Real-Time 6D Object Pose Estimation on CPU

We propose a fast and accurate 6D object pose estimation from a RGB-D image. Our proposed method is template matching based and consists of three main technical components, PCOF-MOD (multimodal PCOF), balanced pose tree (BPT) and optimum memory rearrangement for a coarse-to-fine search. Our model templates on densely sampled viewpoints and PCOF-MOD which explicitly handles a certain range of 3D object pose improve the robustness against background clutters. BPT which is an efficient tree-based data structures for a large number of templates and template matching on rearranged feature maps where nearby features are linearly aligned accelerate the pose estimation. The experimental evaluation on tabletop and bin-picking dataset showed that our method achieved higher accuracy and faster speed in comparison with state-of-the-art techniques including recent CNN based approaches. Moreover, our model templates can be trained only from 3D CAD in a few minutes and the pose estimation run in near real-time (23 fps) on CPU. These features are suitable for any real applications.Comment: accepted to IROS 201

Serum amyloid alpha 1-2 are not required for liver inflammation in the 4T1 murine breast cancer model

がんに起因して起こる宿主の肝臓の急性期応答と炎症 --血清アミロイドαは乳がんモデルにおける肝臓の炎症の原因ではない--. 京都大学プレスリリース. 2023-02-06.Cancers induce the production of acute phase proteins such as serum amyloid alpha (SAA) in the liver and cause inflammation in various host organs. Despite the well-known coincidence of acute phase response and inflammation, the direct roles of SAA proteins in inflammation in the cancer context remains incompletely characterized, particularly in vivo. Here, we investigate the in vivo significance of SAA proteins in liver inflammation in the 4T1 murine breast cancer model. 4T1 cancers elevate the expression of SAA1 and SAA2, the two major murine acute phase proteins in the liver. The elevation of Saa1-2 correlates with the up-regulation of immune cell-related genes including neutrophil markers. To examine this correlation in detail, we generate mice that lack Saa1-2 and investigate immune-cell phenotypes. RNA-seq experiments reveal that deletion of Saa1-2 does not strongly affect 4T1-induced activation of immune cell-related genes in the liver. Flow cytometry experiments demonstrate the dispensable roles of SAA1-2 in cancer-dependent neutrophil infiltration to the liver. Consistently, 4T1-induced gene expression changes in bone marrow do not require Saa1-2. This study clarifies the negligible contribution of SAA1-2 proteins in liver inflammation in the 4T1 breast cancer model

Neonatal asphyxia as an inflammatory disease: Reactive oxygen species and cytokines

Neonatologists resuscitate asphyxiated neonates by every available means, including positive ventilation, oxygen therapy, and drugs. Asphyxiated neonates sometimes present symptoms that mimic those of inflammation, such as fever and edema. The main pathophysiology of the asphyxia is inflammation caused by hypoxic-ischemic reperfusion. At birth or in the perinatal period, neonates may suffer several, hypoxic insults, which can activate inflammatory cells and inflammatory mediator production leading to the release of larger quantities of reactive oxygen species (ROS). This in turn triggers the production of oxygen stress-induced high mobility group box-1 (HMGB-1), an endogenous damage-associated molecular patterns (DAMPs) protein bound to toll-like receptor (TLR) -4, which activates nuclear factor-kappa B (NF-κB), resulting in the production of excess inflammatory mediators. ROS and inflammatory mediators are produced not only in activated inflammatory cells but also in non-immune cells, such as endothelial cells. Hypothermia inhibits pro-inflammatory mediators. A combination therapy of hypothermia and medications, such as erythropoietin and melatonin, is attracting attention now. These medications have both anti-oxidant and anti-inflammatory effects. As the inflammatory response and oxidative stress play a critical role in the pathophysiology of neonatal asphyxia, these drugs may contribute to improving patient outcomes

Cellular Responses of Human Lymphatic Endothelial Cells to Carbon Nanomaterials

One of the greatest challenges to overcome in the pursuit of the medical application of carbon nanomaterials (CNMs) is safety. Particularly, when considering the use of CNMs in drug delivery systems (DDSs), evaluation of safety at the accumulation site is an essential step. In this study, we evaluated the toxicity of carbon nanohorns (CNHs), which are potential DDSs, using human lymph node endothelial cells that have been reported to accumulate CNMs, as a comparison to fibrous, multi-walled carbon nanotubes (MWCNTs) and particulate carbon black (CB). The effect of different surface characteristics was also evaluated using two types of CNHs (untreated and oxidized). In the fibrous MWCNT, cell growth suppression, as well as expression of inflammatory cytokine genes was observed, as in previous reports. In contrast, no significant toxicity was observed for particulate CB and CNHs, which was different from the report of CB cytotoxicity in vascular endothelial cells. These results show that (1) lymph endothelial cells need to be tested separately from other endothelial cells for safety evaluation of nanomaterials, and (2) the potential of CNHs as DDSs.ArticleNANOMATERIALS. 10(7):1374 (2020)journal articl

