Hierachical Delta-Attention Method for Multimodal Fusion

In vision and linguistics; the main input modalities are facial expressions, speech patterns, and the words uttered. The issue with analysis of any one mode of expression (Visual, Verbal or Vocal) is that lot of contextual information can get lost. This asks researchers to inspect multiple modalities to get a thorough understanding of the cross-modal dependencies and temporal context of the situation to analyze the expression. This work attempts at preserving the long-range dependencies within and across different modalities, which would be bottle-necked by the use of recurrent networks and adds the concept of delta-attention to focus on local differences per modality to capture the idiosyncrasy of different people. We explore a cross-attention fusion technique to get the global view of the emotion expressed through these delta-self-attended modalities, in order to fuse all the local nuances and global context together. The addition of attention is new to the multi-modal fusion field and currently being scrutinized for on what stage the attention mechanism should be used, this work achieves competitive accuracy for overall and per-class classification which is close to the current state-of-the-art with almost half number of parameters

Flow: Per-Instance Personalized Federated Learning Through Dynamic Routing

Personalization in Federated Learning (FL) aims to modify a collaboratively trained global model according to each client. Current approaches to personalization in FL are at a coarse granularity, i.e. all the input instances of a client use the same personalized model. This ignores the fact that some instances are more accurately handled by the global model due to better generalizability. To address this challenge, this work proposes Flow, a fine-grained stateless personalized FL approach. Flow creates dynamic personalized models by learning a routing mechanism that determines whether an input instance prefers the local parameters or its global counterpart. Thus, Flow introduces per-instance routing in addition to leveraging per-client personalization to improve accuracies at each client. Further, Flow is stateless which makes it unnecessary for a client to retain its personalized state across FL rounds. This makes Flow practical for large-scale FL settings and friendly to newly joined clients. Evaluations on Stackoverflow, Reddit, and EMNIST datasets demonstrate the superiority in prediction accuracy of Flow over state-of-the-art non-personalized and only per-client personalized approaches to FL

Determining the effects of low-dose ultraviolet radiation on the circadian rhythm of thermogenesis in brown adipose tissue of mice fed a high fat diet.

Obesity and its resulting co-morbidities place a huge burden on the Australian healthcare system and economy. Alterations to the body’s normal circadian rhythm increase the risk of developing obesity and metabolic dysfunction. Like most metabolically active tissues, circadian rhythm has been observed in brown adipose tissue (BAT) a site of thermogenesis, whereby heat is released via the process of uncoupled respiration, involving uncoupling protein-1 (UCP-1). Activation of thermogenesis in BAT has potential to treat metabolic dysfunction. We have previously shown that ongoing exposure to low dose ultraviolet radiation (UVR) curbed weight gain and limited metabolic dysfunction in mice fed a high fat diet through mechanisms involving skin release of nitric oxide(1). We hypothesised that regular exposure to low dose UVR (1 kJ/m2 UVB radiation, twice a week) would alter the circadian rhythm of thermogenesis in BAT of mice fed a high fat diet, through skin release of nitric oxide. The circadian rhythm of thermogenesis in BAT was examined by monitoring expression of the UCP-1, using UCP-1 luciferase transgenic (‘thermomouse’, FVB/NJ background, n=12/treatment) male mice. In this mouse, UCP-1 expression in the interscapular BAT (iBAT) was tracked by monitoring bioluminescence following their injection with the substrate luciferin. The circadian rhythm analyses involved measuring UCP-1 bioluminescence in iBAT, as well as blood glucose and and interscapular skin temperature at 4-6 hourly intervals over a 28 hours time-course. This was done at baseline, and after 6 and 12 weeks of feeding mice a high or low fat diet.. There were four treatment groups in this 12-week study: 1. Mice fed a low-fat diet, and mock-irradiated (n=20); 2. Mice fed a high fat diet, and mock-irradiated (n=20); 3. Mice fed a high fat diet, and exposed twice a week to low dose UVR (1 kJ/m2)(n=20); or, 4. Mice fed a high fat diet and exposed twice a week to low dose UVR (1 kJ/m2) and topically treated with the nitric oxide scavenger, cPTIO (1 mM) (n=20). Signs of adiposity and metabolic dysfunction were also monitored by weighing mice, performing glucose and insulin tolerance tests, and measuring levels of liver steatosis via histopathology. Weak trends of circadian rhythmicity was noted in interscapular skin temperature during week 12. Ongoing UVR exposure to mice fed a high fat diet had moderately altered the level of UCP-1 expression in interscapular brown adipose tissue. Ongoing UVR exposure seemed to increase the potential of metabolic buffering in response to the high fat diet, and thus reducing the need for diet induced thermogenesis. More so, ongoing UVR suppressed the development of fatty liver disease in mice fed a high fat diet. The outcome of this study provides evidence that UVR exposure may suppress need for metabolic compensation in terms of diet-induced thermogenesis. The suppressive effects of UVR on signs of adiposity (e.g. hepatic steatosis and reduced WAT weights) were not linked with increased rates of thermogenesis in iBAT, in the absence of a circadian rhythm of UCP-1 expression in iBAT). And so if it is not the thermogenesis in BAT, it is important to examine the effects of UVR on other metabolic pathways and tissues as future focus

