High-Resolution Deep Image Matting

Image matting is a key technique for image and video editing and composition. Conventionally, deep learning approaches take the whole input image and an associated trimap to infer the alpha matte using convolutional neural networks. Such approaches set state-of-the-arts in image matting; however, they may fail in real-world matting applications due to hardware limitations, since real-world input images for matting are mostly of very high resolution. In this paper, we propose HDMatt, a first deep learning based image matting approach for high-resolution inputs. More concretely, HDMatt runs matting in a patch-based crop-and-stitch manner for high-resolution inputs with a novel module design to address the contextual dependency and consistency issues between different patches. Compared with vanilla patch-based inference which computes each patch independently, we explicitly model the cross-patch contextual dependency with a newly-proposed Cross-Patch Contextual module (CPC) guided by the given trimap. Extensive experiments demonstrate the effectiveness of the proposed method and its necessity for high-resolution inputs. Our HDMatt approach also sets new state-of-the-art performance on Adobe Image Matting and AlphaMatting benchmarks and produce impressive visual results on more real-world high-resolution images.Comment: AAAI 202

Investigation of the Effect of Dimple Bionic Nonsmooth Surface on Tire Antihydroplaning

Inspired by the idea that bionic nonsmooth surfaces (BNSS) reduce fluid adhesion and resistance, the effect of dimple bionic nonsmooth structure arranged in tire circumferential grooves surface on antihydroplaning performance was investigated by using Computational Fluid Dynamics (CFD). The physical model of the object (model of dimple bionic nonsmooth surface distribution, hydroplaning model) and SST k-ω turbulence model are established for numerical analysis of tire hydroplaning. By virtue of the orthogonal table L16(45), the parameters of dimple bionic nonsmooth structure design compared to the smooth structure were analyzed, and the priority level of the experimental factors as well as the best combination within the scope of the experiment was obtained. The simulation results show that dimple bionic nonsmooth structure can reduce water flow resistance by disturbing the eddy movement in boundary layers. Then, optimal type of dimple bionic nonsmooth structure is arranged on the bottom of tire circumferential grooves for hydroplaning performance analysis. The results show that the dimple bionic nonsmooth structure effectively decreases the tread hydrodynamic pressure when driving on water film and increases the tire hydroplaning velocity, thus improving tire antihydroplaning performance

HMGB1 cytoplasmic translocation in patients with acute liver failure

<p>Abstract</p> <p>Background</p> <p>High-mobility group box 1 (HMGB1) is a late mediator of lethal systemic inflammation. Acute liver failure (ALF) has been shown to trigger systemic inflammation in clinical and animal studies. To evaluate the possibility of HMGB1 cytoplasmic translocation in ALF, we determined whether HMGB1 is released in hepatocytes and end organ in patients with liver failure/injury.</p> <p>Methods</p> <p>HepG2 cell were stimulated with LPS or TNF-α, the increase of HMGB1 extracellularly in the culture medium and intracellularly in various cellular fractions were determined by western blot or immunocytochemistry. To observe sub-cellular location of HMGB1 in hepatocytes, liver specimens were obtained from 6 patients with ALF caused by HBV infection, 10 patients with chronic viral hepatitis B, 6 healthy controls, as well as animals model of ALF by intraperitoneal administration of D-GalN (600 mg/kg) and LPS (0.5 mg/kg).</p> <p>Results</p> <p>In HepG2 cell culture, LPS or TNF actively induced HMGB1 cytoplasmic translocation and release in a time- and dose-dependent fashion. In animal model of ALF, cytoplasmic HMGB1 translocation was observed in hepatocyts as early as 3 hours post onset of ALF. In patients with ALF caused by HBV infection, cytoplasmic HMGB1 translocation was similarly observed in some hepatocytes of the liver specimen.</p> <p>Conclusions</p> <p>Cytoplasmic HMGB1 translocation may occur during ALF, which may potentially contribute to the pathogenesis of liver inflammatory diseases.</p

Modulation of Excited State Property Based on Benzo[a, c]phenazine Acceptor: Three Typical Excited States and Electroluminescence Performance

Throwing light upon the structure-property relationship of the excited state properties for next-generation fluorescent materials is crucial for the organic light emitting diode (OLED) field. Herein, we designed and synthesized three donor-acceptor (D-A) structure compounds based on a strong spin orbit coupling (SOC) acceptor benzo[a, c]phenazine (DPPZ) to research on the three typical types of excited states, namely, the locally-excited (LE) dominated excited state (CZP-DPPZ), the hybridized local and charge-transfer (HLCT) state (TPA-DPPZ), and the charge-transfer (CT) dominated state with TADF characteristics (PXZ-DPPZ). A theoretical combined experimental research was adopted for the excited state properties and their regulation methods of the three compounds. Benefiting from the HLCT character, TPA-DPPZ achieves the best non-doped device performance with maximum brightness of 61,951 cd m−2 and maximum external quantum efficiency of 3.42%, with both high photoluminescence quantum efficiency of 40.2% and high exciton utilization of 42.8%. Additionally, for the doped OLED, PXZ-DPPZ can achieve a max EQE of 9.35%, due to a suppressed triplet quenching and an enhanced SOC

