in the midlatitudes and subsequently decrease the probability of droughts, a finding that is reflected in the enhanced JJA mean soil moisture. However, some drylands like the eastern edges of the Gobi desert present marginal or even opposite changes in coupling strength, meaning a limited effect of vegetation on relieving droughts. Therefore, given limited financial and human resources, acupuncture-like afforestation, i.e., concentrated tree planting in a particular region where the coupling strength can be substantially reduced by vegetation, is an effective strategy to secure long-standing desertification mitigation

Mitochondrial Dysfunction Induces Formation of Lipid Droplets as a Generalized Response to Stress

Lipid droplet (LD) formation is a hallmark of cellular stress. Cells attempt to combat noxious stimuli by switching their metabolism from oxidative phosphorylation to glycolysis, sparing resources in LDs for generating cellular reducing power and for anabolic biosynthesis. Membrane phospholipids are also a source of LDs. To elucidate the formation of LDs, we exposed mice to hyperoxia, hypoxia, myocardial ischemia, and sepsis induced by cecal ligation and puncture (CLP). All the above-mentioned stressors enhanced the formation of LDs, as assessed by transmission electron microscopy, with severe mitochondrial swelling. Disruption of mitochondria by depleting mitochondrial DNA (ρ0 cells) significantly augmented the formation of LDs, causing transcriptional activation of fatty acid biosynthesis and metabolic reprogramming to glycolysis. Heme oxygenase (HO)-1 counteracts CLP-mediated septic shock in mouse models. In HO-1-deficient mice, LD formation was not observed upon CLP, but a concomitant decrease in “LD-decorating proteins” was observed, implying a link between LDs and cytoprotective activity. Collectively, LD biogenesis during stress can trigger adaptive LD formation, which is dependent on mitochondrial integrity and HO-1 activity; this may be a cellular survival strategy, apportioning energy-generating substrates to cellular defense

Melittin restores proteasome function in an animal model of ALS

Amyotrophic lateral sclerosis (ALS) is a paralyzing disorder characterized by the progressive degeneration and death of motor neurons and occurs both as a sporadic and familial disease. Mutant SOD1 (mtSOD1) in motor neurons induces vulnerability to the disease through protein misfolding, mitochondrial dysfunction, oxidative damage, cytoskeletal abnormalities, defective axonal transport- and growth factor signaling, excitotoxicity, and neuro-inflammation

Carbon monoxide inhibits Fas activating antibody-induced apoptosis in endothelial cells

<p>Abstract</p> <p>Background</p> <p>The extrinsic apoptotic pathway initiates when a death ligand, such as the Fas ligand, interacts with its cell surface receptor (<it>ie</it>., Fas/CD95), forming a death-inducing signaling complex (DISC). The Fas-dependent apoptotic pathway has been implicated in several models of lung or vascular injury. Carbon monoxide, an enzymatic product of heme oxygenase-1, exerts antiapoptotic effects at low concentration <it>in vitro </it>and <it>in vivo</it>.</p> <p>Methods</p> <p>Using mouse lung endothelial cells (MLEC), we examined the antiapoptotic potential of carbon monoxide against apoptosis induced by the Fas/CD95-activating antibody (Jo2). Carbon monoxide was applied to cell cultures <it>in vitro</it>. The expression and/or activation of apoptosis-related proteins and signaling intermediates were determined using Western Immunoblot and co-immunoprecipitation assays. Cell death was monitored by lactate dehydrogenase (LDH) release assays. Statistical significance was determined by student T-test and a value of <it>P </it>< 0.05 was considered significant.</p> <p>Results</p> <p>Treatment of MLEC with Fas-activating antibody (Jo2) induced cell death associated with the formation of the DISC, and activation of caspases (-8, -9, and -3), as well as the pro-apoptotic Bcl-2 family protein Bax. Exposure of MLEC to carbon monoxide inhibited Jo2-induced cell death, which correlated with the inhibition of DISC formation, cleavage of caspases-8, -9, and -3, and Bax activation. Carbon monoxide inhibited the phosphorylation of the Fas-associated death domain-containing protein, as well as its association with the DISC. Furthermore, carbon monoxide induced the expression of the antiapoptotic protein FLIP and increased its association with the DISC.</p> <p>CO-dependent cytoprotection against Fas mediated apoptosis in MLEC depended in part on activation of ERK1/2-dependent signaling.</p> <p>Conclusions</p> <p>Carbon monoxide has been proposed as a potential therapy for lung and other diseases based in part on its antiapoptotic effects in endothelial cells. In vitro, carbon monoxide may inhibit both Fas/caspase-8 and Bax-dependent apoptotic signaling pathways induced by Fas-activating antibody in endothelial cells. Strategies to block Fas-dependent apoptotic pathways may be useful in development of therapies for lung or vascular disorders.</p