Multiple emission lines of Hα\alpha emitters at z∼2.3z \sim 2.3 from the broad and medium-band photometry in the ZFOURGE Survey

We present a multiple emission lines study of $\sim$1300 H$\alpha$ emitters (HAEs) at $z \sim 2.3$ in the ZFOURGE survey. In contrast to the traditional spectroscopic method, our sample is selected based on the flux excess in the ZFOURGE-$K_s$ broad-band data relative to the best-fit stellar continuum. Using the same method, we also extract the strong diagnostic emission lines for these individual HAEs: [OIII]$\lambda\lambda4959,5007$, [OII]$\lambda\lambda3726,3729$. Our measurements exhibit good consistency with those obtained from spectroscopic surveys. We investigate the relationship between the equivalent widths (EWs) of these emission lines and various galaxy properties, including stellar mass, stellar age, star formation rate (SFR), specific SFR (sSFR), ionization states (O32). We have identified a discrepancy between between HAEs at $z\sim2.3$ and typical local star-forming galaxy observed in the SDSS, suggesting the evolution of lower gas-phase metallicity ($Z$) and higher ionization parameters ($U$) with redshift. Notably, we have observed a significant number of low-mass HAEs exhibiting exceptionally high $EW_{\mathrm{[OIII]}}$. Their galaxy properties are comparable to those of extreme objects, such as extreme O3 emitters (O3Es) and Ly$\alpha$ emitters (LAEs) at $z\simeq2-3$. Considering that these characteristics may indicate potential strong Lyman continuum (LyC) leakage, higher redshift anaglogs of the low-mass HAEs could be significant contributors to the cosmic reionization. Further investigations on this particular population are required to gain a clearer understanding of galaxy evolution and cosmic reionization.Comment: 24 pages, 13 figures, submitted to Ap

Murine breast cancers disorganize the liver transcriptome in a zonated manner

がんが宿主の臓器に及ぼす悪影響を捉えた --がんをもつ個体における「肝機能の空間的制御」の破綻--. 京都大学プレスリリース. 2023-02-01.The spatially organized gene expression program within the liver specifies hepatocyte functions according to their relative distances to the bloodstream (i.e., zonation), contributing to liver homeostasis. Despite the knowledge that solid cancers remotely disrupt liver homeostasis, it remains unexplored whether solid cancers affect liver zonation. Here, using spatial transcriptomics, we thoroughly investigate the abundance and zonation of hepatic genes in cancer-bearing mice. We find that breast cancers affect liver zonation in various distinct manners depending on biological pathways. Aspartate metabolism and triglyceride catabolic processes retain relatively intact zonation patterns, but the zonation of xenobiotic catabolic process genes exhibits a strong disruption. The acute phase response is induced in zonated manners. Furthermore, we demonstrate that breast cancers activate innate immune cells in particular neutrophils in distinct zonated manners, rather than in a uniform fashion within the liver. Collectively, breast cancers disorganize hepatic transcriptomes in zonated manners, thereby disrupting zonated functions of the liver

Excessive daytime napping independently associated with decreased insulin sensitivity in cross-sectional study – Hyogo Sleep Cardio-Autonomic Atherosclerosis cohort study

BackgroundAlthough excessive daytime napping has been shown to be involved in diabetes occurrence, its impact on insulin secretion and sensitivity has not been elucidated. It is speculated that excessive napping disrupts the sleep-wake rhythm and increases sympathetic nerve activity during the day, resulting in decreased insulin sensitivity, which may be a mechanism leading to development of diabetes. We previously conducted a cross-sectional study that showed an association of autonomic dysfunction with decreased insulin sensitivity, though involvement of autonomic function in the association between napping and insulin sensitivity remained unclear. Furthermore, the effects of napping used to supplement to short nighttime sleep on insulin secretion and sensitivity are also unknown. In the present cross-sectional study, we examined the relationships of daytime nap duration and autonomic function with insulin secretion and sensitivity in 436 subjects enrolled in the Hyogo Sleep Cardio-Autonomic Atherosclerosis (HSCAA) Cohort Study who underwent a 75-g oral glucose tolerance test (75-g OGTT), after excluding those already diagnosed with diabetes.MethodsDaytime nap duration was objectively measured using actigraphy, with the subjects divided into the short (≤1 hour) and long (>1 hour) nap groups. Insulin secretion and sensitivity were determined using 75-g OGTT findings. Standard deviation of normal to normal R-R interval (SDNN), a measure of autonomic function, was also determined based on heart rate variability. Subgroup analysis was performed for the associations of napping with insulin secretion and sensitivity, with the results stratified by nighttime sleep duration of less or greater than six hours.ResultsSubjects in the long nap group exhibited lower insulin sensitivity parameters (QUICKI: β=-0.135, p<0.01; Matsuda index: β=-0.119, p<0.05) independent of other clinical factors. In contrast, no associations with insulin secretion were found in either group. Furthermore, the association of long nap duration with insulin sensitivity was not confounded by SDNN. Specific subgroup analyses revealed more prominent associations of long nap habit with lower insulin sensitivity in subjects with a short nighttime sleep time (β=-0.137, p<0.05).ConclusionLong daytime nap duration may be a potential risk factor for decreased insulin sensitivity