Therapeutic potential of HMGB1-targeting agents in sepsis

Sepsis refers to a systemic inflammatory response syndrome resulting from a microbial infection. The inflammatory response is partly mediated by innate immune cells (such as macrophages, monocytes and neutrophils), which not only ingest and eliminate invading pathogens but also initiate an inflammatory response upon recognition of pathogen-associated molecular patterns (PAMPs). The prevailing theories of sepsis as a dysregulated inflammatory response, as manifested by excessive release of inflammatory mediators such as tumour necrosis factor and high-mobility group box 1 protein (HMGB1), are supported by extensive studies employing animal models of sepsis. Here we review emerging evidence that support extracellular HMGB1 as a late mediator of experimental sepsis, and discuss the therapeutic potential of several HMGB1-targeting agents (including neutralising antibodies and steroid-like tanshinones) in experimental sepsis

Novel Mechanisms of Herbal Therapies for Inhibiting HMGB1 Secretion or Action

High mobility group box 1 (HMGB1) is an evolutionarily conserved protein and is constitutively expressed in virtually all types of cells. In response to microbial infections, HMGB1 is secreted from activated immune cells to orchestrate rigorous inflammatory responses. Here we review the distinct mechanisms by which several herbal components inhibit HMGB1 action or secretion, such as by modulating inflammasome activation, autophagic degradation, or endocytic uptake. In light of the reciprocal interactions between these cellular processes, it is possible to develop more effective combinational herbal therapies for the clinical management of inflammatory diseases

RIS-based IMT-2030 Testbed for MmWave Multi-stream Ultra-massive MIMO Communications

As one enabling technique of the future sixth generation (6G) network, ultra-massive multiple-input-multiple-output (MIMO) can support high-speed data transmissions and cell coverage extension. However, it is hard to realize the ultra-massive MIMO via traditional phased arrays due to unacceptable power consumption. To address this issue, reconfigurable intelligent surface-based (RIS-based) antennas are an energy-efficient enabler of the ultra-massive MIMO, since they are free of energy-hungry phase shifters. In this article, we report the performances of the RIS-enabled ultra-massive MIMO via a project called Verification of MmWave Multi-stream Transmissions Enabled by RIS-based Ultra-massive MIMO for 6G (V4M), which was proposed to promote the evolution towards IMT-2030. In the V4M project, we manufacture RIS-based antennas with 1024 one-bit elements working at 26 GHz, based on which an mmWave dual-stream ultra-massive MIMO prototype is implemented for the first time. To approach practical settings, the Tx and Rx of the prototype are implemented by one commercial new radio base station and one off-the-shelf user equipment, respectively. The measured data rate of the dual-stream prototype approaches the theoretical peak rate. Our contributions to the V4M project are also discussed by presenting technological challenges and corresponding solutions.Comment: 8 pages, 5 figures, to be published in IEEE Wireless Communication

Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis

Colonic tissues in Inflammatory Bowel Disease (IBD) patients exhibit oxygen deprivation and activation of hypoxia-inducible factor 1α and 2α (HIF-1α and HIF-2α), which mediate cellular adaptation to hypoxic stress. Notably, macrophages and neutrophils accumulate preferentially in hypoxic regions of the inflamed colon, suggesting that myeloid cell functions in colitis are HIF-dependent. By depleting ARNT (the obligate heterodimeric binding partner for both HIFα subunits) in a murine model, we demonstrate here that myeloid HIF signaling promotes the resolution of acute colitis. Specifically, myeloid pan-HIF deficiency exacerbates infiltration of pro-inflammatory neutrophils and Ly6C+ monocytic cells into diseased tissue. Myeloid HIF ablation also hinders macrophage functional conversion to a protective, pro-resolving phenotype, and elevates gut serum amyloid A levels during the resolution phase of colitis. Therefore, myeloid cell HIF signaling is required for efficient resolution of inflammatory damage in colitis, implicating serum amyloid A in this process

A Hepatic Protein, Fetuin-A, Occupies a Protective Role in Lethal Systemic Inflammation

A liver-derived protein, fetuin-A, was first purified from calf fetal serum in 1944, but its potential role in lethal systemic inflammation was previously unknown. This study aims to delineate the molecular mechanisms underlying the regulation of hepatic fetuin-A expression during lethal systemic inflammation (LSI), and investigated whether alterations of fetuin-A levels affect animal survival, and influence systemic accumulation of a late mediator, HMGB1.LSI was induced by endotoxemia or cecal ligation and puncture (CLP) in fetuin-A knock-out or wild-type mice, and animal survival rates were compared. Murine peritoneal macrophages were challenged with exogenous (endotoxin) or endogenous (IFN-γ) stimuli in the absence or presence of fetuin-A, and HMGB1 expression and release was assessed. Circulating fetuin-A levels were decreased in a time-dependent manner, starting between 26 h, reaching a nadir around 24-48 h, and returning towards base-line approximately 72 h post onset of endotoxemia or sepsis. These dynamic changes were mirrored by an early cytokine IFN-γ-mediated inhibition (up to 50-70%) of hepatic fetuin-A expression. Disruption of fetuin-A expression rendered animals more susceptible to LSI, whereas supplementation of fetuin-A (20-100 mg/kg) dose-dependently increased animal survival rates. The protection was associated with a significant reduction in systemic HMGB1 accumulation in vivo, and parallel inhibition of IFN-γ- or LPS-induced HMGB1 release in vitro.These experimental data suggest that fetuin-A is protective against lethal systemic inflammation partly by inhibiting active HMGB1 release