Indium as an efficient ohmic contact to N-face n-GaN of GaN-based vertical light-emitting diodes

We propose indium (In), a low work function and nitride-forming element, as an efficient ohmic contact layer to N-face n-GaN. While conventional Al-based ohmic contacts show severe degradation after annealing at 300 C, In-based ohmic contacts display considerable improvement in contact resistivity. The annealing-induced enhancement of ohmic behavior in In-based contacts is attributed to the formation of an InN interfacial layer, which is supported by x-ray photoemission spectroscopy measurements. These results suggest that In is of particular importance for application as reliable ohmic contacts to n-GaN of GaN-based vertical light-emitting diodes.open3

Differential effect of corn oil-based low trans structured fat on the plasma and hepatic lipid profile in an atherogenic mouse model: comparison to hydrogenated trans fat

<p>Abstract</p> <p>Background</p> <p><it>Trans </it>fat are not desirable in many aspects on health maintenance. Low <it>trans </it>structured fats have been reported to be relatively more safe than <it>trans </it>fats.</p> <p>Methods</p> <p>We examined the effects of low <it>trans </it>structured fat from corn oil (LC), compared with high <it>trans </it>fat shortening, on cholesterol and fatty acid metabolism in apo E deficient mice which is an atherogenic animal model. The animals were fed a high <it>trans </it>fat (10% fat: commercial shortening (CS)) or a low <it>trans </it>fat (LC) diet for 12 weeks.</p> <p>Results</p> <p>LC decreased apo B and hepatic cholesterol and triglyceride concentration compared to the CS group but significantly increased plasma total cholesterol and triglyceride concentration and fecal lipids with a simultaneous increase in HDL-cholesterol level, apo A-I, and the ratio of HDL-cholesterol to total cholesterol (HTR). Reduction of hepatic lipid levels by inclusion of LC intake was observed alongside modulation of hepatic enzyme activities related to cholesterol esterification, fatty acid metabolism and fecal lipids level compared to the CS group. The differential effects of LC intake on the plasma and hepatic lipid profile seemed to be partly due to the fatty acid composition of LC which contains higher MUFA, PUFA and SFA content as well as lower content of <it>trans </it>fatty acids compared to CS.</p> <p>Conclusions</p> <p>We suggest that LC may exert a dual effect on plasma and hepatic lipid metabolism in an atherogenic animal model. Accordingly, LC, supplemented at 10% in diet, had an anti-atherogenic effect on these <it>apo E</it>^{<it>-/- </it>}mice, and increased fecal lipids, decreased hepatic steatosis, but elevated plasma lipids. Further studies are needed to verify the exact mode of action regarding the complex physiological changes and alteration in lipid metabolism caused by LC.</p

Effects of Bee Venom on Glutamate-Induced Toxicity in Neuronal and Glial Cells

Bee venom (BV), which is extracted from honeybees, is used in traditional Korean medical therapy. Several groups have demonstrated the anti-inflammatory effects of BV in osteoarthritis both in vivo and in vitro. Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS). Changes in glutamate release and uptake due to alterations in the activity of glutamate transporters have been reported in many neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. To assess if BV can prevent glutamate-mediated neurotoxicity, we examined cell viability and signal transduction in glutamate-treated neuronal and microglial cells in the presence and absence of BV. We induced glutamatergic toxicity in neuronal cells and microglial cells and found that BV protected against cell death. Furthermore, BV significantly inhibited the cellular toxicity of glutamate, and pretreatment with BV altered MAP kinase activation (e.g., JNK, ERK, and p38) following exposure to glutamate. These findings suggest that treatment with BV may be helpful in reducing glutamatergic cell toxicity in neurodegenerative diseases