Rescue from Stx2-Producing E. coli-Associated Encephalopathy by Intravenous Injection of Muse Cells in NOD-SCID Mice

Shiga toxin-producing Escherichia coli (STEC) causes hemorrhagic colitis, hemolytic uremic syndrome, and acute encephalopathies that may lead to sudden death or severe neurologic sequelae. Current treatments, including immunoglobulin G (IgG) immunoadsorption, plasma exchange, steroid pulse therapy, and the monoclonal antibody eculizumab, have limited effects against the severe neurologic sequelae. Multilineage-differentiating stress-enduring (Muse) cells are endogenous reparative non-tumorigenic stem cells that naturally reside in the body and are currently under clinical trials for regenerative medicine. When administered intravenously, Musecells accumulate to the damaged tissue, where they exert anti-inflammatory, anti-apoptotic, anti-fibrotic, and immunomodulatory effects, and replace damaged cells by differentiating into tissue-constituent cells. Here, severely immunocompromised non-obese diabetic/severe combined immunodeficiency (NOD-SCID) mice orally inoculated with 9 × 109 colony-forming units of STEC O111 and treated 48 h later with intravenous injection of 5 × 104 Muse cells exhibited 100% survival and no severe after-effects of infection. Suppression of granulocyte-colony-stimulating factor (G-CSF) by RNAi abolished the beneficial effects of Muse cells, leading to a 40% death and significant body weight loss, suggesting the involvement of G-CSF in the beneficial effects of Muse cells in STEC-infected mice. Thus, intravenous administration of Muse cells could be a candidate therapeutic approach for preventing fatal encephalopathy after STEC infection

Rescue from Stx2-Producing E. coli-Associated Encephalopathy by Intravenous Injection of Muse Cells in NOD-SCID Mice

Shiga toxin-producing Escherichia coli (STEC) causes hemorrhagic colitis, hemolytic uremic syndrome, and acute encephalopathies that may lead to sudden death or severe neurologic sequelae. Current treatments, including immunoglobulin G (IgG) immunoadsorption, plasma exchange, steroid pulse therapy, and the monoclonal antibody eculizumab, have limited effects against the severe neurologic sequelae. Multilineage-differentiating stress-enduring (Muse) cells are endogenous reparative non-tumorigenic stem cells that naturally reside in the body and are currently under clinical trials for regenerative medicine. When administered intravenously, Musecells accumulate to the damaged tissue, where they exert anti-inflammatory, anti-apoptotic, anti-fibrotic, and immunomodulatory effects, and replace damaged cells by differentiating into tissue-constituent cells. Here, severely immunocompromised non-obese diabetic/severe combined immunodeficiency (NOD-SCID) mice orally inoculated with 9 × 109 colony-forming units of STEC O111 and treated 48 h later with intravenous injection of 5 × 104 Muse cells exhibited 100% survival and no severe after-effects of infection. Suppression of granulocyte-colony-stimulating factor (G-CSF) by RNAi abolished the beneficial effects of Muse cells, leading to a 40% death and significant body weight loss, suggesting the involvement of G-CSF in the beneficial effects of Muse cells in STEC-infected mice. Thus, intravenous administration of Muse cells could be a candidate therapeutic approach for preventing fatal encephalopathy after STEC infection

Environmental impact on star-forming galaxies in a z∼0.9z \sim 0.9 cluster during course of galaxy accretion

Galaxies change their properties as they assemble into clusters. In order to understand the physics behind that, we need to go back in time and observe directly what is occurring in galaxies as they fall into a cluster. We have conducted a narrow-band and $J$-band imaging survey on a cluster CL1604-D at $z=0.923$ using a new infrared instrument SWIMS installed at the Subaru Telescope. The narrow-band filter, NB1261, matches to H$\alpha$ emission from the cluster at $z=0.923$. Combined with a wide range of existing data from various surveys, we have investigated galaxy properties in and around this cluster in great detail. We have identified 27 H$\alpha$ emitters associated with the cluster. They have significant overlap with MIPS 24$\mu$m sources and are located exclusively in the star forming regime on the rest-frame $UVJ$ diagram. We have identified two groups of galaxies near the cluster in the 2D spatial distribution and the phase-space diagram, which are likely to be in-falling to the cluster main body. We have compared various physical properties of star forming galaxies, such as specific star formation rates (burstiness) and morphologies (merger) as a function of environment; cluster center, older group, younger group, and the field. As a result, a global picture has emerged on how the galaxy properties are altered as they assemble into a denser region. This includes the occurrence of mergers, enhancement of star formation activity, excursion to the dusty starburst phase, and eventual quenching to a passive phase.Comment: 19 pages, 15 figures. Accepted for publication in ApJ. Error bars in Table 2 correcte