Natural Image Reconstruction from fMRI Based on Node-Edge Interaction and Multi-Scale Constraint.

Reconstructing natural stimulus images using functional magnetic resonance imaging (fMRI) is one of the most challenging problems in brain decoding and is also the crucial component of a brain-computer interface. Previous methods cannot fully exploit the information about interactions among brain regions. In this paper, we propose a natural image reconstruction method based on node-edge interaction and a multi-scale constraint.

Explaining Orientation Adaptation in V1 by Updating the State of a Spatial Model.

In this work, we extend an influential statistical model based on the spatial classical receptive field (CRF) and non-classical receptive field (nCRF) interactions (Coen-Cagli et al., 2012) to explain the typical orientation adaptation effects observed in V1. If we assume that the temporal adaptation modifies the "state" of the model, the spatial statistical model can explain all of the orientation adaptation effects in the context of neuronal output using small and large grating observed in neurophysiological experiments in V1.

Key regulators of sensitivity to immunomodulatory drugs in cancer treatment.

Immunomodulatory drugs (IMiDs) include thalidomide, lenalidomide, and pomalidomide, which have shown significant efficacy in the treatment of multiple myeloma (MM), myelodysplastic syndrome (MDS) with deletion of chromosome 5q (del(5q)) and other hematological malignancies. IMiDs hijack the CRL4 ubiquitin ligase to target cellular proteins for ubiquitination and degradation, which is responsible for their clinical activity in MM and MDS with del(5q). However, intrinsic and acquired resistance frequently limit the efficacy of IMiDs.

ERK signaling mediates resistance to immunomodulatory drugs in the bone marrow microenvironment.

Immunomodulatory drugs (IMiDs) have markedly improved patient outcome in multiple myeloma (MM); however, resistance to IMiDs commonly underlies relapse of disease. Here, we identify that tumor necrosis factor (TNF) receptor-associated factor 2 () knockdown (KD)/knockout (KO) in MM cells mediates IMiD resistance via activation of noncanonical nuclear factor κB (NF-κB) and extracellular signal-regulated kinase (ERK) signaling. Within MM bone marrow (BM) stromal cell supernatants, TNF-α induces proteasomal degradation of TRAF2, noncanonical NF-κB, and downstream ERK signaling in MM cells, whereas interleukin-6 directly triggers ERK activation.

Recent advances in the molecular mechanism of thalidomide teratogenicity.

Thalidomide was first marketed in 1957 but soon withdrawn because of its notorious teratogenicity. Studies on the mechanism of action of thalidomide revealed the pleiotropic properties of this class of drugs, including their anti-inflammatory, antiangiogenic and immunomodulatory activities. Based on their notable activities, thalidomide and its analogues, lenalidomide and pomalidomide, have been repurposed to treat erythema nodosum leprosum, multiple myeloma and other haematological malignancies.

The effect of jet lag on the human brain: A neuroimaging study.

Jet lag is commonly experienced when travelers cross multiple time zones, leaving the wake-sleep cycle and intrinsic biological "clocks" out of synchrony with the current environment. The effect of jet lag on intrinsic cortical function remains unclear. Twenty-two healthy individuals experiencing west-to-east jet lag flight were recruited.

Novel immunomodulatory drugs and neo-substrates.

Thalidomide, lenalidomide and pomalidomide are immunomodulatory drugs (IMiDs) effective in the treatment of multiple myeloma, myelodysplastic syndrome (MDS) with deletion of chromosome 5q and other hematological malignancies. Recent studies showed that IMiDs bind to CRBN, a substrate receptor of CRL4 E3 ligase, to induce the ubiquitination and degradation of IKZF1 and IKZF3 in multiple myeloma cells, contributing to their anti-myeloma activity. Similarly, lenalidomide exerts therapeutic efficacy via inducing ubiquitination and degradation of CK1α in MDS with deletion of chromosome 5q.

Improving color constancy by selecting suitable set of training images.

With very simple implementation, regression-based color constancy (CC) methods have recently obtained very competitive performance by applying a correction matrix to the results of some low level-based CC algorithms. However, most regression-based methods, e.g.

Underwater Image Enhancement Using Adaptive Retinal Mechanisms.

We propose an underwater image enhancement model inspired by the morphology and function of the teleost fish retina. We aim to solve the problems of underwater image degradation raised by the blurring and nonuniform color biasing. In particular, the feedback from color-sensitive horizontal cells to cones and a red channel compensation are used to correct the nonuniform color bias.

Combining Bottom-Up and Top-Down Visual Mechanisms for Color Constancy Under Varying Illumination.

Multi-illuminant-based color constancy (MCC) is quite a challenging task. In this paper, we proposed a novel model motivated by the bottom-up and top-down mechanisms of human visual system (HVS) to estimate the spatially varying illumination in a scene. The motivation for bottom-up based estimation is from our finding that the bright and dark parts in a scene play different roles in encoding illuminants.