Metabolic dysfunction induced by a high-fat diet modulates hematopoietic stem and myeloid progenitor cells in brown adipose tissue of mice

Brown adipose tissue (BAT) may be an important metabolic regulator of whole-body glucose. While important roles have been ascribed to macrophages in regulating metabolic functions in BAT, little is known of the roles of other immune cells subsets, particularly dendritic cells (DCs). Eating a high-fat diet may compromise the development of hematopoietic stem and progenitor cells (HSPCs)-which give rise to DCs-in bone marrow, with less known of its effects in BAT. We have previously demonstrated that ongoing exposure to low-dose ultraviolet radiation (UVR) significantly reduced the 'whitening' effect of eating a high-fat diet upon interscapular (i) BAT of mice. Here, we examined whether this observation may be linked to changes in the phenotype of HSPCs and myeloid-derived immune cells in iBAT and bone marrow of mice using 12-colour flow cytometry. Many HSPC subsets declined in both iBAT and bone marrow with increasing metabolic dysfunction. Conversely, with rising adiposity and metabolic dysfunction, conventional DCs (cDCs) increased in both of these tissues. When compared with a low-fat diet, consumption of a high-fat diet significantly reduced proportions of myeloid, common myeloid and megakaryocyte-erythrocyte progenitors in iBAT, and short-term hematopoietic stem cells in bone marrow. In mice fed the high-fat diet, exposure to low-dose UVR significantly reduced proportions of cDCs in iBAT, independently of nitric oxide release from irradiated skin [blocked using the scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO)], but did not significantly modify HSPC subsets in either tissue. Further studies are needed to determine whether changes in these cell populations contribute towards metabolic dysfunction .</p

Characterising nitric oxide-mediated metabolic benefits of low-dose ultraviolet radiation in the mouse: a focus on brown adipose tissue

AIMS/HYPOTHESIS: Exposure to sunlight has the potential to suppress metabolic dysfunction and obesity. We previously demonstrated that regular exposure to low-doses of ultraviolet radiation (UVR) reduced weight gain and signs of diabetes in male mice fed a high-fat diet, in part via release of nitric oxide from skin. Here, we explore further mechanistic pathways through which low-dose UVR exerts these beneficial effects.METHODS: We fed mice with a luciferase-tagged Ucp1 gene (which encodes uncoupling protein-1 [UCP-1]), referred to here as the Ucp1 luciferase transgenic mouse ('Thermomouse') a high-fat diet and examined the effects of repeated exposure to low-dose UVR on weight gain and development of metabolic dysfunction as well as UCP-1-dependent thermogenesis in interscapular brown adipose tissue (iBAT).RESULTS: Repeated exposure to low-dose UVR suppressed the development of glucose intolerance and hepatic lipid accumulation via dermal release of nitric oxide while also reducing circulating IL-6 (compared with mice fed a high-fat diet only). Dietary nitrate supplementation did not mimic the effects of low-dose UVR. A single low dose of UVR increased UCP-1 expression (by more than twofold) in iBAT of mice fed a low-fat diet, 24 h after exposure. However, in mice fed a high-fat diet, there was no effect of UVR on UCP-1 expression in iBAT (compared with mock-treated mice) when measured at regular intervals over 12 weeks. More extensive circadian studies did not identify any substantial shifts in UCP-1 expression in mice exposed to low-dose UVR, although skin temperature at the interscapular site was reduced in UVR-exposed mice. The appearance of cells with a white adipocyte phenotype ('whitening') in iBAT induced by consuming the high-fat diet was suppressed by exposure to low-dose UVR in a nitric oxide-dependent fashion. Significant shifts in the expression of important core gene regulators of BAT function (Dio2, increased more than twofold), fatty acid transport (increased Fatp2 [also known as Slc27a2]), lipolysis (decreased Atgl [also known as Pnpla2]), lipogenesis (decreased Fasn) and inflammation (decreased Tnf), and proportions of macrophages (increased twofold) were observed in iBAT of mice exposed to low-dose UVR. These effects were independent of nitric oxide released from skin.CONCLUSIONS/INTERPRETATION: Our results suggest that non-burning (low-dose) UVR suppresses the BAT 'whitening', steatotic and pro-diabetic effects of consuming a high-fat diet through skin release of nitric oxide, with some metabolic and immune pathways in iBAT regulated by UVR independently of nitric oxide.</p