Restriction of hepatitis B virus replication by c-Abl-induced proteasomal degradation of the viral polymerase.

About 257 million people with chronic infection of hepatitis B virus (HBV) worldwide are at high risk of developing terminal liver diseases. Reactivation of virus replication has been frequently reported in those patient populations receiving imatinib (an Abl kinase inhibitor) or bortezomib (a proteasome inhibitor) to treat concurrent diseases, but the underlying mechanism for this reactivation is unknown. We report that the HBV polymerase protein is recruited by Cdt2 to the cullin-RING ligase 4 (CRL4) for ubiquitination and proteasome degradation and that this process is stimulated by the c-Abl nonreceptor tyrosine kinase.

CRL4 antagonizes SCFFbxo7-mediated turnover of cereblon and BK channel to regulate learning and memory.

Intellectual disability (ID), one of the most common human developmental disorders, can be caused by genetic mutations in Cullin 4B (Cul4B) and cereblon (CRBN). CRBN is a substrate receptor for the Cul4A/B-DDB1 ubiquitin ligase (CRL4) and can target voltage- and calcium-activated BK channel for ER retention. Here we report that ID-associated CRL4CRBN mutations abolish the interaction of the BK channel with CRL4, and redirect the BK channel to the SCFFbxo7 ubiquitin ligase for proteasomal degradation.

Improving color constancy by discounting the variation of camera spectral sensitivity.

It is an ill-posed problem to recover the true scene colors from a color biased image by discounting the effects of scene illuminant and camera spectral sensitivity (CSS) at the same time. Most color constancy (CC) models have been designed to first estimate the illuminant color, which is then removed from the color biased image to obtain an image taken under white light, without the explicit consideration of CSS effect on CC. This paper first studies the CSS effect on illuminant estimation arising in the inter-dataset-based CC (inter-CC), i.

A portable image-based cytometer for rapid malaria detection and quantification.

Increasing resistance by malaria parasites to currently used antimalarials across the developing world warrants timely detection and classification so that appropriate drug combinations can be administered before clinical complications arise. However, this is often challenged by low levels of infection (referred to as parasitemia) and presence of predominantly young parasitic forms in the patients' peripheral blood. Herein, we developed a simple, inexpensive and portable image-based cytometer that detects and numerically counts Plasmodium falciparum infected red blood cells (iRBCs) from Giemsa-stained smears derived from infected blood.

Activation of c-Abl Kinase Potentiates the Anti-myeloma Drug Lenalidomide by Promoting DDA1 Protein Recruitment to the CRL4 Ubiquitin Ligase.

Cullin-RING ligase 4 (CRL4), a complex of Cul4 and DDB1, regulates the cell cycle, DNA damage repair, and chromatin replication by targeting a variety of substrates for ubiquitination. CRL4 is also hijacked by viral proteins or thalidomide-derived compounds to degrade host restriction factors. Here we report that the c-Abl non-receptor kinase phosphorylates DDB1 at residue Tyr-316 to recruit a small regulatory protein, DDA1, leading to increased substrate ubiquitination.

A Retinal Mechanism Inspired Color Constancy Model.

In this paper, we propose a novel model for the computational color constancy, inspired by the amazing ability of the human vision system (HVS) to perceive the color of objects largely constant as the light source color changes. The proposed model imitates the color processing mechanisms in the specific level of the retina, the first stage of the HVS, from the adaptation emerging in the layers of cone photoreceptors and horizontal cells (HCs) to the color-opponent mechanism and disinhibition effect of the non-classical receptive field in the layer of retinal ganglion cells (RGCs). In particular, HC modulation provides a global color correction with cone-specific lateral gain control, and the following RGCs refine the processing with iterative adaptation until all the three opponent channels reach their stable states (i.

A Retina Inspired Model for Enhancing Visibility of Hazy Images.

The mammalian retina seems far smarter than scientists have believed so far. Inspired by the visual processing mechanisms in the retina, from the layer of photoreceptors to the layer of retinal ganglion cells (RGCs), we propose a computational model for haze removal from a single input image, which is an important issue in the field of image enhancement. In particular, the bipolar cells serve to roughly remove the low-frequency of haze, and the amacrine cells modulate the output of cone bipolar cells to compensate the loss of details by increasing the image contrast.

Boundary detection using double-opponency and spatial sparseness constraint.

Brightness and color are two basic visual features integrated by the human visual system (HVS) to gain a better understanding of color natural scenes. Aiming to combine these two cues to maximize the reliability of boundary detection in natural scenes, we propose a new framework based on the color-opponent mechanisms of a certain type of color-sensitive double-opponent (DO) cells in the primary visual cortex (V1) of HVS. This type of DO cells has oriented receptive field with both chromatically and spatially opponent structure.